Cardiovascular year 2(1)

what are 3 different macroscopic features of an atheroma?

fatty streak simple atheroma complex atheroma-Atheromas with ulceration and/or mobile components were defined as complex atheromas, according to a previously published definition.

Summarize the steps involved in calculating the mean QRS complex

Inspect limb leads I and II. If the QRS is primarily upward in both, then the axis is normal and you are done. If not, then proceed to the next step. Inspect the six limb leads and determine which one contains the QRS that is most isoelectric. The mean axis is perpendicular to that lead. Inspect the lead that is perpendicular to the lead containing the isoelectric complex. If the QRS in that perpendicular lead is primarily upward, then the mean axis points to the (+) pole of that lead. If primarily negative, then the mean QRS points to the (−) pole of that lead.

How might you investigate intermittent claudication?

- doppler ultrasonography -ABPI is the ratio of pressure in the foot compared to the arm. ABPI is usually greater than 1. An ABPI <0.9 suggests intermittent claudication and an ABPI of less than 0.5 indicates critical ischaemia. -Duplex scan- can show blood flow within vessels and any turbulence/ increased velocity which may be encountered with a stenosis. -angiogram

Describe the renin-angiotensin- aldosterone pathway in the regulation of blood pressure.

1) Decrease in the renal perfusion causes the JGA to produce the hormone renin. 2) Angiotensinogen produced by the liver is converted by renin into angiotensin I 3) ACE produced in the pulmonary endothelium causes angiotensin I to be converted into angiotensin II 4) angiotensin II has numerous effects: It increases sympathetic activity; increases the tubular NaCl and water rebsorption and K+ excretion; it causes vasoconstriction; increases aldosterone secretion from the adrenal glands and ADH secretion from the pituitary gland. 5) aldosterone is released from the zona glomerulosa of the cortex.

Describe the sequence of analysis of the ECG

1) check the voltage calibration- for some patients with increased QRS complexes (left ventricular hypertrophy or bundle branch blocks) this is adjusted so that the signals fit on the page. 2) check the rhythm- it may be a sinus bradycardia or tachycardia or arrythmia/ dysrhythmia 3) check the HR: if it is irregular then you should measure 30 large squares (6 seconds) and the amount of QRS complexes in the square and then x10 OR 1500/ number of small squares in the RR interval 4)Look at the intervals- PR, QRS and the QT -look at the P waves-are they regular? -PR interval should be less than 3-5 small squares -are they followed by a QRS complex? are these regular? -The QRS complex should be less than 3 small squares -do all the signals sit on the isoelectric line? -are there any P wave abnormalities? - are there abnormalities of the QRS wave (hypertrophy, bundle branch block or infarction. -are there any abnormalities of the ST segment or the T wave?

Describe CNS ischaemic response

1) severe decrease in blood flow to the brain causes cerebral hypoxia 2) the vasomotor centre is strongly stimulated 3) powerful constriction occurs due to the action of noradrenaline. 4) BP and blood flow increases

what triggers the secretion of aldosterone?

1)high potassium 2) angiotensin II

How would you diagnose tachyarrythmias on ECG?

1. Is the tachycardia regular? -regular- sinus tachycardia (ST), sinus node re-entry tachycardia, atrial tachycardia, AVRT (atrioventricular re-entrant tachycardia), AVNRT (AV node re-entrant tachycardia) -irregular- Atrial tachycardia or atrial flutter with variable block, AF 2. is the QRS broad (>120m/s) - suggests it is ventricular origin -SVT (sudden ventricular tachycardia)- young, no history of cardiac problems, normal ventricular function 3. Is there a P wave present? what is its morphology? normal P waves in sino-atrial tachyarrythmias, focal atrial tachyarrythmias near the sino-atrial nodes Abnormal p waves are seen in FAT, AVRT or AVNRT no P waves can be seen in AVRT and AVRT 2:1 or 3:1 Focal atrial tachycardia (FAT) or macro-re-entrant atrial tachycardia with AVN block P> 250 bpm in atrial flutter (macro-entrant tachycardia) 4. what is the response to adenosine or carotid massage? -terminated in AVNRT and AVRT -not terminated in macro-entrant tachycardia and FAT

Describe the placement of the limb lead electrodes and which are bipolar and unipolar leads

A complete eCG is produced by recording the electrical activity between the electrodes in specific patterns and this results in six reference axes of the bodys frontal plane (limb leads) and six in the transverse plane Limb leads are unipolar- aVR- positive deflection when it travels in the direction of the right arm aVL- positive deflection when moving to the left arm aVF-positive deflection when going tothe left leg bipolar- I-left arm to right arm II-right arm to left leg III- left arm to right leg

Describe the pathophysiology of hypertneson

A number of factors increase BP, including (1) obesity, (2) insulin resistance, (3) high alcohol intake, (4) high salt intake (in salt-sensitive patients), (5) aging and perhaps (6) sedentary lifestyle, (7) stress, (8) low potassium intake, and (9) low calcium intake. Furthermore, many of these factors are additive, such as obesity and alcohol intake. Variations in BP can be genetically determined and they are called "inherited BP," although we do not know which genes cause BP to vary;

What are the stages of fatty streak development?

A) The fatty streak develops as a result of endothelial dysfunction, lipoprotein entry and oxidation of LDL, leukocyte recruitment, and foam cell formation. B) Plaque progression is characterized by migration of smooth muscle cells into the intima, where they divide and elaborate extracellular matrix. The fibrous cap contains a lipid core. C) Hemodynamic stresses and degradation of extracellular matrix increase the susceptibility of the fibrous cap to rupture, allowing superimposed thrombus formation.

Describe the normal ventricular depolarisation shown by the limb leads

A. In the resting state, the surface is homogeneously charged so that the leads do not record any electrical potential. B. The first area to depolarize is the left side of the ventricular septum. This results in forces heading away from aVL (downward deflection on aVL recording) but toward the (+) region of aVF, such that an upward deflection is recorded by that lead. C. and D. Depolarization continues; the forces from the thicker-walled left ventricle outweigh those of the right, such that the electrical vector swings leftward and posteriorly toward aVL (upward deflection) and away from aVF. E. At the completion of depolarization, the surface is again homogeneously charged, and no further electrical forces are recorded.

Describe the orientation of the precordial (chest) leads

A. The cross-sectional plane of the chest. B. Arrangement of the six chest electrodes shown in the cross-sectional plane. Note that the right ventricle is anterior to the left ventricle.

what are the differnt characteristics of ulcers and the features you should look for? how do they differ in severity?

Edge- is it infected, ischaemic or have signs of granulation? Depth- how deep is it? Discharge- serous, serosanguinous (blood and serum) or purulent Local: cellulitis, pulses and neurology lymphnodes systemic: possibly RA?

Describe the different stages in the lifecycle of plaque development.

A. The fatty streak develops as a result of endothelial dysfunction, lipoprotein entry and modification, leukocyte recruitment, and foam cell formation. B. Plaque progression is characterized by migration of smooth muscle cells into the intima, where they divide and elaborate extracellular matrix. The fibrous cap contains a lipid core. C.Hemodynamic stresses and degradation of extracellular matrix increase the susceptibility of the fibrous cap to rupture, allowing superimposed thrombus formation.

what are the types of AV conduction disturbance? What causes them?

AVN (nodal) or His-Purkinje (infranodal) Atrial activation is conducted to the ventricles with a delay or not at all when not expected to be refractory Damage or fibrosis to the conduction system -LEV's disease can be idiopathic (hetart block due to fibrosis and calcification of the electrical conduction system); progressive (overtime there is greater fibrosis); part of the ageing process, seen in the elderly; or, it can be hereditary, presenting in younger patients. -IHD- heart attacks can lead to scar tissue formation in the conduction system (20% of those with heart attacks develop heart blocks). Cardiomyopathies and myocarditis can also cause heart block It is common cause for the insertion of a pacemaker. • Congenital • Neuromuscular disease • Conduction system fibrosis • IHD - acute infarction/ischaemia • Infection - endocarditis, myocarditis • Valvular - calcified aortic stenosis • Cardiomyopathy - haemochromatosis, amyloidosis, sarcoidosis • Hypothermia • Hypothyroid • Hyperkalaemia • Hypoxia • Trauma, cardiac surgery • Radiotherapy • CTD - SLE, scleroderma, RA • Anti-arrhythmics, BB, CCB

Describe the pathphysiology of atrioventricular re-entrant tachycardia

AVRT is a type of supraventricular tachyarrythmia. There are two pathways: the normal conduction pathway and the accessory pathway The accessory pathway is an extra pathway between the atria and the ventricles. Conduction can either be in an anterograde or retrograde. This depends on the timing of refractory period of the accessory pathway as well as the direction from which signals are coming towards the accessory pathway. The signal goes around causing tachyarrythmia. The most classical example of AVRT is wolf parkinson white syndrome. There is ventricular stimulation through the AV node and the accessory pathway. AV node slows the signal in the normal conduction pathway but this does not occur in the accessory. Shortened PR interval <0.12 secs (less than 3-5 small squares) and because there is depolarisation over a longer period of time then you get a delta wave (classical of WPW). When the signal passes back to the accessory then the myocardiocytes are no longer in a refractory period and you get the signal conducted around and around that you get in AVRT.

what are the three types of atrio-ventricular tachyarrythmias? what are there characteristics?

AVRT, AVNRT and junctional tachycardia They can be congenital arrythmias

what specific findings on ECG may help distinguish between a broad complex tachyarrythmia that is ventricular origin and one that is supraventricular in origin?

Absence of typical RBBB or LBBB morphology Extreme axis deviation ("northwest axis") Very broad complexes (>160ms) AV dissociation (P and QRS complexes at different rates) Capture beats — occur when the sinoatrial node transiently 'captures' the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration. Fusion beats — occur when a sinus and ventricular beat coincides to produce a hybrid complex. Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen. Brugada's sign - The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms Josephson's sign - Notching near the nadir of the S-wave RSR' complexes with a taller left rabbit ear. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller. Image shown- the first of the narrower complexes is a fusion beat (the next two are capture beats).

Describe the definition of an atheroma

An atheroma is the degneration of the walls of the arteries due to the formation in them of fatty plaques and scar tissue. It is the accumulation of degenerative material in the inner layer of the artery wall. The material containing macrophage cells, or debris, containing lipids, calcium and variable amounts of fibrous connective tissue. The accumulated material formas a swelling in the arterial wall which causes narrowing and restriction of blood flow. Atheroma formation occurs in atherosclerosis, one of the three subtypes of arteriosclerosis (which are atherosclerosis, mockenbergs arteriosclerosis and arteriolosclerosis) The plaque is divided into three distinct components: -The atheroma, which is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery -Underlying areas of cholesterol crystals -Calcification at the outer base of older or more advanced lesions.

Describe the main formas of peripheral vascular diesease

Arterial -atherosclerosis: an atheromatous lesion consists of a patch or a plaque of intima thickening due mainly to lipid accumulation, smooth muscle proliferation and the formation of fibrous tissue. -ischaemia Venous -Incompetence -hypertension

wha are the classifications of leg ulcers?

Arterial: -atherosclerosis -Burger's disease -vasculitis -raynauds Venous: -chronic venous insufficiency -varicous veins -post sclerotherapy lymphatic (chronic lyphedema)

what is the definition of arteriosclerosis?

Arteriosclerosis is the arterial wall thickening and the loss of elasticity of arteries Three patterns are recognised: -arteriolosclerosis: the thickening and hardening of smaller arterioles -Monckeberg medial sclerosis: or medial calcific sclerosis is seen mostly in the elderly, commonly in arteries of the extremities. -Atherosclerosis: narrowing of arteries from a build up of atheromatous plaque, usually made up of cholesterol, fatty substances, cellular waste products, calcium and fibrin, inside the arteries. This affects large and medium-sized arteries. a video explaining arteriosclerosis and atherosclerosis: https://en.wikipedia.org/wiki/Arteriosclerosis

What are the symptoms and signs of bradycardia

Asymptomatic- SV maintaining CO fatigue, muscle weakness and exercise intolerance confusion, pre-syncope, syncope hypotensive AF palpitations oligouria Heart failure.

Describe the typical findings you would see on a narrow complex tachycardia

Atrial Rate = 140 Ventricular Rate = 140 Rhythm = Regular QRS complex = 0.08 (2 small squares) P-R interval = 0.16 (4 small squares)

Describe the pathophysiology of AVNRT

Atrialventricular nodal re-entrant tachycardia (AVNRT) is a type of supraventricular tachyarrythmia. It is the commonest in those with a young, normal heart and has a benign prognosis. It causes severe palpitations in the neck. There is no re-entrant tachycardia and the mechanism involves only the AV node whereby local circuits are formed. Part of the AV node is fibrosed and this creates two pathways of conduction: a slow pathway through the diseased tissue and a fast pathway through the normal conduction tissue. The fast pathway has a longer refractory period than the slow pathway. The fast pathway is conducted first and passes to the ventricles, causing contraction and then entering the refractory period (which is longer) In the meantime the slow pathway is conducted and enters its shorter refractory period which ends sooner. If there is a premature beat that comes in when the fast track is recovering from the refractory period but the slow tract has finished. The slow pathway will allow conduction and if the fast pathway has finished its refractory period then you get the conduction going back up the fast pathway in a retrograde fashion which can then activate the slow pathway again causing a circuit which can cause repeat firing from the AV node causing a HR of around 100-250 bpm and the ECG will appear as a supraventricular tachycardia with narrow QRS (normal conduction in hte purkinje system) and a heart rate that is greater than 100bpm. Treatment: Ablation is curative- Your doctor uses heat, cold, or radio energy to scar some tissue inside your heart, where the irregular beats are triggered. The treated tissue helps get your heartbeat regular again. Some people with known AVNRT may be able to stop their attack by using various physical maneuvers to increase the activity of the vagus nerve on the heart (specifically on the atrioventricular node. These maneuvers include carotid sinus massage (pressure on the carotid sinus in the neck) and the Valsalva maneuver (increasing the pressure in the chest by attempting to exhale against a closed airway by bearing down or holding one's breath). Medical therapy can be initiated with medications that slow electrical conduction through the AV node of the heart such as adenosine (which is a form of pharmacologic cardioversion), beta blockers, or non-dihydropyridine calcium channel blockers (such as verapamil or diltiazem). Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma.

Describe the sequence of ventricular polarisation in lead I when the mean axis is +90

Because the mean axis is perpendicular to limb lead I, an isoelectric QRS complex (height of upward deflection = height of downward deflection) is recorded by that lead (see text for details). when the upward and downward deflections of a QRS are of equal magnitude, it is termed an isoelectric complex Thus, when an ECG limb lead inscribes an isoelectric QRS complex, it indicates that the mean electrical axis of the ventricles is perpendicular to that particular lead. Therefore, an easy way to determine the mean QRS axis is to glance at the six limb lead recordings and observe which one has the most isoelectric-appearing complex: the mean axis is simply perpendicular to it. the isoelectric complex appears in lead I; therefore, the next step is to inspect the perpendicular lead, which is aVF (see Fig. 4.5 if this relationship is not clear). Because the QRS complex in aVF is primarily upward, the mean axis points toward its (+) pole, which is in fact located at +90°.

how would you distinguish between an acute STEMI and a MI that happened months ago?

Both would show pathologic Q waves. However, in the case of an acute STEMI there would be a temporal sequence of ST and T wave abnormalities. The initial abnormality is the elevation of the ST segment, often with a peaked appearance of the T wave. At this early stage the myocardial cells are still viable and the Q waves have not yet developed. If the patient has successful acute coronary reperfusion (through thrombolytics and percutaneous coronary interventions) then the ST segments will return to baseline.

what is brugada?

Brugada syndrome (BrS) is a genetic disease that is characterised by abnormal electrocardiogram (ECG) findings and an increased risk of sudden cardiac death. It is an autosomal dominant condition with variable penetrance Na channel loss of function The pattern seen on the ECG is persistent ST elevations in the electrocardiographic leads V1-V3 with a right bundle branch block (RBBB) appearance, with or without the terminal S waves in the lateral leads that are associated with a typical RBBB. A prolongation of the PR interval (a conduction disturbance in the heart) is also frequently seen. The ECG can fluctuate over time, depending on the autonomic balance and the administration of antiarrhythmic drugs. Adrenergic stimulation decreases the ST segment elevation, while vagal stimulation worsens it

what is sinus tachycardia?

Can be induced by exercise etc and has a normal sinus rhythm It originates in the SA node

what are the short term mechanisms of control of blood pressure?

Changes in the blood pressure occurine within seconds or minutes occurs due to the: -autonomic nervous system -chemicals Rapidity of response, beginning within seconds and oftern increasing the pressure to greater than 2x normal in 5-10 secs. sudden inhibiton of the nervous cardiovascular stimulation can increase the arterial pressure by 3/2 times normal in 10-40 seconds. Nervous system- BP contol by changing the blood distribution around the body and the blood vessel diameter. sympathetic and parasympathetic nervous system affects the heart rate, contractility as well as the vessel diameter of veins and arteries. vasomotor centre: found in the medulla which sends efferent fibers to the smooth muscle of the blood vessels. Increased sympathetic activity leads to vasoconstriction and decreased sympathetic activity leads to the vasodilation. Baroreceptors in the carotid sinus (IX), the aortic body (X)and walls of the large arteries respond progressively to BP between 60-180mmHg. They respond more rapidly to changing pressure than stationary pressure. Nerve fibres from baroreceptors entered the medulla via the tractus solitarius. secondary signals inhibit the vasoconstrictor centre of the medulla and excite the vagal parasympathetic centre There is vasodilation of arterioles and veins and decreased HR and contractility. Therefore, the Excitation of the baroreceptors by high pressure in the arteries reflexely causes the arterial pressure to decrease as there is an increase in PR and CO From the cardioregulatory centre and the vasomotor centre the vagus nerve carries parasympathetic vagus efferents to the heart and sympathetic nerves pass to the sympathetic chain and then to the blood vessels and heart smooth muscle. Th vasomotor centre is a cluster of smooth muscle cells found within the medulla. It sends efferent motor fibres which innervate the smooth muscle of the blood vessels.

Describe cushings reaction to ischaemia

Cushings reaction is a special type of CNS ischaemic response 1) Increased pressure of CSF 2) increased intracranial tension 3) compression of whole brain and arteries inthe brain 4) CNS ischaemic response is initiated and the arterial pressure continues to rise. 5) relief of brain ischaemia but pressure continues to rise- compression of the brain parenchyma Cushings triad is defined as an increase in systolic BP, decrease in heart rate and decrease in respiratory rate. This is the opposite to shock (increase HR and RR and decrease BP)

Describe the normal depolarisation shown by the chest leads

Depolarization begins at the left side of the septum. The electrical vector then progresses posteriorly toward the thick-walled left ventricle. Thus, V1, which is an anterior lead, records an initial upward deflection followed by a downward wave, whereas V6, a posterior lead, inscribes the opposite. E. In the normal pattern of the QRS from V1 to V6, the R wave becomes progressively taller and the S wave less deep.

what are the properties of class V anti-arrythmics?

Digoxin • Slows conduction through AVN • Increase vagal activity leads to an increase in ACh production, stimulating AVN M2 receptors Adenosine • AVN blocking and slowing • Terminate SVT, reduction of junctional tachycardias • Very short t1 /2 • Side effects - chest tightness, "impending dome"

What are the clinical complications of peripheral vascular disease?

Due to embolic events-cardiac events cerebral events (stroke, TIA's) peripheral vascular disease- aortic aneurysma and peripheral ischaemia chronic limb ischaemia -persistent pain at rest that requires regular adequate analgesia for at least two weeks, with resting ankle pressure of less than 50mmHg. Presence of gangrene/ ulcer on the foot/ toes with the same resting pressure stages: I) asymptomatic II) intermittent claudication limiting lifestyle III) rest pain due to ischaemia IV) ulcer/ gangrene due to ischaemia (fontaine classification) acute limb ischaemia- there is a sudden lack of blood flow either caused by an embolism (people presenting with symptoms for less than 2 weeks). 6 P's -pain -pallor -parasthesias -pulselessness -perishingly cold -paralysis Eventually it may lead to amputation.

how many sec does a small square and large square represent on ECG?

ECG recording speed is 25mm/sec and therefore each small square is 0.04 secs and the larger square is 0.2seconds.

how would you treat venous incompetence?

Endovenous lazer ablation and radiofrequency ablation (EVLA and RFA) Endovenous ablation is an image-guided, minimally invasive treatment for varicose veins. It uses radiofrequency or laser energy to cauterize (burn) and close the varicose veins.

what is essential hypertension?

Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes such as renovascular disease, renal failure, pheochromocytoma, aldosteronism, or other causes of secondary hypertension or mendelian forms (monogenic) are not present. Essential hypertension accounts for 95% of all cases of hypertension. Essential hypertension is a heterogeneous disorder, with different patients having different causal factors that lead to high BP. Essential hypertension needs to be separated into various syndromes because the causes of high BP in most patients presently classified as having essential hypertension can be recognized.

what may cause endothelial dysfuncntion in the formation of atheroma?

Exposure to toxic chemical environment- higher leves of circulating lipids, chemicals from tobacco smoke and diabetes. Also haemodynamic stresses. All of these promote the formation of reactive oxygen species- superoxide anion- which interact with the intracellular molecules to influence metabolic and synthetic function of the endothelium, promoting local inflammation.

Describe what is meant by a fatty streak and the characteristics of this

Fatty streaks are the earliest visuble lesions of atherosclerosis and they appear as yellowish discolourations on the lining of vessels, however they do not impede blood flow. They do not cause symptoms and in some regions they may regress over time. FORMATION endothelial dysficntion (haemodynamic stress or chemical irritants) allows the entry and the modification of lipids which act as pro-inflammatory mediators which initiate leukocyte reacruitment and foam cell formation- the pathological hallmarks of a fatty streak.

Describe the different grades of retinopathy?

Grade 1- toruosity (twisting) of retinal arteries with increased reflectiveness (silver wiring) Grade 2: grade 1 + AV nipping (thickened areteries passing over rentinal veins) Grade 3: Grade 2 + flame haemorrhage and cotton wool exudates (due to small infarct) Grade 4: Grade 3 plus papilloedema (blurry margin of the optic disc)

Describe the homeostasis of cholesterol

HMG-CoA reductase is the rate limiting step in the synthesis of cholesterol denovo and is increased when intracellular cholesterol is low. When cholesterol is in excess, there is efflux to the lipid-poor circulating Apo-AI (synthesised by the liver and the intestines) Free cholesterol is acquired by HDL. Most cholesterol esters in HDL can ve exchanged in the circulating with any Apo-B containing lipoproteins (VLDL, IDL and LDL) which transport cholesterol back to the liver. HDL can also transport cholesterol to the liver and steroid producing tissues.

what is the definition for tachycardia?

HR greater than 100bpm

Explain the vascular causes of tissue hypoxia. Can the peripheral tissue become hypoxic even if there is adequate blood supply?how has this prompted a new definition of hypoxia?

Hypoxia is the presenceof tissue PO2 levels which are low enough to have an adverse effect on the tissue Yes, Hypoxic hypoxia is due to the low PO2 (lung disease) Anaemic hypoxia is due to the inadequate tissue oxygen delivery by haemoglobin and can result from anaemia (low iron) or carbon monoxide poisoning. circulatory hypoxia is inadequate blood flow to the tissue reulting in a critical fall in the tissue oxygen levels. It can affect either the whole body (cardiogenic shock) or can be localised (for example single limbs where a torniquet has been fitted. Histotoxic hypoxia- can be due to cyanide poisoning. Cyanide inhibits the enzyme cytochrome oxidase int he ECT and results in oxygen being unable to combine with hydrogen in the final stage. This prevents oxidative phosphorylation. In this case the PaO2 is normal or elevated. NEW DEFINITION- hypoxia is present when oxidative phosphorylating stops due to the inadequate oxygen utilisation. vascular causes of hypoxia: hypotension- bleeding, arrhythmias, cardiogenic shock, sepsis, cardiac tamponade Infarction/ thromboembolism peripheral vascular disease

Describe the complications of atherosclerosis

If a plaque ruptures there may be formation of the blood clot Occlusion of an artery of more than 70% causes ischaemia and cellular injury downstream Coronary arteries- angina Internal carotid or middle cerebral- stroke Popliteal- intermittent claudication and gangrene Renal- tricks kidney into thinking there is poor perfusion and activates the RAAS system and causes hypertension

what conditions may affect the QT interval?

If the QT is less than half the distance between two consecutive QRS complexes, then it is in the normal range It is decreased in hypercalcaemia and tachycardia It is increased in hypocalcemia, hypokalaemia, hypomagnesem and myocardial ischaemia, congenital prologation of the QT and toxic drug effect (antiarrythmic drugs)

how does the activation of the endothelial cell allow the passage of lipoproteins into the cell wall? how does hypertension exacerbate tis effect?

Increased permeability of the activated endothelial cells which can no longer serve as a barrier to the to the passage of circulating lipoproteins. LDL passes into the intima, which is facilitated by high levels of circulating LDLs. Accumulation of lipids in the endothelial space occurs by the binding of ECM (proteoglycans). The increased residence time allows for the chemical modification of the lipoprotein, critical to the development of the atheroma. Hypertension promotes the retention of lipoproteins in the intima by accentuating the binding of LDL binding proteoglycans to smooth muscle cells.

what are the characteristics of 1st, 2nd (type I and II) and 3rd degree heart block?

In a first degree heart block every stimulus is conducted to the ventricles; a prolonged PR interval of greater than >200ms (more than 3-5 large boxes) is seen on ECG. There are usually no symptoms and treatment may involve identifying electrolyte imbalances or sometimes no further treatment may be necessary. In a second degree heart block (mobitz type I, wenckebach) the PR interval prolongs until the P wave is blocked completely and you get a 'dropped beat' where the signal is not conducted to the ventricles (no QRS complex after P wave. As time increases, say after 2 seconds, the ventricular pacemaker cells take over and you will get a ventricular escape beat. Usually there are no symptoms although sometimes the patient may experience light headedness, dizziness and syncope. Mobitz type II- Similar to type I as you get intermittent dropped beats although they happen randomly and there is no gradual lengthening of the PR interval. There is usually a ratio of conducted: dropped beats and they are sometimes expressed as 2:1 mobitz type II AV block. Symptoms are present and can include dyspnoea, fatigue, chest pain and syncope. 3rd degree occurs when there are no signals being conducted to the ventricles and therefore you get regular P waves with random escape beats coming from the ventricles that struggle along at approximaely 30 beats per minute. Symptoms are always present and include syncope, confusion, dyspnoea and severe chestpain. Patients with this type of heart block are at risk from dying. When someone has AV block it is important to identify the underlying cause and treat it e.g. by stopping a medication or treating the infection. Transcutaneous pacing through electrodes on the skin of permanent pacemakers to monitor the rhythm (if it detects a delay it sends impulses to allow the ventricles to contract regularly).

Describe the characteristics and pathophysiology of Atrial fibrilation

In atrial fibrilation there are unorganised conduction waveforms in the atria which leads to atria spasming. As a result the AV node is being stimulated erratically leading to irregular contraction In atrial fibrilation the rhythm is said to be irregularly irregular and there are no distinct P waves due to atrial spasms. Instead there are squiggly lines showing the spasming. Atrial fibrillation is common and its incidence increases with age. Co-ordinated function is lost and there is a rapid, irregular ventricular rate and the atria dilate. Atrial fibrillation results from diseased atrial tissue: -age -inflammation: from cardiac surgery, myocarditis and pericarditis etc. -enlarged atria- high blood pressure, valve disease, lung disease (COPD) and previous Afib, IHD Hormonal abnormalities such as hyperthyroidism Metabolic- obesity Alcohol abuse Patients that have recently suffered from AF are at risk of clot formation in the atria due to the pooling blood which can increase the risk of stroke. Thereby, patients tend toe be put on blood thinners. • Irregularly irregular rhythm. • No P waves. • Absence of an isoelectric baseline. • Variable ventricular rate. • QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction. • Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm). • Fibrillatory waves may mimic P waves leading to misdiagnosis. https://www.youtube.com/watch?v=6FLE6HWiImM

Describe the different lipoproteins and the components of liprotein transport system

In order of increasing density: chylomicrons, VLDL, ILDL, LDL, HDL Exogenous pathway: Dietary fats are absorbed by the small intestine and repackaged as chylomicrons, accompanied by apo B-48. Chylomicrons are large particles, particularly rich in triglycerides, that enter the circulation via the lymphatic system. Apo E and subtypes of apo C are transferred to chylomicrons from HDL particles in the bloodstream. Apo C (subtype CII) enhances interactions of chylomicrons with lipoprotein lipase (LPL) on the endothelial surface of adipose and muscle tissue. This reaction hydrolyzes the triglycerides within chylomicrons into free fatty acids (FFA), which are stored by adipose tissue or used for energy in cardiac and skeletal muscle. Chylomicron remnants are removed from the circulation by the liver, mediated by apo E. One fate of cholesterol in the liver is incorporation into bile acids, which are exported to the intestine, completing the exogenous pathway cycle. Endogenous (Hepatic) Pathway: Because dietary fat availability is not constant, the endogenous pathway provides a reliable supply of triglycerides for tissue energy needs: The liver packages cholesterol and triglycerides into VLDL particles. The triglyceride content of VLDL is much higher than that of cholesterol, but this is the main means by which the liver releases cholesterol into the circulation. VLDL is catabolized by LPL (similar to chylomicrons, as described in step 3), releasing fatty acids to muscle and adipose tissue. During this process, VLDL also interacts with HDL, exchanging some of its triglyceride for apo C subtypes, apo E, and cholesteryl ester from HDL. The latter exchange (important in reverse cholesterol transport, as described in the next section) is mediated by cholesteryl ester transfer protein (CETP). Approximately 50% of the VLDL remnants (termed intermediate-density lipoproteins [IDL]) are then cleared in the liver by hepatic receptors that recognize apo E. The remaining IDL is catabolized further by LPL and hepatic lipase (HL), which remove additional triglyceride, apo E, and apo C, forming LDL particles. Plasma clearance of LDL occurs primarily via LDL receptor-mediated endocytosis in the liver and peripheral cells, directed by LDL's apo B-100 and apo E.

Describe the ECG evolution that occurs during an acute ST elevation myocardial infarction.

In patients that do not ahieve successful reperfusion myocytes begin to die and this causes a loss of amplitude of the R waves and Q waves begin to be inscribed. During the first few days of infarction the ST segment remains elevated, the T wave inverts and the Q wave deepens. Several days later the T wave remains inverted and the pathological Q waves persist but the ST segment will return to its normal level. Persistence of the Q waves is a permanent marker of MI. If the ST segment is elevated weeks later is likely that a bulging fibrotic scar (ventricular aneurysm) has developed at the site of infarction.

how would you distinguish right ventricular hypertrophy from posterior infarction?

In posterior infarction and right ventricular hypertrophy there are large R waves. However, right ventricular hypertrophy has right axis deviation.

what are the neural factors involved in the regulation of blood pressure?

Increased discharge of sympathetic nerves causes vasoconstriction decreased discharge from the sympathetic nerves and the activation of symapthetic cholinergic vasodilator nerves causes decreased blood vessel tone.

Describe the aetiology of bradycardia

Intrinsic: -iodpathic degeneration (young) -Infiltrative (sarcoid, amyloid and haemochromatosis) -collagen vascular disease- SLE, RA and scleroderma -myotonic muscular dystrophy -Trauma- valve, transplant -congenital -Infectious disease- diptheria, Chagas or endocarditis Extrinsic: -training and athletes -vasovagal syncope, carotid sinus hypersensitivity, vomiting and pain -negative chronotropic drugs- Beta blockers, calcium channel blockers, amiodarone -Electrolyte: hypo and hyperkalaemia -Metabolic: anorexia, hypothyroid and hypothermia -neurological- ICP -Obstructive sleep apnoea

how does NO produced by endothelial cell act as an anti thrombotic agent?

It acts as a vasildilator, an inhibitor of platelet aggregation and an anti-inflammatory agent.

what is arrythmogenic right ventricle dysplasia?

It i caused by genetic defects of the proteins that form desmosomes (interconnecting proteins) It is a type of nonischaemic cardiomyopathy and is characterised by hypokinetic areas involving the free wall of the right ventricle and fibrofatty replacement of the right venricle myocardium that is associated with arrythmias of the right ventricular myocardium and worsening RV function It is an important cause of arrythmias in adults and children The most common ECG abnormality is T wave inversion in leads V1 to V3 although this finding is non-specific. RBBB due to delayed activation of the right ventricles epsilon wave- terminal notch in the QRS wave due to slowed intraventricular condction

Describe the formation of acute non-ST elevation MI. What are the characteristic eatures that are observed on an ECG?

It is a more limited type of infarction which results from a partially occlusive thrombus. There is ST segment depression and/ or T wave inversion rather than elevation that overlies the infarcting myocardia. The extent of myocardial damage is less than in STEMI involving only the subendocardiallayers of the myocardium. As a result, the pathological Q waves do not develop because the remaining viable cells are able to generate some elctrical activity.

what is the definition of atherosclerosis?

It is a slowly progressive disease of large-to-medium sized muscular and elastic arteries. Lesions are characterised by intimal based plaques, usually made up of cholesterol, fatty substances, cellular waste products, calcium and fibrin, inside the arteries.

Describe the characteristics of the focal atrial tachycardia

It is a type of atrial tachycardia narrow complex tachycardia with irregular atrial rhythm and HR is greater than 100 It occurs when the atria are enlarged; HF, COPD coronary heart disease although it is also seen in those without increased atria. Risk factors include increased calcium in the cardiac myocytes which leads to spontaneous calcium release and untimely depolarisation (e.g. during the refractory period. Several pathological processes can cause this: hypokalaemia, hypomagnesemia, hypoxia, acidaemia ( seen in sepsis, MI and COPD) Focal atrial tachycardia occurs when the atrial cells are firing rather than the sino-atrial node and this usually occurs in paroxysmal bursts. It can occur in normal or abnormal hearts and may terminate with adenosine. On ECG you will see a HR greater than 100, more than 3 different types of P wave morphology and PR interval variation. There are also narrow QRS complexes (less than 0.12 secs) which suggests that the abnormality is coming from the atria. The QRS complexes are usually preceded by an abnormal P wave. Treatment is symptomatic or incessant-Beta blockers or calcium channel blckers. Class Ic antiarrythmics (flecainide or propafenone) or class III (amiodarone or sotalol) may suppress. RFA is a cure

Describe the abnormalities seen on ECG with fascicular blocks (both anterior and posterior)

Left anterior fascicular block: Left ventricular activation behins via the left posterior fascicle alone, the the posterior papillary muscle and spreads to the rest of the ventricle. Because the left posterior fascicle first activates the posterior, inferior, medial region of the left ventricle, the initial impulses are directed downward (i.e., toward the feet) and toward the patient's right side there is a positive deflection (initial small R wave) in leads II, III and aVF. As depolarization then spreads upward and to the left, toward the "blocked" anterior, superior, and lateral regions of the left ventricle, a positive deflection (R wave) is inscribed in leads I and aVL, while a negative deflection (S wave) develops in the inferior leads. The predominance of these leftward forces, resulting from the abnormal activation of the anterior superior left ventricular wall, results in left axis deviation (generally more negative than −45°). Left posterior fascicular block is less common and the ventricular activation begins in via the left anterior fascicle at the base of the anterior papillary muscle. There is an upward deflection (positive R wave) in the lateral lead (1 and aVL) and posterior deflection (negative S wave) in the inferior leads II, III and aVF as there is depolarisation of the aterosuperior left ventricular region. As the impulse then spreads downward and to the right toward the initially blocked region, an S wave is inscribed in leads I and aVL, while an R wave is recorded in leads II, III, and aVF. Because the bulk of these delayed forces head toward the patient's right side, right axis deviation of the QRS mean axis occurs There is no widening of the QRS as seen in left and right bundle branch blocks. Also, although LBBB and RBBB it is the chest leads you analyse for abnormalities, in anterior and posterior it is the limb leads that are the most helpful.

what is Long QTsyndrome?

Long QT syndrome (LQTS) is a rare congenital or acquired heart condition in which delayed repolarization of the heart following a heartbeat which increases the risk of torsades de pointes (TdP)- a form of irregular heartbeat that originates from the ventricles. These eposodes may lead to fainting or sudden cardiac death due to VF. The condition is named for the appearance of the electrocardiogram (ECG/EKG) on which a prolongation of the QT interval occurs. Normally, the QT interval duration is between 350 and 440 milliseconds. In some individuals, the QT prolongation occurs after the administration of certain medications (antiarryhtmics such as flecainide, sotalol and smiodarone), which may be dangerous. In addition to medications, long QT syndrome can be acquired from too low blood potassium or low blood magnesium, as in anorexia nervosa, antihistamines, antidepressants, antipsycochitcs, hypothermia, hypothyroid

Describe the differences in an atherosclerotic arterial wall

Noxious elements can disturb the normal homeostasis and pave a way for atherogenesis. endothelial and smooth muscle can be activated by inflmmatory mediators such as IL-1 and TNF-a but they also produce them when activated- therefore its not just immune cells that produce these cytokines. Realising this has led to investigation of endothelil cells and smooth muscle cells in artherogenesis. Several components play a part int he inflammatory process including endothelial cell dysfuncion, accumulation of lipids in the intima, recruitment of leukocytes and smooth muscle cells to the vessel wall, formation of foam cells (as macrophages take up oxidised LDL's) Various cells interact and compete with eachother in the formation of a fatty streak. 1) accumulation of lipids in the intima 2) oxidative stress due to the oxidation of LDL which induces local cytokine elaboration 3) cytokines produced cause increased expression of adhesion molecules (Monocyte chemoattractant protein-1 or MCP-1) that allows for the migration of leukocytes into the intima. 4) After the monocytes enter the cell wall in response to chemoattractants molecules (MCP-1) they encounter stimuli such as macrophage colony-stimulating factor (M-CSF) that augment their expression of scavenger receptors. 5) scavenger receptors mediate the uptake of modified lipoprotein particles and they promote the development of foam cells. Macrophage foam cells are a source of additional cytokines and effector moleules such as superoxide anion and matrix metalloproteinases. They release their contents when theu die and this creates an extracellular lipid core towards the inner surface of the plaque) 6) Smooth muscle cells migrate into the intima from the media. Note the increasing intimal thickness. 7) Intimal smooth muscle cells proliferate and elaborate extracellular matrix, promoting matrix accumulation in the growing atherosclerotic plaque. In this manner, the fatty streak evolves into a fibrofatty lesion. There is recruitment of T cells and lipid accumulation. 8) In later stages, calcification can occur (not depicted) and fibrosis continues, sometimes accompanied by smooth muscle cell death (including programmed cell death, or apoptosis), yielding a relatively acellular fibrous capsule surrounding a lipid-rich core that may also contain dying or dead cells. IL-1, interleukin 1; LDL, low-density lipoprotein are all released.

what are the main intervals you should look for in an ECG?

PR interval is the beginning of the P wave to the beginning f the QRS QT is the beginning of the QRS to the end f the T The QRS- from beginning to the end of the QRS wave

what are the common conditions associated with abnormal PR, QRS and QT intervals

PR- the beginning of the P wave to the start of the QRS and is normally 3-5 small boxes increased in: first degree AV block Decreased in pre-excitation syndrome and junctional rhythm

Describe the common abnormalities of the Q wave

Pathological Q waves are associated with one type of myocardial infarction: STEMI When there is infarction and tissue necrosis (due to coronary vessel occlusion) small Q waves are often seen in aVF and v6 due to septal depolarisation. Compared to the small P waves seen in a normal depolarisation, pathologic Q waves are prominent and they are greater than 1 small square and have a depth greater than 25% of the total height of the QRS complex.

what are the clinical features and commonly encountered complications of essential hypertension?

Quite often, there will be no clinical symptoms. However, hypertension may cause headaches and have a negative impact on memory and mental function. In an emergency: CNS perfusion issues and epileptic fits Heart failure and ischaemia Stroke, visual loss and pulmonary oedema End organ damage: damage to large vessels, small vessels, damage to the eye, damage to the heart and the kidneys

What is the possible cause of ventricular tachycardia in a normal heart?

Right ventricular outflow tract (RVOT) tachycardia is a form of monomorphic VT originating from the outflow tract of the right ventricle or occasionally from the tricuspid annulus. It is usually seen in patients without underlying structural heart disease, although may also occur in the context of arrhythmogenic right ventricular dysplasia (ARVD). it is associated with two conditions: idiopathic VT and arrythmogenic right ventricular dysplasia- an inherited myocardial disease with associate paroxysmal ventricular arrythmias and sudden cardiac death. It is characterised by pathological fibrofatty replacement of the right ventricular myocardium. Diagnostic features: Heart rate > 100 bpm. QRS duration > 120 ms. LBBB Morphology. Rightward / inferior axis (around +90 degree). Atrioventricular dissociation. palpitations with exercise treatment with verapamil or BB- RFA curative exlude arrythmogenic right ventricle cardiomyopathy

what are the pathophysiological causes of bradycarda?

SA node may be slowed or absent -junctional rhythms occur when the AV node takes over the pacemaker activity. However, the AV node is less efficient than the SA node and this leads to decreased HR (50). If both the SA and the AV node are not functioning then you get ventricular escape rhythms starting from the purkinje system and this causes the HR to be even lower (approximately 25)

Describe the characteristics of sick sinus syndrome/ sino-atrial disease

Sick sinus disease is also called sino-atrial disease or sinus dysfunction, is a subset of arrythmias caused by the malfunction of the sino-atrial node. Sinus bradycardia occurs when the resting heart rate is less than <60bpm Chonotropic incompetence Sinus pauses, sinus arrest and sino atrial exit block AV conduction disturbances paroxysms atrial or junctional tachyarrythmias -Disorders that cause scarring, degeneration, or damage to the sinoatrial node can cause sick sinus syndrome, including sarcoidosis, amyloidosis, hemochromatosis, Chagas' disease, and cardiomyopathies. -Age related degeneration and fibrosis -Ischaemia and infarction (supplied by the RCA) -Excessive vagal stimulation -Myocarditis -It can be caused or worsened by medications such as digoxin, calcium channel blockers, beta-blockers, sympatholytic medications, and anti-arrhythmics. -Congenital SSS can be due to mutations of the gene responsible for formation of Alpha subunit of sodium channel but this is rare. ECG changes are used to diagnose sick sinus syndrome and may show any of the following: Inappropriate sinus bradycardia Sinus arrest Sinoatrial block Tachy-Brady Syndrome- often seen in those with atrial fibrilation- Atrial fibrillation with slow ventricular response

Describe the main risk factors for PVD

Smoking Diabetic (obesity) hypertension (obesity) family history male age- older patients

what does the P wave represent and how would the abnormalities be shown on an ECG

The P wave represents superimposition of right atrial (RA) and left atrial (LA) depolarization. It is best visualised in lead II as it is the most parallel to the electrical conductance. RA depolarization occurs slightly earlier than LA depolarization. In RA enlargement, the initial component of the P wave is prominent (>2.5 mm tall) in lead II. In LA enlargement, there is a large terminal downward deflection in lead V1 (>1 mm wide and >1 mm deep). Normally, V1 inscribes a P wave with an initial positive deflection reflecting right atrial depolarization (directed anteriorly), followed by a negative deflection, owing to the left atrial forces oriented posteriorly to the right atrium Left atrial enlargement is therefore manifested by a greater-than-normal negative deflection (at least 1 mm wide and 1 mm deep) in lead V1

Describe the position of the SAN and AVN and the blood supply to the electrical conduction system

The SA node is high in the lateral right atrium below the SVC. Blood supply to the to SA node is supplied by the RCA. The AVN is anterior to the coronary sinus and superior to the tricuspid valve. Sinus node & atrioventricular (AV node) nodal arteries: originates from the right coronary artery Sinus nodal artery: supplies the right atrial myocardium. https://www.slideshare.net/ramachandrabarik/blood-supply-to-cardiac-conduction-system

Describe the typical findings that you would see on ECG when there is broad complex tachycardia

The atrial rate is undetectable as there are no P waves Ventricular rate of 220 Rhythm- regular QRS- wide (e.g. 0.2 secs or 4 small squares There are no P waves and therefore no PR interval

Describe the changes that take place when blood pressure falls

The baroreceptors are inhibited There are fewer impulses to the brain Decreased parasympathetic and increased sympathetic the heart increases contractility, vessels undergo vasoconstriction and there is increases release of epinephrine from the adrenal glands.

Describe the cardiac action potential

The cardiac cells show automacity (spontaneously depolarising) and do not rely on the nervous system. Inward positive ion flow occurs during diastole and these are spread via the gap junctions. 4- Na+, Ca2+ channels are closed and K+ rectifier channels are open, keeping the TMP stable at -90mV. 0- Rapid Na+ influx through the open fast sodium channels 1-Na+ channels close and the K+ channels open and there is K+ efflux (early rapid repolarisation) 2- Influx of calcium through the L-type calcium channels and this is balanced through the K+ efflux through the delayed rectifier K+ channels (olateau phase) 3- Ca2+ channels close but delayed rectifier K+ channels remain open and return the TMP to -90mV (late rapid repolarisation) which returns the membrane potential to -90mV

Describe the location of the chemoreceptors and their function in maintaining BP

The carotid bodies are located on the external carotid arteries near their bifurcation with the internal carotids. They are supplied by the glossopharyngeal nerve. Hypoxemia, hypercapnia and acidosis lead to an increase in carotid body receptor firing. When hypoxemia results in a PO2 lower than about 80 mmHg (threshold PO2), receptor firing is stimulated (normal arterial PO2 is about 95 mmHg). Any elevation of PCO2 above a normal value of 40 mmHg, or a decrease in pH below 7.4 causes receptor firing. central chemoreceptors are in the venterolateral medullary surface in the vicinity to the exit of the 9th and 10th cranial nerves and are sensitive to pH in their environemt. They detect pH change in the CSF fluid that are indicative of altered oxygen or carbon dioxide concentrations available to brain tissues. An increase in carbon dioxide causes tension of the arteries, often resulting from decreased CO2 output (hypercapnia), indirectly causes the blood to become more acidic; the cerebral spinal fluid pH is closely comparable to plasma, as carbon dioxide easily diffuses across the blood/brain barrier. However, a change in plasma pH alone will not stimulate central chemoreceptors as H+ are not able to diffuse across the blood-brain barrier into the CSF. Only CO2 levels affect this as it can diffuse across, reacting with H2O to form carbonic acid and thus decrease pH. Central chemoreception remains, in this way, distinct from peripheral chemoreceptors. Chemoreceptor activity, however, also affects cardiovascular function either directly (by interacting with medullary vasomotor centers) or indirectly (via altered pulmonary stretch receptor activity). Stimulation of the cardioacceleratory and vasomotor centre causes increased CO. HR and vasoconstriction BP is increased (speeding the return of the blood to the heart and lungs)

what dies left and right axis deviation mean?

The mean QRS axis represents the average of the instantaneous electrical forces generated durin the ventricular depolarisation as measured in the frontal plane. The normal value is between -30 and +90 A mean axis more negative than -30 is called a left axis deviation and greater than +90 represents right axis deviation. To determine whether the axis is normal or abnormal, examine the QRS complexes in limb leads I and II. The QRS is primary positive in both the of these leads (the upward deflection is greater than the downward deflection. If it is not upward then the axis is abnormal and the approximate axis should be identified by a more precise method.

Describe the structure of a normal arterial cell wall

The tunic intima consists of endothelial cells which form a metabolically active barrier between the blood and the vessel wall. The tunica media is a layer of smooth muscle and extracellilar matrix whic subserves as the contactile and elastic functions of the vessel. Boundaries of elastin: the internal and the external laminae seperate the smooth muscle from the intima and the adventitia, respectively. The elastic fibres are more prominent in the larger vessels and they stretch during the pressure of systole and then recoil during diastole, propelling the blood forward. The muscular component is more prominent in the smaller arterioles where contraction and relaxation can alter the veseel resistance and therefore the luminal blood flow. I The adventitia contains nerves, lymphatics and blood vessels (vasa vasorum) that nourish the arterial cell wall.

Describe the characteristics and the pathophysiology of atrial flutter

There are numerous other automacity foci that reside in the atria and they serve as a back-up pacemaker if the SA node fails to fire. In atrial flutter there is an irritable automacity foci that fires repeatedly at around 250-300bpm and local circuit of conduction is formed. However, the ventricles do not contract as rapidly due to the built in protective mechanism of the AV nodes refractory period which prevents it being stimulated. The ventricles therefore contact at a rate of approximately 150bpm. On an ECG you will see multiple P waves with regular R-R intervals. There will be some QRS complexes when the AV node is not in its refractory period. If there is 3 p waves for every p wave that cause a QRS complex is called a 3:1 conduction. Classical atrial flutter is said to have a saw tooth pattern- the saw teeth represented by the P waves. https://www.youtube.com/watch?v=FdRhsEtz2qo

Describe the difference between the short and long term control of blood pressure

There are two basic mechanisms to blood pressure regulation; the short term mechanisms and the long term mechanisms. Short term control mechanisms regulate the blood vessel diameter, heart contractility and rate. The long term mechanisms include changes to the blood volume. Blood pressure is CO x peripheral vascular resistance. Any change to the CO, blood volume or the peripheral resistance will lead to the change in blood pressure.

what are the properties of type I antiarrythmics?

They are membrane stabalising agents that reduce excitability • Ia lengthens the action potential (right shift) • Ib shortens the action potential (left shift) • Ic does not significantly affect the action potential (no shift)

What are the functions of the vascular smooth muscle cells?

They have both contractile and synthetic capabilities -Agonists include angiotensin II (circulating), Ach (released from nerve terminals) and endothelin and NO (produced by the overlying endothelium) -They synthesise collagen, elastin and proteoglycans which form part of the extracellular matrix. They also synthesis vasoactive and inflammatory mediators such as IL-6 and TNF alpha which promotes proliferation and endothelial expression of leukocyte adhesion molecules. These synthetic functions become more prominent in the formation of an atherosclerotic plaque. extracellilar matrx regulates the growth of resident cells; native fibrillar collagen inhibits smooth muscle proliferation. The matrix bound cells respond in a specific manner to GF's and are less likely to undergo apoptosis.

what are the different types of atrial tachyarrythmias?

They occur within the atria or the SAN They are also called supraventricular tachycardias and sinus tachycardia They may be physiological (emotion, stress, exercise) or pathological- hypovolaemia, anaemia, caffeine, salbutamol, hyperthyroidism, hypoxia, pain and pyrexia sinus node re-entrant tachycardia -rare -circuit within the SAN Atrial tachycardia -focal atrial tachycardia -macro-reentrant tachycardia Atrial fibrillation

what are the function of the endothelial cells?

They perform structural, metabolic and signalling functions and they maintain the homeostasis of the vessel wall. -antithrombotic molecules on the surface of the endothelial cells (heparin sulfate and thrombomodulin) and released into the circulation (prostacyclin and NO). However hen subject to various stressors, they can also produce prothrombotic molecules. -They produce vasoconstictors (endothelin) and vasodilators (NO and prostacyclin) -inhibit the proliferation of smooth muscle cells -The modulate the immune response and resist leukocyte adhesion, opposing local inflammation. However post-capillary venules produce chemokines in response to injury which causes the endothelial cells to produce adhesion molecules allowing for mononuclear cells to adhere and facilitaing their migration into the site of injury

Describe what you would see on the ECG of an anteroseptal MI

Typical changes are seen in the leads over the infarction and reciprocal changes in the leads opposite. For example in an anteroseptal MI these changes will be observed in V1 and V2 although reciprocal changes (ST depression) will be seen in the leads overlying the opposit (inferior) region- namely II, III and aVF.

where is the most common site of atheroma formation?

Usually at the branch points of arteries such as the common carotid and left coronary artery (due to greater turbulence in the blood flow). It impairs the athero-protective endothelial measures.

what are the local factors that regulate vasoconstriction and vasodilation

Vasoconstriction is caused by a drop in temperature locally Vasodilation is caused by increased CO2, decreased O2, decreased pH, adenosine, increased potassium and lactate

what are the circulating neurohormonal agens that cause vasoconstriction and vasodilation?

Vasoconstriction: epinephrine (apart from in the skeletal muscle and the liver), norepinephrine, angiotensin II, neuropeptide Y and arginine vasopressin Vasodilation: epinephrine in skeletal muscle and the liver, substance P, vasoactive intestinal polypepide, histamine, ANP and calcitonin G-related protein

what is the difference between a polymorphic and monomorphic ventricular tachyarrythmia

Ventricular Tachycardia (VT) is a broad complex tachycardia originating in the ventricles. There are several different varieties of VT — the most being Monomorphic VT. Monomorphic tachycardia has the characteristic features: Regular rhythm. Originates from a single focus within the ventricles. Produces uniform QRS complexes within each lead — each QRS is identical (except for fusion/capture beats). In monomorphic ventricular tachycardia, all the beats look the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle. The most common cause of monomorphic ventricular tachycardia is myocardial scarring from a previous myocardial infarction (heart attack). This scar cannot conduct electrical activity, so there is a potential circuit around the scar that results in the tachycardia. This is similar to the re-entrant circuits that are the cause of atrial flutter and the re-entrant forms of supraventricular tachycardia. Other rarer congenital causes of monomorphic VT include right ventricular dysplasia, and right and left ventricular outflow tract VT. Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration. The commonest cause of PVT is myocardial ischaemia. Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, in particular in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High-dose magnesium is often used as an antidote in cardiac arrest protocols.

what ar the possible causes of broad complex tachycardias?

Ventricular origin: AV dissociation -independent P waves -capture beats -fusion beats QRS broadened but there is QRS concordance sustained >30sec or requiring cardioversion (DCCV) may be monomorphic or polymorphic supraventricular origin: -SVT with aberrancy due to BBB -SVT and pre-excitation: Pre-excitation refers to early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway (WPW) PR interval <120ms Delta wave - slurring slow rise of initial portion of the QRS QRS prolongation >110ms ST Segment and T wave discordant changes - i.e. in the opposite direction to the major component of the QRS complex -antidromic AVRT (WPW): In antidromic AVRT anterograde conduction occurs via the accessory pathway with retrograde conduction via the AV node. Wide QRS complexes due to abnormal ventricular depolarisation via accessory pathway. usually 200-300 bpm. -SVT with flecainide

what are the differnt types of ventricular tachyarrythmias and their characteristics?

Ventricular tachyarrythmias are contained within the ventricles. The electricle conduction does not originate from the AV node More than 3 consectutive Premature ventricular contractions causes ventricular tachycardia. This causes the HR to go above 100bpm and can be extremely dangerous leading to sudden cardiac death when HR>250bpm chest pain, syncope dizziness can result Focal automacity: abnormal automacity that originates elsewhere in the ventricles If some of the ventricular cells become stressed or irritated or stressed they may cause rapid depolarisation. This stress may result from medications, elicit drugs (cocaine or methylamphetamine), electrolyte imbalances and ischaemia. More commonly, Vtachycardia is re-entrant. cardiac myocytes may become stressed altering their cnduction speed or refractory period. Damage leads to scar tissue formation and a split pathway forming- re-enterant pathway may be formed. ECG when all the QRS complexes look the same then they are monomorphic- re-enterant and focal (if one group of cells is responsible) polymorphic- signals originating from different parts of the ventricles (numerous focii) which can result due to several areas becoming stressed- seen in severe hypoxia. V. tachycardia can lead t V. Fibrillation Treatment: Cardioversion using drugs to lower the heart rate to a normal rhythm or electrical impulses (delivered on the R waves) Radifrequency ablation implantable cardioverter defibrillator https://www.youtube.com/watch?v=xAfj5AHxC2I

Describe the pathophysiology of deep vein thrombosis and the clinical complications? how would you treat DVT?

Virchows triad: vessel wall, flow and blood constituents all contribute to the formation of DVT -post thrombotic syndrome is a medical condition that may occur as a complication of DVT. Signs and symptoms include pain, heaviness, itching or tingling, swelling (oedema), varicous veins, brownish/ redish discolouration of the skin and sometimes venous uleration. Inflammation is thought to play a role as well as damage to the venous valves from the thrombus itself. This valvular incompetence combined with persistent venous obstruction from thrombus increases the pressure in veins and capillaries. Venous hypertension induces a rupture of small superficial veins, subcutaneous hemorrhage and an increase of tissue permeability. That is manifested by pain, swelling, discoloration, and even ulceration. Anticoagulants should be given and compression socks.

what is the treatments involved in PVD?

best medical therapy: -Give up smoking -exercise -Diabetic control -antiplatelets -statins -BP control Angioplasty Endarterectomy Bypass- anatomic and extra-anatomic (does not follow the normal anatomic pathway- such as axillofemoral)

Describe the aetiology of tachy-arrythmias

cardiac- IHD, LV aneurysm, pericarditits, mitral valve disease, congenital heart disease, pre-excitation and LQTS Drugs- antiarrythmics, beta 2 agonists, antidepressants aminophylline, caffeine, alcohol, smoking. metabolic- hypo and hyperkalaemia, hyo/hypercalcaemia, hypomagnesium, hypoxia, hypercarbia, acidosis. Endocrine- thyrotoxicosis and phaechromocytoma (catecholamine secreting tumour) infections, fever and emotions.

what are the characteristics of ventricular fibrillation?

chaotic tachyarrythmia with no discrete QRS complexes. They are initially coarse, degenerate to fine The muscle fibers begin to quiver and contract in an unco-ordinated fashion and is decribed as a bag of worms. ventricular fibrillation can lead to death in minutes Cause- usually stressed or damaged- the tissue is structurally or electrically changed -medications, drugs, electrolyte imbalances and ischaemia of the ventricular myocytes. If a group of myocytes fires at the worng time then the signal is transmitted and leads to premature ventricular contraction (>3PVC's in a row is ventricular tachycardia) ways of inducing fibrilation: •Functional re-entry due to two areas conducting at different speeds •Anatomical re-entry- scar tissue not contracting so the signal moves around •External electrical stimulation- when stimulated on the upslope of the T wav, this can induce fibrillation- some cells may be sufficiently repolarised to contract but some won't leading to abnormal conduction and a similar re-entry phenomenom. One of the only ways to stop ventricular fibrillation is external simulation- high energy shock to depolarise everything or the critical mass of cells and stop the re-entry spirals. Implantable cardioverter defibrillator is a surgically implantable device that monitors the patients ECGand recognises VF, administering a shock. Medications can also help to prevent future episodes.

what is the definition for chronic venous insufficiency and chronic venous ulcer?

chronic venous insufficiency occurs when there is irreversible skin damage as a result of sustained ambulatory venous hypertension (>25mmHg) Chronic venous ulceration is defined as a break in the skin, present for more than 6 months above the maleoli and the tibial tuberosity that is presumed wholly or partially due to venous disease. Macrovascular pathology: -muscle pump dysfunction. ageing, MSK neurological lower limb pathologies -valvular reflux (90%) and can be primary (lack of collagen and elastin) or secondary (valvular incompetence) -venous hypoplasia/ agenesis -venous obstruction Microvascular pathology: -venous stasis and hypoxia -AV fistulas (stealing the blood from the skin -leucocyte migration -capillary proliferation

Describe the different classes of antiarrythmics according to the vaughan williams classification

class I- sodium chnnels 1a (moderate)- quinidine and procainmide Ib (weak)- lidocaine, phenytoin Ic (strong) flecainide, propafenone class II- anti-sympathetic agents such as propanolol and metoprolol (BB) class III- affect K+ efflx amiodarone and sotalol class IV- affect calcium channels and AVN (verapamil and dilitiazem) class V-agents that work by another mechanism

what are the common causes of ventricular tachycardia in an impaired ventricle?

common causes include •ischaemic heart disease •cardiomyopathy- dilated, hypertrophic, arrythmogenic right ventricle •re-entry around scar •channelopathies-LQTS, Brugada, CPVT CPVT (Catecholaminergic polymorphic ventricular tachycardia) or familial polymorphic ventricular tachycardia (FPVT) is a rare inherited heart rhythm disturbance found in young people and children •ventricular tachycardia may deteriorate to VF •antiarrythmics are neutral on prognosis and reduce the incidence of ventricular tachycardia

Describe the common abnormalities of the QRS complex due to ventricular hypertrophy

hypertrophy of the left or the right ventricle causes the affected chamber to produce a greater signal. Right is usually smaller than the left ventricle in the magnitude of the signal. A greater than normal upward signal in leads V1 and V2 (R wave becomes taller than the S) occurs when there is right ventricle hyperthrophy. In addition the increased righ ventricular mass shifts the mean axis of the heart so it is >+90 In left ventricle hyperttrophy leads to the chest leads V5 and 6 and aVL and I to show taller than normal R waves. Leads on the opposite side show the opposite- deeper than normal S waves and diminished T waves.

what is a sinus pause and what are the characteristics on the ECG

is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart, such as the atrio-ventricular junction or the ventricles, begins pacing and restores the heart action. This condition can be detected on an electrocardiogram (ECG) as a brief period of irregular length with no electrical activity before either the sinoatrial node resumes normal pacing, or another pacemaker begins pacing. If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm. If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest. The interval between the P waves is longer than 2 seconds and is not a multiple of the normal PP interval (stand still for >150% of the cardiac cycle length). It occurs due to the inability for the SAN to generate impulses.

what medications can be used to control the heart rate and the rhythm

rate is controlled by: -beta blockers -calcium channel blockers -digoxin rhythm: -flecainide: Flecainide works by blocking the Nav1.5 sodium channel in the heart, slowing the upstroke of the cardiac action potential. This thereby slows conduction of the electrical impulse within the heart. Its effect increases with HR and therefore it is used to treat tachyarrythmia. -sotalol: beta blocker activity (decreasing the strength and the rate of contraction) and type III antiarrythmic action (acting on potassium channels and delaying relaxation). This effectively prolongs the frequncy of ventricular contraction to treat tachycardia. -amiodarone if poor LV function NB: control thrombotic risk- CHADS2VASC score

Describe how you would localise myocardial infarction

localisation can be done by analysing the pattern of the ECG leads which have pathological Q waves. They develop over the overlying infarcted tissue because the necrotic muscle does not generate forces and rather the electrode over the region detects electrical currents from the opposite regions of the ventricle ehich are directed away from the infarcted tissue and the recording electrodes, producing a downward defection. Q waves are permanent evidence of an ST elevation type myocardial infarction. Inferior- II, III, aVF (RCA) Anteroseptal-V1-V2- LAD Anteroapical V3-V4- LAD (distal) Anterolateral V5-V6, I, aVL (CFX) Posterior V1-V2 (tall R wave, not Q wave) (RCA in most cases) If an abnorml Q wave appears in one single ECG then it is not diagnostic of an infarction. For example, if a pathologic Q wave is present in lead III but not in II or aVF, it likely does not indicate an infarction. in the case of a posterior wall myocardial infarction, it is not pathologic Q waves that are evident on the ECG. Because standard electrodes are not typically placed on the patient's back overlying the posterior wall, other leads must be relied on to indirectly identify the presence of such an infarction. Chest leads V1 and V2, which are directly opposite the posterior wall, record the inverse of what leads placed on the back would demonstrate. Therefore, taller-than-normal R waves in leads V1 and V2 are the equivalent of pathologic Q waves in the diagnosis of a posterior wall MI. Also, Q waves are disregarded in lead aVR because electrical forces are normally directed away from the right arm. In the presence of LBBB, Q waves are usually not helpful in the diagnosis of MI because of the markedly abnormal pattern of depolarization in that condition.

what are the clinical manifestations of atheroma formation?

myocardial ischaemia myocardial infarction cerebral ischaemia mesenteric ischaemia & infarction peripheral vascular disease

what are the signs and symptoms of tachycardia?

palpitations dyspnoea heart failure hypotensive reduced cosciousness, pre-syncope and syncope cool peripheries oligouria

Describe the involvement of the kidneys in hypertension

renal injury causes decreased sodium excretion and this increases blood pressure. A hyperactive SNS, stimulated renin-angiotensin system, low potassium diet and cyclosporine use leads to renal vasocostriction This causes preglomerular arteriopathy- smooth muscle proliferation and tubular ischaemia and interstitial inflammation (arteriopathy can exacerbate ischaemia). There is increased vasoconstrictor expression and decreased vasodilator expression (exacerbating arteriopathy and causing a viscious cycle). It also causes increased sodium reabsorption due to the perceived low flow rate by the macula densa. Decreased sodium filtration results from arteriopathy (reduction in GFR) Sodium retention increases the BP and tubular ischaemia diminishes and sodium handling returns to a normal

What is a sino-atrial node exit block? what are the characteristic features on the ECG?

sinoatrial exit block- the expected P wave is absent but the following one occurs at the expected time (the exact pauses are exact multiples of the basic PP interval) Sino-atrial exit block is due to failed propagation of pacemaker impulses beyond the SA node. The sino-atrial node continues to depolarise normally but there is failure of the propagation of impulses through the myocardium Some of the sinus impulses are "blocked" before they can leave the SA node, leading to intermittent failure of atrial depolarisation (dropped P waves). Differential diagnosis of sinus arrest and sino-atrial block can be made by examining the exact length of the interruption of cardiac activity. If the next available pacemaker takes over in the following order: 1. Atrial escape (rate 60-80): originates within atria, not sinus node (normal P morphology is lost). 2. Junctional escape (rate 40-60): originates near the AV node; a normal P wave is not seen, may occasionally see a retrograde P wave. 3. Ventricular escape (rate 20-40): originates in ventricular conduction system; no P wave, wide, abnormal QRS. causes include: vagal tone, aging and fibrosis, myocarditis, cardiovascular accidents, iatrogenic (digoxin toxicity and antirhythmics) Treamtment includes stopping any medications that might stop the SA node (betablockers, calcium channel blocker and digitalis); the patient may need pacing.

what are the different stages of hypertension- NICE guidelines?

stage 1 hypertension- the blood pressure is greater than 140/90 or home blood pressure monitoring greater than 135/85 stage 2 hypertension- the blood pressure is greater than 160/100 or HBPM is greater than 150/95 stage 3 hypertension- in clinic the blood pressure is greater than 180/110 or higher

Describe the adrenal glands function in the regulation of BP

sympathetic stimulation causes the release of adrenaline from the adrenal glands.

Describe the pathophysiology of tachycardia's may you get?

tachycardia is a rate greater than 100bpm may be narrow complex (impulses are initiated above the ventricles and follow the normal conductive pathway) Broad complexed (impulses are initiated at the ventricles or are aberrantly (abnormally) conducted throughout the ventricles

What conditions may affect the QRS complex?

the QRS complex is usually less than 3 small squares. It is increased in: bundle branch blocks ventricular ectopic beat toxid drug effects: antiarrhythmic drugs severe hyperkalaemia

Where is the vasomotor and the cardiovascular centre found? what are the main inputs to these areas?

the cardiovascular centre contains the cardioacceletrator centre, the cardioinhibitory centre and the vasomotor centre

what are the endothelial products involved in vasodilation and vasoconstriction

vasoconstriction: endothelin-1, locally released platelet serotonin, thromboxane A2 This works by increasing vascular amooth muscle cells Calcium and vise versa for dilations vasodilation: NO, kinins and prostacyclin

Describe the investigations used to investigate between an arterial and venous ulcer.

venous ulcers tend to occur above the medial/ lateral maleoli Arterial ulcer may occur on the anterior shin, over the malleolus, under the heel or over the toe joints (pressure points) Neuropathic- similar to arterial but not found on the shi and they can be found on the inner side of the first metatarsal or under the metatarsal Arterial: • Hx- they occur most often in cases of diabetes/ hyperlipidaemia/ hypertension/ overweight/ smokers; very severe pain. • Exam - Pulses: diminished pulse - Ulcer characteristics- they usually have a punched out, regular appearance and are deeper than venous ulcers; unhealthy appearance of the wound bed with nectotic tissue and fixed slough; there is not typically much exudate unless it becomes infected; dry and shiny skin. • ABPI • Duplex • MRA • CTA • DSA Venous investigations: • Hx- most venous ulcers accompany varicous veins and they may have had a cramping, aching pain (minimal pain) • Exam - Pulses: the pulse is present and is usually full and bounding - Ulcer characteristics- more superficial; most commonly effect the distal leg and ankle; they are painful and exudative; often recurrent; they exhibit varying depths, even within the same ulcer; they are typically sloping and tend to very large; accompanied by oedema. (compared to arterial); reddish-blue coloured skin. • ABPI • Duplex

Describe the common abnormalities of the QRS complex due to bundle branch block

widened QRS complex in the affected branch (due to the relatively slow myocyte-myocyte spread of electrical activity in the ventricle rather than the purkinje fibers. The normal QRS duration is less than 2.5 small squares. If it is between 2.5-3 there is an incomplete bundle branch block greater than 3 shows a complete bundle branch block RBBB Prolonged depolarization process widens the QRS complex and produces a late depolarization current in the direction of the anteriorly situated right ventricle. The appearance of the QRS complex in lead V1 in RBBB (upward R, downward S, then upward R′) is often described as having the appearance of "rabbit ears." LBBB: the normal depolarisation of the left septum does not occur, the right interventricular septum is the first to depolarise. Therefore, an initial downward deflection is recorded in V1 and the normal small Q wave in V6 is absent. It is only after the depolarisation of the right ventricle that the slow cell-to cell spread reaches the left ventricular myocytes. The slow conducted forces show up as a widened QRS complex with abnormal terminally upward deflections in the leads of V5 and V6

Describe the pathophysiology of wolf parkinson-white syndrome

wolf parkinson white syndrome is due to an alternate pathway the atria and the ventricles. Some action potentials are not going to be delayed in the AV node and parts of the ventricles are going to depolarise faster and contract early (pre-excitation) - The PR interval is very short; the Q wave is sloped due to only partially depolarising the ventricle; there is a long QRS complex and there may be ectopic P waves with no ventricular contaction. Sometimes the accessory pathway can facilitate some arythmias such as atrial fibrilation. The accessory pathway provides an alternate pathway and there is no longer blcking of the abnormally rapid AP from the atria leading to ventricular tachyarrythmia (This is when it is called WPW syndrome) and can lead to cardiogenic shock Re-entry circuits can be caused (the signal moves back up the accessory pathway and back into the atria, called atrioventricular reenterrant tachycadia). This type of conduction is called orthodromic conduction. https://www.youtube.com/watch?v=9MDRKId2d0Q

what are the clinical signs of hypercholesterolaemia

xanthelasma Arcus senilis-An opaque ring, gray to white in color, that surrounds the periphery of the cornea

what are the properties of class II anti-arrythmicS?

• Beta blockers • Block catecholamines on β1-adrenergic receptors • Reduce sympathetic activity • Decrease conduction through AVN

what are the properties of class III anti-arrythmics?

• Predominantly block K channels • Amiodarone • Dronedarone • Sotalol • Prolong repolarization • Prolongation of the action potential duration and refractory period, prevents re-entrant arrhythmias • Can prolong the QT interval (proarrhythmic)

what are the properties of class IV anti-arrythmics?

• Slow Ca channel blockers • Verapamil • Diltiazem • Decrease conduction through AVN • Shorten phase 2 reducing contractility • may be inappropriate in heart failure