Y3 Cardio

Recognise the signs of peripheral vascular disease on physical examination

● Acute Limb Ischaemia - surgical emergency - 6 Ps o Pain o Pale o Pulseless o Paralysis o Paraesthesia o Perishingly Cold ● Other symptoms: o Atrophic skin o Hairless o Punched-out ulcers (often painful) o Colour change when raising leg (to Buerger's angle)

Define ventricular fibrillation

● An irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death. ● MEDICAL EMERGENCY

Identify the possible complications of heart block

● Asystole ● Cardiac arrest ● Heart failure ● Complications of any pacemaker inserted

Define tricuspid regurgitation

● Backflow of blood from the right ventricle to the right atrium during systole § Usually presents with fatigue, dyspnoea, and lower extremity oedema. Additional complaints may include abdominal distension and early satiety. § The clinically most important form is secondary to left-sided cardiac disease, with tricuspid annular dilation.

List drugs that can be used in chronic heart failure

**ABCD2** § ACEi - give to all pts with LV dysfunction (treats the HTN) § beta blocker - reduce O2 demand on heart § Cardiac resynchronization therapy - aims to improve timings of contraction of atria and ventricles § Diuretics - for fluid retention § Digoxin - positive inotrope, improves symptoms but not mortality § ALSO, Hydralazine + nitrates - considered in Afro-Caribbean patients

Hypertensive retinopathy grades

**SAFE acronym: § Silver wiring § Arteriovenous napping § Flamed shape haemorrhage and cotton wool exudates (due to small infarct) § papilloEdema

What is the first-line treatment option for STEMI? Describe how NSTEMI patients should be managed.

**STEMI: § Percutaneous coronary intervention (GOLD STANDARD) § Thrombolysis § NOTE: this should be done within 12 hours of onset of pain (ideally within 1 hour) **NSTEMI: § If haemodynamically unstable - immediate angioplasty § Other NSTEMI patients should be risk stratified - high risk patients should receive angioplasty

Symptoms of the different murmurs and systolic vs diastolic

*SYSTOLIC: § Exertional dyspnoea §Heart failure signs § Patients may be ASx a) AS: Exertional chest pain, syncope 40% - arrhythmia or postural hypotension b) MR: Decreased exercise tolerance, lower extremity oedema, c) TR: Palpitations, irregular heart rhythm *DIASTOLIC: § Dyspnoea § Fatigue § Orthopnoea § Palpitations § Patients mat be ASx a) AR: Dyspnoea (pulmonary oedema or progressive LV dysfunction), weakness b) MS: Dyspnoea (Increased LA pressure à pulmonary congestion)

•What is the main distinguishing difference between Unstable Angina and NSTEMI?

*remember STEMI can also be something with new LBBB

In what conditions does troponin increase

-NSTEMI/STEMI, PE, heart failure, myocarditis, renal failure, sepsis, tachyarrhythmia

Localised amyloidosis and brain function

1) Alzheimer's 2) Amyloid angiopathy --> weakens walls of BV in brain --> risk of haemorrhage **overall inflammation --> decreased brain functions (e.g. memory)

Systemic amyloidosis and nerves

1) Peripheral nerves - sensory and motor 2) Autonomic nerves - digestion and BP

3 mechanisms for SOB

1. Not enough oxygen reaching the lungs: Breathing issues E.g. asthma, COPD, anaphylaxis 2. Not enough oxygen getting into the blood: V/Q mismatch E.g. pulmonary embolism, pulmonary oedema, pulmonary fibrosis. 3. 3. Not enough oxygen reaching the rest of the body: Heart issues (or anaemia, shock etc.)

Which statin is recommended by NICE for primary and secondary prevention of Cardiovascular Disease

Atorvastatin is the statin which is recommended by NICE for primary and secondary prevention of Cardiovascular Disease, but this is not related to falls risk.

The presence of 'F' waves is diagnostic of?

Atrial fibrillation

Venous ulcers can scar leading to white patches of scarred skin. What is this feature called?

Atrophie blanche

Define Angina pectoris

Chest pain or discomfort due to myocardial ischaemia which is brought on by exertion and relieved by rest.

What is amiodarone?

Class III antiarrhythmic - potassium channel blocker. Used to treat atrial, nodal and ventricular tachycardias

Recognise the presenting symptoms of pulmonary embolism

Depends on the SITE and SIZE of the embolus: ● Small - may be ASYMPTOMATIC ● Moderate o Sudden-onset SOB o Cough o Haemoptysis o Pleuritic chest pain ● Large (or proximal) o As above and: ▪ Severe central pleuritic chest pain ▪ Shock ▪ Collapse ▪ Acute right heart failure ▪ Sudden death ● Multiple Small Recurrent o Symptoms of pulmonary hypertension

Management of acute heart failure

ECG changes summary: § asystole = flat line § AF = narrow complex, irregular, no P wave § ventricular tachycardia = borad tachycardia § VF = no QRS complexes

46 year old man gets chest pain when walking up hill and stops when he stops. What is first step you do?

ECG. First ECG is normal. Then do exercise and take his ECG again. In this next ECG, tachycardia and has ST depression in V4, V5, V6 - this means chronic stable angina (because of a partly blocked coronary artery)

A 67-year-old lady with a history of hypertension complains of feeling generally weak. As part of the work-up an ECG is ordered. What explains the changes in ECG?

Hypokalaemia, This patient has U waves which are pathognomonic of hypokalaemia. There is also a borderline PR interval. It is possible that this lady is on a thiazide-like diuretic for hypertension which can cause hypokalaemia. § ECG features of hypokalaemia o U waves o small or absent T waves (occasionally inversion) o prolong PR interval o ST depression o long QT **One registered user suggests the following rhyme In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

What treatment may be considered in patients with severe ventricular dysfunction and conduction block?

Implantable cardioverter defibrillator (ICD)

Congestive heart failure

LHF + RHF. whole heart congested

Management of pericarditis

NSAIDs, aspirin, colchicine

5 P's of pleuritic chest pain

PE, pneumothorax, pneumonia, pericarditis, pleurisy. Also rib fractures and costrochondritis

Which tow statements are true when prescribing low molecular weight heparin for DVT treatment? The dose depends on the age of the patient, The dose depends on the weight of the patient in kilograms, The dose depends on the renal function of the patient, The dose of heparin does not vary between patients

The dose depends on the weight of the patient in kilograms, The dose depends on the renal function of the patient. § The dose of low molecular weight heparin depends on the patient's weight in kilograms. Low molecular weight heparin should be used with caution in severe renal failure due to increased risk of bleeding.

Figure 3a shows an image in the axial plane of a transthoracic echocardiogram through the heart. It has labels A to G. Match the letter labels with the correct anatomical structure.

There is a large defect present in the ventricular septum. This is well visualised using colour doppler assessment with flow turbulence and communication between right and left ventricle (Figure 3c).

Which heart valve is most commonly affected in intravenous drug users?

Tricuspid. The tricuspid valve is most exposed through repeated injection of foreign material (and infection entering) into the venous circulation.

Causes of pericarditis

Viruses: Most common Post MI Renal failure Endocarditis

What can compartment syndrome of the anterior compartment of the forearm lead to?

Volkmann's contracture - permanent flexion of the wrist due to ischaemia and necrosis of the anterior forearm compartment muscles

What is Buerger's test? Describe how it is performed and what a positive result indicates.

Whilst the patient is supine, raise the leg up until it goes paleNOTE: in normal people, the leg should remain pink even at 90 degreesThe angle at which it goes pale is 'Buerger's angle'Then the leg is put back downWith positive Buerger's sign - the leg will slowly turn pink but then it will go red (this is due to reactive hyperaemia)

Mr Williams' (19 y/0) examination is unremarkable. What first-line investigations would you request for blackout and why?

You should perform the following investigations on anyone with loss of consciousness: 1) Oxygen saturations: may reveal hypoxia, e.g. secondary to a pulmonary embolism (PE). 2) Bloods: a) Capillary blood glucose: you should exclude hypoglycaemia. You will also be looking for undiagnosed diabetes which can lead to polyuria and dehydration, and which in established diabetics is associated with autonomic dysfunction that can lead to hypotension and blackouts. Although diabetes mellitus is also a risk factor for cerebrovascular disease, strokes and TIAs rarely cause blackouts. b) Full blood count (FBC): to look for an anaemia that may be a contributing factor. c) Urea and electrolytes (U&Es): exclude an electrolyte abnormality. 3) Electrocardiogram (ECG): the European Society of Cardiology 2004 Guidelines state that this is only warranted when there is a high pre-test probability of an arrhythmia being a cause (e.g. a young patient with sudden blackout with no warning and for no obvious reason), in which case you might look for evidence of arrhythmia or conduction defect including bundle branch block, a short PR or long QT interval. An ECG can be helpful if it shows an abnormality, but if it is normal it does not exclude a cardiac cause as arrhythmias can be intermittent, particularly if the patient is asymptomatic at the time of the recording. 24-hour ambulatory ECG (HOLTER) monitoring is rarely helpful as few patients have arrhythmias every day and a positive result is just as likely in elderly patients who have experienced a blackout as in those who haven't. As a consequence, the guidelines suggest such recordings are useful only in patients whose symptoms occur daily. ***There are a number of investigations you wouldn't carry out initially on everyone with an episode of loss of consciousness, but only if your history and examination suggest certain diagnoses: a) A cardiac abnormality such as a valve lesion, consider an echocardiogram. b) Carotid sinus sensitivity, consider a carotid sinus massage (see the viva question on this topic). c) Epilepsy, consider an electroencephalogram (EEG) and brain scan (computed tomography (CT) or magnetic resonance imaging (MRI)) .

Williams Syndrome

a genetic condition characterized by mental retardation in most regards but surprisingly good use of language relative to their other abilities

aortic insufficiency

aka aortic regurgitation. inability of the aortic valve to perform at the proper levels, which results in blood flowing back into the left ventricle from the aorta

An 83-year-old woman is admitted with a left intertrochanteric neck of femur fracture. On examination the patient is found to have an ejection systolic murmur loudest in the aortic region. There is no radiation of the murmur to the carotid arteries. Her ECG is normal.

aortic SCLEROSIS. The most likely diagnosis is aortic sclerosis. The main differential diagnosis is of aortic stenosis, however as there is no radiation of the murmur to the carotids and the ECG is normal, this is less likely.

Different causes of syncope

arrhythmia, cardiac, orthostatic, reflex

CHADVASC score in AF

assess for risk of stroke · CHA2DS2-VASc Score - Stroke Risk Stratification o One point for each risk factor · Heart failure · Diabetes · Hypertension · Vascular disease · Aged >65 · Female o Two points for · Prior TIA/stroke/thromboembolism · Age greater than/equal to 75 · o Males: Score of 1 or more - consider oral anticoagulation o Females: score of 2 or more - consider oral anticoagulation

intermittent claudication

cramping pain in the leg muscles that occurs during exercise and is relieved by rest

A 55-year-old woman presents to the emergency department with a sudden onset of central chest pain while she was at rest. The pain was not relieved by her glyceryl trinitrate spray. She has a past history of angina and hypertension. ECG and cardiac biomarkers were positive for an ST-elevation myocardial infarction (STEMI).A few minutes later, she complained of worsening shortness of breath. On examination, her pulse was weak and thready. Her jugular venous pressure is increased. On chest auscultation, there was a new systolic murmur. Her pulse rate was 130 beats per minute and blood pressure was 80/55 mmHg. There were no new acute changes to the ECG.Which of the following is the most likely diagnosis? § Arrhythmia § Aortic regurgitation § Aortic stenosis § Mitral regurgitation § Left ventricular aneurysm

d) Mitral regurgitation The most likely diagnosis is a post-myocardial infarction (MI) acute mitral regurgitation. Due to the rupture of the papillary muscles secondary to an MI, there is abnormal leaking or backflow of blood back into the left atrium, ultimately leading to heart failure and cardiogenic shock in this patient. Arrhythmia and left ventricular aneurysm are also complications of an MI but would not normally present with a systolic murmur. Furthermore, ECG did not show any new acute changes. Aortic regurgitation and aortic stenosis are uncommon in a post-MI situation. **Complications of MI: 1) Cardiac arrest: This most commonly occurs due to patients developing ventricular fibrillation and is the most common cause of death following a MI. Patients are managed as per the ALS protocol with defibrillation. 2) Cardiogenic shock: If a large part of the ventricular myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the patient develops cardiogenic shock. This is difficult to treat. Other causes of cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture as listed below. Patients may require inotropic support and/or an intra-aortic balloon pump. 3) Chronic heart failure: As described above, if the patient survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure. Loop diuretics such as furosemide will decrease fluid overload. Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure. 4) Tachyarrhythmias: Ventricular fibrillation, as mentioned above, is the most common cause of death following a MI. Other common arrhythmias including ventricular tachycardia. 5) Bradyarrhythmias: Atrioventricular block is more common following inferior myocardial infarctions. 6) PericarditisPericarditis in the first 48 hours following a transmural MI is common (c. 10% of patients). The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram.Dressler's syndrome tends to occur around 2-6 weeks following a MI. The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers. It is characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR. It is treated with NSAIDs. 7) Left ventricular aneurysm: The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated 8) Left ventricular free wall rupture: This is seen in around 3% of MIs and occurs around 1-2 weeks afterwards. Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). Urgent pericardiocentesis and thoracotomy are required. 9) Ventricular septal defect: Rupture of the interventricular septum usually occurs in the first week and is seen in around 1-2% of patients. Features: acute heart failure associated with a pan-systolic murmur. An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion. Urgent surgical correction is needed. 10) Acute mitral regurgitation: More common with infero-posterior infarction and may be due to ischaemia or rupture of the papillary muscle. Acute hypotension and pulmonary oedema may occur. An early-to-mid systolic murmur is typically heard. Patients are treated with vasodilator therapy but often require emergency surgical repair.

You review the ECG of Dorothy, who has been experiencing 30 minutes of severe crushing chest pain and see ST elevation in leads II, III, aVF. Which coronary artery has been affected? a.Left anterior descending artery b.Left circumflex artery c.Left main stem occlusion d.Right coronary artery

d.Right coronary artery

Acute limb ischaemia two main causes

embolic and plaque thrombosis

The closure of which valve causes the first part and which causes second part of the second heart sound

first part - aortic second part - pulmonary

AL amyloidosis

is Associated with Multiple Myeloma.

What is IHD?

is a term describing the chronic process of atherosclerosis in the coronary arteries. ACS is an umbrella term for three acute conditions: unstable angina, NSTEMI and STEMI

What diagnosis from this ECG?

left bundle branch block. § wide QRS

What are the five things that occur in rheumatic fever

myocarditis --> heart murmur, arthritis, brain (chorea), erythema marginatum, subcutaneous nodules.

When can ACS be silent?

old / diabetics

Myocarditis pain

pain worse lying down

Cause of mitral stenosis

rheumatic heart disease, young patient

If inferior STEMI, which artery occluded?

right coronary artery

sign of severe AS

soft S2

At what vertebral level does the aorta bifurcate?

§ The aorta bifurcates at the level of L4 which correlates to the level of the UMBILICUS. Don't forget, therefore, that a AAA is palpated above the umbilicus and if an expansile mass is felt below, it is most likely an iliac aneurysm. Get in the routine of ALWAYS palpating for a AAA in an abdominal examination.

Scoring system for DVTs

§ The pre-test probability of a patient having a DVT can be estimated using the Wells' scoring system for DVT

Management of AF

§ for DOAC no need to monitor INR

SVT tachycardia ECG

§ no P waves § tachycardic

list 3 causes of aortic stenosis

§ reverse splitting S2 - aortic valve closing after the pulmonary valve § Pulse - slow-rising § BP - narrow pulse pressure § Palpation - apex not displaced, heaving (LVH) § Auscultation: red/absent S2 - signs of severity Reverse splitting S2 **Ejection Systolic Murmur: § Loudest over aortic area radiating to carotids and apex *Sit patient forward, ask to hold breath on expiration to accentuate murmur*

Management from this CXR

§ shows HF - bilateral airspace shadowing (pulmonary oedema), breathlessness, orthopnea, fine crepitations, raised JVP and peripheral oedema § sit them up and give high flow oxyten § BiPAP - for T2RF

Summary of ulcer examination

§ site § ulcer characteristic § associated signs

What emergency treatments are there for acute limb ischaemia?

§ surgical embolectomy, intra-arterial thrombolysis, intravenous heparin § The limb should NEVER be re-warmed as this enhances tissue damage. § Either embolectomy or thrombolysis can be performed. There is no overall difference in limb salvage or 1 year survival between the two treatments. § The increased risks of surgery are balanced by the increased risk of thrombolytic complications. § The decision should be made on case-by-case basis. § Intra-venous heparin can be used as sole treatment if the limb is viable or whilst awaiting transfer to a vascular centre. Heparin minimises clot propagation and improvement may occur through natural clot lysis and opening of collaterals.

Causes of tricuspid regurgitation

§ systolic murmur

60 y/o man with severe central crushing chest pain. What do you think was on his ECG? He died 3 days later.

§ thinking ACS, also aortic dissection can present acutely and is severe (give BP lowering medication) § early stages get peaked T waves --> ST elevation --> Q waves days following MI § this can lead to thinning of vessel and rupture --> sudden death. Also a fatal arrhythmia (VF/VT) § See atrial fibrillation after MI commonly. If RCA affected --> affects AV node and can cause bradyarrhythmia and heart block.

8 y/o boy comes to GP. right 2nd ICS murmur and facial features of short nose, broad forehead and rosy cheeks. What is most likely murmur?

§ this is aortic stenosis - william's syndrome (learning difficulties, broad forehead, short nose)

Management for chronic heart failure

§ treat underlying cause § treat exacerbating factors § lifestyle modifications § medications: ABD : ACEi, Beta blockers, diuretics

Managing SVT

§ vagal manoeuvres § adenosine § ablation

What one significant feature does his chest X-ray show?

§ widened mediastinum and dilated ascending aorta. § The heart is enlarged but not massively so. The chances are that this is due to hypertension. The main pathological feature is a substantially enlarged ascending aorta widening to the right immediately after it arises from the aortic ring. Dilatation or disruption of the aortic ring itself will account for the early diastolic murmur of aortic regurgitation in this patient.

Immediate ACS management

•ABCDE •MONA -Morphine •IV diamorphine 2.5-5mg -Oxygen •If SpO2 <94%, 15L NRB -Nitrates •GTN spray -Antiplatelets •All patients- Aspirin 300mg chewable •Either Clopidogrel/ Ticagrelor/ Prasugrel (dependent on local trust policy)- dose dependent (higher in STEMI)

Prophylaxis for stable angina

•Retrosternal chest discomfort occurring predictably upon exertion and relieved by rest and nitrates. •Same risk factors as ACS **Acute Tx: -Rest and GTN relieves pain -If not relieved and lasting >15 minutes consider ACS **Prophylaxis: -Lifestyle advice -GTN for relief of symptoms -1st line: Beta blocker/ calcium channel blocker -2nd line: •Isosorbide mononitrate/ nicorandil, ivabradine/ ranolazine - If symptom control poor on maximum dose, consider switching/ adding in another class of drug

What is rheumatic fever caused by?

•Rheumatic fever is always associated with Group A Beta haemolytic streptococcal infections -Recent infection is invariable •Even patients who do not have clinical infection have antibody evidence of recent infection -Site is important •Only associated with pharyngeal infections •Not associated with cutaneous infections

Summarise the epidemiology of arterial ulcers

● 22% of leg ulcers ● Prevalence increases with age and obesity

Define arterial ulcer

● A localised area of damage and breakdown of skin due to inadequate arterial blood supply. Usually seen on the feet of patients with severe atheromatous narrowing of the arteries supplying the legs.

Identify appropriate investigation for tricuspid regurgitation

● Bloods o FBC o LFT o Cardiac enzymes o Blood cultures ● ECG o P pulmonale (>2.5mm height)- due to right atrial hypertrophy ● CXR o Right-sided enlargement of cardiac shadow ● Echocardiography o Extent of regurgitation can be estimated using Doppler ultrasound o May show valve prolapse and right ventricular dilation ● Right Heart Catheterisation o Rarely necessary but may be useful for assessing pulmonary artery pressure

Identify appropriate investigations for gangrene and necrotising fasciitis

● Bloods: § FBC- leukocytosis, haemoconcentration, or anaemia (LDH elevated in haemolytic anaemia) § glucose § CRP - elevated § blood culture - see if positive for infective organism § U&Es - may indicate metabolic acidosis, liver derangement, renal failure ● Wound Swab, Pus/Fluid Aspirate - MC&S ● X-ray of affected area - may show gas produced in gas gangrene, /or indicate underlying osteomyelitis. May do CT in abnormal cases of gas gangrene ● Doppler ultrasonography - may indicate presence and severity of arterial or venous obstruction **in ischaemic gangrene may see reduced ABPI index

Recognise the presenting symptoms of pericarditis

● CHEST PAIN o Sharp and central o May radiate to the neck or shoulders o Worse when coughing and deep inspiration (pleuritic pain) o Relieved by sitting forward o Worse when lying flat ● Dyspnoea ● Nausea

Identify appropriate investigations for constrictive pericarditis

● CXR - small heart +/- calcification of the pericardium ● Echocardiogram - usually diagnostic and helps distinguish from restrictive cardiomyopathy ● MRI - allows assessment of thickness of pericardium ● CT - same role as MRI ● Pericardial biopsy - may be indicated (especially if suspected infective cause)

Identify appropriate investigations for cardiac arrest

● Cardiac Monitor o Allows classification of the rhythm ● Bloods o ABG o U&E o FBC o X-match o Clotting o Toxicology screen o Blood glucose

Cardiac electrical activity

● Cardiac muscle can undergo spontaneous depolarisation and generate action potentials, in certain areas, hence it is its own NATURAL PACEMAKER. ● An excitation signal is created by the sinoatrial node. ● The wave of excitation spreads across the atria, causing depolarisation and atrial contraction. ● The signal reaches the atrioventricular node, where it is delayed allowing atrial emptying The wave is then conducted into the bundle of His, down the interventricular septum. The bundle of His and Purkinje fibres spread the wave impulses along the ventricles, causing ventricular depolarisation and contraction.

Summarise the prognosis for patients with atrial fibrillation

● Chronic AF in a diseased heart does not usually return to sinus rhythm

Recognise the presenting symptoms of aortic regurgitation

● Chronic AR o Initially ASYMPTOMATIC o Later on, the patient may develop symptoms of heart failure (e.g. exertional dyspnoea, orthopnoea, fatigue) o Also: palpitations, angina and syncope, CCF ● Severe Acute AR: medical emergency! o Sudden cardiovascular collapse (left ventricle cannot adapt to the rapid increase in end-diastolic volume) o sudden onset pumonary oedema, hypotension or cardiogenic shock ● Symptoms related to aetiology (e.g. chest or back pain caused by aortic dissection/myocardial ischaemia)

Identify possible complications of ventricular tachycardia

● Congestive cardiac failure ● Cardiogenic shock ● VT may deteriorate into VF

Define pulmonary embolism

● DEFINITION: occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the pulmonary vascular system from another site ● Clots break off and pass through the veins and the right side of the heart before lodging in the pulmonary circulation.

Diastolic murmurs

● Diastolic murmurs: occur between S2 and S1 ⇒ Decrescendo murmur - occurs due to aortic or pulmonary regurgitation ⇒ Decrescendo murmur with brief increase in intensity during atrial contraction - occurs due to mitral or tricuspid stenosis.

Summarise the epidemiology of tricuspid regurgitation

● Differs based on cause ● Infective endocarditis is the MOST COMMON cause

Recognise the presenting symptoms of cardiomyopathy

● Dilated o Symptoms of heart failure - fatigue, dyspnoea o Arrhythmias o Thromboembolism o Family history of sudden death ● Hypertrophic o Usually NO SYMPTOMS o Syncope o Angina o Arrhythmias o Dyspnoea o Palpitations o Family history of sudden death ● Restrictive - similar to constrictive pericarditis o Dyspnoea o Fatigue o Arrhythmias o Ankle or abdominal swelling o Family history of sudden death

Identify appropriate investigations for pericarditis

● ECG - widespread saddle-shaped (concave) ST elevation, tachycardia, PR depression later followed by T wave flattening and inversion ● Echocardiogram - assesses pericardial effusion and cardiac function ● Bloods o FBC - WCC o U&Es o ESR/CRP o Cardiac Enzymes (usually normal) o Other investigations for cause: blood cultures, ASO titres, ANA, rheumatoid factor, viral serology ● CXR o Usually normal o May be globular if there is a pericardial effusion

Expiration increases --- murmurs Inspiration increases --- murmurs

● Expiration increases lEft-sided murmurs. Inspiration increases rIght-sided murmurs. Because, during inspiration, there is more negative( intra-thoracic pressure which pulls more venous blood into the heart (to the right side) so there is increased preload to R side. At same time, during inspiration, pulmonary blood volume increases and there is a decrease in blood flow from lungs to left atrium so there is decreased preload to L side.

Recognise the presenting symptoms of infective endocarditis

● Fever with sweats/chills/rigors o NOTE: this might be relapsing and remitting ● Malaise ● Weight loss ● Arthralgia ● Myalgia ● Confusion ● Skin lesions ● Ask about recent dental surgery or IV drug use

Define DVT

● Formation of a thrombus within the deep veins (most commonly in the calf or thigh)

Summarise the prognosis of ventricular tachycardia

● GOOD if treated RAPIDLY ● Long-term prognosis depends on the underlying cause

Summarise the prognosis for patients with hypertension

● Good prognosis if well controlled ● Uncontrolled hypertension is associated with increased mortality ● Treatment reduces incidence of renal damage, stroke and heart failure ● Causes 50% of all vascular deaths

Identify appropriate investigations for peripheral vascular disease

● History + vascular exam ● FIRST LINE: ABPI (Ankle-Brachial Pressure Index) o Marker of cardiovascular disease o Ankle SBP/Brachial SBP o ABPI < 0.8 = do NOT apply a pressure bandage because this will worsen ischaemia o Note: calcification of arteries can occur in DIABETES and CHRONIC RENAL FAILURE which can alter results and cause high ankle pressures due to incompressible arteries. o Normal: 1-1.2 o Peripheral arterial disease: 0.5-0.9 (claudication) o Critical limb ischaemia: <0.5 with tissue loss <0.2 ● Then: Colour DUPLEX Ultrasound o Non-invasive o Shows site and degree of stenosis ● GOLD STANDARD: MRI/CT angiogram. But is invasive, requires contrast. ● Full cardiovascular risk assessment o Blood pressure o FBC - anaemia will worsen ischaemia o Fasting blood glucose o Lipid levels o ECG - check for pre-existing coronary artery disease o Thrombophilia screen - for patients < 50 yrs o U&E - renal disease **TREATMENT wise - thrombolysis (tPA) or embolectomy/fogarty catheter or thrombectomy

S1 and S2 normal sounds

● In notes, I + II + O represents normal heart sounds with no added sounds ● S1: due to AV valves closing (mitral is loud, tricuspid is soft) ● S2: due to SL valves closing (usually occur simultaneously in expiration to produce single sound but in inspiration, mild physiological splitting can occur with first part due to aortic and second due to pulmonary) ● S2 is shorter than S1 ● Systole follows S1 representing ventricular emptying ● Diastole follows S2 representing ventricular filling ● The carotid pulse is palpable between S1 and S2 - blood is ejected in to the systemic circulation as ventricles contract during systole after mitral valve closes but before aortic valve closes. This is why palpating the pulse when auscultating heart sounds help work out where lub and dub are and interpret any added sounds.

Define infective endocarditis

● Infection of intracardiac endocardial structures (mainly heart valves)

Relationship between ECG leads and the side of the heart

● Inferior: II, III, aVF (supplied by right coronary artery) ● Anterior: V1-V5/6 (left anterior descending artery) ● Lateral: I, aVL, V5/6 (left circumflex artery) ● Posterior: Tall R wave and ST depression in V1-3

Define pericarditis

● Inflammation of the pericardium - it may be acute, subacute or chronic

Recognise the presenting symptoms of peripheral vascular disease

● Intermittent claudication - cramping pain in the calf, thigh or buttock after walking for a given distance (claudication distance) and relieved by rest o Calf claudication = FEMORAL disease o Buttock claudication = ILIAC disease ● Features of Critical Limb Ischaemia o Ulcers o Gangrene o Rest pain o Night pain (relieved by dangling leg over the edge of the bed) ● Leriche Syndrome (aortoiliac occlusive disease) o Buttock claudication o Impotence, erectile dysfunction o Absent/weak distal pulses (femoral) ● Fontaine Classification of Peripheral Vascular Disease: o Asymptomatic o Intermittent Claudication o Rest pain o Ulceration/gangrene

Identify possible complications of ventricular fibrillation

● Ischaemic brain injury due to loss of cardiac output ● Myocardial injury ● Post-defibrillation arrhythmias ● Aspiration pneumonia ● Skin burns ● Death

Recognise the presenting symptoms of venous ulcers

● Large, shallow, relatively painless ulcer with an irregular margin situated above the medial malleoli (most of the time) ● Features of the history: o Varicose veins o DVT o Phlebitis o Fracture, trauma or surgery o Family history o Other symptoms of venous insufficiency: ● Swelling ● Itching ● Aching

Define venous ulcers

● Large, shallow, sometimes painful ulcers usually found superior to the medial malleoli. They are caused by incompetent valves in the lower limbs leading to venous stasis and ulceration.

Define vasovagal syncope

● Loss of consciousness due to a transient drop in blood flow to the brain caused by excessive vagal discharge.

Recognise the signs of aortic dissection on physical examination

● Murmur on the back (below the left scapula), descending to the abdomen ● Hypertension ● Blood pressure difference between the two arms > 20 mm Hg ● Wide pulse pressure ● Hypotension may suggest tamponade o Check for pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration o This may indicate: ● Tamponade ● Pericarditis ● Chronic sleep apnoea ● Obstructive lung disease ● Signs of Aortic Regurgitation o High volume collapsing pulse o Early diastolic murmur over aortic area ● Unequal arm pulses ● There may be a palpable abdominal mass

Recognise the signs of aortic stenosis on examination

● Narrow pulse pressure ● Slow-rising pulse ● Thrill in the aortic area (only if severe) ● Heaving, undisplaced apex beat ● Ejection systolic murmur at the aortic area, radiating to the carotid artery ● Second heart sound may be softened or absent (due to calcification) ● A bicuspid valve may produce an ejection click **can get paradoxically split S2L With more severe stenosis, aortic valve closure may become so delayed that it follows pulmonic valve closure during expiration, producing the paradoxically split S2. May be accentuated by left bundle branch block.

Recognise the signs of mitral stenosis on physical examination

● Peripheral cyanosis ● Malar flush (image) - due to dec CO ● Irregularly irregular pulse (if in AF) ● Low volume pulse ● Apex beat undisplaced and tapping ● Parasternal heave (due to right ventricular hypertrophy secondary to pulmonary hypertension) ● Loud S1 with opening snap ● Mid-diastolic murmur heard best in expiration with patient lying on their left ● Graham Steell murmur may occur ● Evidence of pulmonary oedema on lung auscultation (if decompensated)

Summarise the epidemiology of aortic stenosis

● Present in 3% of 75 yr olds ● More common in males ● Those with bicuspid aortic valve present earlier

Summarise the epidemiology of cardiomyopathy

● Prevalence of dilated and hypertrophic cardiomyopathy is 0.05-0.20% ● Restrictive is even rarer

Define DC Cardioversion

● Procedure to convert arrhythmias into sinus rhythm using direct current electricity. ● Synchronised electrical cardioversion uses a therapeutic dose of electric current to the heart at a specific moment in the cardiac cycle, restoring the activity of the electrical conduction system of the heart. Note: defibrillation (unsynchronised) uses a therapeutic dose of electric current to the heart at a random moment in the cardiac cycle - used for resuscitation in cardiac arrest i.e. ventricular fibrillation/tachycardia

Recognise the presenting symptoms of myocarditis

● Prodromal flu-like illness with: o Fever o Malaise o Fatigue o Lethargy ● Breathlessness (due to pericardial effusion/myocardial dysfunction) - dyspnoea, orthopnoea ● Palpitations ● Sharp chest pain (suggesting there is also pericarditis)

Recognise the presenting symptoms of pulmonary hypertension

● Progressive breathlessness ● Weakness/tiredness ● Exertional dizziness and syncope ● LATE STAGE - oedema and ascites ● Angina and tachyarrhythmia

Identify the possible complications of cardiac failure

● Respiratory failure ● Cardiogenic shock ● Death

Recognise the presenting symptoms of DVT

● Swollen limb ● May be painless ● Mild fever

Systolic murmurs

● Systolic murmurs: occur between S1 and S2 ⇒ Mid-systolic murmur - occurs due to aortic stenosis or pulmonary stenosis. If semi-lunar valves are narrowed, there will be reduced blood flow through them during systole. These murmurs have a crescendo-decrescendo character. ⇒ Pan-systolic murmur - occurs due to mitral or tricuspid regurgitation. If AV valves are leaky, there will be a murmur heard during ventricular contraction.

Define AAA

● The abdominal aorta is a direct continuation of the descending aorta, and supplies blood to much of the abdominal cavity. ● AAA: A localised enlargement of the abdominal aorta such that the diameter is > 3 cm or > 50% larger than normal diameter. o NOTE: normal diameter of the aorta = 2 cm ● A true aneurysm is an abnormal dilatation involving all layers of the arterial wall. These can be fusiform (most AAAs) or sac-like ● False aneurysms (pseudoaneurysms) involve a collection of blood in the outer layer only (adventitia) which communicates with the lumen e.g. after trauma.

Explain the aetiology/risk factors of WPW syndrome

● The accessory pathway (bundle of Kent) is likely to be congenital ● Associations: o Congenital cardiac defects o Ebstein's anomaly (congenital malformation of the heart characterised by displacement of septal and posterior tricuspid leaflets) o Mitral valve prolapse o Cardiomyopathies (e.g. HOCM)

Define varicose veins

● Veins that become prominently elongated, dilated (>3mm) and tortuous, most commonly the superficial veins of the lower limbs. § some are asympotmatic

What is the likely cause of S3 in a 63 year old man

volume overload and congestive HF - because can hear thud of blood hitting ventricle

Which drugs may be used to reduce the thromboembolic risk in patients at risk of a cardiovascular event?

§ Aspirin § ADP-receptor antagonists (e.g. clopidogrel and prasugrel)

List some surgical options for varicose veins

§ Avulsion/phlebectomy § Stripping § Injection sclerotherapy § Radiofrequency ablation

What treatments do in chronic stable angina?

§ CABG - alternative route § Angiogram § Angioplasty - put wire in in right/left femoral artery and blow up balloon to break up the blockage in coronary artery. If don't do this, then within a year 1 or 2 may get acute MI

Systemic amyloidosis and heart problems

§ CHF § Arrhythmias

List some possible interventions for acute limb ischaemia

§ Embolectomy § Percutaneous thrombolysis § Revascularisation angioplasty § Bypass surgery § Amputation

Key points in an ulcer history

§ about ulcer: pain and presentation § associated symptoms § risk factors

Surgery for PAD

§ above knee anastamosis is better success § dacron or in situ vein

Define the three ways to categorise heart failure

§ acute vs chronic § left vs right § high output vs low output

Summarise the epidemiology of varicose veins

● COMMON ● Incidence increases with age ● 10-15% of men ● 20-25% of women

Kerley B lines

(horizontal lines in the left lower zone). a radiological change of pulmonary venous hypertension

Summarise the indications for CABG

● Left main stem disease ● Multi vessel disease - triple vessel disease involving proximal part of the left anterior descending ● Multiple severe stenosis ● Unsuitable for angioplasty ● Failed angioplasty ● Refractory angina, angina unresponsive to drugs ● When CABG and PCI are both clinically valid options, NICE recommends that the availability of new stent technology should push the decision towards PCI.

Recognise the presenting symptoms of mitral stenosis

● May be ASYMPTOMATIC ● Fatigue ● Exertional dyspnoea ● Chest pain ● Orthopnoea ● Palpitations (related to AF) ● Systemic emboli ● Rare symptoms: chronic bronchitis type picture o Cough o Haemoptysis o Hoarseness caused by compression of left recurrent laryngeal nerve by an enlarged left atrium

Sydenham's chorea

A form of chorea (involuntary muscle twitching) associated with rheumatic fever, usually occurring in childhood. AKA St Vitus' dance

Define peripheral vascular disease

● Occurs DUE TO ATHEROSCLEROSIS causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors

Recognise the presenting symptoms of atrial fibrillation

● Often ASYMPTOMATIC ● Palpitations ● Syncope (if low output) - dizzy, faints ● Symptoms of the cause of AF

Summarise the epidemiology of pulmonary embolism

● Relatively COMMON (especially in hospitalised patients) ● Occur in 10-20% of patients with confirmed proximal DVT

What does left coronary artery divide into?

Also known as left stem. LAD and circumflex.

List different systems that can cause chest pain

Bornholme's is costochondritis but caused by infection

T wave inversion and ST depression on ECG is suggestive of...

NSTE-ACS

NSTE-ACS management

* initial A to E and MONA. § add heparin § then GRACE

In aortic regurgitation what other sign are you likely to find?

quinke's sign. represents the visualization of capillary pulsations upon light compression applied to the tip of the fingernail bed.

Define heart block

**Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles. The severity of the conduction abnormality is described in degrees: first-degree; second-degree, type I (Wenckebach or Mobitz I) or type II (Mobitz II); and third-degree (complete) AV block. This classification scheme should be applied only during sinus rhythm and not during rapid atrial arrhythmias or to premature atrial beats. ● 1st Degree AV Block: prolonged conduction through the AV node ● 2nd Degree AV Block: o Mobitz Type I (Wenckebach): progressive prolongation of AV node conduction until one atrial impulse fails to be conducted through the AV node (PR interval gradually increases and then P wave is not followed by QRS). The cycle then begins again. o Mobitz Type II: intermittent or regular failure of conduction through the AV node. PR interval is fixed in duration but not every P is followed by a QRS. Also defined by the number of normal conductions per failed one (e.g. 2:1 means there are two P waves for each QRS) ● 3rd Degree (Complete) AV Block: no relationship between atrial and ventricular contraction. Failure of conduction through the AV node leads to ventricular contraction generated by a focus of depolarisation within the ventricle. QRS complexes can have abnormal shape and prolonged duration.

Flowchart for investigating suspected DVT using 2-level Wells test

**Clinical probability simplified score § DVT likely: 2 points or more § DVT unlikely: 1 point or less **If a DVT is 'likely' (2 points or more): § a proximal leg vein ultrasound scan should be carried out within 4 hours: o if the result is positive then a diagnosis of DVT is made and anticoagulant treatment should start o if the result is negative a D-dimer test should be arranged. A negative scan and negative D-dimer makes the diagnosis unlikely and alternative diagnoses should be considered § if a proximal leg vein ultrasound scan cannot be carried out within 4 hours a D-dimer test should be performed and INTERIM therapeutic anticoagulation administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed WITHIN 24 hours): o interim therapeutic anticoagulation used to mean giving low-molecular weight heparin o NICE updated their guidance in 2020. o They now recommend using an anticoagulant that can be continued if the result is positive. o this means normally a direct oral anticoagulant (DOAC) such as apixaban or rivaroxaban § if the scan is negative but the D-dimer is positive:stop interim therapeutic anticoagulation AND offer a repeat proximal leg vein ultrasound scan 6 to 8 DAYS later **If a DVT is 'unlikely' (1 point or less): § perform a D-dimer test: this should be done within 4 HOURS. If not, interim therapeutic anticoagulation should be given until the result is available § if the result is negative then DVT is unlikely and alternative diagnoses should be considered § if the result is positive then a proximal leg vein ultrasound scan should be carried out within 4 hours § if a proximal leg vein ultrasound scan cannot be carried out within 4 hours interim therapeutic anticoagulation should be administered whilst waiting for the proximal leg vein ultrasound scan (which should be performed within 24 hours) **D-dimer tests: § NICE recommend either a point-of-care (finger prick) or laboratory-based test § age-adjusted cut-offs should be used for patients > 50 years old

Factors that predispose to rheumatic fever?

**Factors that predispose to rheumatic fever: -Severity of infection and magnitude of immune response •Higher antibody titres associated with greater risk -Positive family history •Specific HLA Class II alleles associated with disease. **•Factors that predispose to Group A streptococcus infection itself: -Age •children from 4 - 9 years old -Sex •Female preponderance in mitral stenosis and Sydenham's chorea -Seasonality •Winter and spring peak -Economic factors •Poverty •Urban environment •Crowding

Clinical diagnosis of Heart failure using Framingham criteria (2+ majors or 1 major and 2 minors)

**Major: •Paroxysmal nocturnal dyspnoea •Bibasal crepitations •S3 gallop •Cardiomegaly •Increased central venous Pressure •Weight loss •Neck vein distension •Acute pulmonary oedema •Hepatojugular reflux **Minor: - bilateral ankle oedema - dyspnoea on ordinary exertion - tachycardia - decrease in vital capacity by 1/3 - nocturnal cough - hepatomegaly - pleural effusion

A 47-year-old female attends the emergency department complaining of sudden onset shortness of breath and chest pain. Her past medical history includes hypothyroidism for which she takes levothyroxine. She doesn't recall any other medical conditions but does remember having a 'leg clot' a few years previously.On examination her airway is patent, however her respiratory rate is 22 breaths/min and her heart rate is 126 beats/min. You take her blood pressure and find it to be 88/42mmHg. She has an urgent chest x-ray followed by a CT pulmonary angiogram which shows a pulmonary embolism in her pulmonary trunk. What must be done next in her management? § Thrombolysis § Perform an ECG § Prescribe apixaban § Give IV fluids § Prescribe LMWH and warfarin

**Massive PE + hypotension - thrombolyse. § Thrombolysis is indicated when there is haemodynamic instability (e.g. hypotension) associated with a massive PE. § Although this patient should have an ECG as part of her investigations, this won't help us further with the diagnosis and management at this time. § DOACs such as apixaban or rivaroxaban should now be offered as first-line treatments for PE. § If neither of these are suitable then LMWH followed by another DOAC such as dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (e.g. warfarin) may be used. § While IV fluids are often appropriate in patients who are hypotensive, in this scenario the PE management is more important as this is causing the hypotension.

Summarise the epidemiology of ventricular fibrillation

● The MOST COMMON arrhythmia identified in cardiac arrest patients ● Incidence of VF parallels the incidence of ischaemic heart disease

Summarise the indications for DC Cardioversion

● Ventricular fibrillation ● Ventricular tachycardia ● Atrial fibrillation ● Atrial flutter ● SVTs if haemodynamically unstable or other treatments failed

Summarise the prognosis for patients with dyslipidaemia

Good if controlled early

What is likely SBP and DBP in patient with atrial regurgitation

Likely SBP - will be high (160), DBP will be low (40)

Mr Woodward is a 69-year-old gentleman who is brought to his GP by a friend after fainting in the street. Mr Woodward has been visiting family for the past couple of days and has been complaining of 'dizzy spells', although this is the first time he has lost consciousness. When asked what he means by 'dizzy spells', he confirms that he means light-headedness rather than vertigo (i.e. there is no rotational component to the sensation). He says this occurs on standing and only started about a month ago. On the occasion on which he lost consciousness, his friend says he came round a few seconds later. He says he wasn't particularly confused afterwards, other than wondering why it happened. His medical history includes hypertension, angina, and benign prostatic hyperplasia for which he takes aspirin, bendroflumethiazide, atenolol, and doxazosin. He has been taking these for several years, except the doxazosin which he started a month ago. What is the most likely diagnosis? What is the physiological basis for this?

Mr Woodward has a history of light-headedness associated with standing that suggests orthostatic hypotension. Th e timing of these symptoms coincides with his new prescription of doxazosin for his prostate problems. This is not uncommon; surprisingly few patients associate the onset of new symptoms (side-effects) with the start of a new medication. § Mr Woodward has good reason to feel lightheaded when he stands up: the diuretic will reduce his circulating blood volume, and the β-blocker and α-blocker will impair the increase in heart rate and vasoconstriction of the large capacitance veins, respectively, when he stands. Therefore Mr Woodward is probably suffering from iatrogenic orthostatic hypotension. § Th is could be confirmed by comparing the lying versus standing blood pressure, looking for a postural drop in blood pressure. § The key to management is to modify his medications by reducing doses to the minimal effective dose, trying different medications altogether (e.g. a different type of α-blocker or a 5α-reductase inhibitor for his benign prostatic hyperplasia), or trying non-medical management of some of his problems (e.g. a transurethral resection of the prostate (TURP) for his benign prostatic hyperplasia).

Arteries supplying heart

The anterior/anterolateral wall is supplied by the left anterior descending artery. The inferior wall is supplied by the right coronary artery of which the RV branch comes off proximally. The left main stem divides into the LAD and then circumflex giving ECG changes normally in more than one territory. The circumflex supplies the posterior and lateral wall.

A 60-year-old man presents to the emergency department with central chest pain. His ECG shows ST depression in leads II,III and aVF. Which of the following may indicate a worse outcome in this patient? § Age <65 § Lung crackles heard on auscultation § Raised 48-hour serum creatinine concentration § 10 pack-year smoking history § Previous history of type 2 diabetes

b) Lung crackles heard on auscultation **Cardiogenic shock is a poor prognostic indicator in acute coronary syndrome § This question is asking about the prognostic factors in acute coronary syndrome. This man has presented with what sounds like a non-ST elevated myocardial infarction with central chest pain and ST depression. In this case, lung crackles heard on auscultation will be a poor prognostic factor as they indicate heart failure has occurred with resultant pulmonary oedema. § Age <65 is not a poor prognostic factor, and in fact the opposite, age >65 is a poor prognostic factor. § It is an initially raised serum creatinine concentration and not a raised 48-hour serum creatinine concentration that is a poor prognostic factor. § A 10 pack-year smoking history has no effect on prognosis as many patients with acute contrary syndrome (ACS) will have some risk factors for cardiovascular diseaseAs with a smoking history, a previous history of type 2 diabetes has no effect on prognosis of ACS *Killip class - system used to stratify risk post myocardial infarction

Diabetic foot

§ 45% neuropathic § 10% Ischaemic § 45% mixed

What would SOCRATES look like for MI?

§ A focussed chest pain history does not take very long and can quickly help you ascertain the origin of the chest pain. § A history involves the SOCRATES approach and acts a robust method in eliciting any pain history. § Key features which suggest a cardiac origin for the pain are as above. § Additionally you know from the type of surgery that the patient has had (EVAR for AAA) that they are likely 'arteriopathic' i.e. their arteries are atherosclerotic with consequent aortic aneurysm formation. § Diabetes is another risk factor and a previous MI is concerning; it suggests underling coronary artery disease. § An MI is a recognised post operative complication. The risk will vary depending on the type and duration of surgery.

List some surgical options for treating arterial ulcers

§ Angioplasty § Bypass surgery § Amputation **Management: § Dress the ulcer to prevent infection § Analgesia § Antibiotics (if signs of infection)

Outline the management of cellulitis

§ Antibiotics § Demarcation of erythematous region to monitor progress § Elevation - helps reduce the swelling and reduce pain § Topical steroids and oral antihistamines - in the case of an inflammatory reaction to an insect bite (may present similarly to cellulitis)

You are doing a medication review on a 79-year-old man. His current medications include aspirin, verapamil, allopurinol and co-codamol. Which one of the following is it most important to avoid prescribing concurrently? Colchicine/ Digoxin/ Simvastatin/ Tramadol/ Atenolol

§ Atenolol - Beta-blockers combined with verapamil can potentially cause profound bradycardia and asystole.

75 year hypertensive ECG

§ Atrial fibrillation - not sinus, irregularly irregular rhythym (random). § AF + weight loss can be from hyperthyroidism (start as tachycardic --> AF) § For fast AF - anticoagulant, beta blockers, digoxin (but not if cause is hyperthyrodism). If cause is hyperthyroidism --> give beta blocker (propanolol, bisoprolol). Also give carbimazole 15-40mg daily for the hyperthyroidism. § metoprolol used for thyroid storm/crises as can be given IV.

Mr Williams' blood glucose, ECG, FBC, U&Es, and oxygen saturations are normal. In light of his age, history, and investigations, what diagnosis for blackout is most likely?

§ Bear in mind that in approximately 50% of cases of loss of consciousness no diagnosis is made. § Given that the patient is young and has an unremarkable history and normal first-line investigations, the most likely diagnosis is vasovagal syncope. § A cardiac arrhythmia is unlikely given the patient's age and the lack of family history of congenital heart problems. § The normal ECG suggests that there is no congenital heart pathology such as Brugada syndrome. Indeed, cardiac arrhythmias in general are unlikely if there is no history of palpitations, no clinical evidence of heart disease, and an entirely normal ECG.

Following defibrillation and two minutes of CPR, you stop for a rhythm check. The rhythm is shown in Figure 2. What is your next step?

§ Check for a pulse. The rhythm strip demonstrates organised electrical activity, this may be compatible with a pulse and therefore change your direction of management from a cardiac arrest algorithm to post arrest management. If your patient did not have a pulse this would be called 'pulseless electrical activity' and you would move over to the non-shockable side of the cardiac arrest algorithm.

Mr Perkins is a 32-year-old investment banker who presents with chest pain. It came on while he was at a party in a bar with friends. He has a family history of cardiovascular disease but no other cardiovascular risk factors. He is normally fit and well, although he says he has had a cold and fever for the past couple of days. His ECG shows >2 mm ST elevation in leads V1-V4 and, as he is at a hospital with the necessary resources, he is scheduled for primary angioplasty. However, no coronary artery occlusion was seen on his angiogram. What is the most likely diagnosis? Which question(s) in particular should you ask on the history?

§ Chest pain and fever suggest an acute inflammation due to, for example, myocarditis/ pericarditis but the ECG does not support this (it would classically show saddle-shaped ST elevation in a number of leads not conforming to the territory of a single coronary artery). § Normal angiography ruled out coronary artery disease. The most likely diagnosis is coronary spasm due to cocaine usage. You should specifically ask about recreational drugs in order to investigate this possibility.

HF: Complications and Prognosis

§ Complications: •Respiratory failure •Renal failure - due to hypoperfusion •Acute exacerbations •Death § Prognosis: • •Very poor, worse than most malignancies •50% of severe HF patients die within 2 years •Acute HF in-hospital mortality = 2-20%

List some clinical signs that are associated with aortic dissection

§ Different blood pressures in the two arms § Aortic regurgitation § Pleural effusion (due to irritation of pleura)

Emergency management of hyperkalaemia

§ ECG § Calcium gluconate 10% 10ml § fix potassium by driving into cells using salbutamol nebs 10mg § insulin 5-10 units BUT hence also give glucose 50% 50mmol **also do regular VBGs

The abdominal radiograph confirms aortic aneurysm calcification. The patient has remained haemodynamically stable and his pain has been well controlled with analgesia. What would you do next?

§ Establish intravenous access § Take blood for cross-match § Discuss case urgently with senior surgical/anaesthetic colleagues § Arrange CT of abdomen/pelvis urgently § Liaise with theatres ***The clinical and radiological picture is now consistent with a probable contained leak from an aortic aneurysm - the patient is stable and it would be reasonable to confirm this with CT, which will also give more information about aneurysm extent. Do get senior help quickly and liaise with vascular surgeon/anaesthetist/theatres. A CT of the leaking aneurysm is shown in Fig. 2; notice the large haematoma around aneurysm (A) with active contrast extravasation (bleeding) also present (B). The aneurysm in the wall of the aorta is also shown (arrows - C) with enhancing lumen (D).

A 26-year-old female is referred to the acute medical unit with chest pain. The pain is sharp, left-sided, worse on inspiration and worsened by lying flat. She has no significant past medical history and is on no regular medications except the combined oral contraceptive pill. She does not drink or smoke.Her observations are heart rate 91 beats per minute, blood pressure 128/84 mmHg, respiratory rate 18/minute, oxygen saturations 98% on room air and temperature 37.4ºC. Clinical examination is unremarkable. An ECG demonstrates widespread ST elevation and PR depression in all leads. Blood tests show high CRP. A transthoracic echocardiogram demonstrates a 0.9cm pericardial effusion. What is the most appropriate immediate management?

§ First line management of acute pericarditis involves combination of NSAID and colchicine § The addition of colchicine to an NSAID reduces symptom duration and frequency of recurrence in acute pericarditis. § Treatment duration should be THREE MONTHS in acute pericarditis. § The diagnosis is acute pericarditis as evidenced by the pleuritic chest pain, worse on recumbency associated with typical ECG changes and pericardial effusion. § While this woman presents with pleuritic chest pain and combined oral contraceptive pill use, there are no other features to suggest a pulmonary embolism and the d-dimer is negative. § Pericardiocentesis is incorrect. This patient has a small pericardial effusion and no clinical features of cardiac tamponade and therefore this intervention is not warranted. **PERICARDITIS: § Features chest pain: may be pleuritic. Is often relieved by sitting forwards other symptoms include non-productive cough, dyspnoea and flu-like symptoms, pericardial rub, tachypnoea, tachycardia. § Causes: viral infections (Coxsackie), tuberculosis, uraemia (causes 'fibrinous' pericarditis), trauma, post-myocardial infarction, Dressler's syndrome connective tissue disease, hypothyroidism, malignancy. § Investigations: A) ECG changes: the changes in pericarditis are often global/widespread, as opposed to the 'territories' seen in ischaemic events', saddle-shaped' ST elevation, PR depression: most specific ECG marker for pericarditis. all patients with suspected acute pericarditis should have transthoracic echocardiography. **Management: treat the underlying cause a combination of NSAIDs and colchicine is now generally used for first-line for patients with acute idiopathic or viral pericarditis

Pathophysiology of Chronic Cardiac Failure

§ In heart failure, the CO declines - but this leads to multiple compensatory mechanisms to help maintain cardiac output. § These changes over months and years can worsen cardiac function and lead to complications such as increasing venous pressure causing oedema and increased afterload on left ventricle, depressing cardiac output further. § Therefore, some of the most effective treatments for chronic heart failure involves modulating non-cardiac factors. Both systolic and diastolic dysfunction leads to increased end-diastolic volume - compensatory to increase SV via Frank Starling mechanism. This can cause high afterload vasodilators. § RAAS is activated but this can increase afterload and increase preload to cause oedema ACEi, ARBs § SNS is activated as compensation to maintain normal arterial pressures in response to a low CO, by constricting arteries. Veins are also constricted to maintain venous pressures. This can increase afterload ACEi and vasodilators Blood volume is increased as RAAS stimulates aldosterone. Can lead to oedema and exertional dyspnea diuretics.

List some features of the cardiovascular examination that may indicate a cardiac cause of collapse.

§ Irregular pulse - AF § Ejection-systolic murmur - aortic stenosis § Carotid bruits - carotid artery stenosis **FOCAL neurological signs: § Peripheral neuropathy may be caused by diabetes § Parkinson's disease can lead to autonomic dysfunction

Why might we perform a Duplex ultrasound scan before varicose vein surgery?

§ It is good practice for all patients to undergo duplex scanning pre-operatively. It should however, be performed in recurrent varicose veins, those who have been diagnosed as having had a DVT in the past and in those patients where the distribution affected is uncertain.

What are contraindications (absolute or relative) for intra-arterial thrombolysis?

§ Limb that is insensate and with fixed skin mottling § Cerebral neoplasm § Oesophageal varices § Abdominal surgery within past 2 weeks ***Contraindications for thrombolysis: (applies equally to thrombolysis in myocardial infarction) § Non-viable limb (irreversible ischaemic change - insensate/fixed skin mottling) § Internal bleeding § Suspected aortic dissection § Prolonged or traumatic CPR § Previous allergic reaction § Heavy vaginal bleeding § Pregnancy or < 18 wks postnatal § Acute pancreatitis § Severe liver disease § Active lung disease with cavitation § Oesophageal varices § Recent trauma or surgery (< 2 wks) § Recent head trauma § Cerebral neoplasm § Recent haemorrhagic stroke § Severe hypertension (>200/120 mmHg) ***Relative contraindications include: § History of severe hypertension § Peptic ulcer § History of CVA § Bleeding diathesis § Anticoagulants

Mr Griffin is admitted to hospital and has a duplex ultrasound that shows moderate stenosis of both the left and right external iliac arteries and severe stenosis (about 80%) of the left superficial femoral artery. He is placed on the waiting list for angioplasty and stenting. On the second night of Mr Griffin's admission the nursing staff bleep the duty junior doctor and ask her to come and see Mr Griffin. He states that he was awoken 2 hours ago because the pain from the ulcer in his left foot had suddenly spread to affect his entire left leg below his knee. He describes the pain as sharp and 8/10 in severity, with a tingling sensation confined to the foot. He was going to wait until the morning until he realized he was unable to move his left ankle. On examination, Mr Griffin's left leg is significantly colder than the right. Both legs have typical Anglo- Saxon pallor but the sole of his left foot is ghostly white compared to his right. His popliteal pulse, dorsalis pedis, and posterior tibial are all impalpable on the left. On the right, dorsalis pedis is palpable but the posterior tibial pulse is not (as per his GP's findings). Sensation remains grossly intact in both legs. What has happened to Mr Griffin? What is your next step?

§ Mr Griffin is a patient with known atherosclerotic disease of both lower limbs who has presented with the cardinal features of acute limb ischaemia which can be remembered as the six Ps: a painful, pale, pulseless, paralysed, perishingly cold leg with paraesthesia. § This is likely to represent either thrombosis at the site of known stenosis or embolism. § Acute limb ischaemia is a surgical emergency that requires urgent intervention by the vascular surgeons to avoid losing the limb from irreversible ischaemic necrosis. § For this reason, the next step should be to refer Mr Griffin to the vascular surgeon on call immediately. § The vascular surgeons will then decide whether to attempt an embolectomy, percutaneous thrombolysis, revascularization angioplasty, bypass surgery, or amputation of the affected limb.

List common side-effects of statins?

§ Nausea and vomiting § Tachycardia § Deranged LFTs § Headache. Patients often complain of headaches, nausea, vomiting and palpitations, which are common side effects of statins. Bloods can often reveal deranged liver function tests, and ECG investigation shows sinus tachycardia.

What ECG abnormalities would you expect in a patient who suffered a full thickness inferior MI 2 years previously? What is the basis for these changes?

§ Old infarcts are visible on ECGs as the infarcted tissue no longer conducts electrical impulses. § If they are full thickness, they can be thought of as a window. Thus an electrode positioned next to an area of fullthickness infarct will look through the window of infarcted tissue and pick up the electrical impulses passing through the myocardium on the other side of the heart. § This is evident in the ECG in the form of deep, so-called pathological, Q waves (>2 mm deep).

What are patients with Boerhaave's perforation prone to developing?

§ Pleural effusion § Pneumomediastinum (presence of air in mediastinum) § Pneumothorax

What are the causes of pericarditis?

§ Pericardium has outer fibrous and inner serous layer § Fibrous layer stops heart overfilling § Serous layer has two sublayers which have fluid in between - typically pericarditis affects these serous layers—> swelling of pericardial sac and pericardial effusion § 3 causes: idiopathic, infectious and non-infectious a) Idiopathic b) Infectious cause is usually viral pericarditis - cocsackie virus; Also bacteria - e.g. strep pyogenes (also causes acute rheumatic fever. In rheumatic fever can get features of pericarditis); Also TB (mycobacteria) can cause pericarditis c) Non-infectious: autoimmune conditions e.g. SLE (immune complexes get deposited in pericarditis), trauma, radiation, drug reaction and following MI (Dresslers syndrome - is because new antigens exposed during MI which stimulates immune response), renal failure (uraemic pericarditis). § tends to be YOUNG age 20-50, MALE § history: centralised retrosternal pain that can move to shoulder; is a sharp pleuritic pain because of fibrous layer irritated by diaphragm when breathing in; relief SITTING UP as less irritation and hence also pain on movement and lying down § 5 Ps of pleuritic chest pain- pneumonia, PE, pneumothorax, pleural effusion and pericarditis acute pericarditis can last for few weeks too; might also get viral prodrome before § On examination - are usually well with usual viral cause; tachycardia (due to pain + heart might be bit compressed so less SV and hence HR), muffling of heart sounds (because increased fluid filled space), pericardial rub (low-pitch sounds like treading on snow during systole and diastole) § Ix: bedside - ECG (global saddle shaped ST elevation, PR DEPRESSION), bloods (raised WCC, CRP, U&Es if uraemia is cause, also troponin if MI (but also raised in pericarditis due to myocyte inflammation), imaging (CXR - to rule out other causes of pleuritic chest pain; USS of heart/ transthoracic echocardiogram; cardiac MRI is GOLD-standard + definitive esp. in chronic pericarditis) § is self-limiting condition so minimal Tx § Tx: 1) conservative - recommend avoid lying down + exercise 2) medical: NSAIDs (e.g. ibuprofen) + COLCHICINE § COMPLICATIONS: A) acute complication: normally 50ml fluid in pericardial sac, but can expand to over a LITRE in severe pericardial effusion which can occur in pericarditis and can cause compression of heart —> acute cardiac tamponade —> do pericardiocentesis B) chronic complication: constrictive pericarditis - inflammation for too long and get fibrosis and calcification —> inflexible shell of pericardium and heart cannot fill or pump properly (reduced stroke volume and causes bottleneck and back up of blood in VC (right sided heart failure)—> Increased JVP and also cause back up in liver (hepatomegaly) and peripheral oedema)

List how, on examination, the nature of the swelling is different in:Septic Arthritis, Compartment Syndrome, Baker's Cyst

§ Septic Arthritis: Swelling around the joint § Compartment Syndrome: Swelling/inflammation is confined to the compartment but spares the joints. § Baker's Cyst: Swelling protrudes backwards from the knee joint into the popliteal fossa **NOTE: rupture of the Baker's cyst can make the swelling run down into the calf

Describe the typical features of compartment syndrome.What are the 5Ps?

§ Tense, shiny, swollen limb that is painful to passive movement § Pain, Paraesthesia, Paralysis, Pallor, Pulseless **high pressures within the compartment in compartment syndrome lead to Neurovascular compromise --> ischaemia and necrosis---> reduced sensation + absent pulses

ECG changes seen in hypothermia

§ The ECG changes associated with hypothermia include: § Bradycardia (<60bpm) and not tachycardia § J waves § Prolonged PR, QT and QRS intervals § Shivering artefacts § VT, VF or asystole **Asystole dominates once the core body temperature drops to below 16ºC. ST-elevation is seen in myocardial infarction. The source of U waves is uncertain, however they are thought to represent the repolarisation of Purkinje fibres and may be seen elevated in patients with hypokalaemia.

Mr Shepherd undergoes angioplasty to an occluded circumfl ex artery and is discharged. Four weeks later he presents again with chest pain. However, he says it is diff erent from his previous pain. This time it radiates to his left shoulder, is worse on deep inspiration, and is aggravated by lying down. You note that he has a fever. What are the complications of an MI, and what has probably happened to Mr Shepherd? How should Mr Shepherd be managed on this admission?

§ The common complications of MI are covered in the mnemonic DARTH VADER: 1) Death 2) Arrhythmia 3) Rupture (either of the septum or the outer walls) 4) Tamponade 5) Heart failure 6) Valve disease 7) Aneurysm 8) Dressler's syndrome (autoimmune pericarditis 2-10 weeks after MI; note that simple post-MI pericarditis is more common than Dressler's syndrome, presenting within 2-4 days) 9) Embolism 10) Re-infarction **Given the timing, fever, and pleuritic and positional aspects of the pain, Mr Shepherd has most likely presented with Dressler's syndrome. As in the management of any patient, you should first assess Mr Shepherd's need for resuscitation (ABC), then confirm his diagnosis. A FBC will show leucocytosis and an ECG may show diffuse saddle-shaped ST elevation across a number of leads without reciprocal ST depression, and may also show PR depression. An echocardiogram may show a pericardial effusion; this may also be visible on chest radiograph. The ECG and chest radiograph will additionally help exclude a re-infarction or pulmonary pathology, respectively. Twelve-hour troponin levels should also be measured on this admission for the same reason. **Having ordered the relevant investigations, Mr Shepherd should immediately be started on analgesia. Large doses of aspirin and other non-steroidal anti-infl ammatory drugs (NSAIDs) may be given and are usually sufficient. If there is a significant effusion, it can be aspirated (pericardiocentesis) to relieve pressure on the heart.

Describe the Stanford criteria for aortic dissection and how this classification influences treatment choice.

§ Type A - ascending aorta - SURGICAL EMERGENCY § Type B - descending aorta - managed medically

How renal artery stenosis increases BP

§ Use MR angiography to detect renal artery stenosis § ACEi contraindicated in bilateral RAS as you want to maintain the pressure in order to maintain the GFR

When may do V/Q scanning instead of CTPA for PE?

§ V/Q scanning is the investigation of choice if there is renal impairment or the equipment for CTPA is not available. § A proximal leg vein ultrasound scan should be considered if CTPA is negative and DVT is suspected. § Thrombolysis is now recommended as the first-line treatment for massive PE where there is a circulatory failure (e.g. hypotension). As this patient is not showing signs of failure this is not indicated. **if 2-level PE Wells score is ≤ 4 and D-dimer is negative then stop anticoagulation and consider alternative diagnosis

Limb viability in acute limb ischaemia

§ also get covid limb (vascular disease)

Intrinsic foci HR in diff parts of heart

§ atrial - 60-80 § junctional - 40-60 § ventricular - 20-40 **hence p waves occur much more frequently than QRS

Risk factors for infective endocarditis

§ need either 2 major/ 1 major + 3 minor/ all 5 minor

DDx of chest pain

§ pericarditis - pleuritic chest pain, relieved by leaning forward

fast AF

§ rapid ventricular response § narrow QRS - less than 3 small squares § if problem in ventricle - get broader complex **slow stable AF - where block AV node e.g. with digoxin. slower rate.

Critical limb ischaemia

§ rest pain requiring opioid analgesia >2 weeks, or tissue loss § in night- might have legs hanging of side § forefoot/ties § gangrene/ulceration § 90% intervention within 1 year; 25% major amputation; 50% dead within 5 years

Acute management of heart failure

§ resuscitate as required e.g. sit upright, O2, diamorphine, GTN § treat precipitating cause if relevant e.g. infection, arrhythmias, MI, anaemia § fluid overload: fluid restriction and loop diuretics (furosemide)

What are the three conditions in ACS

§ unstable angina may also have ECG changes

Define Wolff-Parkinson-White Syndrome

● A congenital abnormality which can result in supraventricular tachycardias that use an accessory pathway (bundle of kent). It is a pre-excitation syndrome. ● Pre-excitation syndrome: early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway.

Recognise the signs of SVT on physical examination

● AVNRT - normal except tachycardia ● Wolff-Parkinson-White o Tachycardia o Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)

Explain the aetiology and risk factors of aortic regurgitation

● Aortic valve leaflet abnormalities or damage: o Bicuspid aortic valve o Infective endocarditis o Rheumatic fever o Trauma o Age ● Aortic root/ascending aorta dilatation: o Systemic hypertension o Aortic dissection o Aortitis o Arthritides (e.g. rheumatoid arthritis, seronegative arthritides) o Connective tissue disease (e.g. Marfan's, Ehlers-Danlos) o Pseudoxanthoma elasticum, Osteogenesis imperfecta ● Pathophysiology o The abnormal backflow of blood leads to pathologic changes - left ventricular chamber enlargement and hypertrophy takes place to maintain a normal CO.

Explain the aetiology/risk factors of mitral regurgitation

● Broadly speaking, it is caused by mitral valve damage or dysfunction, which, in turn could be caused by any of the following: o Rheumatic heart disease (MOST COMMON) o Infective endocarditis o Mitral valve prolapse o Papillary muscle rupture or dysfunction (secondary to IHD or cardiomyopathy) o Chordal rupture and floppy mitral valve associated with connective tissue disease (e.g. Ehlers-Danlos syndrome, Marfan's syndrome) o Functional: LV dilatation o Annular calcification (elderly) o Congenital o Cardiomyopathy o Appetite suppressants e.g. fenfluramine

Identify appropriate investigations for cardiomyopathy

● CXR o May show cardiomegaly o May show signs of heart failure - pulmonary oedema ● ECG o All Types ● Non-specific ST changes ● Conduction defects ● Arrhythmias o Hypertrophic ● Left-axis deviation ● Signs of left ventricular hypertrophy ● Q waves in inferior and lateral leads o Restrictive ● Low voltage complexes ● Echocardiography o Dilated ● Dilated ventricles with global hypokinesia and low ejection fraction ● MR, TR, LV thrombus o Hypertrophic ● Ventricular hypertrophy (asymmetrical septal hypertrophy) o Restrictive ● Non-dilated non-hypertrophied ventricles ● Atrial enlargement ● Preserved systolic function ● Diastolic dysfunction ● Granular or sparkling appearance of myocardium in amyloidosis ● Cardiac Catheterisation ● Endomyocardial Biopsy ● Pedigree or Genetic Analysis

Define constrictive pericarditis

● Chronic inflammation of the pericardium with thickening and scarring of the pericardial layers. It limits the ability of the heart to function normally, as it is encased in a rigid pericardium

Summarise the epidemiology of rheumatic fever

● Common in developing countries but increasingly rare in the West ● Peak incidence between 5 and 15 years ● Mean incidence 19/100,000

Identify the possible complications of dyslipidaemia and its management

● Coronary artery disease --> MI, ischaemic cardiomyopathy, sudden cardiac death ● Stroke (ischaemic) ● Peripheral vascular disease --> erectile dysfunction, claudication, and acute limb ischaemia. ● Very high levels of TGs can cause PANCREATITIS ● Statin toxicity

Explain the aetiology/risk factors of DVT

● Deep veins in the legs are more prone to blood stasis, hence clots are more likely to form (Virchow's triad) ● Risk Factors o Age o COCP (synthetic oestrogen) o Post-surgery o Prolonged immobility - ASK ABOUT TRAVEL o Obesity o Pregnancy o Dehydration o Smoking o Polycythaemia o Thrombophilia (e.g. protein C deficiency) o Malignancy o Trauma o Past DVT

Summarise the prognosis for patients with SVT

● Dependent on the presence of underlying structural heart disease ● If structurally normal heart - GOOD PROGNOSIS ● People with pre-excitation have a small risk of sudden death

Identify appropriate investigations for varicose veins

● Duplex Ultrasound o Locates sites of incompetence or reflux o Allows exclusion of DVT

Identify appropriate investigations for mitral stenosis

● ECG o May be NORMAL o May see p mitrale (broad bifid p wave caused by left atrial hypertrophy) if in sinus rhythm o May see AF o Evidence of right ventricular hypertrophy may be seen if there is severe pulmonary hypertension ● CXR o Left atrial enlargement - double shadow in right cardiac silhouette o Cardiac enlargement o Pulmonary congestion/oedema o Mitral valve calcification (occurs in rheumatic cases) o Kerley B lines ● Echocardiography - **diagnostic** o Assesses functional and structural impairments o Transoesophageal echocardiogram (TOE) gives a better view ● Cardiac Catheterisation o Measures severity of heart failure

Identify appropriate investigations for dyslipidaemia

● FBC: serum lipid profile - measured total cholesterol, TG, HDL cholesterol, calculated LDL cholesterol and VLDL ● Fundoscopy ● Tests for secondary causes of dyslipidaemia: fasting glucose, HbA1c, liver enzymes, creatinine, TSH, urinary protein ● Screening involves fasting lipid profile - screen all those at risk of hyperlipidaemia or of CVD.

Summarise the epidemiology of ventricular tachycardia

● Fairly common ● It is one of the shockable rhythms that is seen in cardiac arrest patients ● VT incidence peaks in the middle decades of life

Summarise the epidemiology of pulmonary hypertension

● Idiopathic pulmonary hypertension is RARE ● More common in severe respiratory and cardiac disease

Summarise the epidemiology of mitral stenosis

● Incidence is declining because rheumatic fever is becoming more and more rare

Recognise the signs of atrial fibrillation on physical examination

● Irregularly irregular pulse ● Difference in apical beat and radial pulse - apical is greater than radial ● 1st heart sound is of variable intensity ● signs of LVF Check for signs of thyroid disease and valvular disease

Identify the possible complications of cardiac arrest AND prognosis

● Irreversible hypoxic brain damage ● Death **Summarise the prognosis for patients with cardiac arrest: ● Resuscitation is less successful if cardiac arrest happens outside the hospital ● Increased duration of inadequate effective cardiac output --> poor prognosis

Identify the possible complications of CABG

● MI ● Bleeding ● Chest infection ● Lung complications ● Stroke

Recognise the presenting symptoms of cardiac arrest

● Management precedes or is concurrent to history ● Cardiac arrest is usually sudden but some symptoms that may be preceded by fatigue, fainting, blackouts, dizziness § also chest pain or dyspnoea.

Recognise the signs of arterial ulcers on physical examination

● Night pain ● Punched-out appearance ● Hairlessness ● Pale skin ● Absent pulses ● Nail dystrophy ● Wasting of calf muscles

Identify possible complications of DVT

● PE ● Venous infarction (phlegmasia cerulea dolens) ● Thrombophlebitis (results from recurrent DVT) ● Chronic venous insufficiency

Recognise the presenting symptoms of ventricular tachycardia

● Symptoms of ischaemic heart disease or haemodynamic compromise due to poor perfusion ● Symptoms: o Chest pain o Palpitations o Dyspnoea o Syncope

Identify the possible complications of atrial fibrillation

● THROMBOEMBOLISM o Embolic stroke risk of 4% per year o Risk is increased with left atrial enlargement or left ventricular dysfunction ● Worsening of existing heart failure

Explain the aetiology/risk factors of cardiomyopathy

● The majority are IDIOPATHIC ● Dilated Cardiomyopathy o Post-viral myocarditis o Alcohol o Drugs (e.g. doxorubicin, cocaine) o Familial o Thyrotoxicosis o Haemochromatosis o Peripartum or postpartum o Hypertension o Autoimmune o Congenital (x linked) ● Hypertrophic Cardiomyopathy o Up to 50% are genetic - autosomal dominant ● Restrictive Cardiomyopathy o Amyloidosis o Sarcoidosis o Haemochromatosis o Scleroderma o Loffler's eosinophilic endocarditis o Endomyocardial fibrosis

Summarise the epidemiology of infective endocarditis

● UK Incidence: 16-22/1 million per year

Generate a management plan for venous ulcers

● elevation, correct malnutrition ● Graduated compression (reduced venous stasis) - compression bandages; elastic stockings o NOTE: must exclude diabetes, neuropathy and PVD before this is attempted ● Debridement and cleaning ● Antibiotics - if infected ● Topical steroids - may help with surrounding dermatitis

Medical management of stable angina

**Medication: § all patients should receive ASPIRIN and a STATIN in the absence of any contraindication § sublingual glyceryl trinitrate (GTN) to abort angina attacks § NICE recommend using either a BETA-BLOCKER OR a CCB (calcium channel blocker) first-line based on 'comorbidities, contraindications and the person's preference' § if a calcium channel blocker is used as monotherapy a rate-limiting one such as verapamil or diltiazem should be used. If used in combination with a beta-blocker then use a long-acting dihydropyridine calcium-channel blocker (e.g. modified-release nifedipine). Remember that beta-blockers should NOT be prescribed concurrently with verapamil (risk of complete heart block) § if there is a poor response to initial treatment then medication should be increased to the maximum tolerated dose (e.g. for atenolol 100mg od) § if a patient is still symptomatic after monotherapy with a beta-blocker ADD a calcium channel blocker and vice versa § if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider one of the following drugs: a long-acting nitrate: ivabradine, nicorandil or ranolazine § if a patient is taking both a beta-blocker and a calcium-channel blocker then only add a third drug whilst a patient is awaiting assessment for PCI or CABG **Nitrate tolerance: § many patients who take nitrates develop tolerance and experience reduced efficacy § NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 HOURS to minimise the development of nitrate tolerance § this effect is not seen in patients who take once-daily modified-release isosorbide mononitrate

Explaining benefits and problems of hypertension medications. Summary of antihypertensive drug treatment.

**benefit = reduce risk of MI and stroke **problem - pt don't feel this benefit until is too late. Only thing they notice is side-effects. § HOT study - if achieved DBP of 100 (minor control) - 6% reduction in risk of MI; target DBP of 80-85 reduced risk to 25-30% so should aim here § UKPDS - tight vs less tight control in people with diabetes. Tight control worked v well § metaanalysis of 354 trails- using 3 drugs at 1/2 standard dose gave better control than one drug at full dose - possibly due to less tolerance and less SEs. § SPRINT study - should pt w/ heart disease we add extra thiazide diuretic to get from 140/80 to 120/80? - giving extra diuretic treatment reduces risk of MI by 2 events and risk of death. SO in patient w/ heart disease need aggressive treatment of BP. **CCBs - can worsen peripheral oedema **

Intermittent claudication vs critical limb ischaemia vs acute limb ischaemia

**intermittent claudication management: ABPI, exercise, antiplatelets + statins **acute limb ischaemia typically from thrombosis from atherosclerotic plaque

Features of Boerhaave's perforation

**note that this is very rare, but it is associated with a high mortality and hence is included. 1) History of sudden-onset severe chest pain immediately following an episode of VOMITING. Shortness of breath and pleuritic pain may develop shortly afterwards due to subsequent pleurisy and effusion. 2) Signs of a pleural effusion after some hours - dullness to percussion, absent breath sounds, decreased vocal resonance. 3) Subcutaneous emphysema is present in a minority of cases. 4) Abdominal rigidity, sweating, fever, tachycardia, and hypotension may be present as the illness progresses but are non-specific.

STEMI management

*done immediate A to E and MONA already. § Additional beta-blockade -5-10mg reduces infarct size and mortality -Caution in COPD/ Asthma § Reperfusion by PPCI-angiography with stenting/ balloon angioplasty •Door to balloon in 2 HOURS ideally! Can be done within 12 hours of onset. Heparin/ fondaparinux given during PCI § Consider thrombolysis if PCI cannot occur within 2h and if presented within 12 hours of onset of symptoms -Unless contraindicated (e.g. if bleeding) § Assessment of LV function whilst admitted (Echo)

CTPA PE

- if the CTPA is positive then a PE is diagnosed - if the CTPA is negative then consider a proximal leg vein ultrasound scan if DVT is suspected **ECG: § the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - 'S1Q3T3'. However, this change is seen in no more than 20% of patients § right bundle branch block and right axis deviation are also associated with PE § sinus tachycardia may also be seen *Chest x-ray: § a chest x-ray is recommended for all patients to exclude other pathology § however, it is typically normal in PE § possible findings include a wedge-shaped opacification

ECG findings in wolff-parkinson-white syndrome

-shortened PR interval -slurred and broad upstroke of the QRS complex (delta wave) -QRS interval widening

An 85-year-old woman was referred by her GP to the Acute Medical Unit having collapsed in her kitchen the night before. She was found by her daughter who described her as confused and disorientated. She has a past medical history of type 2 diabetes mellitus, hypertension, ischaemic heart disease and depression. On examination, she appeared frail, weight 45kg and dehydrated with an AMT of 6/10. Her temp was 37.8°C, BP 95/65 mmHg, RR 22 and HR 80bpm. Her heart sounds were normal and she had left sided crackles. Investigations revealed the following: Creatinine baseline was 60 approx. 1 month ago. Hb 103 WCC 15.5 Plt 205 Neut 14 Na+ 125 K+ 4.8 Ur 15 Cr 195 CK 64 Glucose6.2 1) Using the Cockcroft-Gault Equation, what is her calculated Glomerular Filtration Rate (GFR)? Cockcroft Gault Equation: (((140 - age in years) x (wt in kg)) x 1.23) / (serum creatinine in micromol/l) 2) Three days later, patient's renal function had stabilised, her sodium levels had returned to normal, however her BP was consistently raised at approximately 170/100 mmHg. Which one of the following agents would be the most suitable as a first line antihypertensive treatment for this patient? 3) The most appropriate treatment was started but three days later her BP was still consistently high. Which of the following antihypertensive agents would you recommend as the most suitable additional treatment?

1) 15.6mls/min. Often, the eGFR when automatically calculated, is not correct and can either over or underestimate the actual renal function. This equation provides a method of calculating it more accurately. If you need help in a clinical setting, pharmacists are well placed to help. 2) Ramipril. § According to the British Hypertension Society (BHS) Guidelines (www.bhsoc.org), the recommended first line treatment of hypertension for an adult over 55years would be a calcium-channel blocker or a thiazide diuretic. § However, this patient is a type-2 diabetic, therefore the most appropriate choice in this case would be an ACE inhibitor. This choice is based on the MICRO-HOPE Study (a substudy of the HOPE Study). § As diabetes mellitus is a strong risk factor for cardiovascular and renal disease the MICRO-HOPE Study investigated whether ramipril can lower these risks in patients with diabetes. The study was stopped 6 months early (after 4.5 years) by the independent data safety and monitoring board because of a consistent benefit of ramipril compared with placebo. § Ramipril lowered the risk of myocardial infarction by 22%, stroke by 33%, cardiovascular death by 37%, total mortality by 24%, revascularisation by 17%, and overt nephropathy by 24%. § Overall, this trial found that ramipril provides a vasculoprotective and renoprotective effect for people with diabetes and should be the first line treatment choice in this population (provided that there are no contraindications to an ACE inhibitor). 3) Amlodipine. § In accordance with the BHS guidelines, diabetic patients aged over 55 years should be treated first line with an ACE inhibitor and second line with a calcium-channel blocker. § Amlodipine is the common drug of choice. § Even though the BHS also suggest a thiazide diuretic in patients over 55 years, they have been associated with HYPOGLYCAEMIA and therefore are not generally recommended in the diabetic population. § Beta-blockers have been found to MASK the symptoms of hypoglycaemia in diabetic patients. § Alpha blockers are usually used LAST LINE when all other classes of antihypertensive have been prescribed and the patient is still not adequately controlled.

A 46-year-old male presents to the ED with an hour sudden onset of severe central chest pain radiating to his back. He is a heavy smoker, 200cm tall, has hypermobile joints and scoliosis. He has a family history of hypertension and sudden death. On examination, he is cold peripherally and sweating profusely with a core body temperature 36.1 ◦C. His BP is 192/110 mmHg and oxygen saturations 94% on air. His JVP is not elevated and he has an early diastolic murmur. 1) Which one of the following is the most likely acute diagnosis? 2) Which four observations / investigations are urgently required? 3) What are the two most appropriate further investigations? 4) What is the one most likely predisposing condition? 5) Which three initial treatments are urgently required?

1) Acute thoracic aortic dissection causes a sudden onset of severe 'shearing' chest pain often radiating to the back. Ischaemic chest is usually gradual in onset. Dissection can be complicated by acute aortic regurgitation (hence the early diastolic murmur), pleural effusion and sometimes myocardial infarction. Patients are often initially hypertensive but this can rapidly deteriorate to shock due to haemorrhage. 2) ECG, Chest X-ray, FBC and U&Es, BP measurement in both arms. Urgent tests in unstable patients should rapidly assist in confirming/refuting a life threatening diagnosis based on history and clinical presentation; they will also aid management. Cardiac troponin is usually only significantly elevated 12 hours after a myocardial infarct, so would not be appropriate when the pain started only an hour ago. A systolic BP change of greater than 20mmHg systolic in both arms is significant. 3) Echocardiography and CT chest with aortogram - The CT will give a very good view of the aorta and the possibility of dissection in the acute situation. (Some centres use MRI for the long-term follow-up of patients at risk from aortic dissection, examining the arch and distal aorta as well.) The echo will help establish the presence of aortic regurgitation, the state of the aortic valve and ring, and the development of a pericardial effusion as well as noting LV hypertophy and function. 4) Marfans syndrome - This gentleman has a Marfanoid body habitus. This has an autosomal dominant pattern of inheritance so a family history of sudden death should raise suspicion. Aortic dissection is a potentially deadly complication of this connective tissue disease 5) IV morphine and antiemetic, IV antihypertensive agents and oxygen. In this patient the most important initial treatment should be analgesia, oxygen and IV antihypertensive agents to reduce blood pressure to a safe and narrow range around 110/70 mmHg. When stabilised a CT chest is the gold standard to confirm diagnosis. Proximal or type A dissections (proximal respond best to cardiothoracic surgical intervention), type B tend to be managed more conservatively, but blood pressure control and monitoring remains crucial.

What are some must exclude diagnosis of chest pain?

1) Aortic dissection? Mr Shepherd's pain was not tearing and did not radiate to his back. His pulse and blood pressure were equal in both arms and chest radiography did not suggest a wide mediastinum. Ultimately, the way to rule out aortic dissection if you strongly suspect it is to do CT angiography of the chest or transoesophageal echo, looking for a false lumen. 2) Pneumothorax? Mr Shepherd did not have areas of the chest that were expanded and hyper-resonant, with decreased air entry. His trachea was not displaced and his chest radiograph is normal. 3) PE? Remember that this is a diagnosis of exclusion, so you have not strictly speaking ruled it out. However, the normal oxygen saturations (98% on room air), the ST depression on ECG, and the large rise in troponin make this unlikely (a small rise in troponin may be seen in PE). A D-dimer level was not requested but may in any case have been raised as a result of his infarction. 4) Boerhaave's perforation of the oesophagus? Mr Shepherd did not give a history of vomiting before the onset of his pain. A perforated oesophagus is a very rare diagnosis and even less likely without previous vomiting. Ultimately, the way to rule it out if you strongly suspect it is to perform a chest radiograph after swallowing a water-soluble contrast agent such as GASTROGRAFFIN.

A 75-year-old male patient with known coronary artery disease, is referred by his General Practitioner with increasing frequency of chest pains for the past 2 weeks. Eight years previously he suffered an acute anterior myocardial infarction for which he was thrombolysed. Coronary angiogram at the time demonstrated a 90% stenosis of the LAD artery and he underwent percutaneous coronary intervention. He is an ex-smoker. No other relevant past medical history. His medications are as follows: Aspirin 75mg OD Atenolol 25mg BD Ramipril 5mg BD Simvastatin 40mg OD Glyceryl tri-nitrate (GTN) spray PRN He has had occasional exertional angina for the past year, but this had become frequent in the past two weeks although they generally lasted less than 20 minutes. He had had episodes at rest today although these were relieved with sublingual GTN spray. On examination, the pulse was slow rising, 80bpm and regular, blood pressure 100/80 mmHg and respiratory rate 16/min. The apex beat was non-displaced, but heaving. Heart sounds demonstrated a grade 2 ejection systolic murmur at the right sternal edge which radiated to the neck. The lungs were clear. 1) Which is the most likely explanation for the heart murmur? 2) Which 2 of the following are the most likely causes of his chest pain? 3) What 4 of the following investigations would you request in the ED? 4) Which 2 further investigations would be most appropriate?

1) Aortic stenosis - Many cardinal features of aortic stenosis are present in this patient with a slow rising pulse, narrow pulse pressure and ejection systolic murmur radiating to the neck. Mitral regurgitation typically produces a pansystolic murmur, which does not radiate to the neck. 2) Unstable angina secondary to coronary artery disease, Angina secondary to aortic stenosis. The patient has known cardiac disease and a classical history of unstable angina. His pain is short lived and relieved by GTN spray which suggests unstable angina rather than a myocardial infarction although troponin levels would have to be performed to exclude infarction. Given that clinical examination reveals likely significant aortic stenosis, the angina could also be caused (or exacerbated) by this. 3) ECG, FBC, troponin, chest X-ray. ECG will be important to rule out other cardiac causes of chest pain. Baseline bloods will be required for this patient, including troponin levels to rule out myocardial infarction. CXR is needed to assess the size of the heart and the lung fields (indicating heart failure) 5) Coronary angiogram, Cardiac echocardiography. Cardiac echocardiography is important to characterize the aortic stenosis. Coronary angiogram to identify any significant coronary occlusions.

What surgical options are there for treating varicose veins?

1) Avulsion/phlebectomy: small incisions are made along the varicose vein and it is then pulled out with forceps. 2) Stripping: small incisions are made at the ends of the varicose vein and an endoluminal hook and wire is used to pull the vein out. 3) Injection sclerotherapy: this involves sealing the vein from within by injecting an irritant sclerosant. Unfortunately, the procedure is associated with skin discoloration in about 10% of patients and a 30% risk of recurrence if there is valvular incompetence, and is thus being used less often. A variant of injection sclerotherapy involves injecting a foam that blocks the vein, but there is a (small) risk of the foam embolizing into the venous system 4) Radiofrequency ablation: an endoluminal catheter is inserted into the long saphenous or short saphenous vein and a tip used to deliver high-energy radio waves (VNUS) that seal the vein from within. A similar procedure involves using a laser (EVLT) rather than radiowaves to achieve the same eff ect.

Identify appropriate investigations for aortic dissection

1) Bloods o FBC o X-match 10 units of blood o U&E - check renal function o Clotting screen 2) CXR o Widened mediastinum 3) ECG o Often NORMAL o If the ostia of the right coronary artery is compromised you may get signs of: ● Left ventricular hypertrophy ● Inferior MI 4) CT angioThorax o Shows FALSE lumen - good for stable pts 5) Echocardiography o good for unstable pts who are too risky to take to CT o TransOESEPHAGEAL echo allows visualisation of aorta and position of dissection

Identify appropriate investigations for hypertension

1) Bloods: o U&Es is KEY (potassium might be low in conns/cushings/phaeo, renal function might be affected) o FBC (polycythaemia) o Glucose - risk of diabetes o Lipid panel - RF o Check renin, aldosterone (Conns - increased aldosterone and low renin) and 24 hour urine for catecholeamines (phaeochromocytoma) o if high renin, high aldosterone and everything else normal - renal artery stenosis / essential HTN o Excluding other secondary causes: potassium low in Conn's, calcium high in hyperparathyroidism o fasting metabolic panel with eGFR 2) Urine Dipstick o Blood and protein (e.g. if glomerulonephritis or renal disease causing HTN) 3) ECG o May show signs of left ventricular hypertrophy (deep S wave in V2 and tall R wave in V5) or ischaemia 4) Ambulatory blood pressure monitoring o Excludes white coat hypertension 5) Other investigations may be performed if a secondary cause of the hypertension is suspected (e.g. renal angiogram, urinary free cortisol, renin, aldosterone, MR aorta)

How is acute coronary syndrome classified?

1) ST-elevation myocardial infarction (STEMI): ST-segment elevation + elevated biomarkers of myocardial damage 2) non ST-elevation myocardial infarction (NSTEMI): ECG changes but no ST-segment elevation + elevated biomarkers of myocardial damage 3) unstable angina. **The management of ACS depends on the particular subtype. NICE management guidance groups the patients into two groups: 1. STEMI 2. NSTEM/unstable angina ***Common management of all patients with ACS: 1) Initial drug therapy (MONA): § aspirin 300mg § oxygen should only be given if the patient has oxygen saturations < 94% in keeping with British Thoracic Society oxygen therapy guidelines § morphine should only be given for patients with severe pain, previously IV morphine was given routinely, evidence, however, suggests that this may be associated with adverse outcomes § nitrates: can be given either sublingually or intravenously; useful if the patient has ongoing chest or hypertension; should be used in caution if patient hypotensive. **The next step in managing a patient with suspected ACS is to determine whether they meet the ECG criteria for STEMI. It is, of course, important to recognise that these should be interpreted in the context of the clinical history.S TEMI criteria clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:: § 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years § 1.5 mm ST elevation in V2-3 in women § 1 mm ST elevation in other leads § new LBBB (LBBB should be considered new unless there is evidence otherwise)

During continuous ECG recording, the patient is given a rapid intravenous bolus of Adenosine which causes immediate cessation of the tachycardia. A repeat 12-lead ECG is performed (shown below). Apart from the ST segment depression, what other abnormalities can you identify? 2) What is the most likely unifying diagnosis? 3) What two further investigations should be organised?

1) Broad QRS complex, Short PR interval, Slurred upstroke to QRS complex. Short PR interval (pre-excitation), slurred upstroke to QRS (delta wave) and broad QRS are present on the ECG. 2) Wolff-Parkinson-White syndrome. The combination of preexcitation on the ECG and paroxysmal narrow complex tachycardia (AVRT) is known as the Wolff-Parkinson-White Syndrome. It is due to the presence of an accessory pathway that links the atria and the ventricles electrically. It is more common for this to be left sided (i.e. between the left atrium and left ventricle) than right sided. It is important not only because it causes symptoms from the AVRT but also because if the patient develops atrial fibrillation, this can be conducted very rapidly down the accessory pathway which may lead to ventricular fibrillation and sudden death (as was the case with patient's younger brother). It is therefore very important that all patients that have preexcitation identified on an ECG are referred to a cardiologist (preferably an electrophysiologist) who can assess whether the pathway is potentially dangerous and if necessary ablate the pathway thereby curing the patient of the syndrome. Hyperkalaemia is associated with tall, tented T waves, widened QRS complex, absent P waves and a 'sine wave' appearance. Torsade de pointes is a form of ventricular tachycardia with a varying access due to an raised QT interval. 3) Echocardiography and thyroid function. It is important to perform a full set of blood tests but thyroid is most important even in the presence of Wolf-Parkinson-White syndrome (WPW=delta wave on ECG + palpitations). In WPW there are rare associated structural abnormalities such as ventricular hypertrophy and also Ebsteins' anomaly which is an offset tricuspid valve. It is more commonly performed to ensure left ventricular function is normal and forms part of the routine investigation for any patient with a diagnosed arrhythmia. An exercise test is not required routinely and neither is coronary angiography as there is no evidence from the history of ischaemia. If a troponin was performed, it could be raised secondary to the arrhythmia rather than any ischaemia, so has to be interpreted with caution. The 24 hr tape is again not required as we have the diagnosis and documented tachycardia already.

Approach to broad-complex tachycardia vs narrow-complex

1) Broad-complex tachycardia: a) Regular: § assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block) § loading dose of amiodarone followed by 24 hour infusion b) Irregular: 1. AF with bundle branch block - treat as for narrow complex tachycardia 2. Polymorphic VT (e.g. Torsade de pointes) - IV magnesium 2) Narrow-complex tachycardia: a) Regular: § vagal manoeuvres followed by IV adenosine § if above unsuccessful consider diagnosis of atrial flutter and control rate (e.g. Beta-blockers) b) Irregular: § probable atrial fibrillation § if onset < 48 hr consider electrical or chemical cardioversion § rate control (e.g. Beta-blocker or digoxin) and anticoagulation

A 45-year-old male with a history of hypertension arrives in the ED complaining of severe central chest pain. He tells you it started 1 hour ago whilst running at the gym. While you are taking the history the patient becomes unresponsive and has agonal respirations. You open the airway and check for signs of life but cannot feel a central pulse. 1) What are your two immediate actions?

1) Call for help, Start CPR. In this situation, the most important first step is commencing basic life support and summoning help in order to proceed to advanced life support.

Mrs Rawlings is a patient on the vascular ward. She suffers from long standing leg ulcers and is in hospital with an infection in them. She has had a surgical debridement and evaluation and has been sent back to the ward. She is maintained on the following regime: § Paracetamol 1G QDS § Morphine sulphate S/R tablets (MST) 15mg BD § Dihydrocodeine 30mg QDS § Morphine sulphate solution 10mg/5ml (oramorph) § Her requirement for PRN oramorph is as follows: o 10mg BD for 2 days o Then 10mg TDS for two days o Now 10mg 6x day 1) She is clearly still in pain. What are your two options to control this? 2) What dose of PRN morphine does this patient need?

1) Change opiate to fentanyl patches 25micrograms, increase regular MST doses. § Cumulatively, her dose is 90mg per day. § There are a few options, either you can increase regular opiate (in this case MST) to 45mg BD or else you could initiate a patch of fentanyl. § 25microgram patches are equivalent to 90mg of morphine. § 100microgram patches are equivalent to 360mg of morphine which would be a massive overdose for this patient. § Differing opiates will have different potencies and effects so 25microgram/hr fentanyl dose may be enough to control pain even though it represents a slight decrease in dose. 2) The PRN usage should always be 1/6th of the daily intake. For example, if this lady is using 90mg of morphine (equivalent daily) then her breakthrough regime is 15mg oramorph every 4 hours PRN. 15mg every 4 hours

Several congenital mutations, acquired diseases, and drugs can all make a patient's blood more likely to clot. Can you name them?

1) Congenital mutations • Factor V Leiden mutation (5% of Caucasians) • Prothrombin G20210A mutation (2% of Caucasians) • Antithrombin III deficiency (0.4% of Caucasians) • Protein C deficiency (0.5% of Caucasians) • Protein S deficiency (0.5% of Caucasians) 2) Diseases • Any form of malignancy • Antiphospholipid syndrome • Disseminated intravascular coagulation • Polycythaemia 3) Drugs: • Combined oral contraceptive pill • Hormone replacement therapy • Heparin-induced thrombocytopaenia (HIT), which can counterintuitively cause thrombosis by an unknown mechanism but which can fortunately be prevented by using LMWH instead of full-length heparin • Procoagulant drugs (e.g. for nosebleeds or menorrhagia), such as tranexamic acid or aprotinin

Generate a management plan for hypertension

1) Conservative: o Stop smoking o Lose weight o Reduce alcohol intake o Reduce dietary sodium o Intensive lifestyle modification 2) Investigate for secondary causes (mainly in young patients) 3) Medical - treatment recommended if systolic > 160 mm Hg and/or diastolic > 100 mm Hg, or if evidence of end-organ damage. Multiple drug therapies often needed. A) ACE Inhibitors or Angiotensin Receptor Blockers - first line if: ● < 55 yrs ● Diabetic ● Heart failure ● Left ventricular dysfunction B) CCBs - first line if: e.g. amlodipine ● > 55 yrs ● Black ● NOTE: thiazide diuretics can be used if CCBs are not tolerated C) Beta-Blockers ● Not preferred initial therapy ● May be considered in younger patients ● CAUTION: combining with thiazide diuretic may increase risk of developing diabetes ● May increase risk of heart failure D) Alpha-Blockers ● 4th line ● May be used in patients with prostate disease 4) Target BP: o <80: aim for 135/85 o >80: aim for 145/85 5) Severe Hypertension Management (Diastolic > 140 mm Hg) o Atenolol o Nifedipine 6) Acute Malignant Hypertension Management: o IV beta-blocker (e.g. esmolol) o Labetolol o Hydralazine sodium nitroprusside o CAUTION: avoid rapid lowering of blood pressure because it can cause cerebral infarction ● This is because the autoregulatory mechanisms within the brain for regulating blood flow will cause vasoconstriction of the vessels in the brain when blood pressure is very high ● Lowering the blood pressure too rapidly would mean that the autoregulatory mechanisms do not adapt to the drop in blood pressure and so the vessels remain constricted ● A rapid drop in blood pressure with constricted vessels will cause an infarction **Use ACEi in patients with diabetes who have microalbuminuria. Aggressive management of BP and lipids improves survival - hence also give aspirin and statin to reduce risk of MI

What are the main contraindications and side-effects of warfarin therapy? What advice would you give a patient starting on warfarin?

1) Contraindications: • Pregnancy (warfarin is teratogenic) • Severe hypertension (risk of haemorrhagic stroke) • Peptic ulcer disease (risk of bleeding ulcer) 2) Side-effects: • Haemorrhage • Nausea, vomiting, diarrhoea, rash (like most drugs!) • Purple toes and skin necrosis • Hepatic dysfunction, jaundice • Pancreatitis 3) Advice for patients • Avoid alcohol, cranberry juice, and St John's wort • Check with GP before taking any other medication • Consult GP if faeces or urine go dark or bloody

A 74-year-old lady is referred to the medical assessment unit by her GP with a 3-week history of a tender, red, swollen right calf. She underwent a right total hip replacement 3 weeks ago. 1) What important diagnosis is the GP wanting you to exclude? 2) Which two of the following are differential diagnoses?

1) Deep vein thrombosis. The GP will be most concerned about a deep vein thrombosis. Lower limb surgery is a risk factor for thromboembolic disease. An undiagnosed deep vein thrombosis could progress to a pulmonary embolism, which could be fatal. 2) Post-operative leg oedema, Cellulitis of the right leg. A dislocated hip would be very painful and usually present with a short, externally rotated leg rather than calf swelling and redness. Post operative swelling is common following a total hip replacement. It should settle over time but may not completely resolve. Congestive cardiac failure would usually cause bilateral leg swelling. A cellulitic leg would also be swollen, red and tender.

Identify appropriate investigations for aortic stenosis

1) ECG o P mitrale (left atrial enlargement) o Signs of left ventricular hypertrophy ● Deep S in V1/2 ● Tall R in V5/6 ● Inverted T waves in I, aVL and V5/6 ● Left axis deviation o LBBB or complete AV block 2) CXR o Post-stenotic enlargement of ascending aorta o Calcification of aortic valve o LVH 3) Echocardiogram - o Visualises structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar) o Estimation of aortic valve area and pressure gradient across the valve in systole o Assess left ventricular function 4) Doppler echo **DIAGNOSTIC**: can estimate gradient across valves § Severe stenosis if gradient >/= 50mmHg and valve area <1cm^2 § If aortic jet velocity >4m/s risk of complications is increased. 5) Cardiac angiography o Allows differentiation from other causes of angina (e.g. MI) o Helps assess valve gradient, LV function and coronary artery disease o Allows assessment of concomitant coronary artery disease ● NOTE: 50% of patients with severe aortic stenosis have significant coronary artery disease

Identify appropriate investigations for atrial fibrillation

1) ECG (gold standard) O Can do 24 hours if paroxysmal o Uneven baseline with absent p waves o Irregular intervals between QRS complexes o Atrial flutter = narrow complex tachycardia, saw-tooth pattern flutter waves, loss of isoelectric baseline 2) Bloods o Cardiac enzymes o TFT o Lipid profile o U&Es, Mg2+ and Ca2+ ● Because there is increased risk of digoxin toxicity with hypokalaemia, hypomagnesaemia and hypercalcaemia 3) Echocardiogram o May show: ● Mitral valve disease ● Left atrial dilatation ● Left ventricular dysfunction ● Structural abnormalities

You are a surgical FY1. Mrs Jones is 70-year-old lady and attended for elective EVAR (endovascular aortic repair) surgery to repair an abdominal aortic aneurysm. 1) Mrs Jones returns to the ward post-op and the nurse bleeps you, concerned that Mrs Jones is experiencing 'chest pain'. You are five minutes away. What two things will you ask the nurses to do whilst you are on your way?

1) ECG, Blood pressure/ heart rate. § When you receive a call, do not be afraid to ask the nurses to do simple tests whilst you are on your way, this is an efficient use of time. When you arrive to the ward, carry out your ABCDE assessment of the patient and contact the cardiology team if you are concerned about the ECG.

Different murmurs

1) Ejection systolic: § aortic stenosis § pulmonary stenosis, hypertrophic obstructive cardiomyopathy § atrial septal defect, tetralogy of Fallot 2) Holosystolic (pansystolic) § mitral/tricuspid regurgitation (high-pitched and 'blowing' in character) § ventricular septal defect ('harsh' in character) 3) Late systolic § mitral valve prolapse § coarctation of aorta 4) Early diastolic § aortic regurgitation (high-pitched and 'blowing' in character) § Graham-Steel murmur (pulmonary regurgitation, again high-pitched and 'blowing' in character) 5) Mid-late diastolic § mitral stenosis ('rumbling' in character) § Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character) 6) Continuous machine-like murmur § patent ductus arteriosus

You find that he localizes the chest pain to his sternum. He says it came on 2 hours earlier in the afternoon as he was gardening and has been there since. He describes it as like 'wearing a shirt two sizes too small' and says it has not moved since it came on. The pain was not exacerbated by breathing, and was not position dependent. He does not have a cough but his pain improved minutes after he was given a glyceryl trinitrate (GTN) spray sublingually in the ambulance, going from 8/10 severity to 3/10 now. He is a smoker with a 40-pack-year history, has hypertension that is managed with a calcium-channel blocker and hypercholesterolaemia for which he takes a statin. His father died of stroke in his 70s and his mother of 'old age' in her late 80s. He is not known to be diabetic. On examination, Mr Shepherd appears relatively comfortable (on pain relief), with arcus but no other peripheral signs of cardiovascular disease. His pulse and blood pressure are taken in both arms and found to be equally regular, 84 bpm and 145/90 mmHg. His oxygen saturation is 98% on room air. Both heart sounds are audible with no added sounds and palpation of the chest does not bring on pain. Carotid bruits can be heard bilaterally on auscultation. His lungs have normal resonance to percussion, good air entry, and no abnormal sounds on auscultation. His trachea is central. His limbs show no signs of inflammation and he is not febrile. In light of Mr Shepherd's history, risk factors, and examination, a certain diagnosis for his chest pain appears increasingly likely. What investigations would you like to request? Think particularly of how you can confirm your expected diagnosis and how you can rule out the 'must exclude' diagnoses listed above.

1) Electrocardiogram (ECG): § Perform ECGs on anyone with suspected cardiac disease, either TWO ECGs 30 minutes apart or, if the patient has continuing chest pain, every 10-15 minutes until the diagnosis is made. § If the patient is admitted, ECGs should be performed daily for 3 days thereafter, as changes may take 24 hours or more to develop. § In the context of chest pain, you are particularly looking for signs of ischaemia and arrhythmias (causing a drop in cardiac output and thus decreasing coronary perfusion). § Note that it is particularly important to look for signs of ST segment elevation or new onset LBBB, as the management protocol for individuals with an ST elevation myocardial infarction (STEMI) differs from that for suspected non-ST elevation myocardial infarction (NSTEMI). 2) Blood tests: • Troponin: this should be measured on ADMISSION and at 12 HOURS from the onset of pain. Troponin levels are extremely useful because of their high sensitivity and specificity for damage to cardiac muscle. The drawback is the minimum 8-HOUR DELAY in increased troponin levels. An alternative is CK-MB, an isotype of the enzyme creatinine kinase, which is released more rapidly following damage but which is less specific for cardiac damage. CK-MB levels fall back to normal within 2-3 DAYS whereas troponin levels remain high for >7 DAYS. Thus, CK-MB levels that are elevated >4 days AFTER an MI suggest that there has been a RE-INFARCTION. Note: troponin levels are specific for cardiac damage but not 100% specific for acute coronary syndrome - you need to consider the context. Other conditions causing a raised troponin include: coronary artery spasm (e.g. from cocaine) or aortic dissection causing ischaemia, myopericarditis, severe heart failure, cardiac trauma from surgery or road traffic accident, and PE. • Serum cholesterol: hypercholesterolaemia is another risk factor for cardiovascular disease that is often undiagnosed and that can be treated. It is worth noting that an MI will result in a DECREASE in total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) within about 24 hours of the infarct, and that levels will not return to normal (for that patient) for 2-3 months post-infarct. Thus, cholesterol levels should be measured ASAP if they are to guide future therapy. • Full blood count (FBC): anaemia from any cause is common and will exacerbate any deficiency in cardiac perfusion, resulting in ischaemic heart disease. • Urea and electrolytes (U&Es): pay particular attention to the POTASSIUM, as this may be the cause of an arrhythmia. • Inflammatory markers: C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and the white cell count (WCC) from the FBC are all measures of inflammation. Accordingly these are elevated in inflammatory processes such as pericarditis and Bornholm's disease (inflammation of intercostal muscles due to Coxsackie B virus infection), but will also be elevated following aortic dissection and MI, which cause inflammation of the affected tissues. • Capillary glucose: there is a significant increase in the risk of cardiovascular disease with diabetes mellitus, particularly if untreated. Type 2 diabetics typically suffer from the complications of diabetes prior to becoming symptomatic for the diabetes itself, and as many as 50% may be undiagnosed. Critically, diabetics are more likely to present with 'SILENT INFARCTS' - that is, an MI in the absence of chest pain. 3) Imaging: § Erect chest radiograph: this should be done to help exclude a pneumothorax and aortic pathology (aneurysm or dissection, giving a wide mediastinum). Note that it is possible to have a normal chest radiograph in aortic dissection. If Boerhaave's perforation of the oesophagus is suspected, a chest radiograph will typically show air around the heart shadow (pneumomediastinum), a pleural eff usion, and/or a pneumothorax. 4) Second line D-dimer levels: elevated D-dimers are simply symptomatic of BREAKDOWN of a fibrin clot due to any cause such as recent surgery or trauma, and are therefore not diagnostic of DVT or PE specifically. However, low D-dimer levels can help RULE OUT a DVT or PE as these are unlikely to occur without any fibrin breaking down. These are not done as standard in chest pain but to exclude PE.

Localised amyloidosis and heart

1) Familial amyloid cardiomyopathy --> restrictive 2) Senile cardiac amyloidosis

Heart block is a common cardiac cause of loss of consciousness. What is the classification of heart block affecting the atrioventricular (AV) node (i.e. not the bundles or fascicles)? How are the different types distinguished on ECG?

1) First-degree (incomplete) heart block: every atrial contraction is transmitted to the ventricles, but conduction is slower than normal. It is caused by damage to the AV node (e.g. from ischaemic heart disease, fibrosis, inflammation). On ECG the gap between atrial contraction (P-wave) and ventricular contraction (QRS complex), the PR interval, is >200 ms (one large square on a normally calibrated ECG). This isn't really a 'block', more a 'slowing down'. 2) Second-degree heart block: some but not every atrial contraction is transmitted to the ventricles. This can be because of excessive vagal stimulation to the AV node or damage to the AV node or bundle of His. Various subtypes are recognized: − Mobitz type I block: each heart beat shows a progressively increased PR interval until eventually a QRS complex is missed entirely, as if the AV node block is getting progressively worse and then resetting itself. This pattern on an ECG is called Wenckebach. 'Wenckebaching' can be normal in ultrafit athletes. − Mobitz type II block: this involves random block of the bundle of His such that on an ECG, QRS complexes are found to be missing randomly. It has a high risk of progressing to complete heart block. − Advanced heart block: this involves a QRS complex missing every second (2:1) or third (3:1) heart beat. AV node conduction is essentially being blocked in an intermittent but regular and predictable manner. 3) Third-degree (complete) heart block: this results in no conduction at all between the atria and ventricles. On ECG the P-waves are unrelated to the QRS complexes, which are broad. Whilst the atria continue to contract at the pace set by the sinoatrial pacemaker, the ventricles rely on spontaneous conduction originating in the bundle of His to contract at a slow rate of about 40 bpm.

List features of acute coronary syndrome

1) History of SUDDEN-onset, central CRUSHING chest pain radiating to either/ both arms and neck, especially in someone with a previous history of angina on exertion or MI and/or cardiovascular risk factors (smoking, hypertension, hypercholesterolaemia, diabetes, family history). 2) Signs of hypercholesterolaemia: cholesterol deposits in small skin lumps on the tendons of the back of the hand or bony prominences like elbows (XANTHOMATA), in creamy spots around the eyes (XANTHELASMA), or a creamy ring around the cornea (ARCUS). Note that arcus is a normal finding in the elderly (senile arcus). 3) Signs of systemic atherosclerotic vascular disease: weak pulses, peripheral cyanosis, atrophic skin, ulcers, bruits on auscultation of carotids. 4) Signs of anaemia. Anaemia can cause or exacerbate ischaemic heart disease. You can look for the following signs of anaemia, and should do in an exam, but they are either unreliable or very rare in developed countries: conjunctival pallor (unreliable), glossitis, angular stomatitis, or koilonychia (all very rare). 5) Signs of arrhythmia. If a patient has underlying ischaemic heart disease and develops poor cardiac output due to an arrhythmia, it is likely that they will develop chest pain because their poorly perfused heart will become ischaemic. Thus, check for an IRREGULARLY IRREGULAR pulse (atrial fibrillation, atrial flutter with variable heart block, or frequent ectopics), a slow pulse (heart block), or a very fast pulse (atrial fibrillation/ flutter-induced tachycardia, re-entry tachycardias, ventricular tachycardia). Also, atrial fibrillation is commonly due to PREVIOUS ISCHAEMIC DAMAGE and therefore offers a clue as to what might be wrong with the patient.

Features of pneumothorax

1) History of sudden-onset PLEURITIC chest pain with BREATHLESSNESS - but beware, it may present as painless breathlessness. 2) A hyperinflated chest wall with impaired expansion. Normally the lack of air in the pleural space creates a vacuum that holds the lungs to the chest wall. If air gets into the pleural space, unopposed elastic recoil of the chest wall will cause it to pop out, whilst at the same time the lungs will shrivel up. (Note this is different from lung collapse, in which a bronchus is obstructed and the air trapped distally in that segment is gradually absorbed into the blood.) 3) Hyper-resonant percussion over the affected area. 4) Absent breath sounds over the affected area. Th e crumpled up area of lung will not have any air getting in or out. 5) Tracheal deviation. In tension pneumothorax, a flap of pleural membrane acts as a valve so that the pleural space gets increasingly inflated with air. It eventually starts to deviate the mediastinum, and can compress the heart leading to cardiopulmonary arrest. Therefore, a trachea that deviates away from a suspected pneumothorax is an emergency requiring urgent insertion of a LARGE-BORE CANNULA in the MCL just above the third rib to allow the air trapped in the pleural space to escape.

A post mortem was performed and his heart was found to look like this: microscopy of the heart showed focal disorganisation of hypertrophied cardiac muscle fibres. 1) What is the most likely diagnosis? 2) What is the MOST likely mechanism of death? 3) The patient in this case had two children. What, if any, is the significance of their father's condition for them?

1) Hypertrophic cardiomyopathy. The marked hypertrophy of the left ventricle in the absence of an identifiable cause (e.g. hypertension, or valvular disease) along with the disorganised arrangement of the hypertrophied cardiac muscle fibres is typical of hypertrophic cardiomyopathy (HCM) which is also called hypertrophic obstructive cardiomyopathy (HOCM). The LV hypertrophy can be asymmetric (e.g. more thickening in the septum than the free wall) but it is more usually symmetric (concentric) evenly affecting the full circumference of the left ventricle. The history of sudden death in a young person during exercise, whilst not specific for this condition, is fairly typical. 2) Arrhythmia. The suddenness of death indicates that it was due to a cardiac arrhythmia and this is the usual mode of death in hypertrophic cardiomyopathy. Arrhythmias occur in this condition because the severe thickening of the left ventricle increases the metabolic demand of the muscle whilst moving the subendocardial region further away from the coronary arterial blood supply on the epicardial surface of the heart. There is often also obstruction to aortic outflow by the thickened ventricular septum. The subendocardial region being at the "end of the line" of the blood supply becomes prone to ischaemia. 3) The condition is autosomal dominant. HCM is an autosomal dominant condition and each child (regardless of sex) has, therefore, a 50% chance of the abnormal gene being passed on to them. Many people with the abnormal gene will not however show any symptoms or die from cardiac problems but may only show evidence of HCM on detailed investigation i.e. the expressivity of the gene varies from individual to individual.

DDx of collapse

1) Hypoglycaemia (DNEFG- do not ever forget glucose) 2) Vasovagal, arrhythmia, outflow obstruction, postural hypotension 3) Seizure

The age of any given patient makes particular causes of loss of consciousness much more likely than others. What is the main cause of loss of consciousness in a patient: (1) aged 25 years? (2) aged 55 years? (3) aged 85 years?

1) In young patients, the commonest cause of loss of consciousness is VASOVAGAL SYNCOPE. Patients describe a warning or PRE-syncopal sensation - an odd sensation in the stomach, going pale and clammy, and knowing they are going to lose consciousness. 2) In middle-aged patients, the most common causes of loss of consciousness are VASOVAGAL syncope (see above) and cardiac ARRYTHMIAS. Th is is because cardiac arrhythmias are usually secondary to ischaemic heart disease, itself more common as patients age and accumulate an increasing burden of atherosclerotic lesions. By this line of reasoning, one would expect cardiac arrhythmias to account for most episodes of lost consciousness in elderly patients as well, but in reality many of the patients who have sufficient ischaemic heart disease to cause arrhythmias in middle age will succumb to an atherosclerosis-related death (usually cardiac or stroke) before reaching 'old age'. Patients typically describe losing consciousness WITHOUT any WARNING or without any obvious trigger (e.g. suddenly passing out whilst sitting in front of the television). Arrhythmias are important as there is a high risk of fatal arrhythmia. 3) In elderly patients, the most common cause of loss of consciousness is ORTHOSTATIC hypotension caused by MEDICATIONS. These include DIURETICS and angiotensin-converting enzyme (ACE) INHIBITORS (reduced blood volume and vasodilatation), β-BLOCKER (inability to increase heart rate on standing), α-BLOCKER (inability to vasoconstrict the major capacitance veins), and CCBs (inability to vasoconstrict and some are negatively inotropic/chronotropic). Many elderly patients are on a number of these drugs simultaneously and find it hard to maintain adequate blood pressure. Patients typically describe losing consciousness after standing up, because their body is unable to compensate for the sudden drop in blood pressure. The condition carries a significant morbidity (from broken bones, loss of confidence and independence) and mortality (from venous thromboembolic disease and infections acquired as a consequence of prolonged bed rest after a fall).

A 45-year-old man presents with a 3-week history of general malaise and night sweats. He has been feverish, tired, lost his appetite and lost 3 kg in weight. He is mildly short of breath on exercise but denies a cough or chest pain. He has no GI symptoms. He had a cystoscopy one month ago to investigate an incidental finding of non-visible haematuria. No abnormality was found but he reports some urinary frequency and discomfort since the procedure. He is not taking any regular medications apart from paracetamol for his febrile episodes. He does not smoke or drink alcohol. He is married with two children and works as a postman. On examination, he looks pale. His temperature is 38.5°C, pulse 90 bpm, regular, and blood pressure 135/85 mmHg. On auscultation of his heart there is evidence of a pansystolic murmur loudest at the cardiac apex radiating to the axilla. Respiratory examination is normal and no nodes are palpable in his neck, axillae or groins. He has mild enlargement of his spleen on abdominal examination. Blood results are available: Hb 108135-180 g/L WCC 164-11 x109/L Plt 225150-450 x109/L MCV 8276-100 fL Na+ 136136-145 mM K+ 4.03.5-5.1 mM Ur 61.7-8.3 mM ESR860-15 mm/h Bili 220-21 µM ALP 2640-129 iu/L AST 460-40 IU/L GGT 3610-71 IU/L 1) What is the most likely diagnosis for his current symptoms? 2) Which five investigations should be performed during an initial assessment for infective endocarditis in this patient?

1) Infective endocarditis - This patient has a fever, raised ESR and a presumed new heart murmur and has infective endocarditis until proved otherwise. Whilst all the other conditions would cause some of the signs and symptoms, infective endocarditis is the most likely to cause all three symptoms above. 2) ECG, Transthoracic echocardiogram, Blood cultures (three sets), Mid-stream urine for culture and sensitivity, Ultrasound abdomen. Three sets of blood cultures are required, and should be taken before starting anti-microbials. Ideally the results of these should also be awaited before the onset of antibiotic treatment if the patient's condition allows. Blood cultures should be taken from a peripheral vein and not taken from indwelling lines. Cultures do not need to be taken at the time of a fever spike and patients with infective endocarditis generally have a persistent bacteraemia. Echocardiography is needed to delineate valves, and look for vegetations and possible peri-valvular abscess - a transthoracic echo should be performed within 24 hours when there is a suspicion of infective endocarditis. The transoesophageal echocardiogram (TOE) is more accurate and should be sought if transthoracic echo does not show vegetations in a patient suspected as having infective endocarditis, but these often take longer to organise. ECG abnormalities may occur, particularly heart block. I In the presence of splenomegaly an ultrasound should be performed to look for possible splenic infarcts. A urine culture is not part of the standard work up for infective endocarditis but is important in this man with urinary symptoms one month after his cystoscopy

Systemic amyloidosis body effects

1) Kidneys - nephrotic syndrome: § proteinuria § hypoalbuminaemia § oedema § hyperlipidaemia 2) Heart - CHF and arrhythmias 3) GI - enlarged liver, spleen, tongue, malabsorption of nutrients 4) Nerves - peripheral (Sensory and motor), autonomic (digestion and BP)

Recognise the presenting symptoms of cardiac failure

1) Left Heart Failure - symptoms caused by pulmonary congestion o Dyspnoea - divided based on the New York Heart Association classification: ● 1 - no dyspnoea ● 2 - dyspnoea on ordinary activities ● 3 - dyspnoea on less than ordinary activities ● 4 - dyspnoea at rest o Orthopnoea o Paroxysmal nocturnal dyspnoea o Fatigue o Poor exercise tolerance o Nocturnal cough (+/- pink frothy sputum) o Wheeze (cardiac 'asthma') o Nocturia o Cold peripheries o Weight loss o Muscle wasting 2) Acute Left Ventricular Failure o Dyspnoea o Wheeze o Cough o Pink frothy sputum 3) Right Heart Failure - venous congestion o Swollen ankles o Fatigue o Increased weight (due to oedema) o Reduced exercise tolerance o Anorexia o Nausea

Recognise the signs of cardiac failure on physical examination

1) Left Heart Failure: o Tachycardia o Tachypnoea o Displaced apex beat (LV dilatation) o Bilateral basal crackles o S3 gallop (caused by rapid ventricular filling) o Pansystolic murmur (due to functional mitral regurgitation) 2) Acute Left Ventricular Failure o Tachypnoea o Cyanosis o Tachycardia o Peripheral shutdown o Pulsus alternans ● Arterial pulse waveforms showing alternating strong and weak beats ● Sign of left ventricular systolic impairment ● Explanation: ▪ In left ventricular dysfunction, ejection fraction significantly decreases leading to a reduction in stroke volume ▪ This causes an increase in end-diastolic volume ▪ This means that the left ventricle is stretched more for the next contraction ▪ Due to Starling's Law, the increased stretch of the left ventricle caused by the increased end-diastolic volume following the previous beat leads to an increase in the strength of the myocardial contraction ▪ This results in a stronger systolic pulse o Gallop rhythm o Wheeze (cardiac asthma) o Fine crackles throughout lung 3) Right Heart Failure o Raised JVP o Hepatomegaly o Ascites o Ankle/sacral pitting oedema o Signs of functional tricuspid regurgitation - pulsation in neck and face o Facial engorgement o Epistaxis o RV heave (pulmonary hypertension)

A 35-year-old mother of 2 attended surgical outpatients complaining of varicose veins. On standing, examination of her right leg showed dilated tortuous veins over the medial aspect of her thigh and calf. 1) What would be the most likely distribution of veins causing this problem? 2) What tests are available to assess incompetence of varicose veins? (List three)

1) Long saphenous. Most cases of varicose veins are due to incompetent valves in the long or short saphenous veins. Incompetence of the long saphenous vein would be noted from the groin to the medial aspect of the lower leg. Below the knee it is more difficult to differentiate between the two, however the short saphenous vein would be located from the popliteal fossa along the calf to the lateral malleolus. 2) Trendelenburg's, doppler and simple tourniquet test. § The tourniquet test is performed thus: a) The patient lies on the bed b) Drain the varicosities of blood by supporting their leg above the level of the bed (and "milking" the veins) c) Tie the tourniquet around the thigh, at or below the level of the sapheno-femoral junction (where the saphenous vein enters the femoral vein, just below the groin). d) Ask the patient to stand. If the veins do not fill this suggests that the sapheno-femoral junction is incompetent. If the veins fill the test can be repeated bringing the tourniquet further down the thigh to assess the perforators. § Trendelenburg's test is a variation of the above test but instead of a tourniquet, a finger is used to control the sapheno-femoral junction. § Hand held Doppler probe can be used to assess reflux in veins. The Doppler is placed over the sapheno-femoral junction and the examiner squeezes the calf on the ipsilateral leg. If there is a SINGLE sound heard with the Doppler this suggests that there is NO incompetence. If there were incompetence in the veins there would be 2 sounds heard with the doppler: the first as the blood flows up the vein when the calf is squeezed, and the second when blood flows back down the incompetent vein when the calf is released.

Mrs McDonald is in town visiting her daughter, who is getting married next week. She arrived yesterday after a 10-hour overnight bus journey and noticed that her right calf started swelling within a few hours of arriving. She can still walk on her affected limb, which is only slightly painful but 'feels very hot'. She thinks the swelling has been the same for the past few hours. She has not noticed any cuts, bites, or wounds in her right leg. She has not had any recent surgery, but started taking hormone replacement therapy last month to help with the unbearable hot flushes that she was getting from her menopause - her last period was 5 months ago and she has had no vaginal bleeding since. She has never had any cancer or radiotherapy, but did have her appendix removed when she was a teenager. Her past medical history is otherwise unremarkable. She has been trying to lose weight recently in preparation for her daughter's wedding but admits to limited success in her efforts as her BMI is still >30 kg/m2. Can you identify risk factors for any of your differential diagnoses in the history?

1) Long-distance travel: several studies have shown an increased risk of venous thrombosis in people who are immobilized through travelling for more than 8 HOURS non-stop. It is important to realize that what matters is the prolonged immobility, and not the type of transport used. Thus, most lay people will (wrongly) associate DVTs with all forms of flying (irrespective of duration) whilst few people will consider long-haul bus, train, or car journeys as a risk for DVT. Also, it is important to note that most studies suggest that the increased risk of DVT associated with long-distance journeys applies only to people with other predisposing risk factors for DVT, although patients may not be aware of these at the time of travelling. 2) Oestrogen- and progesterone-based therapies: several studies have shown that medications involving oestrogen and/or progesterone analogues (e.g. contraceptive pills in fertile women, hormone replacement therapy for menopausal women, tamoxifen in breast cancer patients) increase the risk of venous thrombosis. However, it is important to note that most people taking oestrogen/ progesterone-based medications will have a low baseline risk of venous thrombosis, and so increasing that risk only moderately will still result in a risk that is low overall. 3) Obesity: obesity also increases the risk of thrombotic disease.

Causes of chronic right heart failure

1) Lungs: pulmonary hypertension, pulmonary embolism, chronic lung disease (ILD, CF) 2) Valvular: triscupid regurgitation, pulmonary valve disease 3) LHF --> Congestive heart failure

A 39-year-old woman presents with a four-week history of night sweats, fevers and weight loss. She is an intravenous drug user of no fixed abode. She has no past medical history and is not taking any prescription medications. Her temperature is 38.2°C. Heart rate is 96 bpm, BP is 112/58 mmHg, respiratory rate is 18 breaths per minute and oxygen saturation is 96% breathing air. 1) Which three of the following differential diagnoses would consider in this patient? 2) Clinical examination of the patient revealed splinter haemorrhages. Which two of the following investigations would be most useful in confirming the underlying diagnosis?

1) Malignancy, Tuberculosis, Infective endocarditis. § Influenza and necrotizing fasciitis do not present with chronic symptoms. The others are all possible at this stage. 2) Three sets of blood cultures, Echocardiogram. This patient has nail splinter haemorrhages and the likely diagnosis is infective endocarditis. This is diagnosed according to the Duke criteria. Acid fast bacilli in the sputum would confirm a diagnosis of tuberculosis. A CT scan is not used as part of the diagnostic criteria for infective endocarditis (although would be useful if suspicious of an alternative diagnosis). HIV serology would not help diagnose infective endocarditis and C3 levels can be low in infective endocarditis but is not specific and not used to make a diagnosis.

Mr Shepherd's ECG is shown in Fig. 9.1. Comment on any abnormalities. He begins to complain of pain once the analgesia wears off . His troponin is 6 ng/mL on admission, (normal range given by the lab <0.4 ng/mL). His chest radiograph is normal. In light of the history (hypertensive, hypercholesteraemia, smoker and central crushing chest pain), examination, and investigations, what is the diagnosis? How else might this condition present?

1) Mr Shepherd's ECG shows ST depression and prominent R waves in V1-V3 but no signs of ST elevation. 2) Mr Shepherd is a 40-pack-year smoker with hypertension and hypercholesterolaemia who has presented with central crushing chest pain. This picture is typical for MI. He has elevation of cardiac troponin levels, suggesting MI. His ECG shows ST depression in leads V1-V3 which would be consistent with an anterior NSTEMI. Remember that transmural infarctions normally result in ST elevation on an ECG and are hence referred to as ST elevation myocardial infractions (STEMIs). However, in the case of posterior wall transmural infarctions, the fact that the ECG chest leads are on the opposite side of the chest wall results depression in leads V1-V3 rather than ST elevation. Thus, this could also represent a posterior infarct, which are treated like STEMIs despite the lack of ST elevation. MIs present in many different ways and you should have a low threshold for suspecting it in anyone with cardiac risk factors. Ultimately, diagnosis depends on an elevated 12-hour troponin. Chest pain is not always a feature, particularly in the elderly and long-standing diabetics who frequently have neuropathy and dulled pain sensation. ECG readings are also non-diagnostic, as changes may not be present in infarction.

You are called to see a 46-year-old patient on the medical assessment unit who has been admitted with a 2-hour history of central chest discomfort. He has also noted severe pain in the left side of his jaw and has felt sweaty. He is not short of breath, but does feel nauseated although he has not vomited. He has not experienced these symptoms before and has no previous medical history of note. He smokes 10 cigarettes a day and has done so since his teens. He drinks alcohol in moderation and is on no medication. He is married with two children. On examination, he is a little clammy, pulse 95bpm and regular, blood pressure 140/85 mmHg and apyrexial. His heart sounds are normal and lungs clear. Physical examination is otherwise unremarkable. 1) Which diagnosis would you want to exclude? 2) Which three further investigations would you arrange immediately?

1) Mycocardial infarction. This clinical history with chest discomfort, nausea and pain in the jaw should suggest a diagnosis of myocardial infarction. The history is not typical for pulmonary embolus or aortic dissection which do not cause jaw pain. There is no clinical evidence of pneumonia. 2) Cardiac enzymes, Chest radiograph, Electrocardiogram (ECG). In addition to routine blood tests (FBC, U&Es, glucose, troponin etc.), pulse oximetry and cardiac monitoring are also indicated. Formal blood gases are not necessarily needed at this stage in the absence of shortness of breath.

A 54-year-old man presents to the emergency department with a 3-hour history of sudden onset, severe crushing central chest pain associated with sweating, shortness of breath and nausea. He had previously been well, although had suffered with what he called 'indigestion' and 'heart burn' for many years for which he regularly took Gaviscon. He had been recently diagnosed with hypertension by his GP who had treated him with Bendroflumethiazide 2.5mg OD. He smoked 20 cigarettes per day and had done so for over 30 years. His mother had suffered with angina in her 70's and later died age 75 from a stroke. On examination, he appeared unwell, was cold and clammy, HR 72 bpm, BP 147/91 mmHg, saturation 95% on room air. His JVP was not elevated, heart sounds were normal and chest clear to auscultation. 1) What is the single most likely diagnosis given this history?

1) Myocardial infarction. Differential includes: Acute coronary syndrome (unstable angina), acute pericarditis, aortic dissection, perforated duodenal ulcer, pulmonary embolus and acute pancreatitis.

The patient received primary angioplasty and recovers on the coronary care unit. Over the next few hours, the patient becomes increasingly short of breath and the following chest x-ray is performed (image below). 1) What does it show? 2) What is the most likely cause of the breathlessness? 3) The patients blood pressure is now recorded at 75/50 mmHG. What is the next step in the management of this patient? 4) Which three of the following investigations would you now consider to investigate the cause for the deterioration?

1) Opacification of air-spaces extending out from the hila 2) Pulmonary oedema secondary to myocardial infarction 3) Continuous Positive Airways pressure - Treatment options limited due to low blood pressure and cardiogenic shock. The only management step here should be to initiate CPAP (continuous positive airway pressure). This method of non invasive ventilation will allow the lung fluid to effectively pushed under pressure back into the vasculature to improve blood pressure. This will then permit drugs such as IV diuretics to be given without risk of further hypotension. Adrenaline and salbutamol are not indicated here. Oxygen alone would not result in resolution of the pulmonary oedema. IV fluids would be dangerous and risky to to this patient who has intravascular fluid in the wrong compartment (lungs). 4) renal function, echocardiogram, ECG. The majority of patients returning to coronary care after a primary PCI will be fine but you need to be aware of some complications, pulmonary oedema being one of them. It is important to consider the cause for the acute left ventricular failure (LVF). Another ECG to see if arrhythmia such as AF. VT. Also to consider whether the stent has occluded already (malpositioned) so ST elevation may be still present. Normally these patient still have ongoing chest pain. Rarely the patient may have pre-existing unknown renal failure and the amount of contrast given during the procedure tips them into acute LVF. Thus routine bloods are important such as renal function. A full blood count may also give some indication of blood loss such as from the arterial puncture site that can be masked in the retroperitoneal space (femoral access less used currently for access and most patients will have radial artery access). Next an echocardiogram would be very helpful to diagnose left ventricular function and if any rupture, valve dysfunction or development of septal VSD (may be early to see this in time frame of presentation). Perhaps a bladder scan may be useful as monitoring urine output with a catheter. CT scan and renal USS not indicated at this point of the process.

What does this chest X-ray show? What complication of pericarditis has occurred?

1) Over the next 2-3 weeks the patient became increasingly short of breath. On examination, she was tachycardic, her JVP was elevated to the angle of the jaw, her apex beat was impalpable and the heart sounds were soft. She had a palpable liver edge 6cm below the costal margin and pitting oedema to the mid shin. A CXR was performed (image below). Which statement best describes the CXR findings? Cardiomegaly and normal pulmonary vasculature. The CXR shows cardiomegaly as the width of the heart is larger than half of the width of the chest. The hila show normal vasculature, with no suggestion of pulmonary congestion 2) Pericardial effusion. The enlarged heart but in the absence of pulmonary vascular congestion indicates the pericardial effusion rather that congestive failure. If there is any degree of pericardial tamponade the JVP will be elevated.

Mr Williams remembers feeling unwell and dizzy before passing out, but seems alright now, half an hour later. His friend tells you that he appeared well earlier in the evening, although he was inebriated. However, immediately before he collapsed his friend says 'the colour drained from his face'. He tells you Mr Williams was unconscious for only a few seconds and was a little surprised but not particularly confused when he came around. Other aspects of the history can also help in the diagnosis of blackouts. What would you particularly ask about in the history?

1) Past medical history • Has it happened BEFORE? If it has happened before, you should ask the same questions about previous episodes and if they are increasing in frequency. • DIABETES? This predisposes to vascular disease, hypoglycaemia, polyuria and dehydration, and autonomic dysfunction that can cause orthostatic hypotension. • CARDIAC illness? Ask about palpitations and chest pain as well as previous diagnoses. The presence of heart disease is a strong predictor of a cardiac cause of syncope. Arrhythmias may arise following infarction. Left ventricular outflow obstruction may occur secondary to aortic stenosis, HOCM, etc. • Peripheral VASCULAR disease? Ask about claudication in case the patient is not aware of having peripheral vascular disease. Peripheral vascular disease is associated with coronary artery disease, as both are manifestations of the same underlying pathological process - atherosclerosis. It is also associated with cerebrovascular events (transient ischaemic attacks (TIAs), strokes), but these are very rarely a cause of transient loss of consciousness. • EPILEPSY? If they have epilepsy, did this episode resemble one of their typical seizures? • ANAEMIA? This can contribute to hypoxia. • PSYCHIATRIC illness? Panic attacks are associated with hyperventilation and loss of consciousness. Non-epileptic 'seizures' are also more common amongst patients with psychiatric comorbidities. 2) Drug history • INSULIN? Oral hypoglycaemics? These will obviously make patients susceptible to hypoglycaemia. • ANTIHYPERTENSIVES? (e.g. diuretics, ACE inhibitors, β-blockers, calciumchannel blockers). All can cause hypotension. • VASODILATORS? (e.g. glyceryl trinitrate (GTN), isosorbide mononitrate). Th ese can also cause hypotension, particularly in elderly patients. • ANTI-ARRYTHMICS? These can paradoxically predispose to arrhythmias. • ANTIDEPRESSANTS? Hypotension can be a side-effect with some antidepressants, e.g. tricyclic antidepressants. 3) Social history • ALCOHOL? Many people who are intoxicated are brought in as 'loss of consciousness of unknown cause', although some might not have lost consciousness but simply become unable to stand anymore. • STIMULANT RECREATIONAL drugs? Drugs such as cocaine and amphetamines stimulate the heart, causing tachyarrhythmias and potentially a drop in cardiac output. 4) Family history • SUDDENT death? Such a history is significant in all cases of unexplained syncope, but is particularly informative regarding exercise-induced syncope. Some cardiomyopathies and arrhythmias are hereditary.

Explain the aetiology/risk factors of hypertension

1) Primary (essential) - treat the hypertension itself: o Essential or idiopathic hypertension o Unknown cause o Responsible for > 90% of cases 2) Secondary - treat the cause: a) Renal ● Renal artery stenosis ● Chronic glomerulonephritis ● Chronic pyelonephritis ● Polycystic kidney disease ● Chronic renal failure ● Renovascular disease b) Endocrine ● Diabetes mellitus ● Hyperthyroidism ● Cushing's syndrome ● Conn's syndrome ● Hyperparathyroidism ● Phaeochromocytoma - nervousness, sweat pouring down face, palpitations, severe episodic hypertension, severe vasoconstriction causes necrotic bowel ● Congenital adrenal hyperplasia ● Acromegaly c) Cardiovascular ● Coarctation of the aorta (congenital) - as aorta goes down it gets poor blood blow to kidneys --> like you have renal artery stones ● Increased intravascular volume d) Drugs ● Sympathomimetics ● Corticosteroids ● COCP e) Pregnancy ● Pre-eclampsia 3) Isolated systolic hypertension (ISH): o Most common form in the UK - affects >50% of the over 60s o Due to stiffening of the large arteries (arteriosclerosis) 4) Malignant (accelerated phase) hypertension o A rapid rise in BP leading to vascular damage (pathological hallmark is fibrinoid necrosis) o Usually there is severe hypertension + bilateral retinal haemorrhages and exudates; papilloedema may or may not be present **RISK FACTORS: § obesity § sodium intake >1.5 g/day § aerobic exercise <3 times/week § low fruit and vegetable intake

Generate a management plan for pulmonary embolism

1) Primary Prevention: o Compression stockings o Heparin prophylaxis for those at risk o Good mobilisation and adequate hydration 2) If haemodynamically stable: o O2 o Anticoagulation with LMWH or rivaroxaban o Switch over to oral warfarin for at least 3 months ▪ Maintain INR 2-3 3) Analgesia: ● If haemodynamically UNSTABLE (massive PE) o Resuscitate o O2 o IV fluids o Thrombolysis with tPA may be considered if cardiac arrest is imminent 4) Surgical or radiological: o Embolectomy o IVC filters - sometimes used for recurrent PEs despite adequate anticoagulation or when anticoagulation is contraindicated

Management of AF in someone who is haemodynamically unstable

1) Rhythm control: § haemodynamically unstable: tachycardic, tachypnoea, hypotensive, low sats despite O2 --> DC cardioversion. § if pt is haemodynamically stable, check timing. § If acute onset --> DC cardioversion if refuse -> chemical cardioversion (flecaeninide or amiodarone) § if chronic onset --> anticoagulation w/warfarin, continue for 3-4 weeks, cardioversion after. 2) Rate control: a) verapamil (non-dihydropyiridine CCB) b) beta-blockers (contraindicated in asthmatics and diabetics) c) digoxin § use CHADVASC to calculate risk of stroke with AF. if low risk no treatment, if medium risk consider treatment, high risk warfarin

An 83-year-old gentleman presents to the ED with sudden onset lumbar back pain which started 2 hours ago and is now associated with sweating and light-headedness. 1) What is the most important diagnosis to exclude?

1) Ruptured AAA. An elderly male is the most common patient to have an abdominal aortic aneurysm (AAA) and they will often go unnoticed for many years until the pressure effect on the lumbar spine causes back pain. In itself this does not indicate rupture but the rapidity of onset suggests a leaking AAA must be excluded. The presence of light headedness suggests reduced cerebral perfusion, in this case due to hypovolaemic shock and sweating is a symptom of the sympathetic response to this.

1) What does this ECG show? 2) Diagnosis? 3) The patient's oxygen saturations are 99% on air. What is the most likely reason the patient had an increased respiratory rate on arrival?

1) ST elevation primarily in anterior leads. There is ST elevation most pronounced in V2-V5, but also to a lesser extent in the lateral leads I and aVL. Note that there is 'reciprocal' ST depression in leads III and aVF. 2)Acute anterolateral myocardial infarction. In the context of acute chest pain, the ECG findings are unequivocal and diagnostic of acute anterolateral myocardial infarction. 3) Pain- Severe pain will increase the respiratory rate and is most likely given there are no clinical features of pulmonary oedema, although this is still a possibility.

Generate a management plan for chronic left ventricular failure

1) TREAT THE CAUSE (e.g. hypertension, valvular disease) 2) TREAT EXACERBATING FACTORS (e.g. anaemia) 3) Diuretics: ▪ Loop diuretics e.g. furosemide ▪ Can correct fluid overload and relieve symptoms ▪ Monitor potassium as can cause low K. 4) ACE Inhibitors ● Consider in all with left ventricular failure ● Inhibits renin-angiotensin system and inhibits adverse cardiac remodelling ● They slow down the progression of heart failure and improve survival 5) Beta-Blockers ● Blocks the effects of a chronically activated sympathetic system ● Slows progression of heart failure and improves survival ● The benefits of ACE inhibitors and beta-blockers are additive 6) Aldosterone Antagonists ● Improves survival in patients with NYHA class III/IV symptoms on standard therapy ● Monitor K+ (as these drugs may cause hyperkalaemia) 7) Spironolactone 8) Angiotensin Receptor Blockers ● May be added in patients with persistent symptoms despite the use of ACE inhibitors and beta-blockers ● Monitor K+ (as these drugs may cause hyperkalaemia) 9) Hydralazine and a Nitrate e.g. hydralazine + isosorbide dinitrate (VASODILATORS) ● May be added in patients (particularly Afro-Caribbeans) with persistent symptoms despite the use of ACE inhibitors and beta-blockers 10) Digoxin ● Positive inotrope ● Reduces hospitalisation but does NOT improve survival 11) N-3 Polyunsaturated Fatty Acids ● Provide a small beneficial advantage in terms of survival 12) Cardiac Resynchronisation Therapy ● Biventricular pacing improves symptoms and survival in patients with a left ventricular ejection fraction < 35%, cardiac dyssynchrony (QRS > 120 msec) and moderate-severe symptoms ● These patients are also candidates for implantable cardioverter defibrillator (ICD) ● They may receive a combined device o CAUTION: avoid drugs that could adversely affect a patient with heart failure due to systolic dysfunction (e.g. NSAIDs, non-dihydropyridine CCBs)

Which 3 of the following statements regarding imaging of aortic stenosis are correct?

1) The CXR in severe cases may be normal 2) Left ventricular hypertrophy is usually seen with severe aortic stenosis 3) Echo is the diagnostic imaging modality of choice The left ventricle is hypertrophied rather than dilated hence the heart can appear to be a normal size on CXR. Echocardiography is the imaging modality that should reliably confirm the diagnosis Prior to surgery, patients will require catheter angiography to establish if there is underlying ischaemia. CT angiography is not indicated

What do you want to know about the history of the ulcer itself, and how would each of the main types differ?

1) The first thing is to ask about the ulcer. You should consider: 1) Is the ulcer painful? − Venous ulcers are caused by venous stasis in the leg and are thus LESS painful when ELEVATED and drained of blood. However, only about 30% of venous ulcers are painful. − Arterial (atherosclerotic) ulcers are caused by ischaemia to the leg and are thus MORE PAINFUL when ELEVATED and drained of blood. Patients often say the ulcers are painful enough to wake them up at night and that they obtain relief by lowering their leg over the side of the bed. − Neuropathic ulcers are caused by loss of sensation (which predisposes to constant trauma) and are thus NOT painful. 2) How long has the ulcer been there? − Venous ulcers are less painful and can therefore present LATE. They often have a long and recurring history. − Arterial ulcers tend to present relatively EARLY because of pain. They often occur secondary to trivial trauma. − Neuropathic ulcers are associated with a loss of sensation and thus often present LATE. − A long history should arouse suspicion of a MARJOLIN ulcer, which only occurs in chronically present ulcers

Generate a management plan for infective endocarditis

1) A to E and supportive care: resuscitation, oxygen therapy, and other supportive measures, 2) Antibiotics for 4-6 weeks ● Blind therapy of native valve: amoxicillin +/- gentamicin ● Blind therapy or prosthetic valve: vancomycin + gentamycin + rifampicin ● On clinical suspicion = EMPIRICAL TREATMENT o Benzylpenicillin o Gentamicin ● Streptococci - continue the same as above ● Staphylococci o Flucloxacillin/vancomycin o Gentamicin ● Enterococci o Amoxicillin o Gentamicin ● Culture Negative o Vancomycin o Gentamicin ● SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics

Identify appropriate investigations for ischaemic heart disease

1) Bloods: o FBC o U&Es o CRP o Glucose o Lipid profile o Cardiac enzymes (troponins and CK-MB) - troponin would be elevated in STEMI/NSTEMI, but not in unstable angina Troponin serum levels (most specific) rise within 3-12 hours from onset of chest pain and peak at 24-48 hours. They decrease to baseline over 5-14 days. Creatine kinase CK-MB isotope levels rise within 3-12 hours from onset of chest pain and peak at 24 hours, returning to baseline after 48-72 hours. Myoglobin levels rise within 1-4 hours from onset of pain. Very sensitive but not specific. o Amylase (pancreatitis could mimic MI) o TFTs o AST and LDH (raised 24 and 48 hours post-MI, respectively) 2) ECG - FIRST THING TO DO: o Unstable Angina or NSTEMI: ● May show ST depression or T wave inversion o STEMI: ● Hyperacute T waves ● ST elevation (> 1 mm in limb leads, > 2 mm in chest leads) ● New-onset LBBB ● Later changes: ▪ T wave inversion ▪ Pathological Q waves ** Relationship between ECG leads and the side of the heart: ● Inferior: II, III, aVF (supplied by right coronary artery) ● Anterior: V1-V5/6 (left anterior descending artery) ● Lateral: I, aVL, V5/6 (left circumflex artery) ● Posterior: Tall R wave and ST depression in V1-3 3) CXR: o Check for signs of heart failure o Cardiomegaly, pulmonary oedema or widened mediastinum (aortic rupture) 4) Exercise ECG: o Indications ● Patients with troponin-negative ACS or stable angina with a high pretest probability of coronary heart disease ● Pretest probability is based on characteristics of chest pain, cardiac risk factors, age and gender ● NOTE: digoxin is associated with giving a false-positive result o Results: ● Positive Test: > 1 mm horizontal or downsloping ST depression measured at 80 ms after the end of the QRS complex ● Failed Test: failure to achieve at least 85% of the predicted maximal heart rate (220-age) and otherwise negative findings (no chest pain or ECG changes) ▪ NOTE: beta-blockers reduce heart rate and so should be stopped before the test ● Resting ECG Abnormalities: e.g. pre-excitation syndrome, > 1 mm ST depression, LBBB or pacemaker ventricular rhythm 5) Radionuclide Myocardial Perfusion Imaging (rMPI): o Uses Technetium-99m sestamibi or tetrofosmin o Can be performed under stress or at rest o Stress testing shows low uptake in ischaemic myocardium 6) Echocardiogram o Measures left ventricular ejection fraction o Exercise or dobutamine stress echo may detect regional wall motion abnormalities 7) Pharmacological Stress Testing: o This is used in patients who are unable to exercise o Pharmacological agents can be used to induce a tachycardia, such as: ● Dipyridamole ● Adenosine ● Dobutamine o These agents are used in conjunction with various imaging modalities (e.g. rMPI, echocardiography) to detect ischaemic myocardium o NOTE: Dypiridamole and adenosine are contraindicated in AV block and reactive airway disease 8) Cardiac Catheterisation/Angiography: o Performed if ACS with positive troponin or if high risk on stress testing 9) Coronary Calcium Scoring: o Uses specialised CT scan o May be useful in outpatients with atypical chest pain or in acute chest pain that isn't clearly due to ischaemia

1) A chest radiograph was also performed (image below). What 2 pathological features does the CXR show? 2) What further investigation is needed?

1) Borderline cardiomegaly. Widened mediastinum. § CXR shows a widened mediastinum due to the aortic dissection. There is also borderline cardiomegaly despite the fact that this is an AP film. This can be subjective however should there be doubt a CT scan of the thorax should be performed. 2) CT thoracic aorta. CT thoracic aorta is the best investigation of choice to quantify the damage and assess for possible repair.

Examples of localised amyloidosis

1) Brain 2) Heart 3) Pancreas

What are the five major criteria for rheumatic fever

1) Carditis (changing heart murmur) 2) Arthritis 3) Erythema Marginatum 4) Sydenham's chorea 5) Subcutaneous nodules

Investigations for someone with chest pain and suspected MI

1) ECG 2) Troponin: +ve --> coronary angiogram. -ve: ETT (exercise tolerance testing) 3) echo

Identify appropriate investigations for WPW syndrome

1) ECG may be normal if the conduction speed of the impulse along the accessory pathway matches the conduction speed down the bundle of His ● Classic ECG findings: o Short PR interval o Broad QRS complex o Slurred upstroke in initial portion of QRS producing a delta wave - this is because ventricles are being excited over a longer period of time. ● Patient may be in SVT (AVRT) 2) Bloods - check for other causes of arrhythmia 3) Echocardiogram - check for structural heart defects

A 67-year-old male smoker is brought to the ED via blue light ambulance with severe central chest pain radiating to his neck and left arm. He had been admitted with unstable angina previously but had been asymptomatic since. He had no other significant past medical history. On examination, he is in pain, is sweaty with a pulse of 100bpm, blood pressure 170/100 mmHg and respiratory rate of 30/min. Oxygen saturations Heart sounds are normal, JVP is not elevated and the chest is clear. 1) What would be your initial management of this patient in the ED?

1) ECG, Aspirin 300mg stat, Diamorphine 20mg, Oxygen saturations measurement. § has had chronic unstable angina (blocked coronary artery) and plaque has ruptured and has had infarction of heart muscle. If don't perfuse the tissue before it dies that will form scar tissue which can't pump as effectively and get heart failure The immediate management from those choices should be ECG, Aspirin 300mg, and oxygen saturation monitoring. Mnemonic MONA= morphine, oxygen, nitrates and asprin. Subsequently, a portable CXR is indicated (the patient should be kept in the resuscitation area and mobile film performed), oxygen saturations can be quickly performed with observations, the patient should be sat up and given oxygen via a face mask if oxygen saturation are less than 90%. Diamorphine is correct but should be titrated to pain (20mg is too high initial dose).

A 67-year-old gentleman attends the the ED with a very painful cold right leg. He woke this morning with a severe dull ache in his calf and foot which has not been helped by co-codamol. There is no recent history of trauma. He is a retired builder, who has smoked 10 cigarettes a day for 40 years. He is on no medications. He is apyrexial, with an irregularly irregular pulse at a rate of 102 bpm and is normotensive. His right leg is cool to touch, pale and has reduced sensation. His left leg is normal. 1)

1) The history suggests acute limb ischaemia, likely to be embolic in origin with a cardiac source (atrial fibrillation). § Compartment syndrome occurs after direct trauma (fractured tibia/fibula) or from pressure effects (rhabdomyolysis following prolonged immobility e.g. CVA). § It can however be a complication of revascularising an ischaemic limb, and can be prevented by doing a fasciotomy after revascularisation. § Morton's neuroma is a condition causing metatarsal pain due to inflammation around the plantar nerve. § Tabes dorsalis is a feature of quaternary syphilis that may present with numb legs and a neuropathic type pain. § Guillan-Barré syndrome is a progressive motor neuropathy. § Charcot arthropathy is secondary to peripheral neuropathy and is therefore painless.

A 35-year-old female presented to her GP with mild central chest pain which did not radiate and was pleuritic in nature and relieved on sitting forwards. She had a viral episode 7 days previously, with malaise and fever from which she was still recovering. There was no significant past medical or family history and she was a non-smoker. She did not report any breathlessness. On examination, she was afebrile, tachycardic with a pulse of 100 bpm regular, blood pressure was 120/80 mmHg and respiratory rate of 16/min. A soft rub was heard on auscultation of the heart. The JVP was not elevated, the lungs were clear and there was no peripheral oedema. Initial troponin level was normal. Shows widespread ST saddle shape ECG. 1) Which is the most likely diagnosis? 2) Which 3 initial tests would you perform next ? 3) What would be the most appropriate therapeutic action?

1) The pattern of presentation is very suggestive of viral percarditis. This is a young female, so the likelihood of coronary disease is very low. The history is longer than you would expect with a pulmonary embolism, though this is always a good diagnosis to consider in anyone with pleuritic chest pain. Musculoskeletal pain is possible - associated with a viral illness, but wouldn't be associated with a pericardial rub. 2) Echocardiogram, serial ECGs and repeat troponin. Troponin levels at 12 hours need to be performed to exclude myocardial insult, but bear in mind it is possible to get a mild elevation in troponin with myopericarditis. The troponin levels may also be elevated if the patient had a silent myocardial infarction several days previously and now has secondary pericarditis. An echocardiogram will further assess the heart and exclude a pericardial effusion. Viral serology is usually requested, but would not take priority in this instance as it takes 2 weeks for the result and rarely changes management 3) NSAIDs are the treatment of choice in pericarditis, unless there are any obvious contraindications to their use

Features of aortic dissection

1) History of sudden-onset TEARING chest pain radiating to the BACK. 2) ABSENT pulse in ONE arm. 3) Hypertension (in about 50% of cases) or hypotension (in about 25% of cases). 4) A DIFFERENCE in blood pressure between arms >20 mmHg (about a third of cases). 5) New-onset aortic regurgitation. This is caused by the new lumen tracking down to the valve and making it incompetent. 6) Pleural effusion, usually on the left. Th is is due to irritation of the pleura by the dissecting aorta.

A 72-year-old man has come to the ED with acute severe lower back pain. He has not done any undue exercise or lifted anything heavy. He has no sensorimotor changes in his perineum or legs. He denies dysuria. His temperature is 37.0°C, pulse 96 bpm and BP is 142/78 mmHg. His BMI is 27 kg/m2. 1) What does AXR show?

1) There is curvilinear calcification present in the wall of an aneurysmal aorta (Fig.1 answer - arrows) and with the history of back pain a periaortic bleed needs to be excluded. CT is the technique of choice to evaluate the aorta and retroperitoneum acutely, but is only indicated in haemodynamically stable patients in whom the diagnosis is in doubt. Patients who are bleeding actively need to go straight to theatre for repair of the aneurysm. **As the patient is haemodynamically stable would next arrange: A CT aorta. would allow the aorta to be visualised and is better at looking for a leak that ultrasound. If there is no evidence of a leak, a CT scan is also useful to look for other pathologies. An unenhanced CT abdomen is useful to diagnose renal stones but is not indicated in this patient.

Explain the aetiology/risk factors of pulmonary embolism

1) Thrombus o 95% arise from DVT in the lower limbs o Rarely arises in the right atrium (in AF patients) 2) Other causes of embolus: o Amniotic fluid o Air o Fat o Tumour o Mycotic o Parasites o Right ventricular thrombus (post MI) o Septic emboli (right sided endocarditis) 3) Risk Factors: o Surgical patients o Immobility o Obesity o OCP o Heart failure o Malignancy o Thrombophilia o Pregnancy o Previous PE

3 general causes of chronic left heart failure

1) Valvular (LHS valves): Aortic stenosis, aortic regurgitation, mitral regurgitation 2) Muscular: ischaemia (IHD), cardiomyopathy, myocarditis, arrhythmias --> (biventricular failure) 3) Systemic: HTN, amyloidosis, drugs (e.g. cocaine, chemo)

1) On examination he is fully alert but in obvious discomfort, tachycardic and hypotensive. On examining his abdomen, you find an 8cm expansile mass in his epigastrium. This confirms your suspicions of a ruptured AAA. List in order your immediate management steps 2) Normal saline was chosen as the first fluid to given in resuscitation but this is not the only fluid which is appropriate. From the selection below which other fluid would it be reasonable to give in this scenario?

1) It is very important to follow the principles of ABC. We know he has a patent airway so after giving oxygen we rapidly move on to C (circulation). Again, it is important to place large diameter lines so that fluid can be administered as quickly as needed. In these cases aim to keep the systolic blood pressure at about 100 mmHg. Remember that a central line is long so actually has high resistance and is NOT for resuscitation. The only person who can save this patient is a vascular surgeon so they should be involved early. A urinary catheter is connected to a urometer to accurately measure urine output which reflects renal perfusion and, therefore, cardiac output. 2) Hartmann's solution. 5% Dextrose is the worst fluid to use for resuscitation purposes. Dextrose (glucose) is only added to make the solution isosmolar to plasma and is of no nutritional value. The glucose is immediately metabolised so what is given is essentially water and this will redistribute throughout the body and very little will stay within the vasculature which is what is required in a resuscitation scenario. Synthetic colloids are very good at staying within the vessels but many have a relatively short half life and also have the small risk if allergy. There is no proven benefit over normal (0.9%) saline. Natural colloids are controversial because they have more risk of anaphylaxis and do not give added benefits over other products in this scenario so are reserved for intensivists.

DDx of elevated JVP

1) Right Heart failure - could be secondary to left heart failure (=CCF), secondary to pulmonary hypertension (e.g. due to PE and COPD) 2) Tricuspid regurgitation (valve leaflets, right ventricle dilatation) 3) Constrictive pericarditis: infection, inflammation, malignancy

You are called to see a 73-year-old male patient with abdominal pain in the ED. He gives a history of generalised abdominal pain over the previous 2 hours, worse in the epigastrium, which radiates through to the back. He felt dizzy and light-headed initially and also nauseated, but now feels a little better. He has not vomited and has not experienced shortness of breath or chest pain. He has no significant bowel or urinary symptoms. He is a smoker, 10 per day but does not drink much alcohol. He has a history of mild hypertension, treated with bendroflumethiazide, but has no other medical history of note. On examination, he is peripherally perfused but mildly clammy. His heart rate is 95bpm and regular, blood pressure 110/65 mmHg and temperature 37.2oC. Cardio-respiratory examination is unremarkable and pulses are present in both wrists and groins. His abdomen appears mildly distended and is diffusely tender and difficult to examine especially in the epigastrium where there is fullness. Bowel sounds are present but quiet. Examination of the lower limbs confirms pedal pulses to be present but there are some scattered purpuric changes noted over the shins. Blood results: Hb 105 135-180 g/L WCC 13 4-11 x109/L Plt 212 150-450 x109/L Na+ 138 136-145 mM K+ 4.2 3.5-5.1 mM Ur 6.8 1.7-8.3 mM Urine dipstick: normal 1) Which four diagnoses would you consider? 2) Which five initial investigations would you arrange?

1) acute pancreatitis, MI, perforated duodenal ulcer, leaking AAA. § The initial diagnosis in this patient is not clear and abdominal examination is difficult. § He does not have a classical palpable, expansile and tender mass to indicate a leaking aortic aneurysm, although the history is suggestive with pain radiating to his back. § The presence of lower limb purpura is also concerning and would be explained by small emboli from the aneurysm. § Acute pancreatitis, duodenal perforation and myocardial infarction do all need to be excluded however. § Gastric volvulus is usually associated with severe pain and vomiting and abdominal distension/pain tends to be more pronounced with sigmoid volvulus (bowel sounds increased). § The history is not typical of renal colic or appendicitis. 2) ECG, serum amylase, abdo X-ray, chest X-ray (erect), cardiac enzymes. Lumbar spine radiographs/IVU are not indicated. This pain is not typical of renal colic and is not lumbar in origin.

1) 36 y/o male w/ LHS dull chest pain for 5 days. Recent sore throat and headache last week which has since resolved. DDx? 2) upon cardio exam --> tachycardic (100bpm), chest pain worse when lie back, nothing else remarkable. What Ix?

1) myocarditis, pericarditis, infective endocarditis, pericardial effusion, MSK trauma 2) § bedside - BP, HR, sats, temp (basic obs), urine dip, ECG § bloods - CRP/ESR, FBC, Troponin T, U&Es, VBG § radiology - CXR, Echocardiogram § other **results - normal CXR, tachycardic, ECG in pic. Bloods- raised WBC, CRP, Troponin T is normal. Hence likely to be pericarditis

Mrs Swanson is no longer confused after a night's sleep and some antibiotics for her pneumonia. She tells you that her ulcer is not really painful but that her legs often 'feel heavy' if she has been standing for a while. Her right ankle has been very itchy lately. She has not noticed any varicose veins and does not get pain in her calves when walking because of arthritis in her hip limiting her mobility. She never gets chest pain or suffers from shortness of breath. Her past medical history is remarkable for bilateral hip osteoarthritis, well-controlled hypertension, a presumed TIA 2 years ago, and chronic glaucoma in her right eye. She takes regular diclofenac with misoprostol for her hip pain, timolol and latanoprost for her glaucoma, and aspirin, simvastatin, ramipril, and bendrofl umethiazide because of her hypertension a previous TIA. She smoked a packet of cigarettes every day from her 20s until her 50s. She has lived at home alone since the death of her husband 2 years ago. What will you look for on examination? Think of what features might distinguish the most common types of leg ulcers. Also think about other signs associated with the underlying pathology that you can look for.

1) Site of ulcer: § Venous ulcers occur where venous pressures are highest, which is the GAITER area of the legs (i.e. the area covered by a long sock). The most commonly affected area is just ABOVE the MEDIAL MALLEOLUS malleolus because this is the site of the medial calf perforators. § Arterial ulcers occur where arterial blood supply is worst, which tends to be the distal areas of the FOOT (e.g. between TOES) and those that are frequently compressed (e.g. BALL of foot, LATERAL malleolus, and bony PROMINENCES). § Neuropathic ulcers are caused by repetitive trauma in a foot that has lost sensation, and thus occur in pressure areas where the foot rubs on poorly fitting footwear (e.g. BENEATH the METATARSAL HEADS). 2) Characteristics of the ulcer? § Venous ulcers: shallow, wet, and with irregular borders that look white and fragile. § Arterial ulcers: deep, punched out, dry, and often elliptical. § Neuropathic ulcers often have very thick, keratinized, raised edges surrounding them (unlike a basal cell carcinoma, which has rolled edges that are not as thick). § Pyoderma gangrenosum (a type of ulcer associated with inflammatory bowel disease or haematological malignancies) often has a characteristic dark blue/purple halo around it. 3) Associated signs? § Venous ulcers are due to increased hydrostatic (venous) pressure, which can also cause OEDEMA, EXTRAVASATION, and death of erythrocytes (skin PIGMENTATION) and eventually scarring of the skin ('ATROPHIE BLANCHE') and underlying tissue ('LIPDERMATOSCLEROSIS'). Superficial varicose veins or a collection of small, dark, engorged superficial veins ('ANKLE FLARE') may be visible. In extreme cases, severe lipodermatosclerosis may lead to an 'INVERTED CHAMPAGNE BOTTLE' appearance to the leg. § Arterial ulcers are due to limb ischaemia and are therefore associated with COLD, PALE limbs with POOR capillary refill, absent or WEAK PULSES, and ATROPHY skin changes (dry, shiny, hairless). BUERGER's TEST may reveal blanching of the foot on elevation to 45 degrees and reactive hyperaemia on lowering the leg, suggesting arterial insufficiency. They usually occur in patients with widespread atherosclerotic disease. Thus, look for popliteal and AAAs, and listen for carotid, femoral, or renal artery BRUITS. § Neuropathic ulcers are due to loss of sensation. Typically, VIBRATION and PROPRIOCEPTION are lost before other modalities. Foot DEFORMITIES may be present due to motor neuropathy or repetitive joint trauma secondary to sensory neuropathy (CHARCOT joints). § Inguinal lymphadenopathy: check for this if you suspect infection or MALIGNANCY as the cause of the ulcer.

Generate a management plan for STEMI

1) Same as UAP/NSTEMI management except: ● Clopidogrel ▪ 600 mg if patient is going to PCI ▪ 300 mg if undergoing thrombolysis and < 75 yrs ▪ 75 mg if undergoing thrombolysis and > 75 yrs ▪ MAINTENANCE: 75 mg daily for at least 1 year ● If undergoing primary PCI: ▪ IV heparin (plus GlpIIb/IIIa inhibitor) ▪ Bivalirudin (antithrombin) 2) Primary PCI: ● Goal < 90 min if available 3) Thrombolysis: ● Uses fibrinolytics such as streptokinase and tissue plasminogen activator (e.g. alteplase) ● Only considered if within 12 hours of chest pain with ECG changes and not contraindicated ● Rescue PCI may be performed if continued chest pain or ST elevation after thrombolysis 4) Secondary Prevention: ● Dual antiplatelet therapy (aspirin + clopidogrel/ticagrelor/ prasugrel) ● Beta-blockers ● ACE inhibitors ● Statins ● Control risk factors - diet, exericse 5) Advice ● No driving for 1 month following MI o CABG 6) Considered in patients with left main stem or three-vessel disease

Stage 1 vs stage 2 hypertension

1) Stage 1 - >= 135/85 mmHg. § Treat if <80 years AND any of the following: (CORD10) -Established CVD -Target Organ damage -Renal disease -Diabetes -10 year CV risk equivalent to 10% or greater 2) Stage 2 >= 150/95 mmHg. Treat all patients regardless of age **Signs of chronic hypertension - LVH (heave), S4, bruits, hypertensive retinopathy

Features of PE (due to deep vein thrombosis (DVT))

1) This is a diagnosis of exclusion as its presentation can be very varied and it is therefore difficult to diagnose clinically. 2) History of sudden-onset shortness of breath and/or haemoptysis and/or pleuritic chest pain in someone with an inflamed limb and/or risk factors for blood clots (e.g. recent surgery, recent stasis, or hypercoagulable blood due to the oral contraceptive pill or malignancy). 3) Signs of hypoxia. The patient may appear pale, have cold peripheries, feel lethargic and/or be drowsy or confused, depending on the degree of hypoxia. 4) Right heart strain evidenced by a raised jugular venous pressure (JVP). 5) You should refer to the Wells' criteria for diagnosis of PE if you suspect this.

1) What birth defects are the following drugs associated with:Sodium Valproate AND Phenytoin 2) Describe the effect of carbamazepine and phenytoin on drug metabolism.

1) § Sodium Valproate: Neural tube defects § Phenytoin: Cleft palate + congenital heart disease 2) They are CYP450 inducersThey cause increased metabolism and, hence, reduced effectiveness of OCP and warfarin

Miss Gokhale is a 15-year-old school student who has come to neurology outpatients with her mother following three suspected seizures in the past 4 months. The first occurred during break time at school, after which she was brought to hospital by ambulance. Two subsequent attacks have taken place, one at home and another at school. Miss Gokhale has no recollection of the episodes, although she knows that she is confused for some time after they occur. Her mother, who spoke to witnesses at school, says that during each attack she 'goes tense and shakes vigorously'. She has not bitten her tongue or been incontinent. The attacks last 5-10 minutes, after which her daughter is confused for around 30 minutes. 1) What is the most likely diagnosis and why? 2) A couple of months later, Miss Gokhale comes back to hospital via ambulance whilst fitting. The seizure started at a dinner with her friends over half an hour ago and she has not regained consciousness at any time. What complication has happened to Miss Gokhale and how should she be managed acutely? What possible causes are there?

1) § Given the stereotyped nature, the lack of vagal symptoms prior to the attacks, and the slow spontaneous recovery with persistent confusion, Miss Gokhale has most likely had epileptic seizures. § § As with the case of Mrs Maxwell above, an EEG and brain CT/MRI was ordered to try to confirm the diagnosis. Neither showed any abnormality. § However, epilepsy is a clinical diagnosis and the neurologist felt there was enough in her history to warrant this diagnosis, so she was commenced on anticonvulsants. 2) Miss Gokhale is in status epilepticus. Th is is a medical emergency and requires urgent attention. § As always, you should start by assessing her airway, breathing, and circulation (ABC). § As part of this she should be given high-flow oxygen, have monitoring set up (continuous ECG, pulse oximeter, blood pressure cuff ), a blood capillary glucose measurement, and two intravenous (IV) lines put in with bloods taken for an FBC, U&Es, Ca2+, and Mg2+. § A selective toxin screen and levels of anticonvulsant medications may be appropriate if the history suggests intoxication or non-concordance. § Two IV lines are necessary, partly because they can be easily disrupted in patients who are convulsing and also because benzodiazepines (used to try to terminate the seizure) should have a dedicated line. § If she is hypoglycaemic you should treat her with 50 mL of 20% dextrose immediately. § Having checked her ABC, you should rapidly assess D and E: disability (Glasgow Coma Scale (GCS) and pupils) and exposure (a quick check for any obvious external signs of injury). § Then you should try to end her seizure. Start by giving her 2-4 mg of lorazepam IV as a slow bolus over 2 minutes. If she is still fitting 10 minutes later, you can repeat this. If 10 minutes after that she is still fitting, you should contact an intensive care consultant and start giving her a PHENYTOIN infusion with a loading dose of 18 mg/kg at a rate of 50 mg/min. Be sure to monitor her ECG and blood pressure when starting the infusion for arrhythmias and hypotension (both side-effects of phenytoin given acutely). By this time the intensive care specialists will have taken over and, if she is still fitting 10 minutes later, may decide to give her a GENERAL ANAESTHETIC such as thiopentone to terminate the seizure. § Once the acute situation has been dealt with, you should investigate the cause of her seizure. **In particular consider: § Poor compliance with anticonvulsant medications § Metabolic causes (hypoglycaemia, electrolyte imbalance - renal or liver failure are unlikely in this patient given her age) § Alcohol or other toxins § Hypoxia § Infection (intercurrent infection lowering the seizure threshold in a known epileptic, encephalitis/meningitis) § Hypertensive encephalopathy § Cerebral (tumour, head injury, or abscess are all possibilities - stroke, arteriovenous malformation, and vasculitis would be unlikely given her age) **In Miss Gokhale's case, the seizure was terminated with the initial dose of lorazepam. She later revealed that she had stopped taking her medications after a month as she had started to gain weight and felt self-conscious. In addition, she had consumed alcohol at dinner, which may have triggered the seizure.

1) Suggestions to relieve postural hypotension symptoms 2) Should these measures not be successful, what medication can be trialled?

1) § Standing gradually from the chair § Avoid standing for long periods **The first line treatment for postural hypotension is non-pharmacological treatment. There are many ways to mitigate the symptoms and they include: o Withdraw offending medication (either substitution ordiscontinuation) o Rise slowly from supine to sitting to standing position o Avoid straining, coughing, and prolonged standing in hotweather o Cross legs while standing o Squat, stooping forward o Raise head of bed 10 to 20 degrees o Small meals and coffee in the morning o Elastic waist high stocking o Increase salt and water intake o Exercise, eg, swimming, recumbent biking, and rowing 2) Fludrocortisone and Midodrine. § Fludrocortisone and Midodrine are the most commonly used agents for treatment in the UK, both are associated with potential side effects. § Fludrocortisone acts by expanding blood volume and reducing salt loss. Therefore it is important to monitor for potential fluid overload and electrolyte imbalance. § Midodrine is last line treatment and therefore is recommended by BNF only for: 'Severe orthostatic hypotension due to autonomic dysfunction when corrective factors have been ruled out and other forms of treatment are inadequate' It has a number of contraindications as it can cause serious cardiac side effects and therefore, it some health care settings can only be prescribed by a cardiologist.

74 y/o female with 2 Month of SoBOE, worsened during last 2 days, swollen legs. BG of STEMI and HTN. Ran out of supply of ramipril 2 days ago. DDx? Ix>

1) § acute decompensation of chronic heart failure § Exam --> 22breaths/min, bibasal inspiratory creps, pitting oedema 2) § bedside - basic obs, ECG, § bloods - FBC, U&Es, BNP, Troponin, ABG, CRP § radiology - CXR, echocardiogram

Summary of antiarrhythmics used for SVT, VT and AF

1)vagal manoeuvres+ adenosine for SVT 2) digoxin for Atrial fib, - beta blocker (chemical cardioversion), electrical cardioversion in younger patients. Also use anticoagulant to prevent clotting and stroke risk e.g. warfarin/NOAC (apixaban). § so for older patient - anticoagulant + beta blocker § younger patient - cardioversion § if is due to hyperthyroidism - treat this first. If idiopathic then just treat AF. **so overall: anticoagulation (warfarin/NOAC), rate control (beta blocker/digoxin). If new onset can give shock, as there is less chance of clot; otherwise give warfarin for 3 months first then shock. 3) amiodarone for VT 4) amlodipine (CCB) for hypertension

LSBP should be assessed with regard to prescribed Atenolol. T or F?

A lying standing blood pressure is an important assessment in an older adult who has fallen and should be undertaken in all patients who present this way. B blockers can exacerbate postural hypotension and this would be a further reason to make such an assessment.

Which three are the clinical features of mitral regurgitation? Atrial fibrillation, Dyspnoea, Pansystolic murmur radiating to the axilla, Pink cheeks, Slow rising pulse

Atrial fibrillation, Dyspnoea, Pansystolic murmur radiating to the axilla. Mitral regurgitation - often presents with dyspnoea, fatigue, palpitations. Signs - atrial fibrillation, displaced hyperdynamic apex, pansystolic murmur at the apex radiating to the axilla. The more severe the larger the ventricle. The cardinal symptoms of mitral stenosis are also fatigue and dyspnoea. Pink cheeks (mitral facies) are a sign associated with mitral stenosis, not regurgitation.

Implanted Cardiac Defibrillator

Automated implantable cardioverter defibrillator implantable inside the body - able to perform cardioversion, defibrillation and SOMETIMES - pacing of the heart Indications - to prevent sudden cardiac death. For primary (not yet suffered lift threatening arrhythmia episode) and secondary prevention (survivors of cardiac arrest secondary to VF/VT

Aston was a 33-year-old male who suddenly collapsed on stage. Although the doctors attempted "love CPR", the patient died, and the post-mortem revealed a hypertrophic heart. What was the most likely cause of death? A. Obstructed flow of blood from the heart B. Arrhythmia C. Reduced pumping of blood due to stiff myocardium D. Stroke E. Sub-arachnoid haemorrhage

B. Arrhythmia. Most likely cause of death from HCM, hypertrophic muscle affects electrical circuits

What are indications for rate or rhythm control in AF?

§ NICE guidelines state that the first line rate control medication is a beta blocker (in this case atenolol ). § This is often enough in patients to normalise their heart rate and limit many of their symptoms. § If this does not completely control the patient's rate, another drug can be added to the beta blocker. § This can be either diltiazem (a calcium channel blocker) or digoxin (the correct answer in this case).Verapamil would not be used alongside a beta blocker due to the risk of heart block in combined use. **Factors favouring rate control: Older than 65 years, History of ischaemic heart disease **Factors favouring rhythm control: § Younger than 65 years § SymptomaticFirst presentation § Lone AF or AF secondary to a corrected precipitant (e.g. Alcohol) § Congestive heart failure **NICE recommends the use of catheter ablation for those with AF who have not responded to or wish to avoid, antiarrhythmic medication. § the aim is to ablate the faulty electrical pathways that are resulting in atrial fibrillation. This is typically due to aberrant electrical activity between the pulmonary veins and left atrium § the procedure is performed percutaneously, typically via the groin § both radiofrequency (uses heat generated from medium frequency alternating current) and cryotherapy can be used to ablate the tissue

A 60-year-old woman presents to the cardiology clinic complaining of multiple episodes of syncope. She said that she gets breathless when climbing the stairs and can't go to the grocery store as often because her chest starts to hurt every time she walks the distance. She claims it has been going on for 2 months. After clinical examination and auscultation, a diagnosis of aortic stenosis is made. Which of the following correlates with severity of the disease? A. Radiation to carotids B. Decreased pulse pressure C. Soft S2 D. Ejection click E. Pulsus parvus et tardus

C. Soft S2

Diabetes mellitus hypertension management?

§ NICE recommends a blood pressure target of < 140/90 mmHg for type 2 diabetics, the same as for patients without diabetes. § Intervention levels for recommending blood pressure management should be 135/85 mmHg unless the adult with type 1 diabetes has albuminuria or 2 or more features of metabolic syndrome, in which case it should be 130/80 mmHg **Because ACE-inhibitors have a renoprotective effect in diabetes they are the first-line antihypertensives recommended for NICE. Patients of African or Caribbean family origin should be offered an ACE-inhibitor plus either a thiazide diuretic or calcium channel blocker. Further management then reverts to that of non-diabetic patients, as discussed earlier in the module. § Remember than autonomic neuropathy may result in more postural symptoms in patients taking antihypertensive therapy. § The routine use of beta-blockers in uncomplicated hypertension should be avoided, particularly when given in combination with thiazides, as they may cause insulin resistance, impair insulin secretion and alter the autonomic response to hypoglycaemia.

Mr Daniels is a 52-year-old man who presents to A&E with a 4-hour history of chest pain associated with nausea and vomiting. His cardiac risk factors include a 15-pack-year history of smoking, although he quit 10 years ago, and a father and brother who had heart attacks in their fifties. He has no other medical history of note and reports no symptoms of reflux disease, but drinks 20 units of alcohol a week. On examination he appears uncomfortable and dyspnoeic. The rest of his examination is unremarkable except for mild consolidation at his left lung base. His ECG and troponin on admission are normal. A chest radiograph confirms a small effusion on the left. What are the most likely diagnoses? If his 12-hour troponin levels are normal, does this change your differential? What complications should you be particularly wary of?

§ Nausea and vomiting are commonly associated with INFERIOR MIs. § However, the small unilateral pleural effusion should alert you to the possibility of Boerhaave's syndrome - a perforation in the oesophagus. This was indeed the case with this patient, whose 12-hour troponin levels proved to be normal. § Note that the vomiting should precede the onset of pain in Boerhaave's: contrast this with MI (pain precedes vomiting), as it is the vomiting that causes the perforation (whereas in infarction, it is the post-infarct inflammation that irritates the diaphragm). § Not unusually, this patient was not a particularly good historian and could not recall which came first. § Patients with Boerhaave's are prone to develop a pleural effusion, pneumomediastinum and/or pneumothorax, perhaps followed by infection with gastrointestinal flora (mediastinitis and sepsis). § Treatment consists of prompt antibiotic therapy and surgical repair of the oesophagus with mediastinal washout. § Prognosis is grim, with a 30% mortality if surgical intervention is initiated within 24 hours, rising to 50-65% if surgery is delayed beyond 24 hours. Whilst it is a rare diagnosis it is important to be aware of it as early diagnosis is critical in increasing the chances of survival.

Necrotising fasciitis

§ Necrotising fasciitis is a life-threatening subcutaneous soft-tissue infection that requires a high index of suspicion for diagnosis § Infection may be polymicrobial in aetiology (type I) due to mixed anaerobic/facultative anaerobic organisms, or due to a single organism (type II), most commonly Streptococcus pyogenes, also called group A streptococcus. **Key diagnostic factors: § presence of risk factors (Patient to patient spread of group A streptococcal infection, varicella zoster infection, cutaneous trauma, non-traumatic skin use, IVDU § anaesthesia or severe pain over site of cellulitis § fever § palpitations, tachycardia, tachypnoea, hypotension, and lightheadedness **Ix: § FBC - abnormally high or low WBC count with or without a left shift (elevated percentage of polymorphonuclear leukocytes and/or bands) § U&E - sodium may be decreased § urea and creatinine and CRP may be elevated § blood and tissue cultures: positive; may indicate polymicrobial or monomicrobial aetiology § ABG -hypoxaemia, acidosis (if resp compromise) § radiography, CT/MRI -oedema extending along fascial plane and/or soft tissue gas § surgical exploration - surgical consultation for inspection, exploration, and debridement of infected tissue should be obtained in every case of suspected necrotising fasciitis

Which BP medication is most likely to cause bilateral ankle oedema?

CCB. And spiro causes gynaecomastia. § ContraIndications of Beta blockers: Asthma; cardiogenic shock; hypotension; marked bradycardia; metabolic acidosis; phaeochromocytoma (apart from specific use with alpha-blockers); Prinzmetal's angina; second-degree AV block; severe peripheral arterial disease; sick sinus syndrome; third-degree AV block; uncontrolled heart failure § Spironolactone induces gynecomastia by decreasing testosterone production, increasing peripheral conversion of testosterone to estradiol § CCBs: cause ankle swelling by increasing capillary pressure leading to leakage of fluids into the surrounding tissues

The same trace is shown again. What three statements are correct regarding this rhythm?

CPR is always required. Defibrillation is always indicated. Hyperkalaemia is a cause. § Ventricular fibrillation is a disorganised electrical activity that will not produce organised myocardial contraction and therefore the patient will be pulseless. CPR and early defibrillation is the treatment for VF. There are multiple causes of VF arrests including electrolyte abnormalities (hyperkalaemia, hypokalaemia, hypocalcaemia), toxins (particularly tricyclic antidepressants taken in overdose), hypothermia, and, less commonly the other causes of cardiac arrest. If you do not know them please look up the "4H's and 4T's" of reversible causes of cardiac arrest and the management of these. **Major points include: § ratio of chest compressions to ventilation is 30:2 § chest compressions are now continued while a defibrillator is charged § during a VF/VT cardiac arrest, ADRENALINE 1 mg is given ONCE chest compressions have restarted after the THIRD shock and then every 3-5 MINUTES (during alternate cycles of CPR). § a single shock for VF/pulseless VT followed by 2 minutes of CPR, rather than a series of 3 shocks followed by 1 minute of CPR § if the cardiac arrested is witnessed in a monitored patient (e.g. in a coronary care unit) then the 2015 guidelines recommend 'up to three quick successive (stacked) shocks', rather than 1 shock followed by CPR § asystole/pulseless-electrical activity: adrenaline 1mg should be given as soon as possible ASAP. Should be treated with 2 MINUTES of CPR prior to reassessment of the rhythm § atropine is no longer recommended for routine use in asystole or pulseless electrical activity (PEA) § delivery of drugs via a tracheal tube is no longer recommended § following successful resuscitation oxygen should be titrated to achieve saturations of 94-98%. This is to address the potential harm caused by hyperoxaemia

Explain the aetiology and risk factors of cardiac failure

Cardiac failure can be classified in different ways: 1) Systolic versus diastolic failure a) Systolic failure/ HFrEF: inability of the ventricle to contract normally, resulting in decreased CO. Ejection fraction <40%. Causes: IHD, MI, dilated cardiomyopathy, long-standing hypertrophy b) Diastolic failure/HPpEF: inability of the ventricle to relax and fill normally, causing increased filling pressures. Caused by long-standing hypertension --> hypertrophy (less room for filling), aortic stenosis, hypertrophic cardiomyopathy, restrictive cardiomyopathy (stiff + less compliant) 2) Acute versus Chronic heart failure a) Acute: new onset acute or decompensation of chronic heart failure characterised by pulmonary and/or peripheral oedema with/without signs of peripheral hypoperfusion b) Chronic: develops slowly. Venous congestion is common but arterial pressure is maintained well until late. 3) LOW OUTPUT Cardiac Failure (reduced cardiac output, failing to rise normally with exertion): a) Left Heart Failure (left ventricular failure) ● Ischaemic heart disease ● Hypertension ● Cardiomyopathy ● Aortic valve disease ● Mitral regurgitation b) Right Heart Failure (right ventricular failure) ● Secondary to left heart failure (in which case it is called congestive cardiac failure) ● Infarction ● Cardiomyopathy ● Pulmonary hypertension/embolus/valve disease ● Chronic lung disease ● Tricuspid regurgitation ● Constrictive pericarditis/pericardial tamponade c) Biventricular Failure ● Arrhythmia ● Cardiomyopathy (dilated or restrictive) ● Myocarditis ● Drug toxicity 4) HIGH OUTPUT Cardiac Failure (increased demand, quite rare, heart is normal but can occur earlier if there if heart disease) o Anaemia o Beri beri o Pregnancy o Paget's disease o Hyperthyroidism o Arteriovenous malformation ***RISK FACTORS: The most common risk factors are advanced age, female sex, hypertension, obesity, chronic kidney disease, diabetes mellitus, and coronary artery disease.

Describe the progression of ECG changes you would expect to see over 7 days in a patient presenting with acute STEMI.

Classically you see the following changes: 1) Tented T waves in the aff ected leads within minutes of the occlusion (due to localized hyperkalaemia following myocyte ischaemia) 2) ST elevation in the aff ected leads with ST depression in the reciprocal leads, lasting 24-48 hours 3) T wave inversion, developing in 1-2 days and persisting for weeks or months 4) Q waves, developing within days and remaining permanently

Which three of the following investigations are used in the diagnosis of DVT? Chest radiograph Colour doppler ultrasound D-dimer estimation Venometry Femoral angiography ESR/CRP

Colour doppler ultrasound, D-dimer estimation, Venometry. A venometer is a machine that uses automated strain gauge plethysmography to detect DVT. It is quick and non-invasive. It is sensitive but not specific for the diagnosis of DVT, i.e. it has a good negative predictive value. A doppler ultrasound uses reflected sound waves to evaluate blood as it flows through a vessel. It is more specific for the diagnosis of DVT. D-dimer is a sensitive, but non-specific test for DVT. It may also be increased in infection, pregnancy, malignancy and post-operatively.

Which five of the following are recognised complications of infective endocarditis?

Complete heart block, Transient ischaemic attack, Acute kidney injury, Heart failure, Vertebral osteomyelitis. § Acute kidney injury is common and often multi-factorial - septic emboli leading to infarction or abscess formation, sepsis, drug-induced acute interstitial nephritis or toxicity and immune-related glomerulonephritis (the latter is now uncommon in the UK) § Acute hepatitis and Pancreatitis are not a recognised complications of endocarditis.

Chest radiograph, amylase and ECG are normal.The abdominal radiograph is shown below. (Fig.1) Which statement best describes the findings?

Curvilinear calcification within an aneurysmal aorta

Mrs McDonald looks systemically well but her right calf is indeed swollen (pitting oedema), red, warm, and tender from just below the knee to just above her ankle. Her right calf is 4.5 cm greater in circumference than her left calf. There are no wounds visible on her leg and no lymph nodes palpable in her right leg or right groin. Palpation of the popliteal fossa reveals no swelling. Slow, passive movement of the ankle and toes does not elicit any pain, only mild discomfort in her right calf. Her sensation to light touch is preserved throughout her right limb. Her posterior tibial pulses are present. Dorsalis pedis is not palpable on either leg, but capillary refill time in the toes of both feet is <2 seconds. Power on dorsiflexion, plantar flexion, and big toe dorsifl exion (extensor hallucis longus) is 5/5 on the MRC scale for both feet. There are no abdominal masses palpable. The history, examination, and risk factors mentioned by Mrs McDonald should have narrowed your differential diagnosis down to just three 'most likely' diagnoses. Which are they?

DVT, ruptured Baker's cyst, or cellulitis.

Why might you measure blood glucose levels in a patient with a suspected ACS?

Diabetic patients can have 'silent infarcts' - MI without chest pain

Silent MI common in...

Diabetics

ECG criteria of a STEMI include

ECG criteria of a STEMI include: § ≥2 mm of ST segment elevation in 2 contiguous precordial leads in men (1.5 mm for women) § ≥1mm in other leads (2 contiguous) § An initial Q wave or abnormal R wave develops over a period of several hours to days

Prolonged PR interval in rheumatic fever

ECG showing heart block in acute rheumatic fever

Echocardiogram confirms probable vegetations on the mitral valve with regurgitation evident. Which four of the following are used as clinical criteria to make a diagnosis of infective endocarditis?

Echocardiogram evidence of valve vegetations, Focal lesions in the spleen on ultrasound, Positive rheumatoid factor, Pyrexia of over 38 °C § Major diagnostic criteria include more than one positive blood culture (typical organism in 2 separate cultures or presistently positive blood cultures), or positive echocardiogram findings of vegetation, abscess or abscess prosthetic valve. ** Minor criteria include: § predisposition (cardiac lesion, IV drug abuse); § fever over 38 °C; § vascular signs, e.g. mycotic emboli, Janeway lesions (painless palmar/plantar macules); § immunological signs e.g. Oslers nodes (painful swelling fingers/toes), positive RhF, glomerulonephritis; § microbiological evidence not fitting major criteria. **Diagnosis is made on 2 major, 1 major/3minor or >5 minor criteria.

A 33-year-old woman presents with sudden onset hemiparesis affecting the right face, arm and leg. On examination you note right sided hemiparesis, aphasia, a right homonymous hemianopia, and a harsh pansystolic murmur. Over the past few weeks she has been complaining of low grade fever.What is the most likely cause of the stroke? Atrial myxoma/ Left ventricular/ thromboembolism/ Cerebral abscess/ Ventricular septal defect/ Emboli from infective endocarditis vegetation

Emboli from infective endocarditis vegetation. § The PANSYSTOLIC murmur and low grade FEVER are suggestive of infective endocarditis. Small amounts of material (e.g. bacteria and thrombi) called vegetations may develop on infected endocardium. Sections of these vegetations may break away and circulate to the brain and other vital organs. This can result in an ischaemic stroke as demonstrated in this case. § An atrial myxoma is a type of primary cardiac tumour. They are usually found in the left atrium. On auscultation, a late diastolic tumour 'plop' may be heard. They are very rare and therefore, combined with the auscultation findings, the best answer in this case would be infective endocarditis

Cardiac cirrhosis

From long-standing severe right-sided heart failure --> venous congestion. § also get ascites, pitting oedema

Which scoring system allows risk stratification of NSTEMI patients.

GRACE score

Gliclazide is safe because it does not cause hypoglycaemia. T or F?

Gliclazide does cause hypoglycaemia and as such is not often the best medication of choice for diabetes in the elderly. A history regarding other possible episodes of hypoglycaemia, blood sugar diary monitoring and HbA1C testing would be helpful in making further judgements about it's appropriate continuation.

1) Which five conditions below can cause sinus bradycardia? 2) What is the prognosis in this patient?

Hypothermia, Hypothyroidism, Aerobic training, Legionnaire's disease, Myocardial infarction. Sinus bradycardia can be normal in athletes, and is also caused by hypothermia, hypothyroidism, vagal stimulation, drugs (e.g. beta blockers), raised intracranial pressure and myocardial infarction. Sinus bradycardia can also be a feature of certain infections including Legionnaire's disease, typhoid fever and Lyme disease. Hypocalcaemia is associated with a prolonged QT interval rather than bradycardia. 2) No adverse prognosis. In a healthy asymptomatic patient, there is no adverse prognosis associated with a sinus bradycardia

What would be the desired reference range for the INR when treating a patient with an uncomplicated DVT?

INR 2.0-3.0. § INR 2.0-3.0 is correct. Treatment for an uncomplicated first DVT usually lasts between 6 and 12 weeks. § INR 1.0-2.0 - Incorrect. This is too low when treating DVT patients. § INR 3.5-4.5 - Incorrect. This value is too high for DVT patients but may be used in patients with a prosthetic heart value.

What is the name of the test which monitors the therapeutic effect of warfarin?

INR. The prothrombin time is used to measure the effect of warfarin, ratio to normal expressed as the INR (international normalised ratio). Heparin is monitored using the APTT, thrombin time measures fibrinogen function, bleeding time for platelet function and the Coombs' test is an antiglobulin test used in autoimmune haemolytic anaemia.

Identify possible complications of venous ulcers AND complications

Identify possible complications of venous ulcers ● Recurrence ● Infection Summarise the prognosis for patients with venous ulcers ● GOOD ● Results are better if patients are mobile with few comorbidities

CHADVASC score

Identify which patients are at greatest risk for thromboembolism, and would benefit from antithrombotic therapy.: if score>4, give warfarin.

Which three of the following statements concerning treatment of infective endocarditis are true?

If possible antibiotic treatment should be commenced once culture results available. Heart failure suggests valve failure and is an indication for urgent surgery. Mortality in native valve endocarditis is estimated to be 80-90% at one year whereas in prosthetic valve endocarditis it is significantly higher, up to 40%. § Prolonged antibiotic treatment (4-6 weeks) is usually necessary § Large vegetations on the mitral valve are an indication for surgery § Surgery is best delayed to allow effective antibiotic treatment if the patients condition allows

What makes up IHD?

In ACS: all due to myocardial ischaemia. Presentations of varying severities of myocardial ischaemia Due to coronary artery plaque rupture/ erosion and intra-luminal thrombosis

What does GRACE score assess?

In NSTE-ACS Risk stratification- Grace score -Assesses risk of 6 month mortality -Categorise the risk of future cardiovascular events 1.Offer coronary angiography within 96 hours of admission •Intermediate/ high risk of adverse cardiovascular events- 6 month mortality > 3% •Consider addition of GPIIb/IIIa inhibitors. § give fondaparinux if no immediate PCI 2.Conservative management without early coronary angiography •Low risk of cardiovascular events- 6 month mortality < 3%. Give ticagrelor. 3.Offer coronary angiography if initially low risk but ischaemia is subsequently experienced/ demonstrated by ischaemia testing ● SECONDARY PREVENTION- SAAB -Statin -Antiplatelet -ACEi -Beta Blocker

ECG was undertaken (image below). What is the diagnosis from the ECG??

Inferior-lateral MI. The ECG demonstrates an inferior-lateral myocardial infarct. This is a result of the dissection involving the right coronary artery (RCA). Aortic dissection can involve any of the branches off the aorta, most commonly involved are renal, spinal, coronary or iliac arteries or as in this case dissect back into the aortic valve resulting in aortic incompetence (early diastolic murmur). This is an important point to remember with patients presenting with atypical histories for MIs. As had this patient been thrombolysed for an MI it could have made the situation drastically worse and most likely resulted in the death of the patient.

What is HOCM?

Inherited genetic disorder (autosomal dominant) of inappropriate LV and/or RV hypertrophy (especially septal). Unexplained syncope is one of the indicators that sudden death may occur and thus rapid treatment is required as well as limiting any strenuous exercise - an implantable cardioverter-defibrillator can be inserted to reduce the risk of sudden cardiac death in HOCM. echocardiogram shows an increased thickness of the interventricular septum which is characteristic of hypertrophic obstructive cardiomyopathy (HOCM).

Which of the following factors are risk factors for the development of infective endocarditis?

Intravenous drug abuse, Pneumonia, Colonic malignancy, Prosthetic valve, Chronic cholecystitis, Miscarriage

What is the term used to describe severe lipodermatosclerosis?

Inverted champagne bottle sign

Investigations for aortic dissection

Ix: 1) ECG -Rule out ACS -Normal or may show LV strain •Bloods (same as in ACS) 2) CXR -Widened mediastinum (>8cm) rare -Irregularity of aortic knuckle + small left pleural effusion 3) Echo -May show aortic root leak, aortic valve regurgitation, pericardial effusion 4) CT/MRI- definitive diagnosis

ECG is shown below. What does this ECG show?

Left bundle branch block. The ECG demonstrates left bundle branch block, with prolongation of all QRS complexes. There is also some evidence of left ventricular hypertrophy in the antero-lateral leads: the depth of the S wave in V2 + height R wave in V5 > 30mm, (although please note that further interpretation of the ECG is difficult in the setting of left bundle branch block).

A 66-year-old woman suddenly develops dyspnoea 10 days after having an anterior myocardial infarction. Her blood pressure is 78/50 mmHg, JVP is elevated and the heart sounds are muffled. There are widespread crackles on her chest and the oxygen saturations are 84% on room air. What is likely complication of MI?

Left ventricular free wall rupture: The prognosis from such a catastrophic event is clearly poor unless this patient has immediate surgery.

Elderly patients presenting to hospital with a loss of consciousness are often seen as an unexciting or unglamorous case, but they are in fact patients who require rapid, effective multidisciplinary team management. Why is loss of consciousness in the elderly so important?

Loss of consciousness in the elderly carries a very high risk of: 1) Morbidity: elderly patients who lose consciousness and fall are likely to: − Injure themselves seriously. Falling can result in head trauma and subdural haematomas; radial fractures that make washing, cooking, and eating difficult; neck of femur fractures that confine them to bed; etc. − Lose their confidence. Ask yourself if you would walk confidently down a flight of stairs if the last time you did so you fell down 15 stairs and broke a hip and both ankles. This often leads to signifi cant anxiety or depression, which needs managing. − Lose their independence. For example, an elderly patient who has fractured a clavicle and radius may go from living alone to being dependent on carers to wash, get dressed, cook, and feed themselves. 2) Mortality: loss of consciousness in an elderly patient may not sound life-threatening, but if the patient suffers, say, a neck of femur fracture, they may need a prolonged hospital stay. Whilst an inpatient, their immobility may lead to a deep vein thrombosis and pulmonary embolus. Or they may get pressure sores, which in turn may get infected. They may get urinary tract infections from indwelling catheters, or pneumonia from the lack of movement and small areas of collapsed lung (atelectasis), leading to poor clearance of mucus. A fractured neck of femur continues to be a major (albeit indirect) cause of death in elderly people in the developed world. 3) Cost: loss of consciousness in the elderly, if accompanied by a fracture, can result in a lengthy hospital stay, prolonged physiotherapy, investment to adapt their house for their new immobility, regular (often daily) visits by carers to help with activities of daily living (ADLs), days off work for caring relatives eager to help, and sometimes moving into a nursing home. All of this entails signifi cant cost to the patient, their family, and the state.

Describe the management of ACS

MONABASH § Morphine - may be given with an anti-emetic e.g. metoclopramide § Oxygen - maintain oxygen saturations of 94% § Nitrates - e.g. GTN or imdur § Anticoagulants - e.g. aspirin + clopidogrel § Beta-blockers - reduce myocardial oxygen demand § ACE inhibitors - reduce adverse cardiac remodeling + antihypertensive § Statins - control cholesterol § Heparin - can be used to reduce future thromboembolic risk

The Doppler ultrasound of Mrs McDonald's right calf showed an occlusion in one of her deep veins consistent with a DVT. Her serum D-dimer was not requested and her FBC was normal. How will you manage Mrs McDonald?

Mrs McDonald has had a diagnosis of DVT confi rmed by Doppler ultrasound. Her management should include: 1) Anticoagulation. This is to prevent clot extension, PE, and recurrence: with LMWH or fondaparinux, then ongoing anticoagulation is achieved with warfarin or rivaroxaban. LMWH is administered via a subcutaneous (SC) injection and is dosed according to the patient's weight. In addition they should be started on warfarin and have their international normalized ratio (INR) measured until it is stable in the target range (2-3) at which point the LMWH can be stopped. The optimal duration of anticoagulation therapy is debated and varies with a number of factors such as location (above/below knee), previous DVTs, and the presence of risk factors. Mrs McDonald will require 3 months on warfarin. 2) Compression stockings. To prevent acute recurrence. Mrs McDonald should also be advised to wear compression stockings on long-haul travel (or at other times of prolonged stasis). 3) Lifestyle advice. Lifestyle advice, e.g. cessation of hormone replacement therapy (HRT) or the combined oral contraceptive pill, weight loss. These are risk factors for DVT that you should address.

Mrs Swanson's admission blood results show leucocytosis and a raised CRP, as expected in a patient with pneumonia. Her ABPI is 0.95. How should Mrs Swanson's ulcer be managed?

Mrs Swanson almost certainly has a VENOUS ulcer. This is the result of prolonged venous stasis in her lower limb, and thus management of venous ulcer involves: 1) Adequate nutrition, vital for any healing process but especially relevant for venous ulcers as they tend to occur in elderly patients who may be MALNOURISHED or deficient in key vitamins and minerals (e.g. vitamin C, zinc). 2) Lifestyle modification: encourage patients to MOBILISE (to encourage venous blood fl ow in the legs). 3) Leg elevation whenever possible, to reduce blood pressure in the lower limb. 4) Compression bandages applied and frequently changed by an experienced nurse, to reduce the pooling of venous blood in the lower limb. This can be done safely given that her ABPI is GREATER THAN 0.8. 5) Graduated class I or II elastic stockings will be helpful once the venous ulcer has healed to prevent recurrence. 6) Varicose vein surgery may also be helpful in preventing recurrence if the ulcer was caused by obvious superficial varicosities and there is no deep vein incompetence (see viva question). **With this management, about 80% of venous ulcers will heal within 26 WEEKS. Those that fail to heal in this way may require skin GRAFTING by the plastic or vascular surgeons.

A 68-year-old male presents to the emergency department with crushing chest pain radiating up his neck. His heart rate is 72 beats/min with a regular pulse. Electrocardiogram demonstrates sinus rhythm with no ST-elevation, however point-of-care troponin is elevated.Although the patient is not at high-risk of bleeding, a joint decision is made that he is not for percutaneous coronary intervention at this point.He has already received aspirin .Which of the following medications should also be administered?

NSTEMI (managed conservatively) antiplatelet choice § aspirin, plus either: a) ticagrelor, if not high bleeding risk b) clopidogrel, if high bleeding risk **Dual antiplatelet therapy (DAPT) is indicated in the conservative management of non-ST elevation myocardial infarction (NSTEMI). § Ticagrelor is the correct option as this is a case of NSTEMI with low bleeding risk, as stated. § Edoxaban is incorrect as an anticoagulant that works by inhibiting factor Xa, and not indicated in use for NSTEMIs. § Warfarin is incorrect as an anticoagulant that inhibits the production of clotting factors II, VII, IX and X and not indicated for use in NSTEMIs. § Digoxin is incorrect in this case, but may be used in the management of heart failure or atrial fibrillation, however neither are present. § Amiodarone is incorrect. There is no arrhythmia present, hence there is no indication for amiodarone.

Contrasting unstable angina vs NSTEMI vs STEMI

NSTEMI/ Unstable Angina -Normal ECG... or... T wave inversion/ flattening, ST depression (no ST-elevation) -Troponin rise in NSTEMI, no raised troponin in unstable angina STEMI -ST elevation/ New LBBB Symptoms -Chest pain of varying severity/ duration -Possible radiation (more likely in NSTEMI and unstable angina) -Often associated SOB and nausea/ vomiting Signs -Pallor -Sweating and anxious -Tachycardia -Shock

Risk factors of ACS

Non Modifiable -Age -Sex (male is increased risk) -Family history Modifiable -Smoking -HTN -DM -Hyperlipidaemia -Obesity

How to assess SOB, orthopnoea, PND in OSCE

OSCE TIPS: 1) Assess SOB: "How far are you able to walk before getting breathless? How many flights of stairs?" 2) Assess orthopnoea: "Have you noticed anything making the SOB worse? What about lying down, standing up?" 3) Assess PND: "Do you ever wake up at night gasping for air? How many pillows do you sleep with at night? Has this changed recently?"

The ECG below shows typical U waves

One registered user suggests the following rhyme In Hypokalaemia, U have no Pot and no T, but a long PR and a long QT

•James is a 24 year old man who presents to ED after experiencing chest pain. He describes the pain as being sharp and centrally located, with radiation to the left arm. He reports feeling 'fluey' 10 days ago and says the pain is worse when he lies down and is relieved by sitting forward. •What is the most likely diagnosis?

Pericarditis

Describe the typical presentation of pneumothorax vs PE

Pneumothorax: Sudden-onset pleuritic chest pain with breathlessness. PE: Sudden-onset pleuritic chest pain with breathlessness § With or without haemoptysis § Patients may also have a swollen/inflamed leg (DVT)

When to consider polypharmacy?

Polypharmacy is an important risk factor for falls and should be considered in all patients prescribed more than four medications.

Which one of the following signs does the chest radiograph below show?

Pulmonary oedema, Acute pulmonary oedema signs on CXR - cardiomegaly, prominent upper lobe veins, diffuse interstitial shadowing, classic perihilar 'bat wings' shadowing.

Torsades de pointes

Rate: 120 - 200 usually P wave: Obscured by ventricular waves QRS: Wide QRS - "Twisting of the Points" Conduction: Ventricular only Rhythm: Slightly irregular **see it going up and down; arctic monkey sign toox

Define aortic regurgitation

Reflux of blood from the aorta into the left ventricle during diastole, due to a weakened aortic valve. Also known as aortic insufficiency

A 46-year-old man develops cardiogenic shock 48 hours after admission with an anterior myocardial infarction. He had intermittent chest pain symptoms for 3 days prior to admission. On admission, he underwent coronary angiography and percutaneous coronary intervention - a stent was inserted in to the left anterior descending artery. His ECG improved but there were anterior Q-waves and a degree of residual ST elevation. A loud pan systolic murmur is heard which is new. Which 4 of the following should be considered in the management of this patient? Repeat coronary angiography Inotropic support Intravenous beta-blockers Transfer to cardiothoracic surgical centre Urgent echocardiography

Repeat coronary angiography, Inotropic support, Transfer to cardiothoracic surgical centre, Urgent echocardiography. § Increasing revascularisation both with coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) has seen reductions in the number of deaths and complications following acute myocardial infarction. However, shock remains the leading cause of death in hospital particularly if patients present several hours or days after symptom onset. It is likely that this patient has developed a post MI ventricular septal defect or acute mitral regurgitation - investigations are aimed at determining this. The use of intravenous beta-blockers in the shocked patient is relatively contraindicated. The mainstay of treatment is therefore supportive and surgical intervention, if appropriate.

What is your immediate management priority once diagnosis of acute anterior myocardial infarction has been made?

Restore coronary blood flow with primary angioplasty (increase blood flow to heart). Salvaging any threatened myocardium is time sensitive. Thrombolysis or primary angioplasty are appropriate. Anticoagulation is not routinely indicated in patients with acute myocardial infarctions. All patients will have cardiac monitoring - there is no need to transfer the patient there before pursuing a strategy for restoring coronary bloodflow.

Generate a management plan for stable angina

STABLE ANGINA: o Minimise cardiac risk factors (e.g. blood pressure, hyperlipidaemia, diabetes) ● All patients should receive aspirin 75 mg/day unless contraindicated o Immediate symptom relief (e.g. GTN spray) o Long-term management ● Beta-blockers ▪ Contraindicated in: ● Acute heart failure ● Cardiogenic shock ● Bradycardia ● Heart block ● Asthma ● Calcium channel blockers ● Nitrates o Percutaneous coronary intervention (PCI) ● Performed in patients with stable angina despite maximal tolerable medical therapy o Coronary artery bypass graft (CABG) ● Occurs in more severe cases (e.g. three-vessel disease)

AA amyloidosis

Seen in a) Chronic inflammatory conditions: RA, IBD, cancers b) Chronic infections: osteomyelitis, TB **Composition of amyloid: b2microglobulin apolipoprotein or transthryretin

Recognise the signs of pulmonary embolism on physical examination

Severity of PE can be assessed based on associated signs: ● Small - often no clinical signs. There may be some tachycardia and tachypnoea ● Sudden onset ● Moderate o Tachypnoea o Tachycardia o Pleural rub o Low O2 saturation (despite O2 supplementation) o Pyrexia o Hypotension ● Massive PE o Shock o Cyanosis o Signs of right heart strain ▪ Raised JVP ▪ Left parasternal heave ▪ Accentuated S2 heart sound ● Multiple Recurrent PE o Signs of pulmonary hypertension o Signs of right heart failure

Interpret this ECG

Sinus rhythm and right bundle branch block. This ECG shows normal sinus rhythm with a normal axis (QRS more positive than negative in leads I and II). The diagnosis of left ventricular hypertrophy, a recognised complication of longstanding hypertension, is often made by voltage criteria, but these are not altogether reliable. This ECG shows R wave in V5 or V6 plus S wave in V1 is greater than 35 mm - but it does have an R wave in aVL of >11mm. False negative LVH diagnoses can be made in patients who are overweight or have emphysema or pericardial effusion; false positive diagnoses can be made in fit young people with thin chest walls. True LVH is often accompanied, as here, by ST-T changes that look remarkably like ischaemia, or even a digitalis effect in the leads with the largest R waves. This pattern is often refered to as a 'strain' pattern with no very clear understanding of what the 'strain' means pathophysiologically.

Virchow's triad

Stasis, hypercoagulability, endothelial damage

Causes of cardiac arrest

Sudden cardiac arrest is a sudden state of circulatory failure due to a loss of cardiac systolic function. Can result from 4 specific cardiac rhythm disturbances: ventricular fibrillation, pulseless ventricular tachycardia, pulseless electrical activity (electrical activity and no cardiac output) and asystole

What is the most common finding on examination of patients with PE?

Tachycardia. Also see S1Q3T3 in PE.

When a patient arrives with chest pain, you need to be thinking about the conditions that present with chest pain that are potentially fatal and require immediate management. Which diagnoses fall into this category? What features are going to alert you to these conditions?

Th e following diagnoses require immediate management and should be kept in mind: • Acute coronary syndrome (unstable angina, or myocardial infarction (MI)) • Aortic dissection • Pneumothorax • PE • Boerhaave's perforation

The pathologies causing ulcers are not limited to the ulcer but will be evident in other symptoms. These will vary depending on the pathology. What other symptoms occur in the most common pathologies causing ulcer (and therefore which symptoms should you ask about)?

The associated symptoms you should ask about are: 1) Venous ulcers: chronic venous insufficiency leads to VARICOSE veins, stasis eczema, leading patients to complain of ITCHINESS, and ankle oedema, leading to complaints of SWOLLEN ankles and a sensation of 'HEAVY FEET'. 2) Arterial ulcers: atherosclerosis is likely to be manifest systemically, thus ask about symptoms of peripheral arterial disease and coronary artery disease. These include CLAUDICATION, COLD EXTREMITIES, and ANGINA or shortness of breath (SOB) on exertion. 3) Neuropathic ulcers: these are associated with SENSORY LOSS, and patients may also have an UNSTEADY GAIT. There is often secondary infection, and if this is by anaerobes the patient may comment on a FOUL SMELL.

1) A CT scan of the aorta was performed (image below). What one of the following options does the CT scan show? 2) Which 2 options would be your immediate course of treatment for this patient? 3) Which is the most appropriate subsequent management?

The axial CT scan shows a type A aortic dissection as this is affecting the ascending aorta. The false lumen is clearly visible. The most common classification of aortic dissections is the Stanford classification. They are split into type A when the ascending aorta is involved and type B when the descending aorta is involved. This also has a relevance on treatment with virtually all type A dissections requiring surgery. 2) IV antihypertensives, Oxygen and analgesia. Patients with an aortic dissection should be admitted to intensive care units, where they are closely monitored. Death can occur a few hours after an aortic dissection begins. Therefore, anti-hypertensives, usually sodium nitroprusside plus a beta-blocker, are given intravenously to reduce the heart rate and blood pressure. Oxygen and analgesia would also be of benefit for symptom control. 3) Transfer to cardiothoracic centre for aortic root replacement/repair/stent. Type A dissections usually require surgical intervention. Surgery is performed via a median sternotomy and on cardiopulmonary bypass. The dissection is excised and the affected aorta is replaced with graft. The aortic valve is preserved if possible. An evolving CVA or established renal failure are contraindications to surgery. Without operation the prognosis for type A dissections is poor. 40% die within 24 hours and 80% die within 2 weeks. Operative mortality is approximately 25%. Type B dissections may be treated without surgery. Requires fastidious blood pressure control. Surgery should be considered if evidence of aortic expansion. Surgery for type B dissections is associated with significant risk of paraplegia.

Mr Williams has no past medical history of note, only childhood asthma. He is not taking any medications. He sheepishly admits to consuming more than 8 units of alcohol earlier that evening, but no other recreational drugs. The history argues in favour of some causes of blackout and against others, but you still need to exclude some of the less likely causes as they are potentially very serious. What signs would you look for on examination?

The examination may be unremarkable, but you should look for the following: a) Tongue: a bitten tongue. Make sure you look at the side of the tongue. b) Dehydration: signs of dehydration (e.g. dry mucous membranes, tachycardia, hypotension), as this can contribute to hypovolaemia and predispose to cerebral hypoperfusion. c) Head trauma: any signs of head trauma (you might expect this to have been mentioned in the history, although perhaps not from this patient if he was overly inebriated!). If there has been head trauma, try to establish whether it came before or after the loss of consciousness, i.e. did they hit their head as they fell? d) Heart: − A slow or irregular pulse, suggesting heart block or atrial fibrillation. − Look at the jugular venous pressure (JVP) for cannon waves. These are exaggerated 'a waves' in the jugular pulse caused by right atrial contraction occurring after ventricular contraction has closed the tricuspid valve. CANNON waves occur in COMPLETE HEART BLOCK, a cause of syncope. − A heart murmur. Aortic stenosis can cause outflow obstructions and cerebral hypoperfusion. e) Carotid bruits: suggest carotid artery stenosis (although loudness of the bruit has no bearing upon severity of the stenosis). f) Blood pressure: check for orthostatic hypotension. Take the blood pressure lying down and within 2 minutes of standing. Orthostatic hypotension is defined as a drop of ≥20 mmHg in systolic blood pressure or ≥10 mmHg diastolic on standing g) Focal neurological signs: look for signs of peripheral neuropathy (e.g. due to diabetes mellitus, chronic alcohol abuse) or parkinsonism that may be associated with autonomic dysfunction (e.g. in multisystem atrophy). In the case of suspected seizures, check that there has been a full neurological recovery.

A 56-year-old male travelling salesman presents to the Emergency department complaining of a 4-hour history of severe sharp central chest pain radiating through to his back. This is described as ripping in nature and came on suddenly and is not helped by taking paracetamol or indigestion medication. There is no radiation of the pain down his arm or jaw. There is no haemoptysis. He does feel unwell, sweaty and nauseated but has no vomiting. He has a known history of hypertension with no other previous medical history of note. On examination, patient looks unwell, pale and clammy but afebrile. His oxygen saturation is 96% on air. BP is 195/110 mmHg with a heart rate of 110bpm in sinus rhythm. He has an early diastolic murmur with a non elevated JVP. Chest was clear. Abdominal and neurology examinations were unremarkable. Screening blood tests (FBC, Urea and electrolytes, LFTs) are within normal ranges. 1) Based on the history and examination what is the most likely diagnosis? 2) Which initial investigations would you perform?

The history is classical for aortic dissection. The differential diagnosis for chest pain is large. However, the nature of the pain is atypical for an myocardial infarction. The position is atypical for a peptic ulcer or pancreatitis. There was no shortness of breath with normal oxygen saturation so making a pulmonary embolus or pneumothorax less likely. Aortic dissection is an important disorder to know as it can be commonly fatal. It is a result of the inner layer of the aortic wall tearing, leading to blood flowing through thereby dissecting the inner from middle layer. Aortic dissection is three times more common in males compared to females. There is also an increased prevalence amongst Afro-Caribbeans. Most aortic dissections occur due to arterial wall deterioration. This is commonly associated with high blood pressure, which is present in over half of people who have an aortic dissection. Aortic dissection may be caused by hereditary connective-tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome. It may also be caused by birth defects of the heart and blood vessels, such as coarctation of the aorta, patent ductus arteriosus, and defects of the aortic valve. Other causes include arteriosclerosis and trauma. 2) ECG, Chest X-ray. Initial investigations should be done to give evidence to your provisional diagnosis or help exclude differential diagnoses. In this case, a CXR would potentially show a widened mediastinum in keeping with an aortic dissection. It would also help rule out a pneumothorax. An ECG would help with many of the differentials for chest pain. We could potentially see if there was any evidence for PE (right heart strain, AF) and identify any areas of ischaemia or infarction.

Mrs McDonald is a 48-year-old cleaning lady who presents to a local hospital complaining of a swollen right calf that has appeared over that last few hours. What is your differential diagnosis for an acutely swollen limb?

The main causes of an acutely swollen limb are: § Deep vein thrombosis (DVT) § Cellulitis § Ruptured Baker's cyst (Swelling of a synovial bursa (usually the semimembranosus bursa) around the knee joint aka a popliteal cyst - CAN BE CLINICALLY V SIMILAR TO DVT) § Muscular strain § Septic arthritis § Lymphoedema § Pelvic tumour (e.g. ovarian) compressing iliac vein § Allergic response to insect bite § Compartment syndrome **Note that it is possible for different pathologies to coexist: a patient may present with a DVT and ruptured Baker's cyst, for example. Also, many patients will get a swollen leg following surgery to that leg, but this shouldn't present much of a diagnostic challenge and therefore is not included in the list above.

Which 2 of the following are true in patients with symptomatic aortic stenosis?

The most common cause under 60 years is a bicuspid aortic valve. Valvular replacement is the treatment of choice. Degenerative valve disease is the most common aetiology in older patients (the commonest group) with aortic stenosis. In younger patients a bicuspid valve is the commonest underlying cause Valve replacement is the treatment of choice in patients fit enough to undergo the procedure. If the patient is unfit for open heart surgery a valvuloplasty or transcatheter aortic valve implantation (TAVI) may be attempted. Exercise testing is contraindicated in aortic stenosis.

How might occlusion of the diff erent coronary vessels be distinguished on ECG?

There are four main patterns of infarction, resulting from occlusion of each of the main coronary arteries § The 'Anterior/Septal leads' correspond to the portion of the heart supplied by the left anterior descending artery. § The 'Right inferior leads' correspond to the portion of the heart supplied by the right coronary artery. § The 'Left lateral leads' correspond to the lateral wall of the left ventricle, supplied by both the left anterior descending and the circumflex arteries. **Anterior infarct: ST elevation in leads V2, V3, and V4 indicates infarction of the anterior surface of the left ventricle, supplied by the left anterior descending artery (LAD). ** Right/inferior infarct: ST elevation in leads II, III, and aVF indicates infarction of the inferior surface, supplied by the right coronary artery (RCA). ** Lateral infarct: ST elevation in leads V5 and V6 indicates infarction of the lateral surface of the left ventricle and may be involved in a circumflex (Cx) or LAD lesion. ** Posterior infarct: ST depression in V1-V3 with tall R waves is indicative of circumflex occlusion, i.e. a true posterior infarct. This can be difficult to distinguish from LAD territory ischaemia: look particularly for a dominant R wave in V1 and inferior lead ST elevation in infarction.

What are the following (rare) cardiac causes of loss of consciousness, and why are they important: HOCM; long QT syndrome; Brugada syndrome; arrhythmogenic right ventricular dysplasia?

These rare causes of loss of consciousness are important as they are associated with sudden cardiac death in young people and athletes. 1) HOCM is a genetic mutation, either inherited (autosomal dominant) or sporadic, resulting in non-physiological left ventricular hypertrophy. Left ventricular outflow obstruction is due to asymmetrical septal hypertrophy which occludes the outflow tract during systole. This is exacerbated by systolic anterior movement of the mitral valve anterior leaflet. The outflow tract gradient is exacerbated by exercise. 2) Long QT syndrome is in fact a collection of disorders with different genetic mutations of cardiac ion channels (sodium and potassium). All of them result in prolonged repolarization and a long QT interval on the ECG, particularly on exertion, and are associated with ventricular tachycardia. TWO acquired causes: Hypomagnesaemia and Hypokalaemia 3) Brugada syndrome is caused by a mutation of the cardiac sodium channel gene, at least in some patients. It is often inherited in an autosomal DOMINANT manner. The ECG findings are a right bundle branch block and saddle-shaped ST elevation in V1-V3 (the QT intervals are normal). The condition is associated with ventricular dysrhythmias. 4) Arrhythmogenic right ventricular dysplasia occurs when the myocardium is partially replaced by fatty or fi brofatty tissue. It occurs primarily in the right ventricle, and results in an arrhythmia, hence the name. The ECG is characterized by T-wave inversion in V1-V3 (a non-specifi c finding), right bundle branch block, and an epsilon wave in 50% of cases (a terminal notch at the end of the QRS complex). In addition there may be ventricular ectopics, which can progress to ventricular tachycardia (VT) or ventricular fi brillation (VF). **An implantable cardioverter defi brillator (ICD) device is the only intervention that can prevent sudden death in all of these patients, although β-blockers have some protective value.

The patient has had a mitral valve replacement; these were the sounds prior to valve replacement. Which of the following statements are true?

This is a recording of a patient with mitral stenosis. This is usually caused by rheumatic fever and causes a tapping apex (palpable and loud first sound) which is non displaced. There is a low rumbling diastolic murmur best heard at the apex with the bell of the stethoscope. § The apex beat is likely to be tapping § The patient has a low rumbling murmur § The most likely cause of the problem is rheumatic fever

Why do some but not all patients with acute MIs get nausea and vomiting?

This is called the Betzhold-Jarisch reflex. Infarction of the inferior myocardium irritates the diaphragm, resulting in vomiting. It is not uncommon for this to happen during angiography (and worth warning patients undergoing angiography about!). Patients with infarcts in other territories will not irritate their diaphragm.

Patient was prescribed Aspirin approximately one year ago after a suspected TIA and was advised of the potential gastro-intestinal side effects of this agent by her pharmacist. She was told to ensure that she took the tablet after food to avoid such side effects. During admission, she revealed that she was no longer taking her aspirin as she found that it gave her 'tummy ache' even when she remembered to take it after food. Which one of the following solutions would you recommend?

To continue Aspirin and prescribe Lansoprazole 15mg OD to reduce the risk of side effects. § Obviously the nature of the abdominal pain should be established before assuming that she is suffering from the GI side-effects of aspirin. § As the patient is a type 2 diabetic with a history of IHD, it is important that she takes regular aspirin as primary prevention against ischaemic events. § Lansoprazole is a Proton Pump Inhibitor (PPI) licensed for the treatment of gastric and duodenal ulceration, NSAID-associated duodenal or gastric ulceration, eradication of H. pylori, Zollinger-Ellison syndrome, GORD and acid-related dyspepsia. § It is also commonly used for the prevention of the GI side-effects associated with aspirin usage. § A dose of 15mg would be sufficient in this patient as she is only taking 75mg aspirin and has no previous history of GORD, duodenal or peptic ulceration. § Gaviscon is an antacid which increases the viscosity of the stomach contents and protects the oesophageal mucosa from acid reflux. § Metoclopramide is a dopamine agonist which stimulates gastric emptying and small intestinal transit and enhances the strength of oesophageal sphincter contraction. It is licensed for the treatment of nausea and vomiting particularly related to GI disorders. It is also commonly used for the treatment of post-operative nausea and vomiting. § Ibuprofen is an NSAID licensed for the treatment of the pain and inflammation associated with rheumatoid arthritis and other musculoskeletal disorders. It can also be used for mild to moderate pain including dysmenorrhoea, postoperative analgesia and migraine. The most common side-effect of ibuprofen AND all of the NSAIDs is gastro-intestinal discomfort and renal failure. NSAIDS should generally be avoided in the elderly population due to these side-effects unless an anti-inflammatory agent is specifically needed in which case careful monitoring of renal function would be required as well as the addition of a PPI to prevent the GI disturbances associated with these agents.

Permanent pacing

Transvenous placement of one or more pacing electrodes within a chamber, or chambers, of the heart while the pacemaker is implanted under the skin under the clavicle. It generates electrical impulses delivered by electrodes to contract the heart muscles and regulate the electrical conduction system of the heart - can be single-chamber, dual-chamber or rate-responsive pacemaker (has sensors that detect changes in physical activity and adjusts pacing accordingly)

What are the earliest biochemical changes in MI? Why do we use troponin levels if they are only reliable after 8 hours?

Troponin levels are used because they have a very high specifi city and sensitivity for cardiac damage. Other biochemical markers rise earlier, specifically myoglobin and CK-MB, one of the isomers of the enzyme creatinine kinase. However, these are far less specific for cardiac damage.

Why is it important to consider the patient's renal function when interpreting troponin results?

Troponins are renally excreted - so a raised troponin in the context of renal failure may NOT be significant

All patients must be asked whether or not they have had a past history of acute rheumatic fever? T or F?

True. It is not caused by bacterial infection of heart it is an autoimmune infection

Patients in whom a diagnosis of DVT is made in the hospital usually managed in the community - is this statement true or false?

True. Out-patient management of DVT is standard practice initially with subcutaneous low molecular weight heparin then anticoagulation with warfarin orally. Or they are initiated on one of the NOAC anticoagulants such as Rivaroxaban or Apixiban.

The patient is connected to the defibrillator and you see the rhythm in Figure 1 What is this rhythm? What do you think the most likely cause of the cardiac arrest is?

Ventricular fibrillation. Ventricular fibrillation is chaotic and irregular electrical activity. Familiarise yourself with these rhythms - you should be able to state the rhythm within 5 seconds. § Thromboembolic. Given the patients presentation with severe chest pain, his age and hypertension history he has most likely gone into cardiac arrest secondary to an acute myocardial infarction, it is also possible he has a pulmonary embolus - both of these would be 'thromboembolic' causes.

This patient has had an anteroseptal myocardial infarction. He was treated with thrombolysis with rapid resolution of ST elevation. On day 3 post-MI, he complained of severe dyspnoea and orthopnoea. On clinical examination, a loud, pan-systolic murmur was audible and he was cold, clammy and tachycardic, BP 80/50mmHg. 1) Which is the most likely diagnosis? 2) Which three initial investigations would you arrange?

Ventricular septal defect post MI. This patient has developed a post-MI VSD as demonstrated by shock and a new systolic murmur. Post-MI, acutely, the myocardium may rupture with profound shock and rapid demise. Papillary muscle rupture may also occur, most often of the mitral valve, with development of mitral regurgitation and cardiac failure. Post-MI deaths have decreased in hospitals due to increasing use of percutaneous coronary intervention (PCI), thrombolysis and coronary artery bypass grafting (CABG). Aortic regurgitation causes a diastolic murmur, not a pan-systolic murmur. Left ventricular aneurysms tend to present with persisting ST elevation on ECG, pain and arrhythmias, although they may rupture with shock and rapid demise. 2) ECG, Echocardiogram, Chest radiograph. Echocardiography is the most important next investigation. It would be useful to determine the cause of the murmur, which echocardiography offers this as a non invasive test.

Once the patient improved from this acute episode, right and left heart catheterisation were performed. The pressure and oxygen saturation data obtained are shown below. Oxygen Sats Pressure (mmHg): Superior vena cava = 74% Right atrium (mean) = 75%, 7mmHg Right ventricle = 87%, 50/12mmHg Pulmonary capillary wedge = 16mmHg Left ventricle = 96%, 140/12mmHg Aorta = 97%, 110/60mmHg. What do these figures reveal as the diagnosis?

Ventricular septal defect. There is a step up in oxygen saturation between RA & RV. This can only occur when there is an abnormal connection between these two chambers i.e. via a VSD. This is confirmed by raised right ventricular pressures.

Below are data obtained during coronary angiography, with right and left heart catheterisation in a patient who is short of breath 5 days post-MI and thrombolysis. Oxygen Saturation Pressure: Superior vena cava 74%, Right atrium (7mmHg) 73%, Right ventricle (50/12mmHg) 89%, Pulmonary capillary wedge pressure 16mmHg, Left ventricle (140/12) 96%, Aorta (110/60mmHg) 97%. Which is the diagnosis?

Ventricular septal defect. These initial figures are intimidating but the answer is actually straight forward. Note from figures the sudden and dramatic rise in pressure from the right atrium to the right ventricle and also of oxygen saturation. This can only happen if there is an abnormal communication between the left and right ventricle (VSD) confirmed by elevated right ventricular pressure. Pulmonary hypertension would cause elevated right heart pressure (not increase oxygen saturation). Mitral stenosis would not directly affect right heart pressures unless causing pulmonary hypertension. Atrial septal defect would affect atrial pressure in addition.

Which 3 of the following are true? § The ECG findings are normal in 10% of patients with acute pericarditis § Bacteria are the most common cause of acute pericarditis § Acute pericarditis may recur in 15-30% of patients § Bloody pericardial effusion is most commonly caused by malignant disease § In pericardiocentesis, the needle is typically inserted anteriorly between the 5th and 6th ribs on the left side

Viral causes of pericarditis are the most common. ECG findings are non-specific and may be normal in about 10%. Acute pericarditis may recur in up to 30% of patients. In pericardiocentesis, the needle is inserted subcostally in the midline aiming towards the left shoulder.

Chronic stable angina cause

When he rests, heart rate decreases and pain goes as lactate is broken down. •Partly blocked coronary artery. •When heart rate rises, ischaemia becomes significant. •Lactate accumulates. •ST depression occurs.

What are the risks of percutaneous angioplasty for arterial ischaemic limb disease?

Whenever you are asked about risks, try to have a structure to help you answer the question: 1) General risks (common to any procedure) § Infection of puncture site § Haemorrhage from puncture site § Haematoma § Reaction to the sedative used during the procedure 2) Specific risks (particular to this procedure): § Thrombosis or embolization, potentially leading to loss of the limb § Perforation of the artery, requiring further surgical intervention § Aneurysm or pseudo-aneurysm of the artery at the site of dilatation and stenting or at the puncture site § Reaction to the contrast dye used in the angiography

A patient who has been diagnosed with having a right femoral DVT is placed on LMWH and warfarin, but continues to throw off clots and suffer from small PEs. Is there any further treatment that can be offered?

You may wish to consider placing an inferior vena cava (IVC) filter using a venous catheter, to catch any clots that become dislodged.

The probability of each type of ulcer is affected by the presence or absence of risk factors. What risk factors should you ask about in the history?

You should make a note of the following risk factors: 1) Venous ulcers usually occur in patients with VARICOSE veins, especially those who are immobile (reduced venous drainage of legs) and/or malnourished (reduced healing). They may also occur in patients with RECURRENT deep vein thrombosis (DVT), an abdominal TUMOUR (compressing the iliac veins), or arteriovenous (AV) malformations (increasing venous pressure). Major JOINT REPLACEMENT (e.g. of a hip or knee) is also a risk factor, as up to about 25% of such operations are associated with subclinical DVTs. 2) Arterial ulcers invariably occur in patients with risk factors for atherosclerosis (smoking, diabetes mellitus, hypertension, hyperlipidaemia, strong family history of atherosclerotic disease, male) and/or evidence of other atherosclerotic disease: CORONARY ARTERY DISEASE (angina, myocardial infarction), CEREBROVASCULAR disease (transient ischaemic attack (TIA), stroke), PERIPHERAL ARTERY disease (claudication, impotence, abdominal aortic aneurysm (AAA)). 3) Neuropathic ulcers mostly occur in patients with DIABETES mellitus or ALCOHOL overuse.

A 58-year-old female on the respiratory ward was admitted with a pulmonary embolism one week ago and was started on warfarin at the time of diagnosis. She was covered with low molecular weight heparin until the INR was > 2 for 24 hours. For the past week she has been taking 4mg of warfarin and her INR four days ago was 2.2. Her INR has been checked today and is 1.3.What is the most appropriate action to take? § Increase dose of warfarin to 6mg and start low molecular weight heparin § Increase dose of warfarin to 6mg § Start low molecular weight heparin and stop warfarin § Continue 4mg of warfarin and start low molecular weight heparin § Re-initiate warfarin using local protocol

a) Increase dose of warfarin to 6mg and start low molecular weight heparin. As her INR is < 2 she needs immediate anti-coagulation with rapid acting low molecular weight heparin. Her warfarin dose should also be increased to 6mg. Her INR should be carefully monitored and the LMWH discontinued when has adequate anti-coagulation.

You see a 65-year-old woman who presents with worsening shortness of breath coupled with decreased exercise tolerance. She had rheumatic fever in her adolescence and suffers from essential hypertension. On examination, she has a murmur heard loudest over the apex with opening snap. Which of the following is a clinical sign associated with the most likely diagnosis? A.Malar flush B.Slow rising pulse C.Austin-Flint Murmur D.Heaving apex beat E.Right ventricular heave

a) malar flush § Slow rising pulse - AS § Austin flint murmur - AR § Heaving apex beat - AS § RV heave - TR § Parasternal heave seen in MS

What happens to JVP in AF?

absence of 'a wave' on jugular venous curve (atrial systole)

The NICE guidelines for the secondary prevention of MI recommend that all patients should be offered ....

an ACEi, dual antiplatelet therapy, a beta-blocker and a statin. e.g. clopidogrel 75 mg od, bisoprolol 2.5 mg od, asprin 75 mg od, ramipril 5mg od, atorvastatin 80 mg od.

Paul is a 60 year old man presenting with chest pain radiating to the back. On examination he is peripherally cold and has unequal radial pulses. Which of the following is most useful in confirming the diagnosis? a.CXR b.CT angiography c.MRA d.Echocardiogram e.ECG

b.CT angiography **ECG would do first, but CT angiography is most useful

what does high potassium cause on ECG in terms of rate?

bradycardia. **stem of this q with falls indicates rhabdomyolysis and this also causes high CK from muscle damage

Carol has presented to ED following experiencing chest pain, which you suspect may be cardiac. Which of the following is most useful in confirming a diagnosis of NSTEMI? a.New LBBB b.ST depression in inferior leads, negative troponin c.Normal ECG, raised troponin at 0 and 6 hours d.Chest pain relieved by GTN spray and rest

c.Normal ECG, raised troponin at 0 and 6 hours

What kind of arrhythmia does WPW cause?

can cause atrial problems --> supraventricular tachycardias

A 76-year-old man is admitted to the emergency department for dizziness, dyspnea and palpitations that began acutely one hour ago. Upon questioning, you discover he has a history of primary hypertension and HFpEF. He is currently medicating with hydrochlorothiazide, lisinopril and aspirin. On physical examination, the patient is afebrile with a blood pressure of 75/60 mmHG, pulse rate is 160 and respiration rate is 27. Oxygen saturation is 76% despite 40% oxygen mask and auscultation reveals bilateral inspiratory crackles and ECG shows irregularly irregular rhythm. Which of the following is the most appropriate treatment? A. Adenosine B. Amiodarone C. Cardioversion D. Diltiazem E. Metoprolol

cardioversion - pt is haemodynamically unstable

Pulmonary oedema in left-sided heart failure

congestion builds up in lungs

David is a 65-year-old Caucasian man who has had hypertension for 2 years. He is not diabetic and there is no other significant medical history. He is currently taking amlodipine at the maximum recommended dose of 10mg.At his medication review at his GP surgery his blood pressure remains elevated - it is 158/95mmHg on average over a number of readings.What medication is the most appropriate next step? § Bisoprolol § Doxazosin § Indapamide § Losartan § Spironolactone2%

d) Losartan **Poorly controlled hypertension, already taking a calcium channel blocker - add an ACE inhibitor or an angiotensin receptor blocker § Bisoprolol is a beta-blocker. They are included in step 4 of NICE guidelines if diuretic therapy is contraindicated or ineffective, therefore are not the correct next step for this patient. § Doxazosin is an alpha-blocker and is part of step 4, alongside beta-blockers, therefore not the correct option. § Indapamide is a thiazide-like diuretic. Step 1 therapy in patients are over 55 (like the patient in the scenario) or of African or Caribbean descent is a calcium channel blocker. If there is oedema or the presence of/risk of heart failure then a thiazide-like diuretic is recommended instead. As there is no evidence of contraindications in the question, the most appropriate step in this patient would be to add losartan. § Spironolactone is a potassium-sparing diuretic and is included in step 4 of the NICE hypertension guidelines, therefore it is not the most appropriate option.

A 23-year-old male is undergoing a medical review at a professional football club when an ejection systolic murmur is found. He is sent for echocardiogram and subsequently diagnosed with hypertrophic obstructive cardiomyopathy (HOCM).Electrocardiogram (ECG) is normal and pulse is regular.Which of the following complications of this condition is most likely to cause sudden death in this athlete? § Myocardial infarction § Ruptured mitral valve § Complete heart block § Ventricular arrhythmia § Wolff-Parkinson White syndrome

d) § Ventricular arrhythmia. **Hypertrophic obstructive cardiomyopathy - is associated with sudden death in young athletes due to ventricular arrhythmia. §The proposed mechanism of sudden death is ventricular tachycardia secondary to ischaemia and this typically occurs in the setting of extreme exertion. § Myocardial infarction (MI) is most commonly associated with atherosclerosis within the coronary arteries. This would be unlikely in a young person. MI in young people may be associated with cocaine use. § Whilst HOCM may lead to a regurgitant mitral valve, rupture of this valve is not a recognised complication. § HOCM may lead to heart block. However, this is uncommon and would be unlikely to cause sudden death. § Wolff-Parkinson White syndrome is associated with HOCM and it can lead to sudden cardiac death but it is not a complication of the condition. **Hypertrophic obstructive cardiomyopathy: features § Hypertrophic obstructive cardiomyopathy (HOCM) is an autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins. The estimated prevalence is 1 in 500. HOCM is important as it is the most common cause of sudden cardiac death in the young. § Pathophysiology: o the most common defects involve a mutation in the gene encoding β-myosin heavy chain protein or myosin-binding protein C o results in predominantly diastolic dysfunction o left ventricle hypertrophy → decreased compliance → decreased cardiac output o characterized by myofibrillar hypertrophy with chaotic and disorganized fashion myocytes ('disarray') and fibrosis on biopsy **Features: § often asymptomatic § exertional dyspnoea § angina § syncope § typically following exercise due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis § sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure § jerky pulse, large 'a' waves, double apex beat § ejection systolic murmur § increases with Valsalva manoeuvre and decreases on squatting § hypertrophic cardiomyopathy may impair mitral valve closure, thus causing regurgitation **Associations: § Friedreich's ataxia § Wolff-Parkinson White **Echo findings - mnemonic - MR SAM ASH o mitral regurgitation (MR) o systolic anterior motion (SAM) of the anterior mitral valve leaflet o asymmetric hypertrophy (ASH) **ECG: o left ventricular hypertrophy o non-specific ST segment and T-wave abnormalities, progressive T wave inversion may be seen o deep Q waves o atrial fibrillation may occasionally be seen

Boris is a 67 year old asthmatic who suffered an MI 2 months ago. A recent echo shows worsening ejection fraction. He is currently taking simvastatin, ramipril and aspirin. Which of the following is most likely to reduce his cardiovascular risk? a.Furosemide b.Bisoprolol c.Isosorbide mononitrate d.Calcium channel blocker

d.Calcium channel blocker **is d because of his asthma. can't give b-blocker for asthma/COPD. SAAB is acronym for secondary prevention

Classification of aortic dissection

debakey 1,2 = stanford A. Debakey 3 = stanford B.

What are the pharmacological treatment options now for WPW patient?

flecainide and amiodarone. The concern for these patients with WPW is the risk of sudden death. This occurs due to rapid conduction of atrial fibrillation forwards down the pathway to the ventricle. As atrial fibrillation conducts at between 300-400 beats per minute (in the atrium alone) then it is possible for the ventricle to beat that fast resulting in degeneration to ventricular fibrillation. Guidelines for the treatment of WPW suggest avoidance of drugs that block the AV node alone (digoxin, verapamil, bisoprolol). You can understand that if the atrial fibrillation cannot conduct down the AV node and is preferentially conducted down the accessory pathway, the higher the chances of the ventricle conducting as fast as the atrium and hence VF. Finally, for that reason we have to do some treatment. Drugs that are safe to use with less AV node blocking ability are flecainide and amiodarone. Ideally these patients will be counselled towards an ablation procedure with a high chance of cure and therefore the risk of death is removed.

What is likely cause of S4

has long standing hypertension and causes pressure overload and ventricular hypertrophy.

Beck's triad

hypotension, JVD, muffled heart sounds

Acute management for aortic dissection

in aortic dissection, BP can either be very high or very low. § SEEK URGENT SENIOR HELP § ABCDE -O2 15L NRB -Monitor BP •Rx shock if hypotensive •Control BP if hypertensive- IV beta blockers -IV access 2 large bore cannulas -X match blood (>6 units) (first blood will have to be group+saved) -IVI and analgesia (IV opioids) •All Type A must be considered for surgery •Type B may be managed medically unless rupture/ organ compromise

Bicuspid aortic valve

is a common cause of aortic stenosis in the US. It is a harsh, crescend-decresecendo systolic ejection murmur heard best in the right second intercostal space to the carotids. § inherited form of heart disease in which two of the leaflets of the aortic valve fuse during development in the womb resulting in a two-leaflet valve (bicuspid valve) instead of the normal three-leaflet valve (tricuspid)

Recurrence of pericarditis?

is self-limiting w/o significant complications or recurrences in 90% of cases

Restrictive cardiomyopathy causes symptoms signs

kussmaul's signs - paradoxical rise in JVP during inspiration

When is pericarditis relieved?

leaning forward. GORD and pericarditis worse on lying down.

Which ulcers may require a biopsy?

marjolin ulcer (sq cell carcinoma on chronically inflamed ulcer)

A 58-year-old man is reviewed in a hypertension clinic, where it is found that his blood pressure is 165/105 mmHg. He is currently on ramipril, amlodipine and Bendroflumethiazide. Which of the following would be your next stage in his management? A.Arrange urinary catecholamine assays B.Add spironolactone to his medication C.Measure serum potassium level D.Add bisoprolol to this medication E.Add doxazocin to his medication

measure serum potassium level to determine whether to give spiro or beta blocker

The closure of which valve causes the first heart sound?

mitral

This patient is likely to have infective endocarditis. Which five of the following statements regarding blood cultures in this condition are true?

o A major diagnostic criterion is the growth of a typical organism in 2 separate cultures o Three sets of cultures should be taken o Cultures should routinely be sent for aerobic and anaerobic incubation o The first two sets of blood cultures are positive in >90% of cases o Some organisms are best identified using serology § Three sets of blood cultures should be taken, but obtaining two positive cultures is a major criterion in diagnosing infective endocarditis and starting antibiotics. Cultures should not be taken from indwelling lines. Serology may be needed for some atypical organisms e.g. Coxiella burnetti (Q fever), Bartonella and Brucella.

Generate a management plan for Unstable Angina/NSTEMI

o Admit to coronary care unit o Oxygen, IV access, monitor vital signs and serial ECG o GTN o Morphine o Metoclopramide (to counteract the nausea caused by morphine) o Aspirin (300 mg initially, followed by 75 mg indefinitely) o Clopidogrel (300 mg initially, followed by 75 mg for at least 1 year if troponin positive or high risk) o LMWH (e.g. enoxaparin) o Beta-blocker (e.g. metoprolol) o Glucose-insulin infusion if blood glucose > 11 mmol/L o GlpIIb/IIIa inhibitors may also be considered (e.g. tirofiban) in patients: ● Undergoing PCI ● At high risk of further cardiac events o If little improvement, consider urgent angiography with/without revascularisation o NOTE: the acute management of ACS can be remembered using the mnemonic MONABASH ● Morphine ● Oxygen ● Nitrates ● Anticoagulants (aspirin + clopidogrel) ● Beta-blockers ● ACE inhibitors ● Statins ● Heparin

CXR signs of left ventricular failure

o Alveolar oedema (shadowing - 'bat's wings') o Kerley B lines (interstitial oedema) o Cardiomegaly o Dilated prominent upper lobe vessels (upper lobe diversion) o Pleural Effusion - blunt costophrenic angles

Complications of pericarditis

pericardial effusion and cardiac tamponade: hypotension, muffled heart sounds, JVD, paradoxical pulse

What is SVT?

regular narrow complex tachycardia with NO p waves § either re-entrant or not

What is VT?

regular wide complex

What does this show

saddle shaped ST elevation widespread

Management of NSTEMI/ unstable angina

same as STEMI (MONA) but with LMWH e.g. fondaparinux / enoxaparin § then determine with GRACE score what to do next

What artery involved in septal MI

septal branch of LAD

65 y/o man present to his GP complaining of headaches and problems with vision. O/E: BP is 190/30 and see optic disc blurred on fundoscopy. What would be next stage in Tx?

specialist referral. then may give labetalol there. Won't give labetalol in GP setting.

Which BP medication is most likely to cause gynaecomastia?

spironolactone

What is most common organism cause of Infective endocarditis

staph aureus

A 22-year-old intravenous drug user is found to have a femoral abscess. The nursing staff contact the on call doctor as the patient has a temperature of 39oC. He is found to have a pan systolic murmur loudest at the left sternal edge at the 4th intercostal space. What murmur?

tricuspid regurgitation. Intravenous drug users are at high risk of right sided cardiac valvular endocarditis. The character of the murmur fits with a diagnosis of tricuspid valve endocarditis.

What is pericarditis often preceded by?

upper resp tract infection. pain worse when lying flat. see in young people

Ventricular tachycardia61%Broad complex tachycardia following a myocardial infarction is almost always due to

ventricular tachycardia.

What is peak age for rheumatic fever? (summary slide)

§ 5-15. § group A strep § affects heart, joints, skin (erythema marginatum, and CNS). § Jones major criteria (CASES) § treat with IM Benzylpenicillin (oral erythromycin if penicilin allergic) § Lancefield group A strep is the main pathogen § Antigenic mimicry: cell-mediated immunity and antibodies to streptococcal antigen cross-react with myocardial antigens. § Histology: Beady fibrous vegetations (verrucae), Aschoff bodies (small giant-cell granulomas) and Anitschkov myocytes (regenerating myocytes) § Commonly affects MITRAL VALVE only (70%) but can affect both mitral and aortic (25%).

hypertrophic cardiomyopathy genetics

§ 50% is familial, autosomal dominant § subtype is HOCM - thickened ventricle obstructs the flow of blood

What are Stokes-Adams attacks? How are they treated?

§ A Stokes-Adams attack is a sudden transient loss of consciousness induced by a slow or absent pulse and subsequent loss of cardiac output. § The underlying problem is either COMPLETE (third degree) heart block OR SINOATRIAL DISEASE § Attacks are not associated with a change in posture or any other trigger. § They usually last seconds but if they go on for more than 15-20 seconds twitching may occur due to cerebral anoxia. § After an attack the patient becomes flushed as the well-oxygenated blood sat in the pulmonary capillaries during circulatory arrest is pumped around. § The term Stokes-Adams attack comes from two physicians who described the condition but is not used much nowadays, as the terms 'cardiogenic syncope' or 'syncope due to cardiac arrhythmia' are preferred. § Stokes-Adams attacks are treated with a pacemaker.

What counts as a positive postural BP test?

§ A drop in systolic BP of 20mmHg or more (with or without symptoms). § A drop to below 90mmHg on standing even if the drop is less than 20mmHg (with or without symptoms). § A drop in diastolic BP of 10mmHg with symptoms (although clinically less significant than adrop in systolic BP).

Mr Shepherd is a 67-year-old man who was referred to accident and emergency (A&E) by his general practitioner (GP) after a 2-hour history of severe chest pain. What are the most common causes of acute chest pain in an individual of this age?

§ A good way to come up with a list of causes is to visualize the anatomy of the affected area and think of what could go wrong. § Thus, in chest pain, there may be pathology of the heart, aorta, lungs, pulmonary vessels, oesophagus, stomach (upper areas), thoracic nerves, or thoracic muscles. Common causes of acute chest pain in an individual aged over 60 include: § Acute coronary syndrome § Stable angina § Pulmonary embolism (PE) § Pleurisy (secondary to infection) § Musculoskeletal† § Oesophagitis (secondary to gastro-oesophageal refl ux disease or hiatus hernia) § Anxiety § Oesophageal spasm § Peptic ulcer disease § Pneumothorax § Myopericarditis § Aortic dissection § Aortic aneurysm § Coronary spasm (e.g. secondary to cocaine) § Boerhaave's perforation of the oesophagus § Cholecystitis § Pancreatitis

What is a tilt table test and what is it used for?

§ A tilt table test is sometimes used to help determine whether there is a vasovagal cause for blackouts. § The patient is placed on a 'tilt table' that swings them from a supine position through 90Åã to upright. The patient is connected to continuous ECG and blood pressure monitoring and asked to report their symptoms every 3-5 minutes. § A baseline is established by monitoring the patient supine for 5 minutes. The patient is then tilted (head up) to between 60Åã and 90Åã for between 10 and 60 minutes (a variety of different protocols are used). The test is considered positive if: a) the patient experiences loss of consciousness with a signifi cant fall in blood pressure or heart rate, in which case they are returned to a supine position; or b) symptoms develop. § If an initial test is negative, it can be repeated whilst infusing drugs that increase the susceptibility to the test by vasodilation (e.g. GTN) or bradycardia (e.g. adenosine). This increases the sensitivity but decreases the specificity of the test - under such conditions as many as 45% of control subjects with no history of syncope may have a positive test! The test is of limited value in patients with situational syncope, e.g. on micturition. It is contraindicated in patients who have orthostatic hypotension. A false negative rate as high as 30% has been reported, although it is difficult to determine, as there is no gold standard for comparison. Thus a negative test cannot be used to exclude a vasovagal cause. The low specificity and sensitivity means that this test is seldom used.

How would your diff erential change if the patient were a 20-year-old woman on the combined oral contraceptive pill?

§ A younger patient is less likely to be suffering from diseases of old age, such as: • Acute coronary syndrome • Stable angina • Myopericarditis (usually post-infarction) • Aortic dissection • Aortic aneurysm § A younger female patient on the combined oral contraceptive pill is more likely to be suffering from: 1) PE (the combined oral contraceptive pill is thrombogenic) 2) Pneumothorax (especially if tall and thin) 3) Cocaine-induced coronary spasm (still rare, but particularly unusual in the elderly!)

What are the different treatment options used to control blood pressure in patients at risk of a cardiovascular event?

§ ACE inhibitors - < 55 yo or white § CCBs or thiazide diuretics - > 55 yo or non-white

Reasons for using/avoiding antihypertensives table

§ ACEi - good if also have HF, diabetic nephropathy too § Alpha blocker - good if have BPH § ARBs for people who can't tolerate ACEi cough § beta-blocker- if also have angina § CCBs - if elderly, isolated systolic hypertension (ISH), angina § thiazide - elderly, ISH, heart failure **if someone 140/80 on beta-blocker, had MI in past. Leave on atenolol or also thiazide to lower to 120/80? - You also give thiazide as strong control lowers MI, death etc.

Long term management of heart failure

§ ACEi and beta blocker (start one at a time) - reduces afterload and negative chronotropic effect of b blocker allows heart to fill --> HAVE MORTALITY benefits with pts with HFrEF § aldosterone antagonist e.g. eplerenone/spironolactone § third line drugs e.g. entresto, hydralizine + nitrate, digoxin, cardiac resynchronisation therapy. Only initiated by specialist

SVT (re-entry circuit) causes

§ AVNRT (AV node re-entry) - re-entry at the AV node. Get SVT with no P waves. no delta wave here. § AVRT (atrioventricular re-entry tachycardia) - accessory pathway, short PR interval and delta wave e.g. WPW **as a result of these re-rentries --> tachycardia § AF - irregularly irregular + no p wave, and SVT - regular + no p wave. § Atrial flutter - sawtooth

DVT Well's Criteria

§ Active cancer (any treatment within past 6 months): 1 point § Calf swelling where affected calf circumference measures >3 cm more than the other calf (measured 10 cm below tibial tuberosity): 1 point § Prominent superficial veins (non-varicose): 1 point § Pitting oedema (confined to symptomatic leg): 1 point § Swelling of entire leg: 1 point § Localised pain along distribution of deep venous system: 1 point § Paralysis, paresis, or recent cast immobilisation of lower extremities: 1 point § Recent bed rest for >3 days or major surgery requiring regional or general anaesthetic within past 12 weeks: 1 point § Previous history of DVT or pulmonary embolism: 1 point § Alternative diagnosis at least as probable: subtract 2 points. **score ≥2: DVT likely (proceed to imaging); score <2: DVT unlikely (proceed to D-dimer)

CT confirms a 7cm aneurysm relating to the infra-renal aorta and there is evidence of a small associated retroperitoneal haematoma. What would you do next?

§ Administer prophylactic broad spectrum antibiotics intravenously § Take patient straight to theatre for surgical repair of aneurysm § Refer patient for urgent vascular surgical opinion

What are the main side-effects and interactions of anticonvulsant drugs in general, and specifically: sodium valproate, lamotrigine, carbamazepine, phenytoin?

§ All anticonvulsants are teratogenic: 2-3% of babies born to patients on one anticonvulsant are affected (around 4-6% if on two or 10% if on three anticonvulsants). § Specific drugs are associated with specific defects: sodium valproate with neural tube defects, phenytoin with cleft palate and congenital heart disease. Although the risk of spina bifida from valproate use can theoretically be reduced by high-dose folate supplementation during the first trimester, current National Institute for Health and Clinical Excellence (NICE) advice is to avoid the use of any anticonvulsants during pregnancy where possible. § Carbamazepine and phenytoin interfere with the hepatic metabolism of the contraceptive pill by inducing cytochrome P450, therefore patients on the pill should be advised to double their dose and/or use barrier contraceptives. By the same mechanism they can interfere with warfarin dosing (requiring a greater dose of warfarin for the same target international normalized ratio (INR)). The specific side-eff ects include: a_ Sodium valproate: weight gain, hair loss and curling, nausea, rash, drowsiness, tremor, drug-induced hepatitis b) Lamotrigine: rash (Stevens-Johnson syndrome), headaches, dizziness, insomnia, vivid dreams c) Carbamazepine: rash, nausea, ataxia, diplopia, agranulocytosis, hyponatraemia d) Phenytoin: acne, rash, ataxia, ophthalmoparesis, sedation, gingival hyperplasia

Which of the following drugs are associated with hyponatraemia? Citalopram/ Gliclazide/ Atenolol/ Bendroflumethiazide/ Aspirin/ Simvastatin

§ All thiazide and loop diuretics are commonly associated with hyponatraemia due to excessive urinary excretion of sodium. This is particularly evident in the elderly female and is a very common cause of confusion. § Citalopram is a Selective Serotonin Reuptake Inhibitor (SSRI). Hyponatremia secondary to the syndrome of inappropriate secretion of antidiuretic hormone is a complication of treatment with the SSRIs. § The risk of hyponatremia seems to be highest during the first weeks of treatment, particularly in elderly females and in patients with a lower body weight.

A 23-year-old woman is investigated after collapsing whilst jogging. She felt briefly unwell and dizzy prior to collapsing but quickly recovered. There has been no previous similar episodes. Routine blood tests are normal but the ECG shows a corrected QT interval of 480ms. What is the most appropriate management? Implantable cardioverter defibrillator/ Propranolol/ Amiodarone/ Reassurance/ Accessory pathway ablation

§ An implantable cardioverter defibrillator is only required in high risk cases, for example if the patient has a QTc > 500ms or previous episodes of cardiac arrest. § Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death. The most common variants of LQTS (LQT1 & LQT2) are caused by defects in the alpha subunit of the slow delayed rectifier potassium channel. A normal corrected QT interval is less than 430 ms in males and 450 ms in females. Causes of a prolonged QT interval: congenital, drugs (e.g. amiodarone), other (hypocalcalcaemia/kalaemia/magnesaemia) **Features § may be picked up on routine ECG or following family screening § Long QT1 - usually associated with exertional syncope, often swimming § Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli § Long QT3 - events often occur at night or at rest sudden cardiac death **Management: § avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise) § beta-blockers*** § implantable cardioverter defibrillators in high risk cases ***note sotalol may exacerbate long QT syndrome

This patient has sustained a post-MI ventricular septal defect (VSD). How would you manage this patient? Select seven. § Analgesia as needed § Arrange urgent transfer to cardiothoracic unit § Consider coronary angiography § Consider intra-aortic balloon pump § Consider positive pressure ventilation § Consider Swann-Ganz pulmonary artery catheter § Inotropic support § Intravenous beta-blockade § Repeat thrombolysis

§ Analgesia as needed § Arrange urgent transfer to cardiothoracic unit § Consider coronary angiography § Consider intra-aortic balloon pump § Consider positive pressure ventilation § Consider Swann-Ganz pulmonary artery catheter § Inotropic support **Thrombolysis and beta-blockers are contra-indicated in this situation (beware use of beta-blockade in a shocked patient). Mainstays of treatment are supportive with inotropes and a balloon pump (counterpulsation inside aorta to augment blood pressure during diastole). Closure of the defect can be considered percutaneously, using the same occlusion device to close atrial septal defects. Cardiac surgery would be a last resort, if the defect cannot be closed via the femoral route. This confers a higher risk to the patient of significant morbidity and mortality. Coronary angiography maybe helpful to confirm and quantify VSD and can be performed at the time of closure.

How do ACEi work?

§ Angiotensin-converting enzyme (ACE) inhibitors are now the established first-line treatment in YOUNGER patients with hypertension and are also extensively used to treat heart failure. § They are known to be less effective in treating hypertensive Afro-Caribbean patients. § ACE inhibitors are also used to treat DIABETIC nephropathy and have a role in the secondary PREVENTION of ischaemic heart disease. § Mechanism of action: inhibit the conversion angiotensin I to angiotensin II ACE inhibitors are activated by phase 1 metabolism in the liver § Side-effects: A) cough occurs in around 15% of patients and may occur up to a year after starting treatment. thought to be due to increased bradykinin levels B) angioedema: may occur up to a year after starting treatment C) hyperkalaemia D) first-dose hypotension: more common in patients taking diuretics **Cautions and contraindications" § pregnancy and breastfeeding - avoid § renovascular disease - may result in renal impairment § aortic stenosis - may result in hypotension hereditary of idiopathic angioedema specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L **Interactions: § patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) - significantly increases the risk of hypotension **Monitoring: § urea and electrolytes should be checked before treatment is initiated and after increasing the dose § a rise in the creatinine and potassium may be expected after starting ACE inhibitors § acceptable changes are an increase in serum creatinine, up to 30% from baseline and an increase in potassium up to 5.5 mmol/l. § significant renal impairment may occur in patients who have undiagnosed bilateral renal artery stenosis

An 82-year-old man is referred to cardiology by his GP with increasing dyspnoea on exertion and a systolic murmur. Examination demonstrates a blood pressure of 100/80 mmHg and a slow rising pulse. What is the most likely cause of his underlying condition?

§ Aortic stenosis - most common cause: a) younger patients < 65 years: bicuspid aortic valve b) older patients > 65 years: calcification **Clinical features of symptomatic disease: § chest pain § dyspnoea § syncope murmur § an ejection systolic murmur (ESM) is classically seen in aortic stenosis § classically radiates to the carotids § this is decreased following the Valsalva manoeuvre **Features of severe aortic stenosis: § narrow pulse pressure § slow rising pulse § delayed ESM § soft/absent S2 § S4 § thrill § duration of murmur § left ventricular hypertrophy or failure **Causes of aortic stenosis: § degenerative calcification (most common cause in older patients > 65 years) § bicuspid aortic valve (most common cause in younger patients < 65 years) § William's syndrome (supravalvular aortic stenosis) § post-rheumatic disease subvalvular: HOCM **Management § if asymptomatic then observe the patient is general rule § if symptomatic then valve replacement § if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery cardiovascular disease may coexist. For this reason an angiogram is often done prior to surgery so that the procedures can be combined § balloon valvuloplasty is limited to patients with critical aortic stenosis who are not fit for valve replacement

What specific questions would you ask Mrs McDonald regarding her swollen leg during your history-taking? Think of questions that will provide key clues to help rule in or rule out particular diagnoses.

§ Are there any risk factors for venous thrombosis? − Hypercoagulable blood? Trauma, surgery within the last month, pregnancy, active cancer, obesity (body mass index (BMI) >30 kg/m2), combined oral contraceptive pill or hormone replacement therapy, family history or past medical history of DVTs − Stasis? Bed rest (>3 days) or long-haul flight (>12 hours) − Vessel injury? Trauma, surgery. § Has she felt breathless, had any chest pain, or coughed up any blood? If DVT is high on your differential list, it would be wise to enquire about symptoms of a possible pulmonary embolism (PE). § Has she had any cuts, insect bites, or other wounds to her right leg? If the patient has recently had a wound in her right leg, infective diseases such as cellulitis and septic arthritis become much more likely. § Is the swelling getting bigger? Cellulitis can spread fairly rapidly along the affected limb, whereas the other pathologies are more likely to remain confined in the short term. § Has she had any abdominal pain? Has she noticed any blood in her faeces? § Has she had any unusual vaginal bleeding? Has she noticed any weight loss, fever, or malaise? If you are considering a pelvic malignancy as the cause of the limb swelling, you can ask for symptoms that are suggestive of colon, ovarian, or uterine malignancies. § Has she recently had radiotherapy or surgery to her right leg or abdomen? Radiotherapy or surgery may have damaged the lymphatic drainage from her affected limb, causing the accumulation of lymph (lymphoedema). § Does moving the joints in her leg elicit the pain? Patients with septic arthritis will tell you that movement of the affected joint brings on excruciating pain in the joint. Patients with compartment syndrome in their calf will tell you that moving the ankles and toes brings on pain in their calf (as this causes the flexors of the foot to move within the compressed compartment of the calf ).

A 68-year-old male presents to the emergency department with a 1-day history of progressive left leg swelling. He reports no other symptoms and has no past medical history of note. You perform an examination which reveals a swollen, erythematous lower left leg. Peripheral pulses are intact and superficial veins are not distended. You calculate the patient's 2-level DVT Wells score, which is 1.What is the most appropriate initial management of this patient? Anti-coagulate with low molecular weight heparin (LMWH)/ Arrange a D-dimer with result available within 6 hours/ Arrange a D-dimer with result available within 4 hours/ Arrange a proximal leg vein ultrasound scan with result available within 4 hours/ Observe for 4 hours then discharge with safety netting

§ Arrange a D-dimer with result available within 4 HOURS. § If a 2-level DVT Wells score is ≤ 1 point then arrange a D-dimer with result within 4 hours or interim anticoagulation whilst awaiting D-dimer § The recommended action is to perform a D-dimer test with the result available within 4 hours. If this is elevated, a proximal leg ultrasound should be arranged with results available within 4 hours. If this is not available the patient should be anticoagulated in the interim with a direct oral anticoagulant (DOAC) and an ultrasound organised with the result available within 24 hours. § 'Observe for 4 hours then discharge with safety netting' is incorrect. If a DVT is suspected (even with a low DVT Wells score) it should be investigated and managed as above

What are the treatments for atrial fibrillation

§ Atrial fibrillation - arrhythmia uncoordinated atrial contraction and thus ventricular contraction. SAN—> AVN—> bundle of his and ventricular contraction. § Have multiple focal mini atrial contractions § Hence AVN doesn't get signal to contract normally and then ventricles contracts irregularly § AF associated with valvular heart disease and coronary heart disease + Hyperthyroid and electrolyte imbalances § Usually asymptomatic, get palpitations, dizzy, light headedness, SOB § On examination - irregularly irregular pulse. Rate is typically 110-160bpm (fast AF). Slow AF is when ventricular rate is below 60bpm and that's caused by hypothermia , digoxin toxicity and sinus node dysfunction § Regularly irregular - e.g. second degree heart block. § Ix for AF - ECG (absent p waves, narrow QRS complex with irregular R-R interval), echocardiogram to rule out structural cause e.g. valve disease/ thrombus § High risk of thrombus as atria doesn't eject blood as efficiently and can get clots in atria and can dislodge in brain to get stroke § Tx depends on if haemodynamically stable or not: 1) if haemodynamically unstable then do electrical DC cardioversion (good if acute AF less than 48 hours), if more than this then do anticoagulation (e.g. IV heparin) for 4 weeks before do cardioversion - this is because if had AF for ages don't know whether they have thrombus and could dislodge to cause stroke 2) When patient is stable do 3 things: rate control, rhythm control, anticoagulation and also any modifiable risk AF a) Rate control - beta blockers e.g. metoprolol or propranolol or verapamil (CCBs) b) Rhythm control - chemical cardioversion e.g. flecainide or amiodarone c) Anticoagulation (based on CHADVASC score) - CHF, HTM, age, diabetes, vascular disease, age, sex, category. If have >1 for male, >2 for female then do anticoagulation. This is done with DOACs e.g. factor 10a inhibitors (apixaban and rivoraxban) or oral direct thrombin inhibitor (dabigatrin) § On top of that, if AF is still refractory can do surgical ablation to find point of atrium that gives off these wrong electrical signals and can get rid of it

Mrs Thompson is a 62-year-old woman with known angina who has been referred by her GP following increasing frequency in her episodes of chest tightness. She says she usually suff ers from angina two or three times a month, but that over the last 2 months her attacks have become more frequent. Some of these episodes are now occurring at rest, often following meals. They are partly alleviated by the GTN spray she has been using for her angina. She is a heavy smoker, blood pressure 163/94 mmHg, and cholesterol 6.5 mM. She had an angiogram 2 years earlier showing mild stenosis of the left circumfl ex artery. Her other medical history includes refl ux disease, but no other conditions. Notably she has no history of gallstone disease and reports no change in stool or urine. On admission her examination and investigations are normal, including the ECG, 12-hour troponin levels, and temperature. The team has a high suspicion of a worsening of her angina and perform a repeat angiography, which is unchanged from her previous angiogram. What diagnoses should you be considering? Which investigations will help you determine the correct one?

§ Attacks of chest pain of increasing frequency and at rest should trigger alarm bells for the progression of her angina from stable to unstable. At the same time, the fact that her angiogram is unchanged should arouse your suspicion of another diagnosis. § The insidious course rules out acute conditions such as infarction or pericarditis. The important diagnoses to exclude are oesophageal spasm, cholecystitis, and acute pancreatitis. § Both oesophageal spasm and cholecystitis are consistent with the history of pain after meals, although a lack of known gallstone disease, unchanged urine and stool, and apyrexia argue against cholecystitis. § Oesophageal spasm may be detected by barium swallow and oesophageal manometry, although a normal result does not exclude it. § Ultimately the diagnosis may come down to a therapeutic trial. § Mrs Thompson was prescribed a proton-pump inhibitor for presumptive oesophageal spasm secondary to reflux. She responded positively, confirming the diagnosis. § If all else had been excluded, you may have considered a diagnosis of coronary artery spasm (sometimes called variant or Prinzmetal angina) or coronary syndrome X. These are diagnoses of exclusion; they are extremely hard to demonstrate and are, in any case, rare in the absence of underlying coronary artery disease. It is best to avoid such 'dustbin diagnoses' until all other causes have been excluded

What is Dressler's syndrome? Treatment?

§ Autoimmune pericarditis that occurs 2-10 weeks after MI § NOTE: this is different from simple post-MI pericarditis (2-4 days after MI) § Treatment: o Analgesia o Anti-inflammatories o Pericardial effusion may need pericardiocentesis

List up to four drugs that can be used to treat chronic stable angina

§ Beta blocker (slow HR down but issue is feel knackered when exert yourself) atenolol 25-100mg once daily § aspirin 75mg daily § GTN - 50micrograms as required § statins - simvastatin 20-80mg

What are the signs of mitral stenosis on ECG?

§ Bifid P waves § No P waves ** Patients with mitral stenosis are often in atrial fibrillation so there may be no P waves. A bifid P wave or P mitrale reflect left atrial enlargement and are sometimes seen before atrial fibrillation. Peaked P waves suggest P pulmonale or right atrial enlargement. Delta waves are seen in Wolf-Parkinson-White syndrome. U waves are seen in hypokalaemia.

A 75-year-old man with a background of type 2 diabetes mellitus and peripheral artery disease is commenced on ramipril for newly diagnosed stage 2 hypertension. Repeat urea & electrolytes (U&Es) are performed 10 days later. Urea and creatinine is slightly elevated. What is the most likely reason for this deterioration in renal function?

§ Bilateral renal artery stenosis. After starting an ACE inhibitor, significant renal impairment may occur if the patient has undiagnosed bilateral renal artery stenosis § Bilateral renal artery stenosis should always be considered in a patient with risk factors for, and evidence of, atherosclerotic vascular disease. In particular, if they are diagnosed later in life with hypertension and have an acute significant drop in renal function following the commencement of an ACE inhibitor. § This acute deterioration in renal function is not in keeping with more longer-term conditions affecting the kidneys such as diabetic and hypertensive nephropathy. § Although possible, there is no evidence from the information given that the patient has glomerulonephritis or has significant pre-renal acute kidney injury from dehydration.

List 2 causes of aortic regurgitation

§ CAUSES •Ascending aortic arch dissection •Connective tissue disease (e.g. Marfan syndrome, Ehlers-Danlos syndrome) § Hands - Quincke's sign § BP - wide pulse pressure § Pulse - collapsing/'water hammer'/Corrigan's pulse § Palpation - displaced apex beat

Scoring system for AF

§ CHADVASC: takes into account CHF, hypertension, age, diabetes, previous stroke, vascular disease, female sex --> gives change of stroke. Risk bigger huge as CHAD score rises; so add up score (e.g. score 5 is then 6% risk of stroke each year is quite high give warfarin/NOAC). If low risk (CHAD risk 0) then don't really need warfarin. But once have score of 1 or 2, consider going on warfarin/ NOAC. § HASBLED - chance of bleeding: abnormal LFTs, bleeding, lable INRs, drugs, alcohol, older. So as HASBLED score rises, risk of bleeding increases a lot so then might not go on warfarin. **so you balance between CHADVASC and HASBLED to see whether to start on warfarin. **sometimes give warfarin and heparin. Because warfarin works about over a week, so if want to prevent stroke from toady start with heparin and warfarin together, then when INR increases and shows warfarin is working, then can stop heparin (is like a bridge).

Causes of right-sided heart failure

§ Chronic lung diseases § Primary pulmonary hypertension § Heart valve disease § Left sided heart failure

As part of the bedside teaching, you were asked to carry out a cardiovascular examination on Mr Henry in bed 5. He exhibits an early diastolic murmur that is louder on expiration and is best heard in the 3rd intercostal space left sternal edge.Given the most likely diagnosis, what is the most likely feature of his pulse? Pulsus paradoxus/ Slow rising pulse/ Jerky pulse/ Pulsus alternans/ Collapsing pulse

§ Collapsing pulse is a feature of aortic regurgitation, PDA, and hyperdynamic states (anaemia, thyrotoxicosis, fever, exercise/pregnancy) § The murmur described is consistent with aortic regurgitation. Collapsing pulse describes a rapid upstroke and a sharp descent. This is seen in chronic aortic regurgitation and other hyperdynamic states e.g. anaemia, thyrotoxicosis, fever, exercise/pregnancy. § Option 1: Pulsus paradoxus describes a fall in systolic blood pressure of more than 10mmHg during inspiration. This is seen in severe asthma and cardiac tamponade § Option 2: Slow rising pulse is seen in aortic stenosis § Option 3: Jerky pulse is seen in hypertrophic obstructive cardiomyopathy § Option 4: Pulsus alternans is a regular alternation of the force of the arterial pulse. This is seen in cases of severe left ventricular failure

Other than ACS, what else can cause a rise in serum troponins?

§ Coronary artery spasm § Aortic dissection § Myopericarditis § Hypertrophic cardiomyopathy § Severe heart failure § PE

Having taken a history, you examine Mrs McDonald. Is there anything in particular you will look for on examination that might help you sort out your differential diagnoses?

§ Cuts, bites, wounds, or superficial infections: patients often haven't noticed small cuts, puncture wounds, or insect bites so look carefully for these all over the affected limb. Also check between the toes for fungal infection as a portal of entry. § Location of the swelling: septic arthritis is likely to produce inflammation that is principally over a joint (e.g. the ankle, the knee). Compartment syndrome is likely to produce inflammation which is confined to the calf or thigh muscle compartments but spares the joints. A ruptured synovial sac in the knee ('Baker's cyst') would emerge from the popliteal fossa and track down into the calf. § Extent of swelling: measure the extent of swelling using a tape measure to compare the circumference of both limbs at the same point (e.g. 10 cm below the tibial tuberosity). Also, mark the area of swelling with a pen so that you can monitor a progressing cellulitis. § Lymphadenopathy: check for swollen lymph nodes along the affected leg and in the inguinal fold, as lymphadenopathy would be highly suggestive of an infection in the limb. § Abdominal masses: an abdominal mass in the right lower quadrant would suggest a tumour that could be compressing the right iliac vein. § Neurovascular status of the limb: it is imperative that you check and document the sensation, motor function, and pulses of the affected limb distal to the swelling. These can be affected by compartment syndrome, and compromise of neurovascular status is a surgical emergency. § Pain on gentle passive movement: septic arthritis will elicit pain in the affected joint whereas pain in the calf is suggestive of compartment syndrome. Note that the joint should be moved gently and slowly to avoid dislodging any DVTs into the circulation.

When are D-dimer levels useful in suspected DVT or PE?

§ D-dimer is the breakdown product of fibrin and is therefore elevated in any inflammatory process, e.g. infection, cancer, thrombosis, trauma. § It is very sensitive but non-specific. § In the context of suspected DVT or PE it is only useful if the likelihood of the patient having a DVT or PE is LOW (i.e. a low Wells' score). § In this case, a negative D-dimer rules out a DVT or PE. § This is referred as negative predictive value. § Remember that if the Wells' score is not low, or there is another inflammatory process ongoing, a D-dimer is of no diagnostic value and you should not request it.

Secondary prevention of STEMI

§ Decrease modifiable risk factors: Smoking, obesity, DM, HTN, High cholesterol § SAAB 1) Statin •Atorvastatin 80mg OD 2) ACEi •Ramipril -1.25mg-10mg OD 3) Antiplatelet •Aspirin 75mg OD lifelong •Ticagrelor/ Clopidogrel for 12/12 4) Beta Blocker •Bisoprolol 1.25mg-10mg OD •Reduce rate of re-infarction

constrictive pericarditis summary slide

§ Definition: Chronic inflammation of the pericardium (outer sac) with thickening and scarring § Causes: •Idiopathic •Infectious (TB, bacterial, viral) •Acute pericarditis •Cardiac surgery and radiation § Signs and Symptoms: Similar to restrictive cardiomyopathy •RHF presentation (raised JVP, oedema) •Kussmaul's sign § Investigations: •CXR: pericardial calcification •Echo: increased pericardial thickness - differentiate from restrictive cardiomyopathy •Cardiac CT/MRI **ECHO helps differentiate constrictive pericarditis from restrictive cardiomyopathy § can cure constrictive pericarditis using pericardectomy (removing pericardium)

ECG changes in dextrocardia

§ Dextrocardia is associated with an inverted P wave in lead I, right axis deviation, and loss of R wave progression § Dextrocardia is a rare cardiac condition where the heart's apex is located on the right side of the body. This means when looking at the conventional axis, the heart is deviated far to the right of what is normally expected. Lead I looks right to left, and as the heart is now is essence 'flipped' in this plane, the electric waveform is reversed, this leads to inversion of the P wave, QRS complex and T wave. Loss of R wave progression is also seen in dextrocardia. § The most common finding in pulmonary emboli (PE) is that of a sinus tachycardia. Right axis deviation can occur, but inverted P waves in lead I is not an associated feature. Other ECG features of PE include right bundle branch block and if the clot is large a right ventricular strain pattern can be seen - T wave inversion in V1-4. § Right ventricular hypertrophy is also associated with right axis deviation, but not P wave inversion in lead I. Other ECG findings are a dominant R wave in V1. § A silent myocardial infarction may be possible due to this patient's diabetes. However, the ECG findings are not consistent with this. Myocardial infarcts typically affect the ST segment, T waves and the Q waves. § Wolff-Parkinson-White syndrome is a condition caused by an accessory conducting pathway, allowing electric activity to bypass the atrioventricular node. In an ECG this is demonstrated by a slurred upstroke of the QRS complex - called a delta wave. **in pic: causes of left axis deviation (LAD) and right axis deviation (RAD)

Lifestyle changes for hypertension management; BP targets for treatment; some new drugs?

§ Diet: low salt (<6/day, ideally 3g), fruit + veg rich, reduce caffeine intake § Stop smoking § Drink less alcohol § Exercise, lose weight

What laxatives with opiates?

§ Don't forget stimulant laxatives (SENNA) with regular opiate. § Lactulose is an osmotic laxative and Fybogel is bulk forming. § Constipation is universal with opiates so always consider laxatives with opiates. § Don't forget DVT prophylaxis, it is very important to assess risk and prescribe as appropriate. This is an avoidable hospital related risk. Fluids MAY be necessary post op as might TPN but weren't the answers sought here.

30 y/o woman with heaviness in legs. Has tortuous superficial leg veins. Compression stockings have not helped. What is most appropriate investigation?

§ Duplex ultrasound scan. § Pt has varicose veins and compression stockings haven't helped. § Duplex § Doppler detects bloow flow, provides waveforms, can be used to confirm non-palpable pulses § Duplex actually allows vein mapping as well as flow - which is necessary for determining Tx for varicose veins. § MRI venogram - maps out veins. Rarely used. § ABPI - is for arterial disease. But might be relevant for someone elderly before compression stockings if have IHD risk factors as the compression stockings can worsen arterial disease

Which four of the following statements are true? § Angina is rare in HOCM § Dyspnoea is a common feature in HOCM § A systolic murmur can be heard in some cases § Drug treatment is of little value § An implantable cardiac defibrillator may be of value § Surgical treatment may be of value

§ Dyspnoea is a common feature in HOCM § A systolic murmur can be heard in some cases § An implantable cardiac defibrillator may be of value § Surgical treatment may be of value Although there may (as in the case presented) be no symptoms prior to death, angina dyspnoea and syncopal attacks are fairly common. In many cases where the septum is thickened there is interference with the movement of the anterior mitral valve leaflet and obstruction to the aortic outflow tract which can combine to produce a systolic murmur. Beta blockers and calcium channel inhibitors can be used to reduce the load on the left ventricle whilst drugs such as amiodarone can reduce the chance of arrhythmias. Implantable defibrillators are sometimes used for high risk patients with intractable arrhythmias. Cardiac surgery may be required where aortic outflow obstruction is severe. **HOCM managment: § Amiodarone § Beta-blockers or verapamil for symptoms § Cardioverter defibrillator § Dual chamber pacemaker § Endocarditis prophylaxis* **Drugs to avoid: nitrates, ACE-inhibitors, inotropes

Bedside, bloods and imaging for Heart failure

§ ECG - good for ruling out MI § Bloods - FBC (anaemia), TFTs (if high output HF), **BNP**, Us and Es, LFTs § Imaging: CXR, Transthoracic echocardiography (TTE) --> GOLD STANDARD

A 26-year-old male presents via ambulance to the emergency department of your local hospital following a motor vehicle accident. He was a restrained passenger. The paramedics have secured his c-spine before transporting him. He is complaining of chest pain and shortness of breath. A primary and secondary survey are undertaken and the following pertinent findings are reported:Young, otherwise healthy looking male in clear pain and respiratory distress.Glasgow coma scale (GCS) of 14.Heart rate of 104/min.Blood pressure of 94/50mmHg.Respiratory rate of 24/min.Oxygen saturation: 99% on 15L non-rebreather.Temperature: 36.8 degrees.There is a tender contusion on the anterior chest. No abnormal chest movements. JVP can been seen at the level of the earlobe. Auscultation reveals soft heart sounds and bibasal crepitations. There is air entry throughout both lung fields.An ECG is performed.Which of the following ECG findings is most likely to be reported in this patient? Electrical alternans/ QT prolongation/ T wave inversion in leads II, III and AVF/ Widespread ST elevation/ Short PR, QRS >120ms and delta waves

§ Electrical alternans is suggestive of cardiac tamponade § Due to history of anterior chest trauma and the presence of Beck's TRIAD (hypotension, raised JVP, soft heart sounds), the most likely cause of this presentation is cardiac tamponade. § Tension pneumothorax is less likely as there is air entry throughout the chest. § Electrical alternans is a relatively specific but non-sensitive ECG sign of cardiac tamponade. § Electrical alternans is characterised by beat to beat variation in QRS amplitude and morphology. § This variability is due to the heart 'swinging' in the pericardial fluid. § Short PR, QRS >120ms and delta waves is a description of Wolff-Parkinson-White syndrome. WPW syndrome is a congenital presence of an accessory with episodes of tachyarrhythmias. It can be found in younger patients and is associated with a small risk of sudden cardiac death. § QT prolongation is usually caused by electrolyte abnormalities (hypokalemia, hypocalcemia) or medications (antipsychotics). QT prolongation is not associated with cardiac tamponade. § T wave inversion in leads II, III and AVF is highly suggestive of inferior myocardial ischaemia. § It is important to remember that cardiac tamponade is a potential complication of a myocardial infarction. § However given this patient's young age and history of trauma, it is unlikely that a myocardial infarction is the cause of this tamponade.It is possible for widespread ST elevation to be present in cardiac tamponade. This occurs when the tamponade is caused by pericarditis, which is unlikely to be the case in this patient. **PIC: An ECG demonstrating electrical alternans. Note the alternation of QRS complex amplitude between beats. **Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure. § Classical features - Beck's triad: hypotension, raised JVP, muffled heart sounds. § Other features: dyspnoea, tachycardia, an absent Y descent on the JVP - this is due to the limited right ventricular filling § pulsus paradoxus - an abnormally large drop in BP during inspiration Kussmaul's sign - much debate about this § ECG: electrical alternans § Management: urgent pericardiocentesis

How would you define epilepsy? How are seizures classified?

§ Epilepsy is defined as a tendency to have recurrent, unprovoked seizures. § A single seizure is not enough to diagnose epilepsy. § A seizure is defined as transient excessive electrical activity with motor, sensory, or cognitive manifestations discernible to the patient or an observer. § Seizures are broadly grouped as generalized or partial, depending on whether the abnormal electrical activity affects the whole brain from the start (generalized) or is focal, at least initially (partial): 1) Generalized seizures can be further subdivided depending on symptoms during the seizure: a) Tonic-clonic ('grand mal'): patients are initially rigid (tonic phase) and then convulse, making rhythmical muscular contractions (clonic phase) b) Absence ('petit mal'): usually in children, the patient loses consciousness and appears vacant and unresponsive to observers for up to 30 seconds c) Atonic: a brief loss of muscle tone, causing the patient to fall to the ground d) Tonic: like the tonic phase of tonic-clonic seizures e) Clonic: like the clonic phase of tonic-clonic seizures f) Myoclonic: an extremely brief muscle contraction (<0.1 second) seen as a jerky movement 2) Partial seizures can be divided into those where consciousness is unimpaired (simple) and those where it is impaired (complex). **Alternatively they may be classified by the brain area affected, e.g. temporal lobe (déjà vu/jamais vu, olfactory/auditory aura, epigastric discomfort), frontal lobe (motor), parietal (sensory), occipital (visual).

Which form of imaging may be used to investigate a patient presenting with chest pain? Describe some pathological signs that you might see.

§ Erect CXR § Allows exclusion of pneumothorax, aortic pathology (e.g. widened mediastinum due to dissection) and boerhaave's perforation (would cause pneumomediastinum, pleural effusion or pneumothorax)

A patient attends A&E with central crushing chest pain. Investigations reveal a normal ECG and normal troponins. All other investigations and examinations are normal, and a presumptive diagnosis of new-onset angina is made. What investigations should you request for a patient such as this presenting with new onset angina?

§ Exercise tolerance test: o An exercise tolerance test may be performed to investigate the possibility of coronary artery disease and therefore the potential benefit to be derived from angioplasty. A patient's ECG and blood pressure are monitored during increasing amounts of exercise (e.g. on a treadmill). ST depression of ≥2 mm, typical symptoms of exertional angina, or ST elevation ≥1 mm usually indicate stenosis of the coronary arteries. A fall in blood pressure during the test is a poor prognostic sign. It is worth noting that this test only has an 80% sensitivity and 70% specificity for detecting ischaemic heart disease (i.e. 30% of positive results will be false positives). § Stress echocardiogram. Some patients cannot perform an exercise tolerance test, for example due to an inability to walk from severe arthritis, severe peripheral vascular disease, or COPD. In these cases a stress echocardiogram can be conducted. The patient is given dobutamine to simulate 'stress' while their cardiac function is assessed by echocardiogram. A normal heart shows increased motility when stressed, whereas ischaemic myocardium is hypokinetic. § Myoview scan. This is an alternative to the tests above and provides a way of looking directly at blood flow within the heart muscle either during exercise (e.g. on an exercise bike) or under medically induced stress. Patients are injected with a radioactive contrast agent (thallium) and a picture taken with a gamma camera. Pictures at rest and immediately after exercise/stress are compared. Areas of the myocardium with good perfusion appear as 'warm' spots on the scan. § Angiography/angioplasty. If any of the tests above are positive, the patient is suitable for angiography to identify if there is stenosis of a coronary artery. If significant coronary artery disease were found, most centres would undertake coronary angioplasty.

Treatment for orthostatic hypotension?

§ Fludrocortisone and midodrine are pharmacological options for treatment of orthostatic hypotension § Fludrocortisone increases renal sodium reabsorption and increases the plasma volume. This helps to counteract the physiological orthostatic vasovagal reflex. **Management of orthostatic hypotension (ESC 2018): § education and lifestyle measures such as adequate hydration and salt intake § discontinuation of vasoactive drugs e.g. nitrates, antihypertensives, neuroleptic agents or dopaminergic drugs § if symptoms persist, consider compression garments, fludrocortisone, midodrine, counter-pressure manoeuvres, and head-up tilt sleeping. **Syncope may be defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery. Note how this definition excludes other causes of collapse such as epilepsy.

Which five questions would you ask in the history when looking particularly for risk factors for thromboembolic disease in a patient presenting with a swollen calf?

§ Have you had an operation recently? § Have you been immobile? § Is there a family history of DVT or PE? § Have you ever had a DVT or PE? § Have you suffered with a malignant disease? Important: § Major surgery requiring a regional or general anaesthetic in the past 12 weeks is a risk factor for thromboembolic disease. Patients undergoing a total hip replacement are usually prescribed prophylactic low molecular weight heparin to reduce the risk. § Being bedridden for > 3 days is a risk factor for thromboembolic disease. § Inherited disorders of coagulation can increase the risk of deep vein thrombosis. § Having previously had a DVT or PE increases your risk of thromboembolic disease. § Active malignant disease is a risk factor for deep vein thrombosis Not necessary: § Diabetes is not a risk factor for deep vein thrombosis. § A drug history is always important but the use of non-steroidal anti-inflammatory drugs does not increase your risk of deep vein thrombosis.

How will the medical team manage Mr Shepherd's NSTEMI acutely? How does the management diff er between full-thickness infarcts (STEMI and posterior infarcts) and partial-thickness infarcts (NSTEMI)?

§ Having assessed the need for resuscitation (airways, breathing, and circulation, ABC), you should consider Mr Shepherd's immediate management. § Given that your differential includes life-threatening conditions, treatment should be started in tandem with your diagnostic screen. § The longer-term management should consider secondary prevention of further cardiovascular events. § Acutely, all patients with any acute coronary syndrome (STEMI, posterior infarcts, NSTEMI, unstable angina) are started on a cocktail of drugs that can be remembered by the mnemonic MONABASH: 1) Morphine, for analgesia, and an anti-emetic such as metoclopramide (although there is some evidence that for patients with no gastrointestinal (GI) disturbance there is no benefit in giving an anti-emetic) 2) Oxygen 3) Nitrates (e.g. GTN, isosorbide mononitrate infusion), for vasodilation 4) Antiplatelets: aspirin, clopidogrel, and glycoprotein IIb/IIIa antagonists, to prevent further coronary thrombosis 5) Beta-blockers, to reduce myocardial oxygen demand. These are contraindicated if the patient is in heart block, has asthma, or has any signs of acute heart failure 6) ACE inhibitors, for multiple reasons including attenuation of post-infarct ventricular remodelling that can cause arrhythmias, reduction of angiotensin II-induced vasoconstriction improving cardiac blood flow and reducing afterload, and beneficial effects on endothelial function 7) Statins, which in addition to reducing cholesterol levels are thought to improve endothelial function, modulate inflammatory responses (e.g. reduce CRP), maintain atherosclerotic plaque stability, and prevent thrombus formation; there is evidence to support their use in the acute setting 8) Heparin (low-molecular weight heparin, LMWH), to prevent coronary thrombosis **STEMI patients (including posterior infarcts) should also receive either primary ANGIOPLASTY or THROMBOLYSIS within 12 HOURS of the onset of pain, the sooner the better, and ideally within 2 hours of the onset of symptoms. Thrombolysis carries significant risks and therefore there are clear indications and contraindications with which you should familiarize yourself before referring a patient for thrombolysis. Angioplasty is superior to thrombolysis if both are equally available, but rapid treatment is even more important so you should not delay thrombolysis if angioplasty is not likely to be achieved within 2 hours of the onset of the symptoms. § NSTEMI patients do NOT receive thrombolysis, as this does not appear to be effective in them. However, NSTEMI patients are candidates for early angioplasty if their TIMI risk score is ≥3

When are beta-blocker contraindicated?

§ Heart block § Asthma § Acute heart failure

Heart and lung signs of Left heart failure

§ Heart: Ø↑HR, ↑RR ØIrregularly irregular heartbeat ØPulsus alternans ØDisplaced apex beat ØS3 Gallop rhythm ØS4 in severe HF ØMurmur (AS, MR, AR) § Lungs: ØFine end-inspiratory crackles at lung bases (pulmonary oedema) Wheeze (cardiac asthma

Mr Bromley is a 28-year-old, tall, thin man with a sudden onset of severe chest pain. He has recently been on a flight from Egypt and had knee surgery 1 month ago. Otherwise he says he has been fit and well, with no previous medical history. He is not known to have Marfan's syndrome, although it has not been investigated, and there is no family history of note. He is a non-smoker with no risk factors for cardiovascular disease. On examination he is pale, sweaty, and breathless. His pulse is weak and thready, but otherwise his examination is normal. What diagnoses are most likely? Which first-line investigations will help you determine the correct one?

§ In a tall, thin, young individual you should immediately be thinking of pneumothorax or Marfan's syndrome predisposing to a dissected aortic aneurysm or aortic dissection. § His recent air travel, although only a short trip, and surgery should alert you to the possibility of a PE. § All of these conditions are associated with high mortality and so you must act fast. § In your assessment of his ABC you should pay particular attention to his blood pressure - patients with an aortic aneurysm are often hypertensive but can become hypotensive if they dissect back into the pericardial space and develop cardiac tamponade (along with muffled heart sounds and distended neck veins). § If they rupture into the chest cavity they tend to exsanguinate before they make it to hospital. § An urgent chest radiograph will rule out a pneumothorax (although you should have detected this when palpating, percussing, and auscultating his chest) and will show a widened mediastinum in most cases of aortic dissection (~80%). § PE is a diagnosis of exclusion, although CT pulmonary angiography (CTPA) can be helpful in making the diagnosis. § Mr Bromley was hypotensive (80/46) but there was no difference in the blood pressure in each arm. His chest radiograph suggested a widened mediastinum. As he was not haemodynamically stable it was felt he should not undergo a CT and a transoesophageal echocardiogram was ordered at the bedside. This showed an aortic dissection near the aortic root and a pericardial effusion. Any dissection involving the ascending aorta, such as this one, is classed as a Stanford type A and is a surgical emergency. § Dissections of the descending aorta, with no involvement of the ascending aorta, are called type B and are managed medically. § However, surgery in type B is indicated if medical treatment fails and complications develop.

Normal INR

§ In healthy people an INR of 1.1 or below is considered normal. § An INR range of 2.0 to 3.0 is generally an effective therapeutic range for people taking warfarin for disorders such as atrial fibrillation or a blood clot in the leg or lung

Mr Williams' is 19 y/o, What questions should you ask about the episode of loss of consciousness itself?

§ In the history, from both the patient and a witness (if available), you should get a detailed description of what happened before, during, and after the episode. Specifically: 1) Before a) Was there any warning? If there was no warning, the cause is most likely a cardiac arrhythmia or a massive pulmonary embolus. Note that sometimes arrhythmias are preceded by palpitations. Patients with other causes of blackout tend to have some warning (e.g. aura preceding an epileptic seizure, dizziness preceding a vasovagal episode). b) Were there any precipitating factors (e.g. exercise, straining, standing up, fear, pain)? Postural triggers suggest orthostatic hypotension. Other precipitating factors are consistent with a vasovagal episode. Loss of consciousness caused by head TURNING suggests carotid sinus hypersensitivity. Blackout whilst sitting or lying down is suggestive of a cardiac arrhythmia. Passing out when exercising suggests structural cardiac pathology such as aortic stenosis or a cardiomyopathy. c) Was there any recent head trauma? This may seem obvious, but patients will not always associate head trauma with an episode of loss of consciousness, especially if there is some delay between the two. Be wary of subdural haemorrhages (particularly in the elderly and alcoholics) which may be precipitated by head trauma days or weeks earlier and may be associated with subsequent seizures. 2) During: a) How long was the patient unconscious - seconds or minutes? Blackouts due to a vasovagal episode or an arrhythmia are short-lived, lasting seconds. b) Did they bite their TONGUE, move their limbs, or were they incontinent of urine or faeces? Note that tongue-biting is virtually pathognomonic of an EPILEPTIC seizure, whereas twitching and incontinence can be features with other causes, e.g. vasovagal. 3) Did they recover spontaneously? If not, how long did it take them to recover? Were they confused after recovery? A spontaneous recovery argues against a metabolic or neurological cause (other than epilepsy). A slow recovery with confusion suggests an epileptic seizure.

What are the main factors to consider when coming up with a differential diagnosis for calf swelling?

§ Is it acute or chronic? § Is it in one leg or both legs?

Miss Patel is a 21-year-old student who has just returned from celebrating the end of her university studies with her friends at a Mediterranean coastal resort in Catalunya. A few days after her return, her left ankle started to swell. She has presented because the swelling has been spreading up her leg and into her foot. She does not use the contraceptive pill. She has never had a 'blood clot in her legs or lungs' before, and has not had any recent surgery. Her past medical history is unremarkable. Her flight back from Catalunya lasted only 2.5 hours. Inspection reveals a red, swollen distal calf, ankle, and dorsum of the foot; although a tape measure reveals that the swelling is actually only 1 cm more than her right limb. The swelling is warm, soft, and tender to touch but has no pitting oedema nor visible superficial veins. A small punctum is visible just next to her lateral malleolus, and she explains that it is a mosquito bite that was particularly itchy. Passive movement of her ankle and toes does not elicit any pain, although it is uncomfortable because of the swelling. No other lumps or bumps are palpable in the leg or abdomen. The patient is apyrexial. What is the most likely working diagnosis and how will you manage this patient?

§ It is likely that Miss Patel has either cellulitis OR an inflammatory response to the mosquito bite over her left ankle. § Her Wells' score is 0 and therefore a DVT is unlikely (and can be ruled out if her serum D-dimer is negative). She has no signs of septic arthritis or compartment syndrome and is young for a pelvic malignancy. **Management of Miss Patel should include: § FBC: looking for signs of bacterial infection (a neutrophilia). § Serum D-dimer: given her Wells' score of 0, a negative D-dimer will rule out a DVT without need for an ultrasound. Unfortunately Miss Patel's D-dimer will be elevated in any case as she has an infection, thus the test will be of no diagnostic value in her case. § Doppler ultrasound: as Miss Patel's D-dimer is unlikely to exclude a DVT, you will need to request an ultrasound of her calf to exclude the possibility of DVT. § Antibiotics: an antibiotic that covers both streptococci and staphylococci should be used, such as flucloxacillin, in case this is cellulitis. § Topical steroids and oral antihistamines: given the story that suggests that the mosquito bite may have triggered the episode, you should also consider that the swelling may simply be an inflammatory response to the mosquito bite (essentially an allergic response to the mosquito bite). If so, the inflammatory response will benefit from topical steroids (to dampen the immune response) and antihistamines (as histamine release by mast cells is likely to be driving the inflammation).

What other distributions of pain can occur with a AAA?

§ It's really important to remember that a AAA can cause pain virtually anywhere in the abdomen even mimicking other pathologies such as renal calculi. § Remember that an elderly male with loin to groin pain who has never had kidney stones before is much more likely to have a AAA. § This is often forgotten by juniors, with fatal consequences. § Remember that they can also present with thromboembolic events, usually affecting one or both of the lower limbs.

What is end point of RAAS?

§ K+ is main intracellular cation § Na+ is main cation in blood

List some causes of mitral stenosis

§ KEY CAUSE is rheumatic heart disease **Face - malar flush § Pulse - 'thready' or irregularly irregular AF is common § Palpation - tapping apex, parasternal heave *Mid diastolic murmur: Loud 1st HS with opening snap.*Listen in left lateral position with bell of stethoscope Low rumbling murmur*. atrial fibrillation.

RHF vs LHF symptoms

§ LHS - from pulmonary veins --> resp symptoms § RHS - from IVC and SVC --> Swelling signs

Describe some features of the affected limb in a patient with neuropathic ulcers.

§ Loss of sensation (gloves and stockings distribution) § Foot deformities (e.g. Charcot foot)

What are the main types of dressings for ulcers?

§ Low-adherence dressings: useful only if there is little exudate that needs soaking up because they have little adherence, but they can often be left in place for 7 days. § Hydrogel dressings: as the name implies, they are useful for hydrating dry ulcers (e.g. arterial) and for encouraging debridement of dead tissue (e.g. diabetic neuropathic ulcers). § Alginate dressings: like the dry algae they are based on, they mop up water and are thus useful for wet ulcers (e.g. venous ulcers, fungating ulcers) that need drying. § Antibacterial dressings: these prevent growth of bacteria by incorporating silver, honey, iodine, or metronidazole. There is little evidence base other than for iodine.

What is the initial pharmacological treatment for T2D?

§ METFORMIN, if not contraindicated and if not tolerated, is the preferred initial pharmacological treatment for T2D (has S/E of diarrhoea, tummy ache). Also exercise and diet combined. § if noninsulin monotherapy at maximum tolerated dose does not achieve or maintain the A1C target after 3 months, ADD a second oral agent, a GLP-1 receptor agonist (increase insulin and decrease glucagon), or basal insulin. § In patients with long-standing suboptimally controlled T2DM and established ATHEROSCLEROTIC cardiovascular disease, empagliflozin (SGLT2 inhibitors) or liraglutide (G1P1 agonist) should be considered as they REDUCE cardiovascular and all-cause mortality when added to standard care. **S/E: § Sglt2- skin mycoses § glp-1 - reactions § dpp4 - pancreatitis and reitnopathy *hence SGLT2 and GLP-1 preferred.

Associated symptoms for cardio

2Ps: chest pain, palpitations 4Ss: SOB, syncope (loss of consciousness), swelling, sweating **After this, do ICE + Effect

How long is the delay between myocardial damage and a rise in troponins?

3 hours

At what size is an elective repair of AAA generally regarded as being required?

5.5cm. § At about 5.5cm the risk of rupture increases significantly from as low as 3% per year in a 5cm aneurysm to as high as 15% in a 6cm aneurysm. § This means that anyone below the threshold is observed with serial ultrasound and anyone above is consented for an elective aneurysm repair. It is not actually that simple and each case is about balancing the risk of operation with the risk of surgery and life expectancy so we reach a different threshold with different patients. In addition, serial monitoring gives an idea of the speed of progression which, amongst other things is a very important factor.

Long-term management of STEMI

§ Manage the patient in the ABCDE approach. § Oxygenation would come first out of the options provided using this approach. § Myocardial muscle needs Oxygen so it is important to put 15L via non-rebreathe mask first and continual cardiac monitoring is also recommended. § Nitrates (GTN spray) is second, because it is easy to administer (under the tongue) and will dilate the coronary arteries. § Then clopidogrel 300mg and aspirin 300mg. § Ultimately the coronary vessel needs to be re-opened via angioplasty, therefore involve cardiology ASAP so that arrangements can be made. § Whilst the nurses are giving the GTN, aspirin and clopidogrel you can get on the phone to the cardiologist. § Tell them concisely the patients ECG findings, the nature of their chest pain and their risk factors (including that they are post-op). Also tell them what you have done so far. § Whilst the cardiologist is coming you can ensure the patient has IV access and take the bloods. § Do a VBG as that will give an instant Hb (anaemia worsens ischaemia). § They will need to take the patient for PCI so tell the nurses in case they need to do any paperwork/ transfer documentation. § Your senior should also be keep up to date. § Long term the patient will need statins and cardiology can decide upon giving beta-blockers and ACE inhibitors.

Miss Takenawa is a 32-year-old lady who has been admitted to hospital for intravenous corticosteroid therapy for a particularly bad flare-up of her ulcerative colitis. During a teaching ward round, a medical student notices that Miss Takenawa has a small ulcer over the lateral aspect of her right leg. Miss Takenawa states that she was bitten by a midge several weeks ago whilst hiking in Scotland and assumes the ulcer has arisen because of the high-dose steroids she is currently receiving. The ulcer has a purplish halo at its border. She says it has been painful although it is now improving. What type of ulcer has Miss Takenawa developed? How should it be managed?

§ Miss Takenawa is a patient with known ulcerative colitis who has developed an ulcer on her leg that has a purple halo around it. In the absence of any other obvious cause for her ulcer this is consistent with PYODERMA GANGRENOSUM, a complication of systemic inflammatory diseases (e.g. Crohn's disease, ulcerative colitis, rheumatoid arthritis) or haematological malignancies. § Management of pyoderma gangrenosum is with good NURSING care (bandages to prevent infection and promote healing) and treatment of the underlying disease. § As Miss Takenawa is already on intravenous corticosteroids, it is likely that the ulcer will improve as her ulcerative colitis settles.

Mitral valve prolapse --> mitral regurgitation and is associated with PCKD.

§ Mitral valve prolapse is associated with polycystic kidney disease

Mr Bullen is a 34-year-old gardener who is on the trauma unit of his local hospital because he has broken his right tibia. He presented yesterday morning having been hit by a car while attempting to cross the road. He was diagnosed with a closed, transverse, minimally displaced fracture of the right tibial shaft which required internal fixation. You have been bleeped by the nurse on the Trauma Unit. Mr Bullen is complaining that his leg is 'excruciatingly painful' and that he cannot feel his toes. You attend and confirm that he cannot feel you touching his cold toes, which protrude from the cast. You immediately cut and remove the cast to reveal a right calf that is red, tender, swollen, and with skin that looks tense and shiny. There is no pitting oedema. Passive movement of his right toes or ankle causes severe pain. Sensation to light touch is diminished over the distal portion of his right calf, over the dorsum of his right foot, and over his toes. His right posterior tibial pulse is palpable but his dorsalis pedis is not, although it is palpable on the left leg. What is the diagnosis? How will you manage this patient?

§ Mr Bullen has features that are strongly suggestive of COMPARTMENT syndrome: a tense, shiny, swollen limb that is painful to passive movement and has neurovascular compromise. § Inflammation due to TRAUMA (accidental or iatrogenic) is the most common cause of compartment syndrome. § Limbs have muscle groups surrounded by tight inelastic fascia. The inflammation in a confined compartment can occlude the deep veins, impeding venous drainage of the limb, which therefore starts to swell - further occluding the deep veins. § Pressures in the affected limb can become high enough to cause ischaemia and necrosis of all the tissues in the limb, leading to an irreversible atrophy of the limb known as VOLKMANN's contracture. § Compartment syndrome is a SURGICAL EMERGENCY requiring urgent decompression via a FASCIOTOMY. The skin, subcutaneous tissue, and tight fascia surrounding the affected limb are all divided and left open for a few days so that the pressure is relieved and the inflammation can resolve. § Two longitudinal incisions are made in the leg in order to decompress all four compartments (anterior and lateral compartments via an anterolateral incision, and superficial and deep posterior compartments via a medial incision)

Mr Cleveland is a 52-year-old patient who has attended his local endocrinology department for a routine follow-up of his type 1 diabetes. During the consultation, Mr Cleveland points out that he has developed a painless ulcer on his right foot and his community nurse has urged him to get it checked. After removing the bandage for inspection, there is a small ulcer over the lateral aspect of the fifth metatarsophalangeal joint. The ulcer has rimmed edges and is deep. After removing some pus, it is obvious that the ulcer extends down to the bone. Mr Cleveland's feet are warm and well perfused. All pulses are palpable in Mr Cleveland's lower limbs and there is no eczema, varicose veins, or lipodermatosclerosis. However, Mr Cleveland has, for several years now, had diminished sensation to vibration in both feet. The registrar confirms that this is still the case, and that Mr Cleveland is now starting to lose his proprioception in both feet as well. What is the likely cause of Mr Cleveland's ulcer? How should the ulcer be managed? What complication should you be concerned about?

§ Mr Cleveland is a patient with known diabetes mellitus who has presented with an ulcer on his foot. § Diabetes mellitus increases one's risk of arterial (atherosclerotic) ulcer. However, this ulcer is directly over a pressure site (where shoes often rub), has rimmed edges, and is painless. § Mr Cleveland has signs of peripheral neuropathy in both feet, whereas there are no signs of arterial disease. § This is therefore a NEUROPATHIC ulcer. § Neuropathic ulcers in diabetics are due to repeated trauma and pressure plus a reduced ability to heal skin breaks and fight infection. For this reason, treatment involves: A) Foot care: avoid tight-fitting shoes until the ulcer is healed. Always wear soft, comfortable shoes thereafter and examine the feet daily. B) Manage diabetes: make sure diabetic control is optimized as uncontrolled hyperglycaemia will hinder ulcer repair and fighting infections. C) Debridement: ulcers in diabetics tend to build up necrotic tissue. This needs debriding either using special bandages (e.g. hydrogel sheets) or surgically. D) Treat infections: if there are clinical signs of infection. ***The major complication to worry about in diabetic foot ulcers is INFECTION. Given that Mr Cleveland's ulcer extends down to the bone you need to exclude OSTEOMYELITIS. § Osteomyelitis should be suspected and investigated by magnetic resonance imaging (MRI) if: • Diabetic ulcer >2 cm2 • Visible or palpable bone in the ulcer (arguably, this represents osteomyelitis by definition) • ESR >70 mm/hour

A 35-year-old Singaporean female attends a varicose vein pre operative clinic. On auscultation a mid diastolic murmur is noted at the apex. The murmur is enhanced when the patient lies in the left lateral position. What murmur?

A mid diastolic murmur at the apex is a classical description of a mitral stenosis murmur. The most common cause is rheumatic heart disease. Complications of mitral stenosis include atrial fibrillation, stroke, myocardial infarction and infective endocarditis.

Why should you ask about symptoms of GI, ovarian and uterine malignancy (e.g. PR bleeding, unusual vaginal bleeding, weight loss) in swollen calf?

A pelvic mass (e.g. a tumour) could compress the iliac veins or IVC leading to leg swelling

Management of VT flowchart

A synchronised cardioversion is the treatment for a unstable patient in VT. Intravenous amiodarone is the pharmacological treatment for chemical conversion of ventricular tachycardia in a stable patient. **For torsades de pointes: § Intravenous magnesium sulphate is the treatment of choice of torsades de pointes, a polymorphic ventricular tachycardia with a prolonged QT interval. § Causes of a prolonged QT interval include drugs, electrolyte disturbances and toxins. § However, in a peri-arrest scenario, if the patient has torsades de pointes, the treatment of choice is ALSO synchronised DC cardioversion.

Marvin presents with a 4-month history of increasing breathlessness and ankle swelling. On examination, he has ascites and Kussmaul's sign is elicited. What would be the most useful diagnostic investigation? A. Echocardiography B. ECG C. Endomyocardial biopsy D. Abdominal X-ray E. CK

A. Echocardiography: Allows differentiation between restrictive cardiomyopathy and constrictive pericarditis. § Endomyocardial biopsy might help you investigate possible causes of restrictive cardiomyopathy (i.e. granulomas in sarcoidosis, amyloid fibrils in amyloidosis)

A 57-year-old man is reviewed in a hypertension clinic, where it is found that his blood pressure is 165/105 mmHg despite standard doses of amlodipine, perindopril, doxazosin and bendroflumethiazide. Electrolytes and physical examination have been, and remain, normal. Which of the following would be your next stage in his management? A.Arrange for his medication to be given under direct observation B.Add spironolactone to his medication C.Arrange urinary catecholamine assays D.Request an adrenal CT scan E.Add verapamil to his medication

A.Arrange for his medication to be given under direct observation

Mr Griffin is a 58-year-old gentleman who presents to his GP because of an ulcer on his left foot which has been present for 2 weeks. The ulcer causes him constant 'sharp pain' that is worse at night unless he sleeps with his foot dangling over the edge of the bed. Mr Griffin gets a stabbing pain in both calves if he walks too fast, but denies any chest pain, shortness of breath, or impotence. He also denies any itch, heaviness, or loss of sensation in his legs. He does not recall any trauma that could have caused the ulcer. His past medical history is remarkable for type 2 diabetes mellitus. He takes metformin, gliclazide, aspirin, simvastatin, and ramipril. He has smoked two packets of cigarettes a day for most of his adult life. His family history is unremarkable. On examination, a well-demarcated, deep, dry ulcer is found over the ball of his left foot. His legs are pale, smooth, and hairless. Both feet are cold and have a capillary refill time of 5 seconds. On the right, dorsalis pedis is palpable but the posterior tibial pulse is not. On the left, neither pulse is palpable. Buerger's test is positive on both legs. The ABPI is 0.45 on the left and 0.65 on the right. Sensation in his lower limb is normal for all modalities. Examination of the rest of his cardiovascular system is unremarkable. His heart rate is 85 bpm (regular) and his blood pressure is 128/76 mmHg. What is the diagnosis of Mr Griffin's ulcer? How should it be managed?

§ Mr Griffin is a gentleman with significant risk factors for atherosclerosis (lifelong smoker, diabetes mellitus) and a history of claudication on exercise. § He has a well demarcated, deep, dry ulcer on his left foot. His feet have poor capillary refill, weak or impalpable pulses, a positive Buerger's test, and an ABPI <0.8. § This all suggests that Mr Griffi n has an ARTERIAL (atherosclerotic, ischaemic) ulcer on his left lower limb. § Furthermore, Mr Griffin has CRITICAL LIMB ISCHAEMIA - he has rest pain, tissue loss (the ulcer), and an ABPI <0.5 in the left leg - and therefore needs urgent REFERRAL to a vascular surgeon. **Management should involve: § Investigations: remember that atherosclerosis is a systemic disease. 1) Duplex ultrasonography of his lower limbs (or magnetic resonance angiography) to assess the patency of the arteries and potential for revascularization or bypass surgery. Alternatively, percutaneous angiography can be performed to allow for assessment and treatment (angioplasty) to be done all in one 2) Electrocardiogram (ECG) 3) Urinalysis looking for proteinuria (?diabetic nephropathy) or haematuria (?vasculitis) 4) Fasting serum lipids, fasting glucose, and HbA1c levels, to see if Mr Griffin's lipid and glucose control are adequate 5) FBC, as anaemia will exacerbate any ischaemia ** Interim management: § Dressing of the ulcer to prevent infection, but take care to avoid the bandage being tight as this will worsen the ischaemia § Analgesia § Antibiotics: if there are any signs of infection and a swab is positive **• Surgical intervention: § Angioplasty and stenting can be performed if an artery is stenotic or there is a short occlusion and there is a patent artery downstream of the occlusion § Bypass surgery using a venous graft or artificial Dacron graft can be performed if angioplasty is not possible

Mr O'Brien is a 42-year-old estate agent who presents to his GP after several episodes of loss of consciousness over the last 2 months. The episodes occurred whilst he was running or rushing, e.g. for the bus. Each was immediately preceded by sweating. He does not recall any palpitations, nausea, chest pain, or shortness of breath. He tells you that some of these episodes were witnessed and he was told that he was only unconscious for a few seconds. He has not bitten his tongue or been incontinent at any time. He says he recovers rapidly and is able to carry on as normal, although he has been taking it a bit easier. He has no known history of cardiovascular disease, epilepsy, or diabetes, and takes no medications. His pulse rate is 72 bpm and regular. There is a slow-rising carotid pulse. His apex beat is undisplaced and there are no heaves or thrills. Heart sounds I and II are both audible and there is a loud ejection systolic murmur which radiates to the carotids. His examination is otherwise unremarkable. His blood glucose, ECG, and U&Es are normal. In light of his heart murmur, you order an echocardiogram. What do you think the echocardiogram would show? How might this account for his episodes of loss of consciousness?

§ Mr O'Brien's echocardiogram showed severe aortic stenosis, consistent with his systolic ejection murmur. § His cardiac output was significantly reduced as a result of the outflow obstruction caused by his aortic stenosis. § It was this that was predisposing him to blackouts. § There are three main causes of aortic stenosis. In a young patient a congenital bicuspid valve is most common. In the elderly, calcification of the valve commonly leads to stenosis. Rheumatic fever is a third cause of aortic stenosis but thankfully is relatively rare in the UK today. § Mr O'Brien's echocardiogram showed a bicuspid aortic valve. § An important differential diagnosis in a young patient presenting like this is HOCM, but this would not account for the slow-rising pulse.

Your consultant agrees that this is most likely a vasovagal attack and decides to discharge Mr Williams. What advice would you give him on discharge? Does he need to be followed up, and if so, by who?

§ Mr Williams has had what is probably a vasovagal attack. § You should explain this and give him lifestyle advice, that is to sit or lie down if he feels like he is going to faint. § Now is also a good opportunity to encourage Mr Williams to avoid excessive alcohol consumption. § You should advise him to see his general practitioner (GP) if he has recurrent episodes, but no follow-up is necessary unless these occur.

Mrs Glenn is an 82-year-old lady who has been referred to the surgeons at her local hospital because of a large ulcer on her right shin. Mrs Glenn lives in a nursing home because she has advanced Alzheimer's dementia. Her GP referral letter states that Mrs Glenn has had a long-standing venous ulcer (fl at, wet, with irregular borders), on her right shin for the past 3 years. Management has been attempted with alginate-based compression dressings changed regularly by the nursing home staff , but the GP has noticed that the ulcer has recently changed: its central area has become raised and indurated, the ulcer smells far worse than usual, and its borders have spread and become raised. On inspection, there is a large fungating ulcer on the right shin, surrounded by an area of lipodermatosclerosis and skin pigmentation. What has most likely happened to Mrs Glenn's ulcer? How should it be investigated? What is the prognosis?

§ Mrs Glenn has had a long-standing venous ulcer over her right pre-tibial region, as suggested by the lipodermatosclerosis, the skin pigmentation, and the GP's letter. § The ulcer is now fungating, suggesting malignancy or infection. § It is likely that Mrs Glenn's chronic venous ulcer has transformed into a SQUAMOUS CELL CARCINOMA - also known as a Marjolin ulcer. § Investigation involves a BIOPSY of the peripheral area of the ulcer (as the central area is likely to contain necrotic tissue which is hard to visualize for a histological diagnosis). § Management of a Marjolin ulcer is by WIDE EXCISION and skin GRAFTING, but the prognosis is poor and she may not be a candidate for surgery given her age and advanced, irreversible dementia.

Mrs Peacock is a 74-year-old woman 2 days post-op (carotid endarterectomy following an ischaemic stroke) who has been referred to the medical team for an episode of chest pain that began half an hour ago. She is a type 2 diabetic, for which she takes metformin and gliclazide. She is also treated for hypertension and hypercholesterolaemia, but has never smoked and has no family history of cardiovascular disease. She usually takes warfarin for atrial fibrillation, but this was stopped prior to her operation. She says the pain is always there but is not severe. On examination she appears unwell lying at 30 degrees in bed, with shallow and rapid breathing. Her lung fields are clear on auscultation. Her pulse is weak and irregularly irregular, but her heart sounds are normal, and her examination is otherwise unremarkable. Her oxygen saturation is 91% on room air. The chest radiograph is normal. Her ECG shows atrial fibrillation but no ST elevation or other abnormalities. Her 12-hour troponin levels are not elevated. What is the most likely diagnosis? What investigation would you order next to investigate this?

§ Mrs Peacock is presenting with an episode of chest pain and breathlessness, on a background of cardiovascular risk factors. § Left heart failure secondary to myocardial ischaemia is a possibility, particularly given her risk factors (atrial fibrillation and recent stroke), with the breathlessness due to pulmonary oedema. § However, if that were the case you would expect bibasal crackles on auscultation of her lungs. The chest radiograph, ECG, and troponin levels also fail to show signs of left heart failure or myocardial ischaemia. § Her recent surgery and reduced mobility following her stroke are both risk factors for a PE, which would explain her breathlessness and reduced oxygen saturation. § PE is a diagnosis of exclusion. § However, the advent of CTPA has made it possible to see the embolus in a large number of cases. Mrs Peacock was indeed sent for CTPA and found to have multiple small clots in both lungs. She was started on low-molecularweight heparin and made a good recovery.

Mrs Swanson has a single, 5 x 5 cm ulcer just above the medial malleolus of her right leg. The ulcer looks wet, has fragile looking irregular borders, and the surrounding skin is deeply pigmented. Her feet (and hands) feel slightly cold but dorsalis pedis and posterior tibial pulses are palpable in both feet. Her capillary refill time is 2 seconds in both feet. The rest of her cardiovascular exam is normal. Sensation is intact in both of her legs. What is the most likely diagnosis? What first-line investigations will you arrange?

§ Mrs Swanson is an elderly lady with limited mobility who has a wet, irregular ulcer on the medial aspect of her right leg (gaiter area). § Sensation is intact. There is surrounding skin pigmentation and no suggestion of arterial insufficiency on examination. § The most likely diagnosis is a VENOUS ulcer. Nonetheless, you should arrange the following investigations IN CASE there is COEXISTING arterial disease, diabetes mellitus, or infection, as these will influence your management: 1) Bloods: full blood count (FBC) (?infection), erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP) (?vasculitis), albumin (?malnutrition), fasting lipids (?hyperlipidaemia, contributing to any atherosclerosis). In Mrs Swanson's case inflammatory markers will be unhelpful as her underlying pneumonia will cause these to be deranged. The FBC and albumin are particularly relevant because ANAEMIA and HYPOALBUMINAEMIA are important factors that IMPAIR HEALING of venous ulcers but which can be addressed. 2) Capillary glucose: a quick and reliable way of assessing whether Mrs Swanson has undiagnosed diabetes mellitus. Remember that up to 50% of type 2 diabetes mellitus is undiagnosed. 3) Urinalysis: looking for glucose (?diabetes mellitus affecting healing) but also haematuria/proteinuria (?vasculitis). 4) Duplex ultrasound: to assess the competence of the sapheno-femoral and sapheno-popliteal junctions, and state of the perforators and deep venous system. 5) Ankle-brachial pressure index (ABPI)†: measured to exclude arterial disease as the cause. This is measured using a manual sphygmomanometer, stethoscope (for brachial pressure), and portable Doppler probe (for dorsalis pedis or posterior tibial pressure). § The ABPI is the ratio of the ankle systolic pressure (either dorsalis pedis or posterior tibial) over the brachial artery systolic pressure. § Even if you are clinically convinced that an ulcer is venous, it is important to measure the ABPI because if the ABPI is <0.8, the patient must NOT have a pressure bandage applied as this suggests the ulcer is actually a mixed venous/ arterial ulcer and compression will make the arterial ischaemia WORSE. If the ABPI is <0.5, or there has been a sudden change, the patient needs URGENT REFERRAL to a vascular surgeon. 6) Swabbing an ulcer for microscopy, culture, and sensitivities (MC&S) is not routinely performed as all ulcers will have some growth. Swabbing may, however, be useful in the case of spreading cellulitis. **† Beware: patients with DIABETES mellitus or chronic renal failure (CRF) can have CALCIFIED (hard) arteries that give falsely HIGH ABPI readings even in the presence of significant limb ischaemia. Oedema may also result in erroneous readings.

What is the investigation of choice for the vascular surgeon before he operates on a patient who is stable enough to not go to theatre immediately?

Abdominal CT. § An abdominal CT is performed as it is quick, readily available and confirms a diagnosis both of the presence of an aneurysm and a rupture. § It also gives the surgeon an idea of the extent of the aneurysm and the size the Teflon graft will need to be. It is particularly important to know if the renal and iliac arteries are involved. § Remember that there are now two commonly used ways of repairing a AAA: Traditionally an open approach is used through a midline laparotomy but endovascular aneurysm repair (EVAR) is becoming more common. Because of the need for greater interdisciplinary involvement at operation EVAR is mainly used for elective repairs, however.

What are arrhythmias?

Abnormal heart rhythm: irregular, too fast (tachycardia) or too slow (bradycardia). e.g. AF, supraventricular tachycardia, WPW, heart block, ventricular tachy, vfib

Compare the mechanism of action of aspirin, clopidogrel, and abciximab/tirofi ban.

All of these are antiplatelet agents with different mechanisms of action: § Aspirin is an irreversible inhibitor of the enzyme cyclooxygenase (COX), which synthesizes inflammatory mediators including the platelet aggregator thromboxane A2. Platelets have no nuclei so cannot synthesize new COX enzymes to compensate for this irreversible inhibition. Aspirin's action is reversed on synthesis of new platelets. 2) Clopidogrel irreversibly blocks the adenosine diphosphate (ADP) receptor on platelet cell membranes that prevents them binding to fibrinogen and hence inhibits platelet aggregation. 3) Abciximab and tirofiban reversibly block fibrinogen binding to the glycoprotein IIb/IIIa receptors on platelet cell membranes that mediate platelet aggregation (abciximab is a monoclonal antibody, tirofiban a small molecule).

What is long QT syndrome>

An inherited condition. Mutations within 13 identified genes result in a variety of channelopathies affecting myocardial repolarisation, thus prolonging the QT interval. QT interval prolongation may also be acquired by certain drugs (e.g., macrolide and fluoroquinolone antibiotics, some antipsychotics). Patients with long QT syndrome should avoid these drugs. ECG shows a prolonged QT interval and abnormal T-wave morphology.[9] Patients are at increased risk for syncope, ventricular arrhythmias (e.g., torsade de pointes) and sudden cardiac death. Treatment may involve avoidance of competitive sport or similar exertion, emotional stress, startling sounds (e.g., alarm clocks) and require QT-prolonging drugs; beta-blocker treatment; and cardioverter-defibrillator implant.

Look at the ECG recorded on. 1) What is the most likely diagnosis 2) The patient is transferred to CCU, attached to a cardiac monitor and an IV cannula inserted. Which four of the following should be given immediately in the management of this patient? 3) What single treatment is the best option for this patient? 4) Given the presentation, what coronary artery is the culprit vessel? 5) The patient is kept in for 3 days and no other complications occur. The patient is mobilising normally without shortness of breath. Prior to discharge, you are asked to check that the patient is being sent home with the appropriate medication following a myocardial infarct. Which five of the following drugs should the patient be discharged on?

Anterolateral myocardial infarction. ECG findings: ST segment elevation leads V2, V3 and leads I and aVL, reciprocal ST segment depression in leads, II, III and aVF. Diagnosis: acute anterior myocardial infarction with lateral extension (acute anterolateral MI). 2) Intravenous opiates, Sublingual GTN, Oral Aspirin 300mg, Intravenous Metoclopramide 10mg. Intravenous opiates, high flow oxygen only if saturations are below the expected range, oral Aspirin 300mg, sublingual GTN, intravenous Metoclopramide 10mg are the immediate management of this patient. Mnemonic: MONA 3) PPCI (primary percutaneous coronary intervention). PPCI (primary percutaneous coronary intervention) is the treatment option. Emergency bypass surgery is also a rarely required and is reserved for cases of failed PPCI +/- stent insertion. 4) left anterior descending. The anterior/anterolateral wall is supplied by the left anterior descending artery. The inferior wall is supplied by the right coronary artery of which the RV branch comes off proximally. The left main stem divides into the LAD and then circumflex giving ECG changes normally in more than one territory. The circumflex supplies the posterior and lateral wall. 5) clopidogrel 75 mg od, bisoprolol 2.5 mg od, asprin 75 mg od, ramipril 5mg od, atorvastatin 80 mg od. Clopidogrel 75mg OD (could also be ticagrelor 90 mg bd or prasugrel 10 mg od which are stronger antiplatelets), Bisoprolol up to 10 mg OD, Ramipril up to 10mg OD, Aspirin 75mg OD, Atorvastatin 80mg OD are correct. The NICE guidelines for the secondary prevention of MI recommend that all patients should be offered an ACEi, dual antiplatelet therapy, a beta-blocker and a statin.

The ECG tracing is shown in Figure 1. What is the most likely diagnosis?

Anteroseptal myocardial infarction. There is ST elevation in the anterolateral leads V1-V4. To confirm that this is an acute STEMI there should be reciprocal changes on the opposite wall: there is T wave inversion in the inferior leads 3 and AVF. Left Ventricular aneurysms can present with ST elevation together with Q waves alone but without the reciprocal changes.

A 72 year old man with a history of 2 previous MI's presents to hospital following sudden tearing chest pain radiating to the back •On examination he has absent radial pulses and CXR shows a widened mediastinum •What is the most likely diagnosis?

Aortic dissection. §Tear in the tunica intima of the aorta allows blood to flow between the layers of the wall of the aorta, creating a false lumen. **Px: -Sudden onset severe chest pain- TEARING in nature -Dizziness -Breathlessness -Sweating -Neurological deficit **Risk factors: -Smoking, obesity, DM, HTN, high cholesterol, FHx, previous IHD **Signs -Unequal radial pulses -Tachycardia -Hypotension/ Hypertension -Brachial pressure difference >15mmHg -Aortic regurgitation -Pleural effusion -Neurological deficit **As the dissection extends, branches of the aorta occlude sequentially leading to hemiplegia (carotid artery), acute limb ischaemia, paraplegia (anterior spinal artery), anuria (renal artery)

What murmur causes a loud early diastolic murmur in the neck

Aortic regurgitation. Likely SBP - will be high (150/160), DBP will be low (40)

A 23-year-old man attends a routine military physical. He is planning to sign up to the army and requires a medical examination beforehand. On auscultation, the army doctor finds a third heart sound, however, the rest of the examination is normal. He is otherwise well with no symptoms or past medical history. Which of the following may be causing this? Atrial fibrillation/ Heart failure/ Normal physiological extra heart sound/ Hypertrophic obstructive cardiomyopathy (HOCM)/ Aortic stenosis

§ Normal physiological extra heart sound § S3 (third heart sound) is considered normal if < 30 years old § Heart failure is another cause for a third heart sound, however, in this young man with no previous history or symptoms, it would be very unlikely.Atrial fibrillation would not cause an extra heart sound, and HOCM or aortic stenosis would cause a fourth heart sound, not a third. **The first heart sound (S1) is caused by closure of the mitral and tricuspid valves whilst the second heart sound ***(S2) is due to aortic and pulmonary valve closure. 1) S1: § closure of mitral and tricuspid valves § soft if long PR or mitral regurgitation § loud in mitral stenosis 2) S2: § closure of aortic and pulmonary valves § soft in aortic stenosis § splitting during inspiration is normal 3) S3 (third heart sound) § caused by diastolic filling of the ventricle considered normal if < 30 years old (may persist in women up to 50 years old) § heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation 4) S4 (fourth heart sound) § may be heard in aortic stenosis, HOCM, hypertension § caused by atrial contraction against a stiff ventricle - therefore coincides with the P wave on ECG § in HOCM a double apical impulse may be felt as a result of a palpable S4

Mr Williams is a 19-year-old student who is brought in by ambulance after collapsing whilst at a university ball. A friend who witnessed the collapse has accompanied him to hospital and confi rms that he lost consciousness. What are the commonest causes of a transient loss of consciousness?

§ Note that the terms 'syncope' and 'loss of consciousness' are not interchangeable as loss of consciousness can be due to either syncopal or non-syncopal causes. Syncope is a form of loss of consciousness in which hypoperfusion of the brain is the cause (from the Greek syn (together) and kopein (to cut), referring to the fact that the blood flow that joins the brain together with the rest of the body has been cut). § Syncopal causes can be subdivided by mechanism as follows: 1) 'Reflex': this is believed to involve activation of a primitive reflex that leads mammals to 'play dead' when faced with danger. Th eir heart rate slows and their blood pressure drops temporarily, reducing cerebral perfusion and leading to syncope. Some people appear to have a low threshold for activating this reflex in specific situations - for example after standing still for a long time, after seeing something frightening (e.g. blood, needles), or when straining (micturition, defaecation). 2) 'Cardiac': pathologies causing a reduction in cardiac output (such as arrhythmias or outlet obstruction) can also lead to syncope. 3) 'Orthostatic': orthostatic hypotension basically means low blood pressure on sitting or standing (as opposed to lying flat). When we stand up there is a sudden drop in blood pressure that we compensate for by vasoconstriction, particularly of the 'capacitance' veins in the legs. Th is reduces the intravascular space, enabling us to maintain the pressure. However, this vasoconstriction takes a few seconds, so to prevent a transient fall in blood pressure every time we stand, there is a temporary increase in heart rate. Patients with reduced intravascular volume (e.g. from dehydration) and/or in whom the normal autonomic response (transient TACHYcardia and peripheral vasoCONSTRICTION) to standing is blunted (e.g. due to drugs or autonomic neuropathy) are vulnerable to blackouts. 4) 'Cerebrovascular': these are non-cardiac structural causes of reduced cerebral perfusion, i.e. obstructions to the blood fl ow between the heart and the brain. Th ey are relatively uncommon.

History presentation in cardiomyopathy

§ OSCE tip: think of sudden unexplained cardiac death <50 years old **cardiomyopathy Definition: A group of diseases in which the myocardium becomes structurally and functionally abnormal •In the absence of coronary artery disease, valvular disease and congenital heart disease •It can affect young people *Primary: •confined to the myocardium. *Secondary: •part of a systemic disease **types: dilated, hypertrophic, restrictive. § Dilated - ventricle dilated, thin walls, reduced ventricular pressure § Hypertrophic - muscle hypertrophies inwards, more rigid, obstruction etc. § Restrictive - basically the same amount of muscle but it's rigid and doesn't pump as well as normal

Management of STEMI Passmed

§ Once a STEMI has been confirmed the first step is to immediately assess eligibility for coronary reperfusion therapy. § There are two types of coronary reperfusion therapy: 1) primary coronary intervention: § should be offered if the presentation is within 12 hours of onset of symptoms AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI) § if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered § drug-eluting stents are now used. Previously 'bare-metal' stents were sometimes used but have higher rates of restenosis § radial access is preferred to femoral access 2) fibrinolysis: § should be offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given § a practical example may be a patient who presents with a STEMI to a small district general hospital (DGH) which does not have facilities for PCI. If they cannot be transferred to a larger hospital for PCI within 120 minutes then fibrinolysis should be given. § If the patient's ECG taken 90 minutes after fibrinolysis failed to show resolution of the ST elevation then they would then require transfer for PCI § If patients are eligible this should be offered as soon as possible. 1) Primary coronary intervention for patients with STEMI: a) Further antiplatelet prior to PCI: this is termed 'DUAL antiplatelet therapy', i.e. aspirin + another drug o if the patient is not taking an oral anticoagulant: prasugrel o if taking an oral anticoagulant: clopidogrel b) Drug therapy during PCI: patients undergoing PCI with radial access: o unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus § patients undergoing PCI with femoral access: bivalirudin with bailout GPI c) Other procedures during PCI: § thrombus aspiration, but not mechanical thrombus extraction, should be considered § complete revascularisation should be considered for patients with multivessel coronary artery disease without cardiogenic shock 2) Fibrinolysis for patients with STEMI: § Fibrinolysis used to be the only form of coronary reperfusion therapy available. § However, it is used much less commonly now given the widespread availability of PCI. § The contraindications to fibrinolysis and other factors are described in other notes. § Patients undergoing fibrinolysis should ALSO be given an ANTITHROMBIN drug. (e.g. unfractionated heparin w/ tenecteplase) § If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.

A 68-year-old female patient was admitted to her local district general hospital after being brought in by ambulance for severe chest pain, 11 hours after symptoms started. Repeat ECGs showed ST segment elevation in the anterior leads. Coupled with a raised troponin level, resulted in a diagnosis of ST elevation myocardial infarction (STEMI). Given the timeframe and logistics involved, she underwent thrombolysis. An ECG repeated 90 minutes after thrombolysis demonstrated the ST elevation was still present, and the patient's symptoms had not changed. Which next step in management should most urgently be undertaken?

§ PCI - If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered § Fondaparinux with outpatient PCI is incorrect - fondaparinux is used in the management of non-ST elevation myocardial infarction (NSTEMI), to those who are not having angiography immediately, but would not be appropriate here. § Arranging an echocardiogram at this moment in time is incorrect - the pressing concern is to transfer to somewhere with PCI capabilities. § Repeating thrombolysis would be incorrect, given the urgent need to transfer her elsewhere for PCI. § Monitoring serial ECGs and waiting for 24 hours is incorrect - this would allow the problem to become worse. **STEMI simplified management in pic §

What are the indications for surgery of varicose veins?

§ Patients with any of the following should be considered for surgery of their varicose veins under the UK National Health Service (NHS): A) Bleeding varicosity B) Unresolving or painful ulcer despite treatment C) Progressive skin changes (pigmentation, lipodermatosclerosis) D) Recurrent thrombophlebitis E) Significant impact on quality of life that has not been improved by conservative management with graded stockings. **The above criteria are based on the current National Institute for Health and Clinical Excellence (NICE) guidelines. As one can see, cosmetic reasons alone do not qualify for surgery under the NHS. **Equally, there is nothing in the guidelines to suggest that a previous venous ulcer warrants surgery to prevent recurrence.

Pneumothorax vs collapsed lung

§ Pneumothorax - If air gets into the pleural space, unopposed elastic recoil of the chest wall will cause it to pop out, whilst at the same time the lungs will shrivel up. 2) Lung collapse - a bronchus is obstructed and the air trapped distally in that segment is gradually absorbed into the blood.

List some potential causes of status epilepticus.

§ Poor compliance with anti-convulsant medications § Metabolic (e.g. hypoglycaemia) § Alcohol and other toxins § Hypoxia § Infection

List some rare causes of angina type symptoms.

§ Prinzmetal angina - angina at rest that occurs in cycles and is caused by vasospasm of the coronary arteries § Coronary syndrome X - signs associated with decreased blood flow to the heart tissue but with normal coronary arteries

Outline the management of pressure ulcers

§ Record the ulcer § Relieve the ulcer § Reduce further ulcers § Reassess ulcer

Mrs Maxwell is a 37-year-old housewife who has been referred to neurology outpatients by her GP after several episodes of loss of consciousness. The GP wonders if she has epilepsy. The GP's letter adds that Mrs Maxwell is an anxious lady with a history of depression. She has come to outpatients with her husband. You ask her about the attacks. She describes a series of different events. On one occasion, she says she was having an argument with her 8-year-old son and then woke up on the floor. On another occasion, she was out shopping with her husband and son and collapsed. She also says she has ended up on the floor at home without knowing how she got there. Her husband corroborates a number of these episodes. There never appears to be any warning or precipitant. Her husband tells you the episodes typically last a few minutes. He says that sometimes she twitches, but not always. Afterwards she appears fine apart from sometimes a headache. She tells you that she frequently suffers with headaches. Given the history, what is the most likely diagnosis? What investigations should you conduct and why?

§ Recurrent, unprovoked losses of consciousness in a woman of this age should raise your suspicion of epilepsy. § However, this is a life-changing diagnosis and you should be sure before making it. § Her history is suggestive of non-epileptic seizures: the episodes are not stereotyped, her recovery is relatively rapid, and there is no post-ictal confusion. § She also has a background of depression and possibly anxiety, which are commonly seen in patients with non-epileptic seizures. § You should nonetheless exclude epilepsy as it is still a possibility. § Accordingly, you should request an EEG (looking for features of epilepsy) and MRI or CT of her brain, to look for any obvious abnormalities that may be triggering the epilepsy.

What does fixed skin mottling indicate?

§ Remember the 6 Ps of an acutely ischaemic limb: pale, pulseless, painful, paralysed, paraesthetic, and 'perishing with cold'. § Fixed skin mottling indicates irreversible limb ischaemia. § The limb may be erythematous when dependent but becomes pale when it is elevated. § Hairless skin and ulcers are signs of chronic ischaemia. § Lipodermatosclerosis is a brown discolouration of hard skin with fibrotic subcutaneous tissues seen in chronic venous insufficiency (which may co-exist with arterial disease).

List some secondary causes of hypertension

§ Renal § Endocrine § Pregnancy § Cardio § Drugs

Which heart sound is heart failure associated with?

§ S3- occurs due to rapid ventricular filling § S4 - is atrium squeezing blood into thickened ventricle (left ventricular hypertrophy can be from longstanding hypertension)

ECG - what does it show?

§ ST depression in V4, V5 and V6 and lead 2

What are the two main ECG signs associated with myocardial infarction?

§ ST elevation § New-onset LBBB

ECG changes for thrombolysis or percutaneous intervention:

§ ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1-V6) § ST elevation of greater than 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, avF, avL) § New Left bundle branch block

What does this ECG show?

§ STEMI - anterior leads (V1 - V4) § ST depression in Lead 3

Mr Shepherd's consultant decided that the prominent R waves on the ECG were more likely to represent a posterior infarct than an anterior NSTEMI. A right-sided ECG confirmed this and Mr Shepherd received primary angioplasty. What advice and medications should Mr Shepherd be discharged on?

§ Secondary prevention is important in patients with ischaemic heart disease. Mr Shepherd should be given the following advice and medication (lifelong): • Lifestyle changes: smoking cessation, low-salt diet, exercise, and weight loss. • Risk factor control with medications: − Blood pressure control: ACE inhibitors if the patient is <55 years and Caucasian. Calcium-channel blockers or diuretic thiazides if the patient is >55 years or non-Caucasian. A mixture of these three classes of drug may be prescribed if the blood pressure cannot be controlled with one drug alone. − Cholesterol reduction: statins, or fibrates if statins are contraindicated. − Diabetic control: tight sugar control is important for cardiovascular risk, although far less important than blood pressure control in diabetics as shown by the United Kingdom Prospective Diabetes Study (UKPDS) trial. • Reduced thromboembolic risk: low-dose aspirin for life and clopidogrel for a period of 1 year. If there is severe left ventricular dysfunction, i.e. an ejection fraction <30% on echocardiogram, there is an increased risk of ventricular arrhythmias and death. Such patients are therefore candidates for implantable cardioversion devices (ICD), which detect the onset of ventricular arrhythmias and shock the heart to stop the arrhythmia.

A concerned patient comes to seek advice on how to prevent DVTs whilst travelling, because their brother suffered from a DVT after a long-haul flight last year. The patient explains that they will be flying from London (Heathrow) to Istanbul (Turkey), before taking a bus to the Cappadocia region of Turkey. The patient wants to know if he should take aspirin and wear compression stockings during the flight.

§ Several studies have shown that the risk of DVT whilst travelling is only increased if the patient is immobile for >8 hours and has other risk factors for DVT (although the patient may not be aware of these). § The flight from London to Istanbul will take less than 8 hours and therefore poses little risk of DVT for this patient. § However, the bus journey from Istanbul to Cappadocia is likely to take >8 hours and involve far less opportunity to mobilize than during the flight, so the patient may wish to wear compression stockings during the BUS journey, rather than the flight. § The Antiplatelet Trialist Collaboration showed that aspirin can reduce the incidence of DVT by up to 25% in post-surgical patients, but as yet there is no evidence of aspirin being beneficial in preventing DVT in long-haul flights.

Define critical limb ischaemia

§ Severe obstruction of the arteries which markedly reduces blood flow to the extremities and has progressed to the point of causing severe pain, ulcers or gangrene. These patients will have rest pain.

Which signs on examination could suggest that the patient has significant risk factors of cardiovascular disease?

§ Signs of hypercholesterolaemia - e.g. xanthelasma, xanthomata, corneal arcus § Signs of peripheral vascular disease - e.g. weak pulses, peripheral cyanosis, cool peripheries, atrophic skin, ulcers, bruits

Which three factors would be the primary indication for surgical treatment of this woman's veins?

§ Skin changes including lipodermatosclerosis § Venous eczema and ulceration § Oedema **Most indications for varicose vein treatment are relative rather than absolute. Some are considered cosmetic rather than medical (e.g. unsightly appearance (a)). Patients should be warned that non-specific symptoms such as aching (c) may not be helped by treatment. These two factors could still be considered in the decision for surgical treatment. § Treatment includes conservative measures, such as graduated compression stockings, or interventional which includes surgery, sclerotherapy or endovenous ablation. § The aim of surgical treatment is to reduce any complications associated with venous insufficiency. § Surgery involves a "high tie and strip" with multiple avulsions. The saphenous vein and its tributaries are ligated. Injection sclerotherapy can also been used for recurrent varicose veins or if the veins are below the knee and not involving the long or short saphenous veins.

List some factors that may precipitate collapse and state the underlying cause of collapse that they are associated with

§ Standing up - postural hypotension (defined as a fall of systolic blood pressure > 20 mmHg on standing) - causes include Hypovolaemia; Autonomic dysfunction: diabetes, Parkinson's; Drugs (diuretics, antihypertensives, L-dopa, phenothiazines, antidepressants, sedatives) Alcohol. § Exercise - cardiac pathology (e.g. aortic stenosis, HOCM, long QT) § Head turning - carotid body hypersensitivity § Vigorous arm activity - subclavian steal syndrome § Vasovagal has many precipitants (e.g. fear, heat, standing for a long time)

Flowchart for diabetes medication

§ Start with metformin § If established ASCVD --> GLP1 agonist and SGLT2 inhibitors § If HF/CKD --> SGLT2 inhibitors **if without ASCVD/CKD: § for weight --> SGLT2 or GLP1 agonist § cost --> use gliclazide (sulphonylureas) (cheaper)

A 55-year-old man who has a history of ischaemic heart disease presents with myalgia. His long-term medications include aspirin, simvastatin and atenolol. Given his statin use a creatine kinase is measured and reported as follows: Creatine kinase: 1,420 u/l (< 190 u/l) His problems seem to have followed the prescription of a new medication. Which one of the following is most likely to have caused the elevation in creatine kinase? § Rifampicin § Clarithromycin § Bisoprolol

§ Statins + erythromycin/clarithromycin - an important and common interaction. Also shouldn't give in pregnancy § This patient can develop statin-induced myopathy secondary to clarithromycin. § Statins should be taken at night as this is when the majority of cholesterol synthesis takes place. § NICE currently recommends the following for the prevention of cardiovascular disease:: atorvastatin 20mg for primary preventionincrease the dose if non-HDL has not reduced for >= 40% atorvastatin 80mg for secondary prevention

Long QT syndrome

§ T wave should finish before half distance between two R waves § abnormal ventricular repolarisation § congenital: e.g. mutations in K+ channels. FH of sudden death § Acquired: low K+, Mg2+, drugs § predisposes you to tachyarrythmia

What is diagnostic test for heart failure

§ TTE and doppler § visualise structure of heart, can calculate Ejection fraction (normal is 50-70%) § if HFrEF is <40% (indicates inability of ventricle to contract) § if HFpEF, EF>50% (inability of ventricles to fill)

What should you, by law, advise patients with an episode of loss of consciousness about driving?

§ The Driver and Vehicle Licensing Agency (DVLA) have very clear guidelines on this matter (http://www.dvla. gov.uk/). § Your actions depend on the cause of the loss of consciousness. For cars and motorcycles: a) If it was a simple faint with prodromal symptoms and a provoking factor can be identified that is unlikely to recur whilst sitting, there are no driving restrictions and there is no need to advise the DVLA. b) If the loss of consciousness was likely due to a transient loss of blood supply to the brain (syncope) with a low risk of recurrence, the patient can drive 4 weeks after the event. c) If the loss of consciousness was likely syncope with a high risk of recurrence, the patient can drive 4 weeks after the event if the cause has been identified and treated, or 6 months after if not identified or treated. d) If the loss of consciousness is unexplained and there are no suggestions it was a seizure, the patient cannot drive for 6 months. e) If the loss of consciousness was associated with seizure markers, the patient cannot drive for one (seizure-free) year. If someone with epilepsy has been on anti-epileptic medication for many years and wants to stop (e.g. due to a desire to be pregnant), they cannot drive for 6 (seizure-free) months after they have stopped

Mr Heyward is a 38-year-old man with increasingly severe chest pain that began during an evening in the pub. The pain has not radiated, and was not alleviated by GTN administered in the ambulance. He has a strong family history with both his father and brother suffering heart attacks in their fifties, and is a heavy smoker with a 50 pack year history. He is not known to have diabetes, hypertension, or high cholesterol. He has no other significant medical history, although you note that he had what sounds like a viral upper respiratory tract infection 3-4 days ago. On examination of his cardiovascular system you find no abnormalities. An ECG taken at the hospital is shown in Fig. 9.2. His other investigations were normal apart from mildly elevated inflammatory markers.

§ The ECG shows ST elevation in leads I, II, aVL, V1-V5, i.e. throughout most leads, and slight PR segment depression. § Acute coronary syndromes typically respond to vasodilators such as GTN. § In addition, MI causes ECG changes which are reciprocal (i.e. ST elevation in some leads, ST depression in opposite anatomical leads). § This is therefore unlikely to be an acute coronary syndrome, although troponin levels 12 hours after the onset of pain should be checked for confirmation. § Pericarditis is the most likely diagnosis despite the atypical sounding pain and lack of a pericardial friction rub, which can be intermittent. A therapeutic trial of NSAIDs was prescribed which diminished the pain. The patient was treated with analgesia as an inpatient for a few days and was discharged once pain free.

As discussed above, current NICE guidelines do not recommend prophylactic surgery of varicose veins to prevent recurrence of healed venous ulcers. Is there any evidence that surgery for varicose veins can reduce the recurrence of venous ulcers?

§ The ESCHAR trial compared the long-term outcomes for patients with venous ulcers who were managed either with compression bandages alone or compression bandages plus surgery for any superficial varicose veins. § The trial found that surgery did NOT accelerate ulcer healing times BUT almost HALVED the rate of recurrence at 4 years. § The trial therefore suggests that it is better to surgically treat superficial varicose veins in patients who have had a venous ulcer as soon as possible, rather than waiting for a recurrent and unresolving ulcer to develop. § The same benefit has not yet been found for deep venous disease.

You are asked to review an ECG of a 76-year-old who has been admitted for a left hemicolectomy:

§ The atrial flutter waves ('sawtooth') are clearly seen on this ECG. The rate suggests 4:1 block is present. **Atrial flutter is a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves. **ECG findings: § 'sawtooth' appearance as the underlying § atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. § For example if there is 2:1 block the ventricular rate will be 150/min § flutter waves may be visible following carotid sinus massage or adenosine **Management: § is similar to that of atrial fibrillation § although medication may be less effective atrial flutter is more sensitive to cardioversion however so lower energy levels may be used § radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

Choice of anticoagulant in DVT

§ The cornerstone of VTE management is anticoagulant therapy. This was historically done with warfarin, often preceded by heparin until the INR was stable. However, the development of DOACs, and an evidence base supporting their efficacy, has changed modern management. &&Choice of anticoagulant: § the big change in the 2020 guidelines was the increased use of DOACs § apixaban or rivaroxaban (both DOACs) should be offered FIRST-line following the diagnosis of a DVT § instead of using low-molecular weight heparin (LMWH) until the diagnosis is confirmed, NICE now advocate using a DOAC once a diagnosis is suspected, with this continued if the diagnosis is confirmed § if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin) **if the patient has active cancer: previously LMWH was recommended; the new guidelines now recommend using a DOAC, unless this is contraindicated **if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA **if the patient has antiphospholipid syndrome (specifically 'triple positive' in the guidance) then LMWH followed by a VKA should be used ****LENGTH of anticoagulation: § all patients should have anticoagulation for at least 3 MONTHS § continuing anticoagulation after this period is partly determined by whether the VTE was provoked or unprovoked § a provoked VTE is due to an obvious precipitating event e.g. immobilisation following major surgery. The implication is that this event was transient and the patient is no longer at increased risk § an unprovoked VTE occurs in the absence of an obvious precipitating event, i.e. there is a possibility that there are unknown factors (e.g. mild thrombophilia) making the patient more at risk from further clots § if the VTE was provoked the treatment is typically stopped after the initial 3 months (3 to 6 months for people with active cancer) § if the VTE was unprovoked then treatment is typically continued for up to 3 FURTHER months (i.e. 6 months in total) § NICE recommend that whether a patient has a total of 3-6 months anticoagulant is based upon BALANCING a person's risk of VTE recurrence and their risk of bleeding § the HAS-BLED score can be used to help assess the risk of bleeding § NICE state: 'Explain to people with unprovoked DVT or PE and a low bleeding risk that the benefits of continuing anticoagulation treatment are likely to outweigh the risks. '. § The implication of this is that in the absence of a bleeding risk factors, patients are generally better off continuing anticoagulation for a total of 6 months

Mrs McDonald has a DVT Wells' score of 2 (pitting oedema, calf swollen >3 cm). Given Mrs McDonald's Wells' score, what investigations will you arrange?

§ The flow chart in Fig. 28.1 is useful for deciding the investigations in suspected DVT using the Wells' score. § Note that D-dimer is used to exclude DVT only if the Wells, score is low (0); ULTRASOUND is used to exclude DVT if the Wells' score is moderate (1 or 2), whilst both D-dimer and ultrasound are used to exclude DVT if the Wells' score is high (3 or more). 1) DOPPLER ultrasound of the right calf: this is the most sensitive, rapid, and non-invasive way of visualizing a DVT in the lower leg (it does not detect isolated thrombi in the femoral or iliac veins). Ultrasound will also enable a ruptured Baker's cyst to be diagnosed. 2) Serum D-dimer levels: D-dimers (fibrin degradation products) can be elevated by DVTs and PE, but also in various other situations such as acute coronary syndromes, atrial fibrillation, pneumonia, vasculitis, sickle cell crises, superficial phlebitis, malignancies, and disseminated intravascular coagulation. Elevated D-dimers have >90% sensitivity for DVT, but only 30-40% specificity. An elevated D-dimer is therefore not useful in positively diagnosing a DVT. However, a normal D-dimer level is useful because it rules out a DVT in someone with a low Wells' score without the need for an ultrasound. Also, an elevated D-dimer in someone with a high Wells' score is an indication for doing SERIAL ultrasounds (rather than a single investigation - if the first ultrasound scan is negative). Ultimately, however, it is the ultrasound that will positively diagnose the DVT. 3) Full blood count (FBC) and clotting studies: a FBC may reveal a high white cell count (WCC; you still haven't ruled out cellulitis) or a high red blood cell count (RBC; polycythaemia - a rare cause of DVT) and clotting studies may reveal deranged coagulation. **Well's score: § < 4 = D-dimer to rule out PE § 4+ = CTPA § >2 + any D-dimer: DVT likely do Doppler § USS<2 & -ve D-Dimer: no USS needed

Management of NSTEMI/unstable angina

§ The management of NSTEMI/unstable angina is complicated and depends on individual patient factors and a risk assessment. § Further drug therapy: a) antithrombin treatment: fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately. b) if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given **Risk assessment: § The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. § It can be calculated using online tools and takes into account the following factors: age, heart rate, blood pressure cardiac (Killip class) and renal function (serum creatinine), cardiac arrest on presentation, ECG findings, troponin levels. § Based on this risk assessment key decisions are made regarding whether a patient has coronary angiography (with follow-on PCI if necessary) or has conservative management. § The detailed pros/cons of this decision are covered in other notes. § Which patients with NSTEMI/unstable angina should have a coronary angiography (with follow-on PCI if necessary)? immediate: a) patient who are clinically unstable (e.g. hypotensive) b) within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk c) coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission 1) Primary coronary intervention for patients with NSTEMI/unstable angina: § Further drug therapy unfractionated heparin should be given regardless of whether the patient has had fondaparinux or not § further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) prior to PCI: o if the patient is not taking an oral anticoagulant: prasugrel or ticagrelorif o taking an oral anticoagulant: clopidogrel 2) Conservative management for patients with NSTEMI/unstable angina: § Further drug therapy further antiplatelet ('dual antiplatelet therapy', i.e. aspirin + another drug) o if the patient is not at a high-risk of bleeding: ticagrelor o if the patient is at a high-risk of bleeding: clopidogrel

Explain the aetiology and risk factors of cardiac arrest

§ The most common underlying causes are ischaemic heart disease and myocardial infarction. In some settings, cardiac arrest is the result of respiratory arrest triggered by opioid toxicity. § The REVERSIBLE causes of cardiac arrest can be summarised as the 4 Hs and 4 Ts ● FOUR Hs o Hypothermia o Hypoxia o Hypovolaemia - dec blood volume o Hypokalaemia/Hyperkalaemia ● FOUR Ts o Toxins (and other metabolic disorders (drugs, therapeutic agents, sepsis)) o Thromboembolic o Tamponade o Tension pneumothorax

The strongest risk factor for developing infective endocarditis is?

§ The strongest risk factor for developing infective endocarditis is a previous episode of endocarditis. § The following types of patients are affected: a) previously normal valves (50%, typically acute presentation) - the MITRAL valve is most commonly affected b) rheumatic valve disease (30%) c) prosthetic valves d) congenital heart defects e) intravenous drug users (IVDUs, e.g. typically causing TRICUSPID lesion) f) others: recent piercings **Causes: § historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries. § Staphylococcus aureus is now the most COMMON cause of infective endocarditis. Staphylococcus aureus is also particularly common in acute presentation and IVDUs coagulase-negative § Staphylococci such as Staphylococcus epidermidis commonly colonize indwelling lines and are the most cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination. After 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause) § Streptococcus viridans still accounts for around 20% of cases. Technically Streptococcus viridans is a pseudotaxonomic term, referring to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis. They are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure. § Streptococcus bovis is associated with colorectal cancer, the subtype Streptococcus gallolyticus is most linked with colorectal cancer § non-infective: systemic lupus erythematosus (Libman-Sacks), malignancy: marantic endocarditis ***Culture negative causes: § prior antibiotic therapy § Coxiella burnetii § Bartonella § Brucella § HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

A 19-year-old female who uses the oral contraceptive pill presents to A&E with a swollen left calf. She has a past medical history of non-Hodgkin's lymphoma for which she received chemotherapy until 2 months ago. A Doppler ultrasound of her leg confirms occlusion of a deep calf vein by a DVT. She is placed on LMWH and warfarin and admitted to hospital for observation. That night, she suffers a thromboembolic stroke. What may have happened?

§ This patient is very young for thromboembolic strokes. § It is possible that her blood is in a highly coagulable state due to underlying malignancy and that this has predisposed to clot formation, but even then it would be hard to explain a clot forming in the fast-flowing arteries that supply the brain. § It is more likely that the clot has formed in the slow-flowing veins and somehow reached the arteries supplying the brain without getting lodged in the lungs. § The most plausible anatomical explanation is that the patient has a patent foramen ovale between her atria which has allowed for the dislodged DVT to cross into the systemic circulation and reach her brain. § This is not as far-fetched as it may sound. § Echocardiographic studies show that 10% of the population have a patent foramen ovale. § About 35% of embolic strokes have no identifiable source and of these, 20% of patients have a patent foramen ovale, which is presumed to have allowed for the 'paradoxical embolus' to reach the brain.

Mr Leroy is a 72-year-old gentleman who limps into hospital using a walking stick. He complains of a painful, swollen right calf since he woke up this morning. He has a past medical history of osteoarthrosis in his right knee and low-grade (papillary) bladder cancer for which he has received a cystoscopic resection and for which he receives ongoing, regular irrigation of his bladder with BCG (Bacille Calmette-Gurin, which is usually used for tuberculosis vaccination). On examination, his right calf is swollen (2 cm), pitting, warm, red, and tender all over (not specifically along the veins), with the inflammation extending up into the popliteal fossa. There are no other masses palpable in his leg or abdomen. His right foot has normal sensation, power, and pulses. Passive movement of his ankle and toes brings on mild pain in his calf. Suspecting a DVT because of his Wells' score (pitting oedema, active cancer = 2), a Doppler ultrasound of his leg is arranged but no occlusion of any deep veins can be seen. What is the most likely diagnosis and how should the patient be managed?

§ This patient probably has a ruptured Baker's cyst. § This is caused by rupture of a synovial sac protruding from the knee in the popliteal fossa, usually in patients with arthropathy of the knee. § The fluid from the ruptured synovial sac ('Baker's cyst') can then track down into the calf, producing signs that are clinically indistinguishable from a DVT. § However, the Doppler ultrasound helps to rule out a DVT, making the diagnosis of ruptured Baker's cyst the more likely one. § Treatment is by ASPIRATION of the fluid and injection of CORTICOSTEROIDS into the knee, to reduce the inflammation and alleviate the pain.

What is screening tool for AAA?

§ Ultrasound is used as a screening tool for aortic aneurysms § They may present with embolic phenomena, such as lower limb purpura § Shocked patients need to go straight to theatre and do not need further imaging § The risk of rupture increases sharply with aneurysms >6cm in size § Aortic stent grafts can be used in the treatment of aortic aneurysms as an alternative to surgery. **Shocked patients need to go to theatre as fast as possible - this should not be delayed by waits for x-rays/CT if the diagnosis is clear. CT is used in stable patients in whom the diagnosis is not clear. Fluid resuscitation is needed, but should not be aggressive as this may cause re-bleeding if initial leak has sealed - aim for a systolic BP of < 100mmHg.

You are called to see a patient by the nurse on your night shift. The patient is a 74-year-old gentleman whose heart rate has suddenly increased to 154 beats/minute. His blood pressure is 130/83 mmHg, his respiratory rate is 18 breaths/minute. He is otherwise feeling well. You order an ECG.The ECG shows a narrow complex tachycardia with left heart strain. There is no ST segment elevation or T wave depression. What is the initial management of this patient? Electrical cardioversion/ Adenosine/ Oral beta-blocker/ IV beta-blocker/ Valsalva manoeuvre

§ Valsalva manoeuvres § is the first-line treatment for supraventricular tachycardia § This patient has a supraventricular tachycardia as demonstrated by the narrow complexes on the ECG. § The initial treatment is a valsalva manoeuvre. Valsalva manoeuvre blocks the atrio-ventricular node and should stop the tachycardia as the tachycardia is caused by a reentrant pathway. § Electrical cardioversion is not indicated as the patient shows no adverse sign such as syncope or shock. If the patient did have adverse signs electrical cardioversion would be the first line treatment. § Adenosine is only indicated if valsalva manoeuvre does not succeed in stopping the tachycardia. § Beta-blockers are not initially indicated as they do not block the atrio-ventricular node and thus would not slow down the tachycardia. § If the tachycardia was to persist after the use of a valsalva manoeuvre and adenosine, atrial flutter should be considered as a diagnosis. § Then beta-blockers and digoxin could be used.

Mrs Swanson is a 72-year-old lady admitted to hospital overnight because of increasing confusion secondary to pneumonia. On the ward round the next morning, the overnight doctor points out that Mrs Swanson also has an ulcer over her right ankle that will need investigating. What is your differential diagnosis for a leg ulcer?

§ Venous ulcer § Mixed arterial/venous ulcer § Arterial (atherosclerotic) ulcer § Neuropathic ulcer § Pressure ulcer § Lymphoedema ulcer § Traumatic ulcer § Malignant ulcer (e.g. a Marjolin ulcer: a squamous cell carcinoma in a long-standing ulcer) § Vasculitic ulcer (e.g. rheumatoid arthritis, pyoderma gangrenosum) § Infective ulcer (e.g. tuberculosis, syphilis, leprosy) § Haemolytic anaemia (sickle cell, hereditary spherocytosis). **Venous ulcers account for by far the MAJORITY (about 70%), with mixed arterial/ venous (about 10%) and arterial (about 10%) most of the remainder. § The other causes are relatively rare with the exception of NEUROPATHIC ulcers in patients with DIABETES mellitus. § Note that many leg ulcers may have a multifactorial aetiology, i.e. they may involve more than one of the pathologies above.

What components of the clotting cascade does warfarin interfere with? What additional drug should all patients starting on warfarin be placed on and why?

§ Warfarin is a competitive antagonist of vitamin K, the cofactor used by liver hepatocytes to synthesize factors II, VII, IX, X, protein C, and protein S. § Warfarin can take a few days to have an effect on clotting because it inhibits the synthesis of coagulation factors, and these have to become depleted. § Also, warfarin can initially cause a paradoxical increase in clotting because of the depletion of protein C and protein S (anticoagulant) before the depletion of other clotting factors (procoagulant). § For this reason, patients are started on LMWH for up to 5 days or until the INR >2 for two consecutive days. **Vitamin K epoxide reductase inhibitor. Inhibits the gamma-carboxylation of factors 2, 7, 9 and 10. Also inhibits the production of protein C and protein S (thus causing a transient hypercoagulable stage). This is why warfarin is started with LMWH until the INR has remained within the target range for > 24 hrs

ECG what does it show

§ Widespread 'saddle shaped' ST elevation. The ST segments are elevated in many leads and are 'saddle shaped' which is classical of pericarditis, although not 100% specific. This will occur in leads with a postive QRS complex. In pericarditis, shallow T-wave inversion may also be seen when adjacent cardiac muscle is affected by the inflammatory process (then strictly a 'myopericaditis'). Unlike in acute myocardial infarction, so-called 'reciprocal' ST segment depression does not occur.

Would your differential diagnosis be different if both of her legs were swollen?

§ Yes, because most of the diseases listed above are local diseases and it would be highly unlikely for the patient to have two similar events in both legs. Instead, it would be more likely that the patient has either a SYSTEMIC PROBLEM or a problem affecting CENTRAL VESSELS. § However, it is worth remembering that a DVT can arise in a patient with pre-existing bilateral leg oedema, so don't rule out a DVT just because both legs are swollen. **Causes for bilaterally swollen legs are: § Right heart failure (in isolation or together with left heart failure) § Pregnancy § Vasodilators (e.g. calcium-channel blockers) § Hypoalbuminaemia: from renal failure (nephrotic syndrome), liver failure, or malabsorption/ malnutrition § Pelvic tumour (e.g. ovarian) compressing the inferior vena cava § Venous insufficiency

An elderly patient complains of regular episodes of loss of consciousness at the weekend when he wears his tie to church. Your consultant suspects carotid sinus hypersensitivity. What simple bedside procedure can you do to test this? How is it performed?

§ You may want to consider performing a carotid sinus massage, whereby an ECG and blood pressure are monitored for bradycardia and/or hypotension induced by the carotid sinus massage. § Carotid sinus massage must not be done in anybody with possible atherosclerotic plaques in the carotids, as these may dislodge, causing a stroke. For this reason, Doppler ultrasound examination of both carotids is recommended before doing a carotid sinus massage in any patient with a history of stroke, TIA, or with a carotid bruit on auscultation. § Patients should be advised that carotid sinus massage always carries a small but real risk of stroke. § Carotid sinus massage should always be done with a patient connected to a 12-lead ECG, with a large IV cannula in situ and a resuscitation trolley (with atropine) at hand, in case the massage triggers a cardiac arrest rather than just a transient blackout. § Ideally, one needs beat-to-beat blood pressure monitoring, which was traditionally done invasively but can nowadays be done non-invasively. § During the test, pressure is applied in a firm circular motion to one carotid sinus at a time (where the carotid artery meets the angle of the jaw) for about 5 seconds. § You should perform the test both with the patient lying down and standing up. § The procedure is considered positive if symptoms are reproduced during or immediately after the massage, in the presence of asystole longer than 3 seconds and/or a fall in systolic blood pressure of 50 mmHg. § There are two possible components to the response: bradycardia and/or reduced blood pressure. Only patients with a significant or predominant bradycardic component may benefit from cardiac pacing.

33 y/o male suddenly collapses. Doctors did CPR, pt died, postmortem showed hypertrophic heart. Most likely cause of death? a) obstructed flow of blood from heart b) arryhthmia c) reduced pumping of blood due to stiff myocardium d) stroke e) Sub-arachnoid haemorrhage

§ although is HOCM, usually the reason of death from HOCM is the Arrhythmia as the thick muscle can't conduct the electrical signals. Obstruction cannot completely block the heart flow to cause death, would see some warning symptoms before

CXR signs of heart failure

§ alveolar oedema § kerley b lines - horizontal lines in peripheries § cardiomegaly § dilated upper lobe vessels § pleural effusion

Management for STEMI

§ angiography - inject dye from femoral artery into heart and then can see how much of heart is affected and then if can do PCI

Causes of hyperkalaemia

§ anti-RAAS § Addison's § renal failure § rhabdomyolysis - breakdown of skeletal muscle --> hence K+ leaks out of cells § metabolic acidosis - decreased pH means trade H+ or K+

46 y/o with chest pain radiating to back but not arms. BP of 155/90mmHg and his HR is 92bpm. ECG is normal. He is distressed and sweaty, not nauseated. Most likely Dx?

§ aortic dissection **Ix: CXR shows widened aorta. BUT Ct/MRI is diagnostic **Tx: oxygen, analgesia, IV beta blocker, consider surgical correction

DDx of systolic murmur

§ aortic stenosis - loudest on right of sternum (aortic area), radiates to neck, slow-rising § mitral regurg = near apex, radiates to axilla, hyperdynamic apex beat § tricuspid regurg = in tricuspid area (left lower sternal edge), elevated JVP § VSD

47 y/o man with buttock pain when exercising and erectile dysfunction. Smokes 40/ day and has previously had a TIA. What is the most likely diagnosis?

§ aorto-iliac occlusive disease - Leriche syndrome. § Triad of leriche: erectile dysfunction, buttock claudication, absent femoral pulses § pain in calf is femoral disease or lower down § pain in buttock is commonly iliac disease **Buerger's disease: thromboangiitis obliterans. Affects young male smokers. Inflammation and thrombosis (arterial and venous). Ulceration of hands and feets. § A non-atherosclerotic vasculitis resulting in segmental occlusions of small and medium-sized arteries. § Highest incidence is in young men of southeast Mediterranean origin and of Middle and Far Eastern origin who smoke. § Presents as an acutely ischaemic limb, more commonly affecting the lower limb. Claudication is rarely described. § Laboratory investigations exclude other vascular disease. Appropriate imaging shows medium and small vessel occlusion. Histological analysis of arterial specimens shows preservation of the internal elastic lamina. Best outcomes are associated with smoking cessation. Life expectancy is not altered. § Patients usually present with rest pain or tissue loss, and rarely present with claudication. Also known as thromboangiitis obliterans.

Heart failure --> arrythmia

§ arrythmia - ventricules out of sync. In this case might get cardiac resynchronisation therapy. or a VAD (ventricular assist devices). IN END-STAGE --> HEART TRANSPLANT

A 73-year-old woman presents to the emergency department complaining of chest pain. She has no past medical history and is not taking any regular medications.An electrocardiogram performed by paramedics displayed sinus tachycardia with ST-segment depression in leads I, aVL, V5 and V6. Point-of-care troponin performed in the emergency department is elevated.This patient is judged to be a suitable candidate for percutaneous coronary intervention.What antiplatelet treatment is indicated? Abciximab alone/ Aspirin alone/ Aspirin and clopidogrel/ Aspirin and ticagrelor/ Clopidogrel alone

§ aspirin and ticagrelor § NSTEMI (managed with PCI) antiplatelet choice: a) if the patient is not taking an oral anticoagulant: prasugrel or ticagrelor b) if taking an oral anticoagulant: clopidogrel § This woman has chest pain, lateral ST-segment depression and a raised troponin. This is in keeping with a diagnosis of non-ST-elevation myocardial infarction (NSTEMI).All patients with a myocardial infarction should be treated with DUAL antiplatelet therapy (DAPT). § Aspirin and ticagrelor is the correct option. § In NSTEMI patients that will undergo percutaneous coronary intervention (PCI) that are not taking an oral anticoagulant, aspirin with either ticagrelor or prasugrel is preferred. § Aspirin and clopidogrel is incorrect. However if this patient were taking an oral anticoagulant, it would be the preferred combination of DAPT. § Abciximab alone, aspirin alone, and clopidogrel alone are all incorrect, as these options all include a single antiplatelet.

branches of aorta

§ atherosclerosis is more of an inflammatory process: endothelial damage (hypertension, hyperglycaemia) --> inflammatory cells infilitrate tunica intima --> macrophages aggregate --> digest lipid from blood --> foam cell --> get fat laid in arteries. § normal diameter of abdominal aorta: 2-3cm. Anything about 3.5 cm is aneurysmal territory. About 5.5. higher risk of rupture. AAA rupture is big emergency - need surgery. So if see aneurysm of 4.5 cm do secondary prevention: weight loss, lowering BP, controlling diabetes, don't really put on anticoagulants.

Sinus tachycardia ECG

§ can see P wave before QRS § caused by sepsis, hypovalaemia (e.g. GI bleed), endocrine (thyrotoxicosis, phaeochromocytoma)

What happens if sodium is replaced too quickly in a hyponatraemic patient?

§ cerebral pontine myelinolysis - middle part of brainstem, myelin sheath has broken apart in pons --> stop breathing and die

Chronic vs acute heart failure

§ chronic - long term condition § acute - rapid onset symptoms; caused by ACS or decompensation of chronic HF

49 y/o with 20 min history of severe crushing chest pain. After giving GTN spray, tells he suffers from hypertension and T2DM and is allergic to aspiring. Most appropriate Tx?

§ clopidogrel

Why combination drug therapy for hypertension?

§ complementary effects § less SEs, lower doses § better compliance § heterogenous patients

Stable angina first line management

§ conservative - Reduce RFs § then go medical

What is most common cause of myocarditis in Europle?

§ coxsackie B virus. Also get pain worse lying down like in pericarditis § can do endomyocardial biopsy - if not resolving after treatment

Left ventricular hypertrophy voltage criteria

§ deep S in V1/2 § and tall R in V5/V6 § is left ventricular hypertrophy --> possibly secondary to hypertension

ECG signs of left ventricular hypertrophy

§ deep S in V1/V2, deep R in V5/6

Investigations for chest pain

§ dipstick - for proteinurea § LDL - IHD § Glucose - diabetes § Troponin - ACS § D- dimer - for PE § amylase - pancreatitis § PE - signs on ECG - sinus tachycardia, S1Q3T3, right axis deviation or RBBB or right ventricular strain (inverted T in V1-V4)

List some causes of tricuspid regurgitation

§ ebstein - abnormal attachment of tricuspid valve *Inspection - raised JVP § Palpation - parasternal heave § Signs of RHF - pleural effusion, hepatomegaly, ascites, pitting oedema, RV heave Visible/palpable hepatic pulsations § Pan-Systolic Murmur § Loudest over tricuspid region *Ask the patient to hold breath on inspiration to accentuate murmur*

Systemic amyloidosis and GI problems

§ enlarged liver, spleen, tongue § nutrient malabsorption

If patient is 29 degrees and in VF what do you do?

§ first warm them up § then defib

When to give adrenaline in non-shockable rhythm?

§ give adrenaline in non-shockable rhythm as soon as possible and then during alternate cycles. § If the rhythm were shockable, adrenaline should be given after the third shock, and then during alternate cycles. Amiodarone should be given after the third shock, and another dose considered after five shocks.

60 y/o man presents to vascular clinic with painful calves on exercise. Smokes 20/ day. Long-standing angina and diabetes mellitus type 2. What is ABPI likely to be?

§ has calf claudication (sign of peripheral vascular disease) § in chronic renal failure and diabetes mellitus the ABPI INCREASES (calcification and less vessel rebound --> increase pressure) § ABPI - ankle brachial pressure index. take systolic BP reading at ankle and brachial artery and compare. Use BP cuff and doppler probe and measure when pulsations become occluded vs not. Take highest reading for both. Divide ankle measurement by brachial measurement. § People with claudication and vascular issues it goes down.

Which three of the following are recognised features of Marfans syndrome?

§ high arched palate § lens dislocation § arachnodactily A patient being unusually tall with long limbs usually invites the clinician to consider a diagnosis of Marfan's syndrome; but there are many normal young people with this body habitus. A clear family history and additional clinical features make the diagnosis more secure. Several are listed here, and the reference listed below gives give a fuller picture of the wide variety of problems faced by patients with the full-blown syndrome. Involvement of the aorta is a serious threat to life

Aetiology of AF

§ hypertension § coronary heart disease § mitral stenosis § alcohol "holiday heart syndrome" § pericarditis § pneumonia **gold standard diagnosis for AF is ECG

BNP in heart failure

§ if is elevated follow up with TTE (Transthoracic echocardiography)

pansystolic murmur louder on inspiration - what kind of murmur?

§ if murmur is louder on inspiration = RIGHT sided murmur. enhanced venous return on inspiration due to lower thoracic pressures. § PSM = mitral regurg or tricuspid regurg § this is tricuspid regurgitation § hence elevated JVP too §right sided valves prone to damage by endocarditis from IVDU § hence also hepatomegaly from backflow

ECG changes in STEMI

§ in start of STEMI , may get tall tented T waves --> ST elevation. Also then pathological Q waves (points sharply downwards) § get ST elevation or NEW LBBB **40% of people can die

Decompensation of heart failure

§ inability of cardiac pump to meet body demands § symptoms: SOB, fatigue, ankle swelling § signs: tachycardia, tachypnoea, bibasal creps, pleural effusion, raised JVP, peripheral oedema § Ejection fraction used to classify as mild, moderate or severe

66 y/o comes with cramps in calves when walk for few mins. Stops when stops walking. DDx?

§ intermittent claudication - has lots of CV risk factors § painful diabetic neuropathy § MSK **in examination: § peripheral vascular exam - pulses, skin changes, cap refill time, thinning of skin, hair loss, buerger's test for arterial insufficiency § CVS examination too **management: ABPI, exercise, antiplatelets + statins

List risk factors and presentation for dilated cardiomyopathy

§ key RF: alcohol § key sign - signs of HD and displaced apex beat § GLOBULAR heart on CXR

Cardiac causes of collapse

§ long QT predisposes to tachycardia (Long QT means it takes longer for the ventricle to contract, so the heart tries to compensate by becoming tachycardic) § slow rising pulse, ejection systolic murmur = aortic stenosis §HOCM = hypertrophic obstructive cardiomyopath

What is low output and high output HF?

§ low output - low cardiac output § high output - cardiac output normal but HIGHER metabolic needs e.g. pregnancy, anaemia, hyperthyroidism

Management for acute heart failure

§ medical emergency § sit patient upright § 60-100% oxygen § IV diamorphine § GTN infusion § IV furosemide **DMONS**

Classification using doppler waveform for peripheral artery disease

§ monophasic - sign of diseased artery as want one more than phase § triphasic is normal § biphasic is probs normal

Definition of cardiomyopathy

§ myocardium becomes structurally and functionally abnormal in the ABSENCE of CAD, valvular disease and congenital heart disease

Collapse case

§ no warning --> vascular? § no tongue biting --> unlikely seizure § not confused --> not tonic clonic § FH of sudden death § most likely cause is tachyarhythmia

What is Right heart failure signs and symptoms

§ nocturia and swelling is quite specific as § Symptoms •Fatigue •Reduced exercise tolerance •Anorexia •Nausea •Nocturia § Signs: •Face: face swelling •Neck: ↑ JVP •Heart/Chest: TR murmur, ↑ HR, ↑ RR •Abdomen: ascites, hepatomegaly •Other: ankle and sacral pitting oedema

NAPMEALS causes of high output heart failure

§ nutritional, anaemia, pregnancy, malignancy, endocrine (e.g. hyperthyroid), AV malformations, liver cirrhosis, sepsis

Measuring BP in OSCE

§ offer to measure in both arms. If difference between both arms > 15mmHg --> repeat --> measure from arm with higher BP § ideally best of 3 measurements: if BP >140/90 --> 2nd --> 3rd --> record lower of last 2 measurement

ECG change in atrial flutter

§ one way to solve atrial flutter is to take big deep breath in and hold it

Define hypertension

§ optimum BP is 120/80 ● Systolic > 140 mm Hg and/or diastolic > 90 mm Hg measured on THREE separate occasions. ● Malignant Hypertension: BP > 200/130 mm Hg ● Defining hypertension is difficult so the value is the value above which risk is significantly increased and benefit of treatment is clear cut. **impt cos increased BP increases risk of stroke and MI. High BP damages walls of arteries supplying body --> so then get blocked. High BP has no symptoms until too late. § need to exclude secondary causes of hypertension e.g. conns and phaeochromocytoma before calling it essential hypertension

Causes of mitral regurgitation

§ papillary muscle rupture secondary to IHD § mitral valve prolapse (back into atria) § LV dilatation secondary to left HF § infective endocarditis § rheumatic fever (BUT chronic rheumatic heart disease causes mitral stenosis)

What are the three types of AF?

§ paroxysmal § persistent § permanent (INSERT MEGED SLIDE)

ECG changes in ACS

§ pathological Q wave - Q wave is just deeper

Systemic amyloidosis and nephrotic syndrome

§ proteinuria § hypoalbuminaemia § oedema § hyperlipidaemia

PERC

§ pulmonary embolism rule-out criteria (the PERC rule) § all the criteria must be absent to have negative PERC result, i.e. rule-out PE § this should be done when you think there is a low pre-test probability of PE, but want more reassurance that it isn't the diagnosis - this low probability is defined as < 15%, although it is clearly difficult to quantify such judgements § a negative PERC reduces the probability of PE to < 2% § if your suspicion of PE is greater than this then you should move straight to the 2-level PE Wells score, without doing a PERC

1) Image below shows his 12-lead ECG on arrival at hospital. What are the two findings? 2) Which of the following is the most likely clinical diagnosis? 3) What three manoeuvres would be helpful to diagnose this arrhythmia?

§ regular rhythm, absent P waves § ECG findings: regular, narrow complex tachycardia, rate of 180/min, T wave inversion in lead aVL. § Absence of P waves suggests either. No normal atrial depolarization, e.g., atrial fibrillation, atrial standstill. The P waves are hidden within the QRS complexes, e.g., ventricular tachycardia, junctional tachycardia. 2) Supra-ventricular tachycardia. The ECG shows a regular, rapid, narrow complex tachycardia. This is therefore a supraventricular tachycardia. There are no discernible P waves and therefore the differential diagnosis includes atrioventricular nodal reentry (AVNRT) or atrioventricular reciprocating tachycardia (AVRT) associated with an accessory pathway.The lack of P waves excludes sinus tachycardia and atrial flutter (no flutter waves). It is not broad complex (excluding VT) and is not irregular (excluding AF). 3) Carotid sinus, valsalva and administration of IV adenosine. Vagal manoeuvres such as the valsalva, carotid sinus massage and administration of IV Adenosine cause slowing within the AV node. If AV block occurs, the tachycardia will terminate and proves that part of the circuit involves the AV node. Only AVNRT and AVRT have the AV node as an integral part of the circuit. Hallpike manoeuvre involves head tilting to diagnose vertigo.

List some causes of mitral regurgitation

§ rupture of chordae tendinae or papillary muscle are consequences of MI too **LISTEN WITH BELL FOR MITRAL REGURGITATION § Pulse - normal/irregularly irregular § Palpation - laterally displaced apex beat *Pan-Systolic Murmur: § Loudest over mitral area, radiating to axilla *Listen in left lateral position with bell of stethoscope Low rumbling murmur

How to control accelerated hypertension

§ severe increase in BP to 180/120mmHg or higher & signs of retinal haemorrhage and/or papilloedema. § associated with target organ damage - malignant hypertension § Specialist referral + IV labetalol **Also remember phaeochromocytoma as a DDx § Hypertensive urgency: BP >180/120 mmHg + stable + no organ dysfunction if no target organ damage is identified, repeat clinic blood pressure measurement within 7 days § CONGESTIVE CARDIAC FAILURE OR ENCEPHALOPATHY! = HEADACHE, FOCAL CNS SIGNS, SEIZURES, COMA § White-coat effect: A discrepancy of more than 20/10 mmHg between clinic and average daytime ABPM or average HBPM blood pressure measurements at the time of diagnosis.

Austin flint murmur

§ sign of severe aoritc regurg: Low pitched rumbling mid-diastolic murmur; Best heard at the apex. §diastolic murmur; regurgitant flow on anterior leaflet mitral valve (aortic regurg) § also de quinke's sign *Early Diastolic MurmurHeard best over LSE and aortic area Severe: radiates to apex*Ask the patient to sit forward hold breath on expiration*

ACS investigations

§ start bedside --> bloods --> imaging/special tests § might see high WCC in ACS § U&Es for when using contrast for scan as well

Cardiac enzymes

§ tend to use troponin nowadays

Hyperkalaemia box on ECG

§ tented T § prolonged PR - as upsetting cardiac contraction § flattened/ absent P § wide QRS (hence get bradycardia); looks like sine wave

Several weeks later, the ulcer has been regularly dressed and debrided and is now healing. You are called to the bedside by the nurse who is concerned that Mrs Rawlings respiratory rate has declined and she is feeling nauseous regularly. She has a normal temperature and you remember she has been drowsy every time you have seen her on the round for the last few days. You look at the chart, she has not required oramorph recently. What do you think is going on here?

§ the pt may be overdosed on opiate § We are very good at stepping up pain control, but not very good at stepping down. It is good practice to monitor the PRN usage both from the viewpoint of increasing but also to decrease the requirement as appropriate. Regular evaluation and follow up of the patient is important.

Comparing cardiac markers

§ troponin is useful as it is very specific for cardiac muscle damage but there is a 3 HOUR DELAY for levels to rise. § CK-MB levels rise faster but only remain high for 2-3 days. § Other causes of high troponin (due to cardiac damage): coronary artery spasm, aortic dissection causing ischaemia, myopericarditis, hypertrophic cardiomyopathy, severe HF, cardiac trauma, PE. § Troponins can also be renally excreted in renal failure! § D-dimers occur as a result of fibrin clot breakdown and are not specifically diagnostic of DVT/PE, but a low D-dimer will help rule out DVT and PE.

What interim anticoagulation whilst waiting for CTPA for PE?

§ updated so now is DOAC - apixaban/rivoraxaban

hypertrophic cardiomyopathy presentation

§ usually asymptomatic, sudden cardiac death is often 1st presentation § signs - ejection systolic murmur, jerky carotid pulse § APEX not displaced as hypertrophy is on inside

Management plan for a patient with SVT & normal BP

§ vagal manoeuvers (e.g. valsalva, carotid massage) § adenosine (cardiac monitor) § DC cardioversion - Restoration of normal heart rhythm by electrical shock

60 y/o attends with an ulcer on her right medial malleolus. It is shallow and contains slough. Has a history of IHD. What is likely aetiology of ulcer?

§ venous as is shallow, near medial malleolus and slough at base. § pic shows diff ulcer types

Events that can occur after MI

§ ventricular arryhthmias (ventricular tachy and fibrillation) - if in VF shock them. § bradyarrhythmia due to sinus bradycardia or AV block in inferior infarction, as a branch of this goes to AV node. As ischaemia of heart tissue progresses, grades of heart block increase from 1 to 3. § if left ventricle dies might get cardiogenic shock (very low BP) **arrhythmias tend to occur within 24 hours, so that's why monitor them in hospital ** RCA --> AV block ** LCA --> heart failure

Features and causes of hypokalaemia

§ weakness § arrhythmia (torsades de point) § polyuria **caused by K+ excretion and vomiting **replacement potassium is irritant to vein hence give slowly via cannula or via central line

Aortic regurg and pulse pressure

§ wide pulse pressure: increases SBP and decreases DBP

ECG - diagnosis?

§ widespread T wave inversion (AVL, lead 2, v4, v5, v6) - could be NSTEMI or unstable angina

Pathogenesis of rheumatic fever

§ •Streptococcal M protein is an alpha helical coiled structure § Alpha helical structures are common in human tissue -found in myosin, collagen, tropomyosin etc § •Patients with severe acute rheumatic fever generate antibodies to M protein •Also bind to human heart muscle -In fatal acute rheumatic fever, antibodies eluted from the heart tissue will bind to Group A streptococci § acute rheumatic carditis is likely to be an autoimmune disease generated through molecular mimicry - causes damage to the heart § basal ganglia was also damaged and causes something called sydenham's chorea

1) Which two of the following does the ECG in figure 2 show? 2) Which five of the following treatments would you initiate? 3) Which three further investigations would you ask for? 4) What four further elements of advice would you give to this patient?

§Anterior myocardial infarction §Sinus rhythm The ECG shows evidence of an anterior ST-elevation myocardial infarction with Q-waves. There are also reciprocal changes in the inferior leads (III and avF) There is no bundle-branch block (The QRS of sinus beats is not broad). L hypertrophy with strain would show increased R-waves in lateral leads (V4-6) - the hypertrophy and ST depression in the lateral lead (the strain) 2) Diamorpine IV, Furosemide, Oxygen therapy, Primary percutaneous angioplasty, Aspirin. This patient has evidence of acute myocardial infarction and heart failure. He requires oxygen therapy as his O2 saturation is currently 90% breathing air. He also needs aspirin immediately and long-term for secondary prevention of further ischaemic events. Unless there is a significant contra-indication, this patient will require dual anti-platelet therapy. He also needs intravenous furosemide is indicated for his pulmonary oedema. He is a candidate for urgent primary percutaneous angioplasty and needs urgent referral to cardiology for possible intervention. Beta-blockers should not be started while the patient has acute pulmonary oedema (but will be started once his fluid overload has been treated). Calcium channel blockers have a negative inotropic effect and should be avoided if possible, particularly in the acute setting. 3) Echocardiogram, Random blood glucose, Lipid profile. This patient must have blood tests to include FBC, U&E, LFT, random blood glucose, lipids. Echocardiogram will assess left ventricular function and also look at his valvular function given that there is a systolic murmur. Lung function tests, urine dipstick and chest CT are not indicated. 4) Stop smoking, Avoid NSAIDs, Graded exercise programme, Reduce saturated fat intake. This patient needs to be given lifestyle advice. He should stop smoking (this is the most important), reduce his saturated fat and increase his intake of whole grains, nuts, fruits and vegetables. intake whilst increasing his fibre and fruit and vegetable intake (DASH or mediterranean diet). Patients are not advised to do the 5:2, Atkins etc diets. NSAIDs have cardiovascular side effects and in particular should not be used in the context of heart failure. Alcohol should be within recommended amounts but does not need to be stopped altogther.

A 35-year-old male presents to the emergency department with a 4-hour history of rapid palpitation and shortness of breath. This is of sudden onset but is not associated with chest discomfort. There has been no antecedent history of URTI or other symptoms, specifically no fevers, sweats or cold intolerance. The patient had suffered with palpitation previously but only for short periods and over the years he had learned various ways to stop his palpitation but none had worked on this occasion. His younger brother had died suddenly at the age of 16 years. He is not taking medication and has no other significant history of note. He was a non-smoker and did not take excess alcohol. 1) The patient described several other manoeuvres which he had used in the past to terminate his attacks. Which of the following could he have used?

§Sticking his fingers down his throat, Pressing hard on his eyeballs, Dipping his face in ice cold water. Valsalva manoeuvre (straining against a closed glottis), sticking his fingers down his throat, dipping his face in ice cold water (diving reflex), pressing hard on his eyeballs, swallowing crushed ice/cold drink. These manoeuvres, like carotid sinus massage, all stimulate the vagus nerve causing AV nodal conduction slowing and may therefore terminate re-entrant arrhythmias using the AV node as part of the circuit.

aortic regurgitation man

•Corrigan's sign - visible distention and collapse of carotid arteries in the neck •De Musset's sign - head bobbing with each heartbeat •Quincke's sign - pulsations are seen in the nail bed with each heartbeat when the nail bed is lightly compressed •Duroziez's sign: •A stethoscope is placed over the femoral arteries •When gentle pressure is applied proximal to the stethoscope a systolic murmur is heard •When gentle pressure is applied distal to the stethoscope a diastolic murmur is heard (as blood flows backwards) •Traube's sign - 'Pistol shot' sound heard when stethoscope placed over the femoral artery during systole and diastole •Muller's sign - uvula pulsations are seen with each heartbeat

•John is a 67 year old male who has been brought in by ambulance after experiencing extreme chest pain at home •What further questions would you like to ask?

•PC Chest Pain •HPC- EXPLODE -S- Central, one sided -O- Sudden vs. gradual onset, exertional/ at rest -C- 'Crushing' / sharp/ dull ache/ tearing pain -R- Radiation to arm/ jaw/ neck/ back -A- Nausea + vomiting, SOB, collapse, palpitations, anxious, reflux -T- >20 minutes? Previous episodes + nature of these -E- Positional, Relation to breathing, Relief with rest/ GTN spray -S- Worst pain you have experienced? Severity out of 10? •PmHx -Medical conditions + risk factors •DHx -Allergies, BP tablets, statin, GTN, Antiplatelets? •FHx -1st degree relative death due to MI? •SHx -Smoker, alcohol, occupation, performance status § central / left-sided --> more likely cardiac § gradual onset might be something musculoskeletal too § dull may also be ACS

Treatment for stable angina

•Retrosternal chest discomfort occurring predictably upon exertion and relieved by rest and nitrates. •Same risk factors as ACS **Acute Tx: -Rest and GTN relieves pain -If not relieved and lasting >15 minutes consider ACS **Prophylaxis: -Lifestyle advice -GTN for relief of symptoms -1st line: Beta blocker/ calcium channel blocker -2nd line: •Isosorbide mononitrate/ nicorandil, ivabradine/ ranolazine - If symptom control poor on maximum dose, consider switching/ adding in another class of drug

Summarise the epidemiology of cardiac failure

● 10% > 65 yrs old

Recognise the presenting symptoms of heart block

● 1st Degree - asymptomatic ● 2nd Degree (Mobitz 1) - usually asymptomatic ● Mobitz Type II and 3rd Degree - may cause Stokes-Adams Attacks (syncope caused by ventricular asystole) o May also cause dizziness, palpitations, chest pain and heart failure

Recognise the presenting symptoms of rheumatic fever

● 2-5 weeks after pharyngeal GAS infection ● General o Malaise o Fever o Anorexia ● Joints o Painful, swollen o Reduced movement/function ● Cardiac o Breathlessness o Chest pain o Palpitations

Summarise the epidemiology of heart block

● 250,000 pacemakers are implanted every year and they are mostly for heart block § age >50-60 years, more in men

Summarise the prognosis for patients with pulmonary embolism

● 30% mortality in those left untreated ● 8% mortality with treatment ● Increased risk of future thromboembolic disease

Summarise the prognosis for a patient with cardiac failure

● 50% with cardiac failure die within 2 years

Summarise the epidemiology of peripheral vascular disease

● 55-70 yrs = 4-12% affected ● 70+ yrs = 15-20% affected ● More common in MALES ● Incidence increases with AGE

Define Aortic Dissection

● A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, creating a false lumen ● Classification of aortic dissection (Stanford): o Type A: ASCENDING aorta (MOST COMMON) 70% o Type B: DESCENDING aorta (distal to the left subclavian artery) 30%

Define coronary angiography and PCI

● A coronary angiography is a minimally invasive procedure to access the coronary circulation and blood filled chambers of the heart using a catheter. ● The catheter is inserted into the heart via the femoral or radial artery or venous system. ● PCI: percutaneous coronary intervention - a non-surgical procedure used to treat narrowing (stenosis) of the coronary arteries. A coronary angiogram is used to visualise the vessels, and then an angioplasty is performed using a balloon catheter. Stents can be used to keep the vessel open.

Define ventricular tachycardia

● A regular broad-complex tachycardia abnormally originating from the ventricles. The rate is usually > 120 bpm. ● MEDICAL EMERGENCY **Non-sustained ventricular tachycardia (NSVT) is an ectopic ventricular rhythm with wide QRS complex (120 milliseconds or greater), rate faster than 120 bpm, lasting for at least 3 beats that spontaneously resolves in less than 30 seconds.[1] It may occur in the absence of any underlying heart disease. However, it is more commonly associated with ischaemic and non-ischaemic heart disease; known genetic disorders such as long QT syndrome, Brugada's syndrome, and arrhythmogenic right ventricular cardiomyopathy; congenital heart disease; metabolic problems, including drug toxicity; or electrolyte imbalance **Sustained ventricular tachycardia (VT) is a ventricular rhythm faster than 100 bpm lasting at least 30 seconds or requiring termination earlier due to haemodynamic instability. VT is defined as a wide complex tachycardia (QRS 120 milliseconds or greater) that originates from one of the ventricles, and is not due to aberrant conduction (e.g., from bundle branch block), at a rate of 100 bpm or greater. 'Idiopathic' VT occurs in the absence of apparent structural heart disease (e.g., prior myocardial infarction, active ischaemia, cardiomyopathy, valvular disease, arrhythmogenic right ventricular cardiomyopathy, left ventricular non-compaction, or other disorders of the myocardium), known channelopathy (e.g., long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT, short QT syndrome), drug toxicity, or electrolyte imbalance. VT can be described as monomorphic or polymorphic. TORSADES DE POINTES is a polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation. Sustained VT usually results in hypotension and symptoms of weakness, syncope, or palpitations; however, the arrhythmia may be present in patients who are asymptomatic and normotensive.

Generate a management plan for ventricular tachycardia

● ABC approach ● CHECK WHETHER THE PATIENT HAS A PULSE OR NOT ● Pulseless VT - follow advanced life support algorithm ● Unstable VT - reduced cardiac output o NOTE: VF and pulseless VT require defibrillation (unsynchronised), BUT other VTs can be treated with synchronised cardioversion o Synchronised DC shock o Correct electrolyte abnormalities o Amiodarone ● Stable VT o These patients DO NOT experience symptoms of haemodynamic compromise o Correct electrolyte abnormalities o Amiodarone o Synchronised DC shock (if steps above are unsuccessful) ● Implantable Cardioverter Defibrillator (ICD) o ICD is considered if: ● Sustained VT causing syncope ● Sustained VT with ejection fraction < 35% ● Previous cardiac arrest due to VT or VF MI complicated by non-sustained VT

Recognise the presenting symptoms of ischaemic heart disease

● ACS: o Acute-onset chest pain lasting > 20 minutes o Central, heavy, tight, crushing pain o Radiates to the arms, neck, jaw or epigastrium o Occurs at rest o More severe and frequent pain that previously occurring stable angina o Associated symptoms: ● Breathlessness ● Sweating ● Palpitations ● Nausea and vomiting ● SILENT INFARCTS occur in the elderly and diabetics (no chest pain). In such patients, presentation includes syncope, pulmonary oedema, epigastric pain and vomiting ● Stable Angina o Chest pain brought on by exertion and relieved by rest

Generate a management plan for DVT

● ANTICOAGULATION: § NICE updated guidelines on VTE in 2020. Some of the key changes include recommending the following: a) the use of direct oral anticoagulants (DOACs) as FIRST-LINE treatment for most people with VTE, including as interim anticoagulants before a definite diagnosis is made b) the use of DOACs in patients with ACTIVE CANCER, as opposed to low-molecular weight heparin as was the previous recommendation c) routine cancer screening is no longer recommended following a VTE diagnosis. o Heparin (LMWH) whilst waiting for warfarin to increase INR to the target range of 2-3. This is because warfarin is prothrombotic for first 48 hours, so must be given with heparin. o Can use NOAC instead of warfarin (Rivoroxaban/apixaban) o DVTs that do NOT extend above the knee may be observed and anticoagulated for 3 months o DVTs extending beyond the knee require anticoagulation for 6 months o Recurrent DVTs require long-term warfarin ● IVC Filter: o May be used if anticoagulation is contraindicated and there is a risk of pulmonary embolisation ● Prevention: o Graduated compression stockings - prevent long term complications like pain and swelling o Mobilisation o Prophylactic heparin (if high risk e.g. hospitalised patients)

Explain the aetiology/risk factors of SVT

● AVNRT: o A localised re-entry circuit forms around the AV node, which conducts to the ventricles faster than normal conduction pathway. ● AVRT: o This occurs when there is normal AV conduction, as well as an accessory pathway present. These form a re-entry circuit between the atria and ventricles. o An accessory pathway is an abnormal conduction pathway. It can conduct impulses either towards the ventricle (anteretrograde) or away from the ventricle (retrograde) or in both directions. o A classic example of AVRT is Wolff-Parkinson-White Syndrome, in which the accessory pathway is called Bundle of Kent. WPW Syndrome can lead to AVRT. **Risk Factors: o Nicotine o Alcohol o Caffeine o Previous MI o Digoxin toxicity

Generate a management plan for pericarditis

● Acute - cardiac tamponade is treated with emergency pericardiocentesis (aspiration of fluid from pericardial space) ● Medical: o Treat underlying cause o NSAIDs for pain and fever relief + aspirin +/- colchicine o May require PPIs to prevent gastric irritation from aspirin/NSAIDs - and monitor renal function ● Recurrent: o Low-dose steroids o Immunosuppressants o Colchicine - consider this before steroids and immunosuppressants ● Surgical: o Pericardiectomy is performed in cases of constrictive pericarditis

Generate a management plan for acute left ventricular failure

● Acute Left Ventricular Failure - medical emergency: a) Treating Cardiogenic Shock: ● This is severe cardiac failure with low blood pressure ● Requires the use of inotropes (e.g. dobutamine) ● Managed in ITU b) Treating Pulmonary Oedema: ● Sit the patient up ● 60-100% Oxygen (and consider CPAP) ● Diamorphine (venodilator + anxiolytic) ● GTN infusion (venodilator --> reduced preload) ● IV furosemide (venodilator and later diuretic effect) ● Monitor: ▪ BP ▪ Respiratory rate ▪ Oxygen saturation ▪ Urine output ▪ ECG ● TREAT THE CAUSE! (e.g. MI, arrhythmia) **IPOD MAN for acute cardiac failure: § IV access § Positioning § O2 § Diuretic § Morphine § Anti-emetic § Nitrates

Recognise the presenting symptoms of mitral regurgitation

● Acute MR - may present with symptoms of left ventricular failure ● Chronic MR - may be asymptomatic or present with: o Exertional dyspnoea o Palpitations if in AF o Fatigue ● Mitral Valve Prolapse - asymptomatic or atypical chest pain or palpitations

Define cardiac arrest

● Acute cessation of cardiac function **VF, pulseless VT, pulseless electrical activity, asystole are four causes

Define myocarditis

● Acute inflammation and necrosis of cardiac muscle (myocardium) **Occurs in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease. It is a clinical syndrome of non-ischaemic myocardial inflammation resulting from a heterogeneous group of infectious, immune, and non-immune diseases.

Summarise the epidemiology of mitral regurgitation

● Affect ~5% of adults ● Mitral valve prolapse is common in young females

Define pulmonary hypertension

● An increase in mean pulmonary arterial pressure which can be caused by or associated with a wide variety of other conditions.

Define rheumatic fever

● An inflammatory multisystem disorder, occurring following group A beta-haemolytic streptococci (GAS) infection

Explain the aetiology/risk factors for angina pectoris

● Angina pectoris occurs because, during exertion, the demand of the cardiac muscle increases but this demand is NOT met. ● Causes: o Most commonly atherosclerosis o Rarely: anaemia, AS, tachyarrhythmias, HCM, arteritis, small vessel disease (microvascular angina, cardiac syndrome X) Syndrome X: combination of angina, ECG changes (i.e. ST depression) but with a normal coronary angiogram - may be due to abnormal function of small coronary arteries. ● Types of angina a) Stable angina: induce by effort, relieved by rest b) Unstable angina: angina of increasing frequency or severity, occurs on minimal exercise or at rest, associated with very high risk of MI - one of the possible presentations of ACS c) Decubitus angina: precipitated by lying flat, usually a complication of HF d) Prinzmetal's angina: due to coronary artery spasm - when they lie down, there is decreased venous pooling and increased myocardial work, precipitated by lying flat or exertion. The angina is associated with transient ST elevation during attacks and negative stress ECG. To investigate, coronary angiography + injection of agents to provoke spasm.

Explain the aetiology/risk factors of ischaemic heart disease

● Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply ● This is usually due to atherosclerosis ● Rarer causes of angina pectoris include coronary artery spasm (e.g. induced by cocaine), arteritis, vasculitis and emboli (A VASE) ● Atherosclerosis pathophysiology: o Endothelial injury leads to migration of monocytes into the subendothelial space o These monocytes differentiate into macrophages o Macrophages accumulate LDL lipids and become foam cells o These foam cells release growth factors that stimulate smooth muscle proliferation, production of collagen and proteoglycans o This leads to the formation of an atherosclerotic plaque - risk of rupture of plaque ** Risk Factors: o Male o Diabetes mellitus o Family history o Hypertension o Hyperlipidaemia o Smoking o Age o Obesity o Sedentary lifestyle o Cocaine use

Explain the aetiology/risk factors of aortic dissection

● Aortic dissection is usually preceded by degenerative changes in the smooth muscle of the aortic media ● Common causes and risk factors: o HYPERTENSION o Aortic atherosclerosis o Connective tissue disease (e.g. Marfan's, Ehlers-Danlos - hypermobility of small joints, translucent skin, SLE) o Congenital cardiac abnormalities (e.g. coarctation of the aorta) o Aortitis o Iatrogenic (e.g. during angioplasty/angiography) o Trauma o Crack cocaine ● NOTE: expansion of the false lumen can lead to obstruction of branches of the aorta: subclavian, carotid, coeliac and renal arteries o Hypoperfusion of the target organs of these major arteries can give rise to other symptoms o e.g. carotid artery --> collapse, hemiplegia o Unequal arm pulses and BP o Anterior spinal artery --> acute limb ischaemia, paraplegia o Renal arteries --> anuria o If dissection moves proximally, may develop aortic valve incompetence, inferior MI and cardiac arrest

Explain the aetiology/risk factors of varicose veins

● Blood from superficial veins of the leg passes into deep veins via perforator veins and at the sapheno-femoral and sapheno-popliteal junctions. Valves prevent blood from passing from deep to superficial veins. If they become incompetent, there is venous hypertension and dilatation of the superficial veins occurs. ● Primary o Due to genetic or developmental weakness in the vein wall o Results in increased elasticity, dilatation and valvular incompetence o Congenital valve absence ● Secondary o Due to venous outflow obstruction ● Pregnancy ● DVT ● Ovarian tumour ● Pelvic malignancy ● Ovarian cysts ● Ascites ● Lymphadenopathy ● Retroperitoneal fibrosis o Due to valve damage (e.g. after DVT) o Due to high flow (e.g. arteriovenous fistula) o Constipation o Overactive muscle pumps e.g. cyclists ** RISK FACTORS: o Age o Female o Family history o Caucasian o Obesity

Recognise the signs of hypertension on physical examination

● Blood pressure should be measured on 2-3 different occasions before diagnosing hypertension ● The lowest reading should be recorded ● Examination may reveal information about causes: o Radiofemoral delay = coarctation of the aorta DISTAL to the left subclavian artery o Renal artery bruit = renal artery stenosis o Palpable kidneys o Signs of phaeochromocytoma or Cushing's o End organ damage signs: LVH, retinopathy, proteinuria (indicates severity and duration of hypertension) Note: unlike in left ventricular dilatation, LVH cannot be detected on clinical examination. In dilatation the heart expands outwards so apex beat displaced but in hypertrophy muscles expand inwards. You may get S4 (atria contracting forcefully in an effort to overcome abnormally stiff ventricle) and a heave o Fundoscopy to detect hypertensive retinopathy. § Keith-Wagner Classification of Hypertensive Retinopathy: A) Grade 1: Silver wiring (silver line down the middle of arterioles) B) Grade 2: Silver wiring + AV nipping (artery crosses the vein and nips it as it crosses, causing vein to become narrow due to high pressure in artery) C) Grade 3: Flame haemorrhage, sometimes cotton wool spots too (means area around it is ischaemic) D) Grade 4: papilloedema (cannot see optic disc) - these can be either due to chronic hypertension or intracranial hypertension (caused by a brain tumour), requires admission. ** if see hypertensive retinopathy: this means that it's hypertension is long standing and severe

Identify appropriate investigations for AAA

● Bloods o FBC, clotting screen, renal function and liver function o Cross-match if surgery is planned ● Scans o Doppler Ultrasound - can detect aneurysm but CANNOT tell whether it is leaking or not o CT with contrast - can show whether an aneurysm has ruptured o MRI angiography o Ultrasound abdo: Definitive test (sensitivity and specificity of 92% to 99% and nearly 100%, respectively). **If not haemodynamically stable - resus and urgent surgery. § Management done in women if 5cm and in men if 5.5cm

Identify appropriate investigations for venous ulcers

● Bloods - check if anaemic, blood glucose (and also urinalysis) ● ABPI o Exclude arterial ulcer o If ABPI < 0.8 - do NOT apply a pressure bandage as this could worsen the ulcer ● Measure surface area of ulcer - allows monitoring of progression ● Swabs for microbiology - if signs of infection ● Biopsy - if possibility of Marjolin's ulcer

Identify appropriate investigations for rheumatic fever and interpret the results

● Bloods: FBC (inc WCC), inc ESR/CRP, rising antistreptolysin O titre; blood culture (no growth - to exclude bacteraemia) ● Throat swab: culture for GAS, rapid streptococcal antigen test ● ECG: saddle-shaped ST elevation and PR segment depression (features of pericarditis), arrhythmias ● Echocardiogram: pericardial effusion, myocardial thickening or dysfunction, valvular dysfunction (mitral/aortic valves regurg) ● CXR - in all cases in which carditis is suspected. Cardiomegaly and/or congestive heart failure in acute rheumatic fever as seen on chest x-ray, results from severe valvular dysfunction secondary to valvulitis. Pericardial effusion should also be considered in cases where significant cardiomegaly is present.

Summarise the epidemiology of ischaemic heart disease

● COMMON ● Prevalence: > 2 % ● More common in males ● Annual incidence of MI in the UK ~ 5/1000

Identify appropriate investigations for pulmonary hypertension

● CXR - exclude other lung diseases ● ECG - right ventricular hypertrophy and strain ● Echocardiography - assess right ventricular function ● Right Heart Catheterisation - directly measure pulmonary pressure and confirm the diagnosis ● Pulmonary function tests ● LFTs - liver damage --> portal hypertension ● Lung biopsy - interstitial lung disease ● Echocardiography - assess right ventricular function ● Right Heart Catheterisation - directly measure pulmonary pressure and confirm the diagnosis

Identify appropriate investigations for aortic regurgitation

● CXR: o Cardiomegaly o Dilatation of ascending aorta o Signs of pulmonary oedema (if accompanied by left heart failure) - in acute ● ECG: o May show left ventricular hypertrophy ● Deep S in V1/2 (left side) ● Tall R in V5/6 (right side) ● Inverted T waves in lead I, aVL, V5/6 ● Left axis deviation ● Echocardiogram - **DIAGNOSTIC** o May show underlying cause (e.g. aortic root dilatation, bicuspid aortic valve) o May show the effects of aortic regurgitation (e.g. left ventricular dilatation, fluttering of the anterior mitral valve leaflet) o Doppler echocardiogram can show AR and indicate severity o Repeat echos allow monitoring of progression (LV size and function) ● Cardiac catheterisation with angiography: o If there is any uncertainty about the functional state of the ventricle or the presence of coronary artery disease o Helps assess severity of lesion, aortic root anatomy, LV function

Recognise the presenting symptoms of angina pectoris

● Central chest tightness or heaviness brought on by exertion and relieved by rest ● May radiate to one or both arms, neck, jaw or teeth ● Associated symptoms: dyspnoea, nausea, sweatiness, faintness

Define ischaemic heart disease

● Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris). May present as stable angina or acute coronary syndrome. ● ACS can be further subdivided into: o Unstable angina - chest pain at rest due to ischaemia but without cardiac injury o NSTEMI - severely occluded coronary artery but not completely blocked o STEMI - ST elevation with transmural infarction o NOTE: MI = cardiac muscle necrosis resulting from ischaemia § primarily due to atherosclerosis of coronary arteries

Define atrial fibrillation

● Characterised by rapid, chaotic and ineffective atrial electrical conduction at 300-600bpm. Often subdivided into: o Permanent o Persistent o Paroxysmal § Atrial fibrillation (AF) is a SUPRAventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction. § Electrocardiographic characteristics include: o Irregularly irregular R-R intervals (where atrioventricular conduction is not impaired) o Absence of distinct repeating P waves o Irregular atrial activations. ● Atrial flutter is a type of supraventricular tachycardia caused by a RE-ENTRY circuit within the right atrium - it leads to continuous atrial depolarisation. Atrial rate of around 200-400 bpm ● The AV node responds intermittently hence an irregular ventricular rate.

Summarise the epidemiology of aortic regurgitation

● Chronic AR often begins in the late 50s ● It is most frequently seen in patients > 80 yrs

Generate a management plan for heart block

● Chronic Block o 1st degree is usually just monitored o Permanent pacemaker (ICD) is recommended in: a) Complete heart block b) Advanced Mobitz Type II c) Symptomatic Mobitz Type I ● Acute Block o If associated with clinical deterioration use IV ATROPINE - causes increased firing of SAN and conduction through AVN. o Consider temporary (external) pacemaker **The goals of therapy are to treat symptoms and to prevent syncope and sudden cardiac death due to very slow or absent ventricular rates.

Recognise the signs of aortic regurgitation on examination

● Collapsing (water-hammer) pulse ● Wide pulse pressure ● Thrusting and heaving displaced apex beat ● Early diastolic murmur over the aortic valve region (aortic regurg - seen in ascending aorta dissection) o Heard better at the left sternal edge when the patient is sitting forward with the breath held at the top of expiration ● NOTE: an ejection systolic murmur may also be heard because of increased flow across the valve (due to increased stroke volume) ● Austin Flint mid-diastolic murmur o Heard over the apex o Caused by turbulent reflux hitting the anterior cusp of the mitral valve causing a physiological mitral stenosis ● Rare signs associated with aortic regurgitation (eponymous signs of AR): o Quincke's Sign - visible pulsation on nail bed o de Musset's Sign - head nodding in time with the pulse o Becker's Sign - visible pulsation of the pupils and retinal arteries o Muller's Sign - visible pulsation of the uvula o Corrigan's Sign - visible pulsation in the neck o Traube's Sign - pistol shot (loud systolic and diastolic sounds) heard on auscultation of the femoral arteries o Duroziez's Sign - systolic and diastolic bruit heard on partial compression of the femoral artery with the stethoscope o Rosenbach's Sign - systolic pulsations of the liver o Gerhard's Sign - systolic pulsations of the spleen o Hill's Sign - popliteal cuff systolic pressure exceeding brachial pressure by > 60 mm Hg

Explain the aetiology/risk factors for tricuspid regurgitation

● Congenital o Ebstein's anomaly (malpositioned tricuspid valve) o Cleft valve in ostium primum ● Functional o Consequence of right ventricular dilation (e.g. due to pulmonary hypertension) o Valve prolapse ● Rheumatic Heart Disease ● Infective Endocarditis (IV drug user) ● Other: carcinoid syndrome, trauma, cirrhosis, iatrogenic ● Drugs e.g. ergot-derived dopamine agonists **RFs: § left sided heart failure § dilated tricuspid annulus § rheumatic heart disease § permanent pacemarker

Recognise the signs of dyslipidaemia

● Corneal arcus - xanthoma of the cornea; grayish white opacification at the periphery of the cornea ● Xanthomas - tendinous, especially Achilles tendon, elbow and knee tendons and over metacarpophalangeal joints. ● Familial hypercholesterolaemia: may also have planar (orange streaks in palmar creases) and tuberous (plaques on elbows and knees) xanthomas ● Xanthelasma - xanthoma of the eyelid; yellowish plaques occurring mostly commonly near inner canthus of the eyelid ● Milky white appearance of retina - seen at very high TG levels

Identify the possible complications of pulmonary embolism

● Death ● Pulmonary infarction ● Pulmonary hypertension ● Right heart failure

Summarise the prognosis for patients with DVT

● Depends on extent of DVT ● Below-knee DVTs have a GOOD prognosis ● Proximal DVTs have a greater risk of embolisation

Summarise the prognosis for patients with ventricular fibrillation

● Depends on the time between onset of VF and medical intervention ● Early defibrillation is essential (ideally within 4-6 mins) ● Anoxic encephalopathy is a major outcome of VF

Summarise the prognosis for patients with pericarditis

● Depends on the underlying cause ● Viral cases have a GOOD prognosis ● Malignant pericarditis has a POOR prognosis ● 15-40% recur

Recognise the signs of venous ulcers on physical examination

● Described above ● Other signs of venous ulcers: o Stasis eczema o Lipodermatosclerosis (inverted champagne bottle sign if SEVERE) o Haemosiderin deposition (dark colour)

Recognise the signs of rheumatic fever on physical examination

● Diagnosis is made using the revised Jones criteria. There must be evidence of recent strep infection + 2 major criteria OR 1 major + 1 minor criteria ● Evidence of GAS infection o Positive throat culture - but usually negative by the time symptoms occur o Rapid streptococcal antigen test +ve o Elevated/rising streptococcal antibody titre o Recent scarlet fever ● Major criteria (CASES) o Carditis: tachycardia, murmurs (mitral/aortic regurgitation), pericardial rub, cardiomegaly, conduction defects o Arthritis: usually affects larger joints o Subcutaneous nodules: small firm painless nodules seen on extensor surfaces, joints and tendons o Erythema marginatum: geographical-type rash with red, raised edges and clear centre mainly on trunk and proximal limbs o Sydenham's chorea: rapid, involuntary, irregular movements with flowing/dancing quality ● Minor criteria (PRAPP) o Pyrexia o Raised ESR/CRP o Arthralgia (only if arthritis not present as major criteria) o Prolonged PR interval (only if carditis not present as major criteria) o Previous rheumatic fever

Recognise the signs of cardiomyopathy on physical examination

● Dilated o Raised JVP o Displaced apex beat o Functional mitral and tricuspid regurgitations o Third heart sound o Tachycardia o Hypotension o Pleural effusion o Oedema o Jaundice o Hepatomegaly o Ascites o AF ● Hypertrophic o Jerky carotid pulse o Double apex beat o Ejection systolic murmur o Systolic thrill at lower left sternal edge ● Restrictive o Raised JVP ● Kussmaul Sign - paradoxical rise in JVP on inspiration due to restricted filling of the ventricles o Palpable apex beat o Third heart sound o Ascites o Ankle oedema o Hepatomegaly

Identify the possible complications of DC cardioversion

● Dislodge of blood clots leading to stroke or PE ● Other arrhythmias ● Skin burns

Identify appropriate investigations for arterial ulcers

● Duplex ultrasonography of lower limbs - assess patency of arteries and potential for revascularisation or bypass surgery ● ABPI ● Percutaneous angiography ● ECG ● Fasting serum lipids, fasting blood glucose and HbA1c (diabetes is a major risk factor) ● FBC - anaemia can worsen the ischaemia

Recognise the presenting symptoms of dyslipidaemia

● Dyslipidaemia itself does not usually cause symptoms but can lead to symptomatic vascular disease such as coronary artery disease, stroke and peripheral vascular disease.

Recognise the signs of angina pectoris on physical examination

● Dyspnoea ● Tachycardia

Identify appropriate investigations for ventricular tachycardia

● ECG o It can sometimes be difficult to distinguish between VT and SVT with aberrant conduction o If in doubt, treat as a VT o ECG Features: ● Rate > 100 bpm ● Broad QRS complexes ● AV dissociation ● Electrolytes - derangement can cause arrhythmias ● Drug levels - e.g. check for digoxin toxicity ● Cardiac enzymes - e.g. troponins to check for recent ischaemic event

Identify appropriate investigations for mitral regurgitation

● ECG o NORMAL o May show AF or p mitrale if in sinus rhythm (indicates left atrial hypertrophy) ● CXR o ACUTE mitral regurgitation may produce signs of left ventricular failure o CHRONIC mitral regurgitation shows: ● Left atrial enlargement ● Cardiomegaly (due to LV dilation) ● Mitral valve calcification (if rheumatic heart disease is the cause) ● Pulmonary oedema ● Echocardiography **Diagnostic** o Performed every 6-12 months in moderate-severe MR o Assess LV function and aetiology ● Doppler echo to assess size and site of regurgitant jet ● Cardiac catheterisation to confirm diagnosis, exclude other valve disease, assess CAD

Identify appropriate investigations for SVT

● ECG o NOTE: acutely, AVRT and AVNRT cannot be differentiated on ECG, as they both appear as narrow complex tachycardia. Only after correcting the tachycardia, you see delta wave in AVRT but no wave in AVNRT. o AVNRT ⇒ Tachycardia ⇒ Narrow QRS ⇒ P waves may be buried in QRS ⇒ Decreased PR interval ⇒ After SVT terminated, ECG appears normal. o AVRT ⇒ Narrow complex tachycardia ⇒ Shortened PR interval ⇒ P waves buried in QRS ● 24 hr ECG monitoring - will be required in patients with paroxysmal palpitations ● Cardiac Enzymes o Check for features of MI (especially if there is chest pain) ● Electrolytes - can cause arrhythmia ● TFTs - can cause arrhythmia ● Digoxin Level - for patients on digoxin ● Echocardiogram - check for structural heart disease

Identify appropriate investigations for heart block

● ECG - GOLD STANDARD o First Degree - fixed prolonged PR interval (> 0.2 s) o Mobitz Type I (Wenckebach) - progressively prolonged PR interval, culminating in a P wave that is NOT followed by a QRS complex. The pattern then begins again. 'Going, going, gone'. o Mobitz Type II - intermittently a P wave is NOT followed by a QRS. There may be a regular pattern of P waves not followed by QRS (e.g. 2:1 or 3:1) o Complete Heart Block - no relationship between P waves and QRS complexes. If QRS is initiated in the: ● Bundle of His - narrow complex ● More distally - wide complex and slow rate (~ 30 bpm) ● CXR o Cardiac enlargement o Pulmonary oedema ● Bloods o TFTs o Digoxin level o Cardiac enzymes o Troponin - acute ischaemia should be aggressively managed and presents a potentially reversible cause of AV block o Potassium/calcium/pH - v high or v low values can cause reversible heart block ● Echocardiogram o Wall motion abnormalities o Aortic valve disease o Vegetations

Identify appropriate investigations for myocarditis

● ECG immediately: o In anyone with chest pain or cardiac symptoms. o Non-specific T wave and ST changes - however, ST-segment elevation and depression frequently occur o Atrial arrhythmias o Transient AV block o PERICARDITIS: widespread saddle-shaped ST elevation ● Bloods o FBC - raised WCC if infective cause o U&E o ESR/CRP - raised o Cardiac enzymes e.g. creatinine kinase/troponin- may be raised - in proper clinical setting, +ve troponin I or T confirms diagnosis o serum B-type natriuretic peptide - may be elevated in response to ventricular distention, such as occurs in CHF due to myocarditis o Negative antimyosin scintigraphy also excludes acute myocarditis o Tests to identify cause (e.g. viral/bacterial serology, ANA, TFT) ● CXR o May be NORMAL o May show cardiomegaly o bilateral pulmonary infiltrates in the setting of myocarditis-induced CHF ● Echocardiography o Assesses systolic/diastolic function o Wall motion abnormalities o Pericardial effusions ● Pericardial Fluid Drainage o Measure glucose, protein, cytology, culture and sensitivity o Helps identify causative organism ● Myocardial Biopsy: Rarely required

Identify appropriate investigations for ventricular fibrillation

● ECG: chaotic irregular deflections of varying amplitude, no identifiable P waves/QRS complexes/T waves ● Cardiac enzymes (e.g. troponins) - check for recent ischaemic event ● Electrolytes - derangement can cause arrhythmias, including VF ● Drug levels and toxicology screen - anti-arrhythmics can (ironically) cause arrhythmia, as can various recreational drugs (e.g. cocaine) ● TFTs - hyperthyroidism can cause tachyarrhythmias ● Coronary angiography - if patient survives VF, to check the integrity of coronary arteries

Explain the aetiology/risk factors of ventricular tachycardia

● Electrical impulses arise from a ventricular ectopic focus - an ectopic focus is an excitable group of cells within the atria/ventricles which cause a premature heart beat outside the normally functioning circulation i.e. abnormal pacemaker sites ● Can impair cardiac output causing hypotension, collapse and acute cardiac failure. ● Risk Factors o Coronary heart disease o Structural heart disease o Electrolyte deficiencies (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia) o Use of stimulant drugs (e.g. caffeine, cocaine)

Define dyslipidaemia

● Elevation of plasma cholesterol, triglycerides or both **Hypercholesterolaemia, an elevation of total cholesterol (TC) and/or low-density lipoprotein cholesterol (LDL-C) or non-high-density lipoprotein cholesterol (HDL-C) (defined as the subtraction of HDL-C from TC) in the blood, is also often referred to as dyslipidaemia, to encompass the fact that it might be accompanied by a decrease in HDL-C, an increase in triglycerides, or qualitative lipid abnormalities. Dyslipidaemia is classified as serum TC, LDL-C, triglycerides, apolipoprotein B, or lipoprotein(a) concentrations above the 90th percentile, or HDL-C or apolipoprotein A-I concentrations below the 10th percentile for the general population. However, these classic percentile cut-off points should not be used too rigidly in defining dyslipidaemia. For example, evidence suggests that lipoprotein(a) ≥80th percentile is abnormal and linked to elevated cardiovascular risk

Recognise the signs of DVT on physical examination

● Examination of the Leg o unilateral leg swelling/pain o Local erythema, warmth and swelling, tenderness o Measure the leg circumference o Varicosities (swollen/tortuous vessels) o Skin colour changes (red/discoloured) o NOTE: HOMAN'sSign - forced passive dorsiflexion of the ankle causes deep calf pain o Pitting oedema ● Risk is stratified using the WELLS CRITERIA (NOTE: this is different from the PE Wells criteria) o Score 2 or more = high risk of DVT present ● Mild fever ● Examine for PE o Check respiratory rate, pulse oximetry and pulse rate

Identify appropriate investigations for angina pectoris

● FIRST LINE: ECG, FBC, lipid profile, fasting glucose ● Then: TSH, stress ECG (gold standard), stress myocardial perfusion imaging, stress echo, coronary angiogram ● ECG: usually normal, may show ST depression, flat/inverted T waves, signs of past MI ● Exclude precipitating factors: anaemia, diabetes, hyperlipidaemia, thyrotoxicosis, temporal arteritis

Recognise the presenting symptoms of tricuspid regurgitation

● Fatigue ● Breathlessness (dyspnoea) ● Palpitations ● Headaches ● Nausea ● Anorexia ● Epigastric pain made worse by exercise ● Jaundice ● Lower limb swelling ● Ascites ● Oedema ● early satiety, dyspepsia, indigestion

Recognise the signs of pericarditis on physical examination

● Fever ● Pericardial friction rub o Heard best at lower left sternal edge, with patient leaning forward during expiration. Sounds like leather rubbing against each other ● Heart sounds may be faint due to a pericardial effusion ● Cardiac Tamponade signs (when fluid in the pericardium builds up resulting in compression of the heart) o Beck's Triad (signs associated with acute CARDIAC TAMPONADE) a) Raised JVP b) Low Blood Pressure (hypoension) c) Muffled Heart Sounds o Tachycardia o Pulsus paradoxus ● Definition: an abnormally large decrease in SBP (> 10 mm Hg drop) and pulse wave amplitude during inspiration ● Constrictive Pericarditis signs: o Kussmaul's sign o Pulsus paradoxus o Hepatomegaly o Ascites o Oedema o Pericardial knock (due to rapid ventricular filling) - early diastolic sound o AF

Identify appropriate investigations for DVT

● First: calculate Well's score. O If score less than or equal to 2: do D-dimer. If D-dimer is normal: DVT excluded o If D-dimer elevated: do duplex USS ● If Well's score >2: do duplex USS (Assesses venous flow by the use of Doppler and vein compression) ● If pregnant: do duplex USS straight away ● Doppler Ultrasound - GOLD STANDARD ● If PE suspected o ECG o CXR o ABG

Generate a management plan for atrial fibrillation

● Firstly, try to treat any reversible causes e.g. thyrotoxicosis, chest infection ● KEY components of AF management o NOTE: in AF, there are randomised atrial contractions which lead to fast ventricular contractions. 1) Rate control - restores ventricular rate to normal range. This leads to slow AF. 2) Rhythm control - restores sinus rhythm 3) Anticoagulation **● ACUTE ATRIAL FIBRILLATION (<48hrs) o If haemodynamically unstable i.e. angina/hypotension/HF ⇒ Requires rhythm control ⇒ O2 --> U&Es --> DC CARDIOVERSION ⇒ If unavailable, chemical cardioversion (IV amiodarone or flecainide) NOTE: flecainide contraindicated in ischaemic heart disease o Then, rate control ⇒ 1st line: verapamil or bisoprolol ⇒ 2nd line: digoxin or amiodarone o Then, anticoagulate o Note: use no anticoagulation if stable sinus rhythm has been restored and no risk factors for emboli and AF recurrence unlikely, i.e. no failed cardioversions, no structural heart disease 2) CHRONIC AF: o Rate control ⇒ 1st line: beta blocker (bisoprolol) or rate control calcium blocker (verapamil) ⇒ If this fails, add digoxin ⇒ Then, consider amiodarone ⇒ Note: do NOT give beta blockers with diltiazem or verapamil (CCBs) - risk of bradycardia. ⇒ Aim for rest rate <90bpm and 200 - age on exertion o Anticoagulate for 3 weeks before elective cardioversion - WARFARIN ⇒ This is as they have had AF for long time so high risk of a clot formation in left atrial appendage so cardioversion can cause clot to dislodge and travel to brain ⇒ Warfarin is the traditional drug used BUT newer drugs known as NOACs can also be used (advantage is that they do not require regular blood tests) o Rhythm control (elective cardioversion) ⇒ Do echo first ⇒ Pre-treat for 4 weeks with sotalol or amiodarone if risk of cardioversion failure ⇒ Flecainide first choice if no structural heart disease ⇒ IV Amiodarone if structural heart disease 3) PAROXYSMAL AF: o Consider pill in the pocket (dose of sotalol/flecainide PRN) o Anticoagulate

Generate a management plan for varicose veins

● For symptomatic superficial vein insufficiency (no PVD) o 1st line: graduated compression stockings o If ineffective: phlebectomy or sclerotherapy o In effective: ablative procedures +/- phlebectomy or sclerotherapy ● For deep vein insufficiency o 1st line: phlebectomy and compression stockings ● Management types explained: o Conservative ▪ Exercise - improves skeletal muscle pump ▪ Elevation of legs at rest ▪ Support stockings o Endovascular treatment - less pain and earlier return to activity than surgery ▪ Radiofrequency ablation: catheter inserted into the vein and heated to 120 degrees destroying the endothelium and closing the vein ▪ Endovenous laser ablation: similar concept but uses a laser ▪ Injection sclerotherapy: liquid injected at multiple sites and vein compressed for a few weeks to avoid thrombosis OR foam injected under ultrasound guidance at a single site and spreads rapidly through the veins, damaging the endothelium. ▪ Phlebectomy: minimally invasive procedure using a small scalpel to remove varicose veins o Surgical - several choices ▪ Saphenofemoral ligation ▪ Stripping of the long saphenous vein - from groin to upper calf (not to ankle as can damage saphenous nerve) ▪ Avulsion of varicosities ▪ NOTE: short saphenous vein isn't stripped because of the risk of damaging the sural nerve ▪ Post op: bandage legs tightly and elevate for 24 hours

Recognise the presenting symptoms of gangrene and necrotising fasciitis

● Gangrene o Pain - There may be a history of chronic claudication-type pain in patients with ischaemic gangrene. By contrast, a sudden onset of pain is usually the first symptom of infectious gangrene. In addition, 50% of patients report a feeling of heaviness in the affected extremity o Discolouration of affected area - BLACK o Often affects extremities or areas subject to high pressure o Gas gangrene: rapid onset of myonecrosis, muscle swelling, gas production, sepsis, severe pain ● Necrotising Fasciitis o Pain - often seems SEVERE and out of proportion to the apparent physical signs o Predisposing event (e.g. trauma, ulcer, surgery)

Recognise the signs of gangrene and necrotising fasciitis on examination

● Gangrene o Painful area = may be oedematous with overlying erythematous region around gangrenous tissue o Gangrenous tissue = BLACK because of haemoglobin break down products o Wet Gangrene - tissue becomes boggy with associated pus and a strong odour caused by the activity of anaerobes o Gas Gangrene - spreading infection and destruction of tissues causes overlying oedema, discolouration and crepitus (due to gas formation by the infection) ● Necrotising Fasciitis o Area of erythema and oedema o Haemorrhagic blisters may be present o Signs of systemic inflammatory response and sepsis (high/low temperature, tachypnoea, hypotension)

Explain the aetiology/risk factors of necrotising fasciitis

● Gangrene o Tissue ischaemia and infarction (critical limb ischaemia) o Physical trauma o Thermal injury o Gas gangrene is caused by Clostridia perfringens ● Necrotising Fasciitis o Usually polymicrobial involving streptococci, staphylococci, bacterioides and coliforms ● Risk Factors: o Diabetes o Smoking o Hypercoagulable states o Peripheral vascular disease o Leg ulcers o Malignancy o Immunosuppression o Steroid use o Puncture/surgical wounds o Trauma o Alcoholism/ drug use o Malnutrition

Summarise the epidemiology of gangrene and necrotising fasciitis

● Gangrene - relatively COMMON ● Necrotising fasciitis and gas gangrene - RARE

Define gangrene and necrotising fasciitis

● Gangrene: tissue necrosis, either wet with superimposed infection, dry or gas gangrene - due to poor vascular supply a) Dry gangrene: necrosis in absence of infection b) Wet gangrene: tissue death and infection c) Gas gangrene: subset of necrotising myositis caused by spore-forming Clostridial species ● Necrotising Fasciitis: a life-threatening infection of deep fascia causing necrosis of subcutaneous tissue. § is either infectious (wet, gas, necrotising fasciitis) or ischaemic (dry) § may result from infection, ischaemia or trauma or combo.

Recognise the presenting symptoms and signs of constrictive pericarditis

● Gradual-onset of symptoms ● EARLY - symptoms and signs may be very subtle ● ADVANCED - jaundice, cachexia, muscle wasting ● Right Heart Failure Signs: o Dyspnoea o Peripheral oedema o Raised JVP o Kussmaul's sign (paradoxical rise in JVP on inspiration) o Pulsatile hepatomegaly o Soft, diffuse apex beat o Quiet heart sounds, S3 o Diastolic pericardial knock o Splenomegaly o Ascites o Oedema

Identify possible complications of SVT

● Haemodynamic collapse ● DVT ● Systemic embolism ● Cardiac tamponade

Identify the possible complications of coronary angiography and PCI

● Haemorrhage ● Contrast reaction ● Loss of peripheral pulse due to dissection/thrombosis/arterial spasm ● Angina ● Arrhythmias ● Pericardial tamponade ● Infection

Summarise the epidemiology of dyslipidaemia

● Half the UK population have a serum cholesterol putting them at significant risk of CVD.

Identify the possible complications of hypertension

● Heart failure ● Coronary artery disease ● Cerebrovascular accidents ● Peripheral vascular disease ● Emboli ● Hypertensive retinopathy ● Renal failure ● Hypertensive encephalopathy ● Posterior reversible encephalopathy syndrome (PRES) ● Malignant hypertension

Recognise the presenting symptoms and signs of ventricular fibrillation

● History of: o Chest pain o Fatigue o Palpitations ● There may be known pre-existing conditions: o Coronary artery disease o Cardiomyopathy o Valvular heart disease o Long QT syndrome o Wolff-Parkinson-White syndrome o Brugada syndrome (SCN5A gene - genetic disorder that can causes a dangerous irregular heartbeat)

Explain the aetiology/risk factors of pericarditis

● IDIOPATHIC ● Infective Most common causative organisms (viruses): o Coxsackie B o Echovirus o Mumps o Streptococci o Fungi o Staphylococci o TB ● Connective tissue disease (e.g. sarcoidosis, SLE, scleroderma) ● Post-MI (within 24-72 hrs of MI - occurs in up to 20% of patients) ● Dressler's Syndrome - pericarditis occurring weeks/months after acute MI ● Malignancy - lung, breast, lymphoma, leukaemia, melanoma ● Radiotherapy ● Thoracic surgery ● Drugs (e.g. hydralazine, isoniazid) ● Others: uraemia, rheumatoid arthritis, myxoedema, trauma

Generate a management plan for SVT

● If Haemodynamically UNSTABLE o DC cardioversion ● If Haemodynamically STABLE o Try VAGAL manoeuvres (e.g. Valsalva, carotid massage) Note: Carotid massage could dislodge atherosclerotic plaques, so is only performed in young patients o If vagal manoeuvres fail: o ADENOSINE 6 mg bolus (can increase to 12 mg) - Contraindicated in ASTHMA as it can cause bronchospasm - in asthma, use VERAPAMIL o Wait 2 minutes - if no change, give 12mg adenosine o Wait another 2 minutes - if still no change, give 12mg adenosine o Wait another 2 minutes - if still no change, IV metoprolol/amiodarone/digoxin/synchronised DC cardiovert ● If unresponsive to chemical cardioversion or tachycardia > 250 bpm or adverse signs (low BP, heart failure, low consciousness) o Sedate and synchronised DC cardioversion o Amiodarone ● Ongoing management of SVT o AVNRT ▪ Radiofrequency ablation of slow pathway ▪ Beta-blockers ▪ Alternatives: fleicanide, propafenone, verapamil o AVRT ▪ Radiofrequency ablation o Sinus Tachycardia ▪ Exclude secondary cause (e.g. hyperthyroidism) ▪ Beta-blocker or rate-limiting CCB

Define cardiac failure

● Inability of the cardiac output to meet the body's demands despite normal venous pressures **The most common risk factors are advanced age, female sex, hypertension, obesity, chronic kidney disease, diabetes mellitus, and coronary artery disease.

Summarise the epidemiology of myocarditis

● Incidence is difficult to measure accurately ● Coxsackie B virus is most common in Europe and USA ● Chagas disease is most common in South America ●age <50 years

Identify the possible complications of ischaemic heart disease

● Increased risk of MI and other vascular disease (e.g. stroke, PVD) ● Cardiac injury from an MI can lead to heart failure and arrhythmias ● Early Complications (within 24-72 hrs): o Death o Cardiogenic shock o Heart failure o Ventricular arrythmias o Heart block o Pericarditis o Myocardial rupture - inferior MI can cause rupture of the posteromedial papillary muscle whilst anterolateral infarctions can cause rupture of the anterolateral papillary muscle. This leads to acute MR. o Thromboembolism ● Late Complications o Ventricular wall rupture o Valvular regurgitation o Ventricular aneurysms o Tamponade o Dressler's syndrome o Thromboembolism ● MNEMONIC for common Complications of MI - DARTH VADER: o Death o Arrhythmias o Rupture - of septum or outer walls o Tamponade o Heart failure o Valve disease o Aneurysm o Dressler's syndrome - autoimmune pericarditis 2-10 weeks after MI due to molecular mimicry o Embolism o Reinfarction

Recognise the signs of varicose veins on physical examination

● Inspection o Inspect when the patient is standing o Oedema, eczema, ulcers, phlebitis, atrophie blanche, lipodermatosclerosis ● Palpation o May feel fascial defects along the veins o Cough impulse may be felt over the saphenofemoral junction o Tap Test - tapping over the saphenofemoral junction will lead to an impulse felt distally (this would not happen if the valves were competent) o Palpation of a thrill or auscultation of a bruit would suggest an AV fistula ● Trendelenburg Test o Allows localisation of the sites of valvular incompetence o Leg is elevated and the veins are emptied o A hand is placed over the saphenofemoral junction o The leg is put back down and filling of the veins is observed before and after the hand is released from the saphenofemoral junction o A Doppler ultrasound can be used to show saphenofemoral incompetence ● Rectal or Pelvic Examination o If secondary causes are suspected ● Signs of Venous Insufficiency o Varicose eczema o Haemosiderin staining o Atrophie blanche o Lipodermatosclerosis o Oedema o Ulceration

Identify appropriate investigations for vasovagal syncope

● Investigations are involved with checking for other causes of syncope o ECG - check for arrhythmia o Echocardiogram - check for outflow obstruction o Lying/standing blood pressure - check for orthostatic hypotension o Fasting blood glucose - check for DM/hypoglycaemia

Identify appropriate investigations for cardiac failure

● Key investigations: BNP + CXR + echo ● NICE: if ECG and BNP are normal - heart failure unlikely. If either abnormal, echocardiography needed. ● Bloods o FBC o U&E o LFTs o CRP o Glucose o Lipids o TFTs ● In ACUTE Left Ventricular Failure o ABG o Troponin o BNP ● Raised plasma BNP suggests diagnosis of cardiac failure (>100ng/L) ● Low plasma BNP rules out cardiac failure (90% sensitivity) ● CXR of left ventricular failure: ABCDE o Alveolar oedema (shadowing - 'bat's wings') o Kerley B lines (interstitial oedema) o Cardiomegaly o Dilated prominent upper lobe vessels (upper lobe diversion) o Pleural Effusion - blunt costophrenic angles ● ECG: o May be normal, can indicate cause o May show ischaemic changes (pathological q waves, t wave inversion) o May show arrhythmia or left ventricular hypertrophy ● Echocardiogram - KEY INVESTIGATION o Assess ventricular contraction o Can indicate the cause (MI, valvular heart disease) and confirm presence/absence of LV dysfunction. o Systolic dysfunction = LV ejection fraction < 40% o Diastolic dysfunction = decreased compliance of the myocardium leads to restrictive filling defect ● Swan-Ganz Catheter Allows measurement of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures

Generate a management plan for dyslipidaemia

● Lifestyle advice o Aim for BMI 20-25 o Diet with <10% calories from saturated fat, high fibre, fresh fruit and veg, omega-3 fatty acids o Exercise ● Treatments will differ for familial or secondary hyperlipidaemia ● Medications o 1st line: statins e.g. simvastatin o 2nd line: fibrates e.g. bezafibrate (usually in mixed hyperlipidaemia) OR cholesterol absorption inhibitors e.g. ezetimibe or a proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor - evolocumab (is a MAB). PCSK9 sits on LDLR and is involved in its recycling - use if statin intolerant, or uncontrolled lipids esp. FH. o Hypertriglyceridaemia responds best to fibrates, nicotinic acid or fish oil ● Treatment priorities o Using statins in primary prevention may cause side-effects and expensive o 1st priority: all those with known CVD o 2nd: all those with DM o 3rd: those with 10 yr risk of CVD >20% o Aim for target plasma cholesterol of less than or equal to 4mmol/L

Explain the aetiology/risk factors of dyslipidaemia

● Lipid travels in blood packaged with proteins as lipoproteins. There are 4 classes: chylomicrons, VLDL (mainly TG), LDL (mainly cholesterol) and HDL (mainly phospholipid). Evidence shows that cholesterol is a big risk factor for CVD. ● HDL correlates inversely with CVD. ● Risk factors for hyperlipidaemia o Family history of hyperlipidaemia o Corneal arcus <50 yrs old o Xanthomata or xanthelesmata ● Types o Common primary hyperlipidaemia: accounts for 70% of hyperlipidaemia Only LDL high o Familial primary hyperlipidaemia: multiple phenotypes o Secondary hyperlipidaemia: due to Cushing's syndrome, hypothyroidism, nephrotic syndrome or cholestasis. Treat cause first. LDL high o Mixed hyperlipidaemia: both LDL and TG high. Due to T2DM, metabolic syndrome, alcohol abuse, chronic renal failure.

Recognise the presenting symptoms of vasovagal syncope AND signs

● Loss of consciousness lasting a short time ● Patients may experience vagal symptoms (sweating, dizziness, light-headedness) before passing out ● There may be some twitching of limbs during the blackout ● Recovery is normally very quick Recognise the signs of vasovagal syncope on physical examination ● Usually NO SIGNS

Explain the aetiology/risk factors for mitral stenosis

● MAIN CAUSE: Rheumatic Heart Disease (90% of cases) ● Rare causes of mitral stenosis: o Congenital mitral stenosis o Mucopolysaccharidoses o Endocardial fibroelastosis o Prosthetic valve o SLE o Rheumatoid arthritis o Endocarditis o Atrial myxoma **RFs: § streptococcal infection § female sex

Recognise the presenting symptoms of aortic dissection

● MAIN SYMPTOM: sudden central 'tearing' pain, it may radiate to the BACK in between the shoulder blades (it can mimic MI) ● Other symptoms caused by obstruction of branches of the aorta: o Carotid artery --> hemiparesis, dysphasia, blackout o Coronary artery --> chest pain (angina or MI) o Subclavian artery --> ataxia, loss of consciousness o Anterior spinal artery --> paraplegia o Coeliac axis --> severe abdominal pain (due to ischaemic bowel) o Renal artery --> anuria, renal failure

Explain the aetiology/risk factors of heart block

● MI or ischaemic heart disease (MOST COMMON) ● Infection (e.g. rheumatic fever, infective endocarditis) ● Drugs (e.g. digoxin) ● Metabolic (e.g. hyperkalaemia) ● Infiltration of conducting system (e.g. sarcoidosis) ● Degeneration of the conducting system

List 10 complications of MI

● MNEMONIC for common Complications of MI - DARTH VADER: o Death o Arrhythmias o Rupture - of septum or outer walls o Tamponade o Heart failure o Valve disease o Aneurysm o Dressler's syndrome - autoimmune pericarditis 2-10 weeks after MI due to molecular mimicry o Embolism o Reinfarction

Recognise the presenting symptoms of aortic stenosis

● May be ASYMPTOMATIC initially ● Think of AS in any elderly person with chest pain, exertional dyspnoea or syncope. ● Angina (due to increased oxygen demand of the hypertrophied left ventricle) ● Syncope or dizziness on exercise (due to outflow obstruction) ● Symptoms of heart failure (e.g. dyspnoea, orthopnoea) ● Others: dizziness, faints, systemic emboli if infective endocarditis, sudden death

Recognise the presenting symptoms of SVT

● May have minimal symptoms or may present with syncope ● Symptoms vary depending on rate and duration of SVT ● Palpitations ● Light-headedness ● Polyuria (due to increased atrial pressure causing ANP release) ● Abrupt onset and termination of symptoms ● Other symptoms: fatigue, chest discomfort, dyspnoea, syncope

Define mitral stenosis

● Mitral valve narrowing causing obstruction to blood flow from the left atrium to the left ventricle § Causes decreased filling of the left ventricle, while simultaneously increasing left atrial pressure, producing the syndrome of heart failure § As disease progresses, pulmonary hypertension and right heart failure occur

Summarise the prognosis for patients with heart block

● Mobitz Type II and 3rd degree block usually indicate serious underlying cardiac disease

Generate a management plan for angina pectoris

● Modify risk factors: stop smoking, encourage exercise, weight loss, control hypertension, diabetes, hyperlipidaemia ● For stable angina § Beta blocker (slow HR down but issue is feel knackered when exert yourself) atenolol 25-100mg once daily § aspirin 75mg daily § GTN - 50micrograms as required § statins - simvastatin 20-80mg ● If poor response to medical therapy, can do percutaneous transluminal coronary angioplasty (PTCA) ● Prinzmetals - treat with CCBs +/- long-acting nitrates - aspirin and b blockers can worsen! ● Syndrome X - CCBs

Summarise the epidemiology of aortic dissection

● Most common in males aged 40-60 yrs

Explain the aetiology/risk factors of infective endocarditis

● Most common organisms causing infective endocarditis: o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis o Staphylococci (35%) - S. AUREUS (most common) and S. epidermidis o Enterococci (20%) - usually E. faecalis o Other organisms: ● Haemophilus ● Actinobacillus ● Cardiobacterium ● Coxiella burnetii ● Eikenella ● Kingella ● Chlamydia ● Histoplasma, Candida, Aspergillus (fungal) ● Other causes: SLE (Libman-Sacks endocarditis), malignancy ● Pathophysiology o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia o The vegetations are made up of platelets, fibrin and infective organisms o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities o Activation of the immune system can lead to the formation of immune complexes 🡪 vasculitis, glomerulonephritis, arthritis **Risk Factors o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease) o Prosthetic heart valves - can occur during surgery or later o Turbulent blood flow (e.g. patent ductus arteriosus) o Recent dental work/poor dental hygiene (source of S. viridans) o indewelling vascular catheters o Dermatitis o IV injections o Renal failure o Organ transplantation o DM o Post-op wounds ● FEVER + NEW MURMUR = endocarditis until proven otherwise ● 50% of all IE occurs on normal valves ● Follows an acute course, presenting with acute heart failure +/- emboli ● Entry is usually via the skin

S3 and S4 meaning

● Murmurs occur due to abnormal movement of blood across valves and between cardiac chambers, causing turbulence ● Systolic murmurs occur during ventricular contraction (systole) ● Diastolic murmurs occur during ventricular filling (diastole) ● S3: heard in early diastole - KEN—TUC-KY Represents thin walled, dilated left ventricle causing decelerated blood flow. Normal in children and athletes, in normal adults can indicate ventricular systolic failure, congestive heart failure. Rapid ventricular filling. ● S4: heard in late diastole just before S1 - TEN-NE—SEE. Occurs due to increased stiffness of left ventricle, or thicker ventricular wall. Atrial wall contracting against ventricular hypertrophy. Associated with severe hypertension and ventricular hypertrophy.

Explain the aetiology/risk factors of constrictive pericarditis

● NOTE: it is often underdiagnosed because it is difficult to distinguish it from restrictive cardiomyopathy and other causes of right heart failure ● Can occur after any pericardial disease process ● More common causes of pericarditis: o Idiopathic o Virus o TB o Mediastinal irradiation o Post-surgical o Connective tissue diseases

Define aortic stenosis

● Narrowing of the left ventricular outflow at the level of the aortic valve. § Aortic stenosis (AS) represents obstruction of blood flow across the aortic valve due to pathological narrowing. It is a progressive disease that presents after a long subclinical period with symptoms of decreased exercise capacity, exertional chest pain (angina), syncope, and heart failure § Characteristic murmur is systolic, mid-to-late peaking with a crescendo-decrescendo pattern, and radiates to the carotids. § Doppler echo is essential to the diagnosis and will show a pressure gradient across the stenotic aortic valve.

Identify appropriate investigations for infective endocarditis

● Note: Duke Criteria for IE 1) Bloods o FBC - high neutrophils, normocytic anaemia o High ESR/CRP o U&Es - elevated urea o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive o LFTs 2) Urinalysis o Microscopic haematuria o Proteinuria 3) Blood Culture o Do 3 SETS at different times from different sites are peak of fever o 85-90% are diagnosed form the first 2 sets. 10% are culture negative o Do microscopy and sensitivities as well 4) CXR - cardiomegaly 5) ECG - long PR interval at regular intervals 6) Echocardiography: **Should be performed in all cases of suspected IE, as early as possible to confirm or rule out the diagnosis** o Transthoracic or transoesophageal (produces better image) o May show vegetation but only if >2mm ** Duke's Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs **Blood cultures should be taken prior to the initiation of antimicrobial therapy, and urgent echocardiography is required

Explain the aetiology/risk factors of peripheral vascular disease

● Occurs due to ATHEROSCLEROSIS in peripheral arteries ● Intermittent claudication and critical limb ischaemia are types of CHRONIC LIMB ISCHAEMIA, separate to ACUTE LIMB ISCHAEMIA. ● Types of PVD include: a) Intermittent claudication - CRAMPING calf pain on exercise and relieved by rest. Exercise increases muscle demand, which cannot be met by supply. Cramping pain is reproducible - claudication distance (how long can walk before claudication). Improvement occurs by maintaining exercise to stimulate angiogenesis , stopping smoking and take statin and antiplatelet. Often don't need to intervene further. 80% chance improves/stable; 20% worse b) Critical limb ischaemia - pain at REST § NOTE: this is the MOST SEVERE manifestation of peripheral vascular disease. § Can lead to tissue loss - gangrene/ulceration. § Gangrene - death of tissue from poor vascular supply, sign of critical ischaemia. § Arterial ulcers - abnormal breaks in an epithelial surface c) Acute limb ischaemia - a sudden decrease in arterial perfusion in a limb, due to thrombotic or embolic causes, or post angioplasty, trauma, iatrogenic - medical emergency requiring revascularisation within 4-6 hours to save limb. Two KEY causes: atherosclerotic plaque and atrial fibrillation **Risk Factors (same as the risk factors for any other atherosclerotic disease): o Smoking o Diabetes o Hypertension o Hyperlipidaemia o Physical inactivity o Obesity o Family history o Renal failure

Recognise the presenting symptoms of hypertension

● Often ASYMPTOMATIC ● Symptoms of complications ● Symptoms of the cause ● Accelerated or Malignant Hypertension: o Scotomas (visual field loss) o Blurred vision o Headache o Seizures o Nausea and vomiting o Acute heart failure

Recognise the presenting symptoms of arterial ulcers

● Often DISTAL - at the dorsum of the foot or between the toes ● Punched-out appearance ● Often elliptical with clearly defined edges ● The ulcer base contains grey, granulation tissue ● NIGHT PAIN - hallmark of arterial ulcers o Pain is worse when supine (because arterial blood flow is further reduced when supine) o Pain is relieved by dangling the affected leg off the end of the bed

Recognise the signs of heart block on physical examination

● Often NORMAL ● Check for signs of a potential cause of heart block ● Complete Heart Block: o Slow large volume pulse (WIDE PULSE PRESSURE) o JVP may show cannon a waves ● Cannon A Waves: waves seen occasionally in the jugular vein of humans with certain cardiac arrhythmias. This occurs when the atria and ventricles contract simultaneously ● Mobitz Type II and 3rd Degree Heart Block o Signs of reduced cardiac output (e.g. hypotension, heart failure)

Explain the aetiology/risk factors for rheumatic fever

● Pathogenic mechanisms remain incompletely understood ● Pharyngeal infection with Lancefield group A beta-haemolytic streptococci triggers rheumatic fever 2-4 weeks later in the susceptible 2% of the population ● An antibody to the carbohydrate cell wall (GAS antigens) of the streptococcus cross-reacts with valve tissue (antigenic mimicry) and may cause permanent damage to the heart valves. ● Risk factors o Genetic susceptibility o Malnutrition o Poverty

Recognise the presenting symptoms of varicose veins

● Patients may complain about the cosmetic appearance ● Aching/cramps in the legs ● Aching is worse towards the end of the day of after standing for long periods of time ● Swelling ● Tingling ● Heaviness and restless legs ● Itching ● Bleeding ● Infection ● Ulceration

Identify the possible complications of pericarditis

● Pericardial effusion - pooling of fluid in pericardial space ● Cardiac tamponade - a large pericardial effusion can put pressure on the heart ● Cardiac arrhythmias

Define cardiomyopathy

● Primary disease of the myocardium. Cardiomyopathy may be: o Dilated - a dilated, flabby heart of unknown cause. Thickening of inner layer of heart chambers, heart muscles stretch and weaken Impairment of contractility (systolic function) o Hypertrophic - thickening of the cardiac muscle Impairment of compliance (diastolic function) o Restrictive - the cardiac cells become replaced with abnormal tissue, such as scar tissue, causing muscle walls of the ventricles to become stiff so the relaxation (filling) phase is abnormal. Impairment of compliance (diastolic function)

Explain the aetiology/risk factors of pulmonary hypertension

● Pulmonary hypertension has a variety of causes o Idiopathic o Problems with smaller branches of the pulmonary arteries o Left ventricular failure o Lung disease (e.g. COPD, interstitial lung disease) o Thromboses/Emboli in the lungs ** Note: cor pulmonale is right heart failure caused by chronic pulmonary arterial hypertension

Recognise the signs of AAA on physical examination

● Pulsatile and laterally expansile mass on bimanual palpation of the abdominal aorta ● Abdominal bruit ● Retroperitoneal haemorrhage can cause Grey-Turner's sign ● Hypotension, tachycardia

Recognise the signs of tricuspid regurgitation on physical examination

● Pulse - irregularly irregular if AF ● Inspection o Raised JVP with giant V waves (which may oscillate the earlobes) o This is caused by transmission of high right ventricular pressures into the great veins o Giant A waves may also be present ● Palpation - parasternal heave ● Auscultation o Pansystolic murmur - heard best at lower left sternal edge o Louder on inspiration (Carvallo sign) o Loud P2 component of second heart sound ● Chest Examination may show signs of: o Pleural effusion o Causes of pulmonary hypertension ● Abdominal Examination may show: o distension o Palpable liver (tender, smooth and pulsatile) o Ascites o Jaundice ● Legs - pitting oedema

Recognise the signs of mitral regurgitation on physical examination

● Pulse may be irregularly irregular (if in AF) ● Laterally displaced apex beat with thrusting (due to left ventricular dilation) ● Pansystolic murmur o Loudest at apex beat o Radiating to the axilla o Soft S1 o S3 may be heard due to rapid ventricular filling in early diastole ● Signs of left ventricular failure in acute mitral regurgitation ● Mitral Valve Prolapse o Mid-systolic click o Late systolic murmur o The click moves towards S1 when standing and away when lying down

Recognise the signs of infective endocarditis on physical examination

● Pyrexia ● Tachycardia ● Signs of anaemia ● Clubbing ● Any new murmur or changing previous murmur ● Frequency of heart murmurs: o Mitral > Aortic > Tricuspid > Pulmonary ● Splenomegaly ● Vasculitic Lesions due to immune complex depositions o Roth spots on retina o Petechiae on pharyngeal and conjunctival mucosa o Osler's nodes (tender nodules on finger/toe pads) o Splinter haemorrhages o Glomerulonephritis ● Embolic phenomena: emboli may cause abscesses in different organs o Janeway lesions (painless macules on the palms which blanch on pressure) - JANE NO PAIN ON PALM **FROM JANE C Fever Roth Spots Osler's nodes Murmur Janeway Lesions Anaemia Nail - splinter hemorrhages Emboli Clubbing

Summarise the epidemiology of constrictive pericarditis

● RARE ● Documented in all ages ● 9% of patients with acute pericarditis will develop constrictive pericarditis ● TB has the HIGHEST TOTAL INCIDENCE out of all causes ● More common in MALES

Summarise the epidemiology of WPW syndrome

● Relatively COMMON ● Most common of the ventricular pre-excitation syndromes ● Found in ALL AGES ● More common in the YOUNG ● Prevalence decreases with age

Define mitral regurgitation

● Retrograde flow of blood from left ventricle to left atrium during systole due to mitral valve insufficiency § Mitral regurgitation (MR) may present with dyspnoea, usually on exertion, palpitations, and/or decreased exercise tolerance. § Typically presents as a holosystolic blowing murmur at the apex, radiating to axilla § Transthoracic echo is the diagnostic test of choice in identifying presence, severity, and mechanism of MR. § Surgical treatment is the best available treatment option,

Recognise the signs of pulmonary hypertension on physical examination

● Right ventricular heave ● Loud pulmonary second heart sound ● Murmur - pulmonary regurgitation ● Tricuspid regurgitation ● Raised JVP ● Peripheral oedema ● Ascites

Summarise the epidemiology of AAA

● Ruptured AAA:125 deaths per million in ages 55-59 ● AAA screening programme being introduced in UK - all males >65 - ultrasound scan ● Unruptured AAA: 3% of >50 yrs, male: female ratio 3:1

Generate a management plan for cardiac arrest

● SAFETY IS IMPORTANT o Approach any arrest scene with caution o The cause of the arrest may pose a threat o Defibrillators and oxygen are hazards ● Basic Life Support: o If the arrest is witnessed and monitored, consider giving a precordial thump (thump the sternum of the patient with the ulnar aspect of your fist) o Clear and maintain the airway with head tilt, jaw thrust and chin lift o Assess breathing by look, listen and feel ● If they are not breathing, give two rescue breaths o Assess circulation at carotid pulse for 10 seconds ● If absent - give 30 chest compressions at around 100/min ● Continue cycle of 30 chest compressions for every 2 rescue breaths o Proceed to advanced life support as soon as possible ● Advanced Life Support: o Attach cardiac monitor and defibrillator o Assess rhythm ● If pulseless ventricular tachycardia or ventricular fibrillation (shockable) rhythms - rhythms caused by aberration in electrical conduction system ▪ Defibrillate once (150-360 J biphasic, 360 J monophasic) ● Make sure no one is touching the patient or the bed ▪ Resume CPR immediately for 2 minutes and then reassess rhythm, and shock again if still in pulseless VT or VF ▪ Administer adrenaline (1 mg IV) after second defibrillation and again ever 3-5 mins ▪ If shockable rhythm persists after 3rd shock - administer amiodarone 300 mg IV bolus (or lidocaine) ● If pulseless electrical activity (PEA) or asystole (non-shockable rhythms) ▪ CPR for 2, and then reassess rhythm ▪ Administer adrenaline (1 mg IV) every 3-5 mins ▪ Atropine (3 mg IV, once only) if asystole or PEA with rate < 60 bpm o During CPR: ● Check electrodes, paddle positions and contacts ● Secure airway ▪ Once secure, give continuous compressions and breaths ● Consider magnesium, bicarbonate and external pacing ● Stop CPR and check pulse only if change in rhythm or signs of life ● Post cardiac arrest treatment o ABCDE approach o Controlled oxygenation and ventilation o 12 lead ECG o Treat precipitating cause o Temperature control/therapeutic hypothermia ● Treatment of REVERSIBLE causes o Hypothermia - warm slowly o Hypokalaemia and Hyperkalaemia - correction of electrolyte levels o Hypovolaemia - IV colloids, crystalloids and blood products o Tamponade - pericardiocentesis o Tension Pneumothorax - aspiration or chest drain o Thromboembolism - treat as PE or MI o Toxins - use antidote for given toxin

Recognise the presenting symptoms and signs of WPW syndrome

● SVT (supraventricular tachycardia) may occur in early childhood ● Often ASYMPTOMATIC - may be an incidental finding of an ECG ● Symptoms: o Palpitations o Light-headedness o Syncope ● Paroxysmal SVT may be followed by a period of polyuria, due to atrial dilatation and release of ANP ● Sudden death - if SVT deteriorates into VF ● Clinical features of associated cardiac defects (e.g. mitral valve prolapse, cardiomyopathy)

Define SVT (supraventricular tachycardia)

● SVT can be used to refer to any tachydysrhythmia arising from above the level of the Bundle of His, usually the atria or AV node. These typically produce a narrow complex tachycardia. ● A regular narrow-complex tachycardia (> 100 bpm) with no p waves and a supraventricular origin. o Technically, AF and atrial flutter counts as a type of SVT o However, SVT generally refers to: ● Atrioventricular Nodal Re-entry Tachycardia (AVNRT) ● Atrioventricular Re-entry Tachycardia (AVRT)

Recognise the signs of ventricular tachycardia on physical examination

● Signs are dependent on the degree of haemodynamic instability o Respiratory distress o Bibasal crackles o Raised JVP o Hypotension o Anxiety o Agitation o Lethargy o Coma

Recognise the signs of myocarditis on examination

● Signs of pericarditis ● Tachycardia ● Soft S1 ● S4 gallop ● Signs of complications (e.g. heart failure, arrhythmia)

Close-Up Images of hypertensive retinopathy

● Silver Wiring ● Arteriovenous nipping ● Flame Haemorrhages, Cotton Wool Exudates and Papilloedema **o Fundoscopy to detect hypertensive retinopathy. Keith-Wagner Classification of Hypertensive Retinopathy: § Grade I: Silver wiring (silver line down the middle of arterioles) § Grade II: Silver wiring + AV nipping (artery crosses the vein and nips it as it crosses, causing vein to become narrow due to high pressure in artery) § Grade III: Flame haemorrhage, sometimes cotton wool spots too § Grade IV: papilloedema (cannot see optic disc) - these can be either due to chronic hypertension or intracranial hypertension (caused by a brain tumour), requires admission

Recognise the signs of ischaemic heart disease on physical examination

● Stable Angina o Check for signs of risk factors ● ACS: o There may be NO CLINICAL SIGNS o Pale o Sweating o Restless o Distress o Low-grade pyrexia o Check both radial pulses to rule out aortic dissection o Pulse high or low o Arrhythmias o Disturbances of BP (high or low) o New heart murmurs o Signs of complications (e.g. acute heart failure, cardiogenic shock) o Signs of heart failure are increased JVP, 3rd heart sound, basal crepitations o Later, a pericardial friction rub or peripheral oedema may develop

Explain the aetiology and risk factors of aortic stenosis

● Stenosis can be secondary to rheumatic heart disease (MOST COMMON WORLDWIDE) ● Congenital: Calcification of a congenital bicuspid aortic valve, William's syndrome ● Calcification/degeneration of a tricuspid aortic valve in the elderly (senile calcification) **RF: § age >60 § congenitally bicuspid aortic valve § rheumatic heart disease § CKD

Meaning of stroke volume, cardiac output, preload, afterload and Frank-starling mechanism

● Stroke volume: the volume of blood pumped by the left ventricle in one contraction ● Cardiac output: the volume of blood pumped by the heart per minute (SV x HR) ● Preload: the filling pressure of the heart at the end of diastole (end diastolic volume) ● Afterload: the pressure against which the heart must work to eject blood in systole ● Frank-Starling Mechanism: the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return ⇒ Increased VR = increased EDV (preload) = increase SV

Define CABG

● Surgical procedure to restore normal blood flow to an obstructed coronary artery. ● Two approaches o Left internal thoracic artery is diverted to the left anterior descending branch of the left coronary artery o A great saphenous vein is removed from a long, one end is attached to the aorta (or one of its major branches) and other end to the obstructed artery immediately after the obstruction to restore blood flow ● Procedure: heart is stopped and blood pumped artificially by a machine outside the body (cardiac bypass). Patient's saphenous vein or internal mammary artery is used as the graft. Severeal grafts may be placed. >50% of grafts close in 10 years.

Summarise the prognosis for patients with ischaemic heart disease

● TIMI score (0-7) can be used for risk stratification o NOTE: TIMI = thrombolysis in myocardial infarction o High scores are associated with high risk of cardiac events within 30 days of MI ● Killip Classification of acute MI can also be used: o Class I: no evidence of heart failure - 6% 30 day mortality o Class II: mild to moderate heart failure (lung crackles, S3) - 17% 30 day mortality o Class III: over pulmonary oedema - 38% 30 day mortality o Class IV: cardiogenic shock - 81% 30 day mortality **%Poor prognostic factors: § age § development (or history) of heart failure § peripheral vascular disease § reduced systolic blood pressure § Killip class* § initial serum creatinine concentration § elevated initial cardiac markers § cardiac arrest on admission § ST segment deviation

Identify appropriate investigations for pulmonary embolism

● The Well's Score is used to determine the best investigation for PE ● If Well's 4 or less (1 or less if used simplified Well's score) o Do D-dimer ▪ If D-dimer negative: PE excluded ▪ If D-dimer raised: do CTPA ● If Well's >4 (>1 if using simplified score): do CTPA and start on LMWH ● Note: if CT is contraindicated (e.g. pregnancy): use V/Q scanning **Additional investigations: ▪ Bloods - ABG (low PaO2 and PaCO2), thrombophilia screen ▪ ECG ● May be normal ● May show tachycardia, right axis deviation or RBBB or right ventricular strain (inverted T in V1-V4) ● May show S1Q3T3 pattern (S waves in lead I, Q waves in III, Inverted T waves in III) ▪ CXR - often NORMAL but helps exclude other diagnoses May show oligaemia of affected segment, dilated pulmonary artery, linear atelectasis, small pleural effusion, wedge shaped opacities ● Spiral CT Pulmonary Angiogram - GOLD STANDARD o Poor sensitivity for small emboli o VERY sensitive for medium to large emboli ● Ventilation-Perfusion (VQ) Scan o Identifies areas of ventilation and perfusion mismatch, which would indicate an area of infarcted lung ● Pulmonary Angiography o Invasive o Rarely necessary ● Doppler US of Lower Limb - allows assessment of venous thromboembolism ● Echocardiography - may show right heart strain

Cardiac cycle

● The cycle can be divided into diastole & systole. Diastole is when ventricles are relaxed, and systole is when they contract and eject blood. The cycle is divided into 7 phases. ● 1 - Atrial contraction: atrial depolarisation. Pressure in atria causes AV valves to open. At end of this, ventricular volumes are maximal (end-diastolic volume) ● 2 - Isovolumetric Contraction: begins with ventricular depolarisation, when ventricle pressure > atrial pressure, AV valves close (1st heart sound). ● 3 - Rapid Ejection: ventricular pressure causes semilunar valves to open and there is rapid ejection of blood into aorta and pulmonary arteries. ● 4 - Reduced Ejection: ventricular repolarisation occurs, and rate of ejection falls. Atrial pressures start to rise due to venous return. ● 5 - Isovolumetric Relaxation: when ventricular pressure fall sufficiently low, semilunar valves close (2nd heart sound) ● 6 - Rapid Filling: when ventricle pressures < atrial pressure, AV valves open to start passive ventricular filling. ● 7 - Reduced Filling: ventricles continue to fill and expand, becoming less compliant as ventricular pressure rises.

The Heart Wall - Anatomy

● The heart wall can be divided into three layers: the endocardium, myocardium and epicardium. 1) Endocardium: ⇒ Innermost layer of cardial wall ⇒ Lines cavities and valves of the heart ⇒ Similar in composition to endothelium of blood vessels ⇒ ENDOCARDITIS: inflammation of endocardium, most commonly occurring on valves which endocardium lines. ● The subendocardial layers lies between the endocardium and myocardium 2) Myocardium ⇒ Composed of cardiac muscle - involuntary striated muscle ⇒ Responsible for contractions of the heart ⇒ MYOCARDITIS: inflammation of the myocardium ● The subepicardial layer lies between the myocardium and epicardium 3) Epicardium (visceral pericardium) ⇒ Outermost layer of the heart, formed by the visceral layer of the pericardium The pericardium consists of two layers: the outer tough fibrous pericardium and internal serous pericardium. The serous pericardium is further divided into the outer parietal layer and the internal visceral layer (aka epicardium) In between the outer and inner serous layer, is the pericardial cavity containing lubricating serous fluid to minimize friction as heart contracts. ⇒ Composed of connective tissue and fat ⇒ PERICARDITIS: inflammation of pericardium

Explain the aetiology/risk factors of arterial ulcers

● The ulcers are caused by a lack of blood flow to the capillary beds of the lower extremities ● Risk Factors o Coronary heart disease o History of stroke or TIA o Diabetes mellitus o Peripheral arterial disease (e.g. intermittent claudication, critical limb ischaemia) o Obesity and immobility

Explain the aetiology/risk factors of ventricular fibrillation

● The ventricular fibres contract randomly causing complete failure of ventricular function ● Most cases occur in patients with underlying heart disease ● Risk Factors: o Coronary artery disease - most common o AF o Hypoxia o Ischaemia o Pre-excitation syndrome o Cardiomyopathy o Drugs o Electrolyte imbalance

Explain the aetiology/risk factors for AAA

● There are NO specific identifiable causes ● Unruptured aneurysms occur due to degeneration of elastic lamellae and smooth muscle loss. ● Ruptured AAAs can leak into retroperitoneal space (relatively haemodynamically stable) or intraperitoneal space (likely to result in shock) ● Risk Factors o Severe atherosclerotic damage to aortic wall o Family history o Smoking o Male o Age o Hypertension o Hyperlipidaemia o Connective tissue disorders: Marfan's syndrome, Ehlers-Danlos syndrome o Inflammatory disorders: Behcet's disease, Takayasu's arteritis

Systemic and pulmonary circulation

● There are two primary circulatory loops - systemic and pulmonary circulation ⇒ Oxygenated blood arrives from the lungs via the pulmonary veins to the left atrium, then left ventricle via the mitral valve. It is pumped out to the body via the aorta, through the aortic valve. Deoxygenated blood arrives from the body via the vena cava to the right atrium, then right ventricle via the tricuspid valve. From here, it is pumped to the lungs via the pulmonary artery, through the pulmonary valve

RHS and LHS valves

● There are two types of valves in the heart: atrioventricular and semilunar valves On the left hand side, there is the mitral (AV) and aortic (SL) valve On the right hand side, there is the tricuspid (AV) and pulmonary (SL) valve

Explain the aetiology and risk factors of atrial fibrillation

● There may be no identifiable cause ('lone AF') ● Secondary causes lead to an abnormal atrial electrical pathway that results in AF ● Systemic Causes o Thyrotoxicosis o Hypertension o Pneumonia o Alcohol o Hypokalaemia o Hypomagnesemia ● Heart Causes o Mitral valve disease o Heart failure o Ischaemic heart disease, MI (seen in 22%) ● Lung Causes o Bronchial carcinoma o PE o Pneumonia ● Others: caffeine, alcohol, post-op ● Rare causes: cardiomyopathy, constrictive pericarditis, sick sinus syndrome, lung cancer, atrial myxoma, endocarditis, rheumatic heart disease, haemochromatosis, sarcoid ● Cardiac output drops by 10-20% as ventricles aren't primed reliably by atria. ● The main risk is embolic stroke. ● Atrial flutter o Ventricular rate is determined by the AV conduction ratio (degree of AV block) o The commonest AV ratio is 2:1, resulting in ventricular rate of 150bpm if atrial rate is 300 bpm o AV blocks of 3:1/4:1 occur due to medications/underlying heart disease

Explain the aetiology/risk factors of venous ulcers

● They are caused by incompetent valves in the lower limbs ● Valve incompetence leads to venous stasis and increased venous pressure ● This results in ulceration ● Risk Factors o Obesity o Immobility o Recurrent DVT o Varicose veins o Previous injury/surgery to the leg o Age

Summarise the epidemiology of pericarditis

● UNCOMMON ● < 1/100 hospital admissions ● More common in males

Ulcers are abnormal breaks in an epithelial surface and can be classified into...

● Ulcers are abnormal breaks in an epithelial surface and can be classified into: ⇒ Venous ⇒ Arterial: large vessel or small vessel ⇒ Neuropathic ⇒ Diabetic: neuropathic, arterial or both ⇒ Lymphoedema ⇒ Vasculitic ⇒ Malignant ⇒ Infective e.g. TB, syphilis ⇒ Traumatic: pressure ⇒ Pyoderma gangrenosum ⇒ Drug induced

Recognise the signs of cardiac arrest on physical examination

● Unconscious ● Not breathing ● Absent carotid pulses

Recognise the presenting symptoms of AAA

● Unruptured o NO SYMPTOMS o Usually an incidental finding o May have pain in the back, abdomen, loin or groin ● RUPTURED o Pain in the abdomen - intermittent or continuous; RADIATES to BACK, iliac fossae or groin o Pain may be sudden or severe o Syncope - low blood pressure o Shock ● NOTE: degree of shock depends on site of rupture and whether it is contained

Explain the aetiology/risk factors of myocarditis

● Usually IDIOPATHIC (50%) ● Viruses o Coxsackie B o EBV o CMV o Adenovirus o Influenza o Hepatitis o Mumps o Rubella o Polio o HIV ● Bacteria o Post-streptococcal o Tuberculosis o Diphtheria o Clostridia o Meningococcus o Mycoplasma o Brucellosis ● Fungal o Candidiasis ● Protozoal o Trypanosomiasis (Chagas disease) ● Helminths o Trichinosis ● Non-infective o Systemic: SLE, sarcoidosis, polymyositis o Hypersensitivity myocarditis: sulphonamides ● Drugs o Chemotherapy agents (e.g. doxorubicin, streptomycin) o Penicillin o Chloramphenicol o Sulphonamides o Methyldopa o Spironolactone o Phenytoin o Carbamazepine ● Others o Cocaine, heavy metals, radiation, toxins, vasculitis **autoimmune disease

Summarise the epidemiology of hypertension

● VERY COMMON ● 10-20% of adults in the Western world

Summarise the epidemiology of SVT

● VERY COMMON ● 2 x more common in FEMALES

Summarise the epidemiology of DVT

● VERY COMMON ● Especially in hospitalised patients

Summarise the epidemiology of venous ulcers

● VERY COMMON ● Increases with age

Summarise the epidemiology of vasovagal syncope

● VERY COMMON ● Syncope (of all causes) affects 40% of people

Summarise the epidemiology of atrial fibrillation

● VERY COMMON in the elderly ● Present in 5% of those > 65 years ● May be paroxysmal

Generate a management plan for ventricular fibrillation

● VF requires urgent defibrillation and cardioversion --> non-synchronised DC shock ● Patients who survive need full assessment of left ventricular function, myocardial perfusion and electrophysiological stability ● Most survivors will need an implantable cardioverter defibrillator (ICD) ● Empirical beta-blockers ● Some patients may be treated with radiofrequency ablation (RFA)

Identify the possible complications of infective endocarditis AND prognosis

● Valve incompetence ● Intracardiac fistulae or abscesses ● Aneurysm ● Heart failure ● Renal failure ● Glomerulonephritis ● Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen **Summarise the prognosis for patients with infective endocarditis ● FATAL if untreated ● 15-30% mortality even WITH treatment

Explain the aetiology/risk factors of vasovagal syncope

● Vasovagal syncope is a very common cause of fainting ● Can be precipitated by: o Emotions (e.g. fear, severe pain, blood phobia) o Orthostatic stress (e.g. prolonged standing, hot weather)

Identify possible complications of varicose veins AND prognosis

● Venous pigmentation ● Eczema ● Lipodermatosclerosis ● Superficial thrombophlebitis ● Venous ulceration ● Complications of Treatment o Sclerotherapy - skin staining, local scarring o Surgery - haemorrhage, infection, recurrence, paraesthesia, peroneal nerve injury **Summarise the prognosis for patients with varicose veins: ● Slowly progressive ● High recurrence rates

Summarise the indications for coronary angiography and PCI

● What is done o Sample blood to assess oxygen saturation and measure pressures o Inject radiopaque contrast medium to image cardiac anatomy and blood flow o Perform angioplasty (+/- stenting), valvuloplasty, and cardiac biopsies, or to do procedures o Perform intravascular ultrasound or echocardiography ● Indications o Coronary artery disease: diagnostic and therapeutic (angioplasty, stent insertion) o Valvular disease: diagnostic to assess severity, therapeutic (valvuloplasty if patient too ill for valve surgery) o Congenital heart disease: diagnostic and therapeutic (balloon dilatation) o Cardiomyopathy o Pericardial disease o Endomyocardial biopsy