Cardiology

pt with many risk factors, what would be most effective in controlling his BP

10% reduction in weight loss NOT smoking weight loss is the most effective nonpharmacologic measure to dec. BP in overweight individuals weight loss has a greater impact on dec. BP than exercise alone

Which medications improve long term survival in patients with LV systolic dysfunction

ACEinhibitors, ARBs, B blockers, mineralocorticoid receptor antagonists and in African americans: hydrazine and nitrates spironolactone and epleronone are mineralocorticoid receptor antagonists that block deleterious effects of aldosterone on the heart and improve survival and hospitalization for HF in patients with LV systolic dysfunction

Cold water immersion during palpitations helps to stop the palpitations by

AV node conductivity, pt with abrupt onset of regular tachycardia that resolves with cold water immersion- consistent with paraxosymal supra ventricular tachycardia, AV nodal re-entry tachycardia is the most common form of PSVT and frequently develops in young patients w/ a structurally normal heart, palpitations are the most common presentation, but some patients have dizziness, SOB or chest pain there are 2 conduction pathways (slow and fast), sinus beats are conducted through the antegrade direction through the fast pathway, if an atrial premature beat occurs at a critical time when the fast pathway is refractory but slow pathway is not, it can initiate AVNRT that is sustained by a re-entry mechanism (the slow and fast pathways form a looped circuit) vagal manuvers (like carotid sinus massage, cold water immersion or diving reflex, valsalva) inc. parasympathetic tone and results in a temporary slowing of conduction in the AV node and inc. the AV node refractory period- leading to termination of AVNRT

17yo comes to ER with palpitations- he previously has episodes of chest fluttering but this episode was sustained he was stressed with school exams and ECG shows narrow complex tachycardia, he gets a medication that stops the tachycardia and the ECG shows WPW

Accessory AV pathway in WPW there is an accessory pathway (bundle of kent) that directly connects the atria to the ventricles by bypassing the AV node- pre excitation of the ventricles and short PR interval, slurred and broad upstroke of QRS complex, and QRS interval widening if there is retrograde conduction from the ventricles to the atria a re-entrant supra ventricular tachycardia may occur

arrhythmia most specific for digitalis toxicity

Atrial tachycardia with AV block- Digitalis can inc. ectopy in the atria or ventricles which can lead to atrial tachycardia (and atrial tachycardia can be distinguished from atrial flutter by it's somewhat slower rate), p waves are present but are different from p waves seen when conduction originates from the SA node, in addition to ectopic rhythms, digitalis can inc. vagal tones and dec. conduction through the AV Node, potentially causing AV block it is rare for ectopy and AV block to occur at the same time, when they do, the combo is specific for digitalis toxicity

Pt with bradycardia, AV block, hypotension and diffuse wheezing with suicide attempt

B blocker overdose,, CCB, digoxin and choleric agents would have similar symptoms but hearing wheezing would be more indicative of B blocker overdose- bradycardia and hypotension leading to cardiogenic shock- as seen by patients cold and clammy extremities- also hypoglycemia, bronchospasm (b2 blockage) and neuro dysfunction the first steps are to secure airway and give isotonic fluids and IV atropine, for the hypotension and bradycardia, in patients with refractory and profound hypotension, the next step is to administer IV glucagon which inc. intracellular levels of cAMP and treats BB and CCB toxicity after that can try IV calcium, vasopressors, (epi and noepi), high dose insulin and glucose and IV lipid emulsion therapy

Greatest sensitivity for diagnosing heart failure

BNP is released from ventricular myocytes in patients with CHF in response to high ventricular filling pressures, and an elevated BNP has a high sensitivity for CHF elevated levels of BNP correlates with severity of LV dysfunction (usually BNP >400) in contrast, clinical signs of HF (bilateral crackles, elevated JVP, LE edema, and a third heart sound) have a high specificity but low sensitivity

Treatment of chronic stable angina

CAD with symptoms and clinical findings of stable angina-mismatch of myocardial oxygen supply and demand, the 3 main medication classes for management of stable angina: B blockers, CCB and nitrates B blockers are first line for controlling anginal symptoms and improving exercise tolerance in patients they reduce myocardial oxygen demand though dec. myocardial HR and myocardial contractility, nondihydropyridine CCB (verapamil and diltiazam) treat angina primarily thought the same mechanism are are an alternative first line therapy in its with b blocker contraindication

Pt with acute arterial occlusion in the left lower extremity due to thromboembolism due to afib pt has acute pain, parasthesia, pallor, and pulselessness (pt has irregular pulse=afib)

CHADS score >2= anticoagulation to reduce risk of systemic embolization Apixiban non-vitamin K antagonist oral anticoagulant (along with dagibitran, rivaroxiban) to reduce the risk of embolization could also use warfarin

Pt with dyspnea, orthopnea, pulm and peripheral edema 1 year ago had an MI

CHF due to LV systolic dysfunction, holosystolic murmur at the apex is likely due to MR (mitral annulus enlargement) with LV dilation and/or papillary muscle displacement due to LV remodeling patients with ischemic cardiomyopathy have dec. CO due to impaired myocardial contractility, the compensatory rise in neurohormonal activity (noepi, renin and ADH) inc. SVR and maintains BP and vital organ perfusion, inc. blood vol b/c of na and water retention inc. preload and results in inc. LVEDV and rise in SV, over time, inc. after load w/ impaired LV contractility leads to dec. CO, inc. L sided pressures, pulm congestion and peripheral edema, CI is low in HF and is CO/ body surface area

Pt with chronic systemic symptoms (fever, weight loss, fatigue) embolic phenomenon ( L sided weakness) and echo findings of mass in LA

Cardiac myxoma (most common beings cardiac tumor), it can cause obstruction of blood flow across the mitral valve- producing an early diastolic sound (tumor plop)- pts present with fatigue, cough, dyspnea orthopnea, pulmonary edema or hemoptysis, and LA tumors can cause systemic embolization (TIA, stroke, splenic infarcts) and >50% of its can report constitutional symptoms (b/c of overproduction of IL6)- like fever/weight loss/raynad's, trans esophageal echo is the most sensitive tx for dx

pt with episode of syncope while working in garden, chest pain and neck pain before syncopal episode and over the last week formed cough, chest tightness, sputum, temp normal , high BP , and high pulse and ECG shows sinus tachycardia, voltage criteria for LVH, no ST segment changes chest xray shown and bestside echo shows moderate sized pericardial effusion what is next step?

CT angiography even though pt doesn't have chest pain or pulse differential, his chest/neck pain, syncope h/o hypertension, evidence of mediastinal widening with pericardial effusion= acute aortic dissection Type A (ascending aorta) can lead into pericardial space and hemopericardium--which can progress to cardiac tamponade and cariogenic shock CT angiographic is the first choice in hemodynamically stable w/ no evidence of renal dysfunction- can show intimal flap and if pt is hemodynamically unstable or has renal insufficnecy- need transesophageal echo pericardiocentesis would be done if patient was hemodynamically unstable

Tx for acute aortic dissection

CT scan shows intimal tears separating true and false lumen, aortic dissection involving the ascending aorta (type A) is surgical emergency tx goals are adequate pain control, reduction of SBP 100-120 mmHG dec. in LV contractility to reduce aortic wall stress IV B blockers (like labetelol) are preferred initial therapy to reduce HR, SBP, and LV contractility pain control w/ morphine

Pt with acute aortic dissection- complicated by cardiac tamponade sudden onset of severe chest pain radiating to the back, widened mediastinum on X-ray, hypotension, tachycardia, distended jugular veins, and respiratory variation in systolic BP (pulsus paradoxes)

Cardiac tamponade can occur as a complication of aortic dissection, with rupture of the aortic and rapid accumulation of blood in the pericardial space, the inc. pericardial pressure causes compression of the cardiac chambers and limited diastolic filling of the right heart chambers- dec. preload and reduced Co causing hypotension and syncope

Improve survival in CHF patients

Captopril, Losartan, Metoprolol, Aspirin, Spironolactone NOT Digoxin- cardiac glycoside that helps to inc. heart contractility- so it helps to improve fatigue and dyspnea and same with furesomede only symptoms

Patient with muscle weakness, recurrent nephrolithiasis, neuropsychiatric symptoms and hypercalcemia

Consistent with primary hyperparathyroidism, the extra parathyroid causes hypercalcemia- due to inc. renal calcium absorption, GI calcium absorption and bone resorption- pt can have bone pain, kidney stones, GI symptoms and neuropsych symptoms 80% due to parathyroid adenoma and primary hyperparathyroidism can cause hypertension, arrhythmias ventricular hypertrophy and vascular and valvular calcification, unclear how it causes hypertension, significant hypertension with primary hyperparathyroid occurs in MEN 2 with pheochromocytoma

Pt with chronic stable angina ( exertional chest pain relieved by rest) with rapid relief of symptoms with nitroglycerin- how nitrates help?

Dec. LV wall stress nitrates- direct vascular SM relaxation causing systemic venodialation and inc. in peripheral venous capacitance and their anti-ischemic effect is by systemic vasodilation and dec. in cardiac preload--> resulting in reduced LV end diastolic and end systolic volume--> reduction in LV systolic wall stress (which reflects after load)-dec in myocardial oxygen demand--relief in anginal symptoms nitrates do also act as coronary vasodilators- but uncertain effect of this mechanism and coronary arteries in flow blocked areas already have their own dilatory mechanism, nitrates actually dec. flow here b/c flow is diverted to the unblocked areas

Tc-99m is used to get assessment of myocardial function and perfusion and then gets a CT scan, specifically single photon emission CT

Dec. tracer uptake both at rest and with exercise (fixed defect) likely indicates scar tissue and decreased perfusion and CAD, but a dec. uptake with stress but normal uptake at rest indicates inducible ischemia and likely CAD as seen with this patients apical images- current guidelines recommend antiplatelet (aspirin) for prevention of MI, b blockers and modifications of patients RF (smoking cessation, lipids and diabetes)

Pt with orthostatic hypotension

Decreased baroreceptor responsiveness postural decrease in BP by 20 systolic or 10 diastolic (sometimes accompanied by an inc. in hR)- insufficient constriction of resistance and capacitance blood vessels in the lower extremities by standing, which may be due to a defect in autonomic reflexes, dec. IV volume, or medications, and some baroreceptor sensitivity is lost as a response to aging overall- arterial stiffness, dec. noei content of sympathetic nerve endings, and reduced sensitivity of the myocardium to sympathetic stimulation contribute to a tendency towards orthostatic hypotension with age

Pt with large anterior ST segment elevation MI and cath showed occlusion of the LAD and they put him on anti platelet therapy and the next day he was having leg pain- cold with mottled appearache, what is next step?

ECHO pt has acute limb ischemia from arterial occlusion caused by cardiac emboli thrombosis (vascular stents, hypercoaguable states) or trauma, and major sources of arterial emboli- LV thrombus, atrial thrombus due to a fib, and aortic atherosclerosis pts with large anterior ST elevation MI are at highest risk for LV thrombus and anteroapical aneurysm formation, these pt's at at high risk for systemic embolization and require immediate anticoagulation and transthoracic echo with contrast to screen for LV thrombus, and vasc surgery consult

Pt with RF of CAD who has chest pain that seem related to ACS what is first step

EKG women, elderly and pts with diabetes are more likely to have atypical symptoms- and dyspnea, epigastric pain, and N/V are atypical presentations

Pt who undergoes CABG, and in days following procedure, there is no drainage from chest tube, lung fields are clear, no heart murmur appreciated, abdomen soft, extremities cool, ECG shows sinus tachycardia and nonspecific T wave changes, pulm artery catheter readings show elevated RAP, RVP and elevated PCWP what is best for management

Echocardiogram pt most likely has post op cardiac tamponade, rare but imp complication of CABG rapid accumulation of blood in the limited pericardial space, leads to inc. diastolic pressure and dec. venous return to the heart, pts have evidence of cardiogenic shock (hypotension, reduced UO, cool extremities) the triad is hypotension, elevated JVP, and distant heart sounds (Beck's triad) characteristically, there is elevation and equalization of intracardiac diastolic pressures (RA, RV and PCWP- suggestive of LA pressure) cardiac tamponade can lead to cardiac arrest if un treated, urgent echo can detect it can identify the pericardial effusion, right atrial diastolic collapse, right ventricular diastolic collapse, and bowing go the inter ventricular septum into L ventricle during inspiration need pericardial window for drainage to relieve elevated intracranial p- to lead to rapid improvement in symptoms and hemodynamic status

pt with lower extremity swelling, htn, DM, hep c, symmetric pitting edema, hepatomegaly, palpate spleen on inspiration, ascites, pos hepatojugular reflex- what is the cause of the edema?

Hepatojugular reflex, elevated jugular venous pressure >3cm then pushing on the abdomen , reflection of a failing RV that cannot sustain the venous return with abdominal compression, constrictive pericarditis, RV infarction, and restrictive cardiomyopathy are the most common causes of hepatojugular reflux, pt previously had TB suggestive of constrictive pericarditis, which is a major cause of right HF, patients get elevated JVP, peripheral edema, ascites, and eventually cirrhosis can also see kussmal's sign, pericardial knock, and pericardial calcifications on chest radiograph

Pt with atrial fibrillation with RVR what other condition can the person have?

Hyperthyroidism

young pt with murmur during sports exam, maternal uncle died during swimming, faint mid systolic murmur heard along LLSB when pt is supine and when pt stands 3/6 crescendo/decrescendo murmur heard- what is the mitral valve anomaly

Hypertrophic cardiomyopathy AD, sarcomere, exertion dyspnea, chest pain, fatigue, palpitations, syncope harsh crescendo-decrescendo systolic murmur with change in intensity on physiologic maneuvers these pts have inc. LV wall thickness, most commonly noted at the basal anterior septum some patients have systolic anterior motion of the mitral valve leading to anterior motion of the mitral valve leaflets towards the inter ventricular septum, contact b/t the mitral valve and the thickened septum leads to LVOT- harsh systolic murmur

Pt with symptoms of hypertrophic cardiomyopathy- what medication to use

Hypertrophic cardiomyopathy: mutation in sarcomere protein genes, autosomal dominant, variable expressivity/penetrance, fatigue, chest pain, palpitations, syncope, complications: sudden cardiac death heart failure, stroke patients with symptoms (syncope, HF, angina)- should be tx with negative ionotrophic agents (b blockers, verapamil, disopyramide), B blockers (metoprolol and atenolol) are most commonly used agents for initial mono therapy, they prolong diastole and inc. myocardial contractility, dec. LVOT obstruction and and improving the symptoms of angina nondihydropyridine CCB (verapamil) is sometimes used despite persistent B blocker therapy,

32yo man with sudden onset excurtiating left sided chest pain high BP, high pulse and high respirations, anxious, agitated and sweating profusely, both pupils dilated, regular heart sounds, no murmurs, lungs clear to auscultation initial electrocardiogram shows ST depression and T wave inversion V1-V4, the first set of cardiac enzymes (CKMB and Troponins were normal) what is next step?

IV Diazepam pt with psychomotor agitation, dilated pupils, atrophic nasal mucosa, hypertension, and acute MI (chest pain/ECG changes)-acute cocaine intoxication inhibits norepinephrine reuptake--stimulation of alpha and beta receptors--coronary vasoconstriction and can inc. the HR, systemic BP, and myocardial oxygen demand and it enhances thrombus formation by promoting platelet activation and aggregation pt should be tx with Oxygen and benzodiazepine and can use aspirin/nitrates and CCB cardioselective BB should not be used in pts with cocaine induced MI or infarction-unopposed alpha stimulation

Pt with PMH of diabetes comes to ER with SOB, BP is 146/92, RR is 26beats/min and auscultation reveals an S3, what is best tx

IV diuretics S3 is believed to result from inflow from the LA strikes blood that is already in in the LV causing reverberation of blood b/t the LV walls, later in life it is a sign of LV failure (and pt has these signs of SOB, tachypnea and hypoxemia)- and the best treatment would be IV diuretics

Pt with exertional SOB, and occasional chest discomfort and headaches and murmur at the L sternal border

Item 4910- listen again early diastolic murmur- aortic regurg, can find water hammer pulses "bounding pulses", inc. SV and an abrupt rise in SBP and dissension of the peripheral arteries, hyper dynamic pulse

Pt with squeezing chest pain that started 2 hours ago and SOB that is worse with lying down, BP 98/60, pulse 110 and auscultation revels holosystolic murmur at the cardiac apex and bibasilar crackles in the lungs and ECG shows ST segment elevation MI in leads II, III, avF what is most likely inc. in pt

LV filling pressures acute inferior MI w/ papillary muscle displacement leading to mitral regurg and pulmonary edema excessive volume of blood leading back into the LA acute mitral regurg leads to excessive diastolic volume overload- elevated LV end diastolic pressure and the pressure is reflected back to the LA and pulm circulation-acute pulm edema dn CHF

hypertrophic cardiomyopathy

LV hypertrophy, most prominent in the basal anterior septum- exertional dyspnea, fatigue, chest pain, palpitations, syncope, and harsh crescendo-decrescendo systolic murmur best heart at the apex and LLSB that changes in intensity with physiologic manuvers HCM is autosomal dominant- mutation in sarcomere genes- encoding myocardial contractile proteins of the heart (cardiac myosin protein C and cardiac B myosin heavy gene)

Woman with high BP on last 2 visits BP 150s/90s, exercises and low slat diet, BP on this visit is also in 150s sinus rhythm and CBC and chem panel are normal what is next step?

Lipid panel and urinalysis most pts with hypertension is usually essential hypertension initial eval should look at secondary causes- urinalysis (for occult hematuria and urine protein/creatinine ratio), chem panel, lipid profile and baseline electrocardiogram and further diagnostic workup for those w/ symptoms suggesting secondary htn (severe/malignant htn, resistant htn >3 drugs, sudden rise in BP and age of onset <30 w/o FH)

Pt with flouroquinoloe and then got torsades de points what is tx?

Magnesium sulfate polymorphic ventricular tachycardia- cyclic or sinusoidal alteration of QRS axis, acquired QT interval prolongation Pt with medication induced prolongation of QT along with h/o alcoholism, cardiomyopathy, and HIV predisposed to getting torsades immediate défibrillation is needed in those patients who are hemodynamically unstable and IV magnesium is the first line in stable pts with episodes of Torsades along with removal of the offending agent

Types of Heart block

Mobitz type I is an intermittent AV nodal block that progressively prolongs the PR interval, it can be due to drugs that block the AV node (digoxin, B blockers, CCB), when the block occurs it causes a nonconducting P wave that does not depolarize the ventricle (dropped QRS), there is a predictable grouping of P-QRS, after every 3 PQRS there is a drop called "group beating", benign rhythm and low risk for complete heart block Mobitz II is due to block in his-purkinje system below the AV node- episodic and unpredictable absence of conduction b/t atria and ventricles, the PR interval is constant and QRS drop suddenly

Pt who recently had an MI, two weeks later having pain in the middle of the chest, can only take shallow breaths because deep breaths make it worse, and leaning forward in the chair makes it better ST segment elevations in all limbs what is next best step in management

NSAIDS pt pain (worse with deep inspiration, improved on leaning forward), suggest pericarditis rather than MI, and EKG findings are classic for pericarditis ( diffuse ST elevation except for reciprocal depression in aVR), post MI acute pericarditis often occurs in the weeks after an MI, this pt most likely has dresser's syndrome, ESR is elevated and NSAID is the mainstay of therapy, corticosteroids may be used in refractory cases anticoagulation should be avoided to prevent development of hemorrhagic pericardial effusion

43 yo woman with fatigue and SOB over the last 2 weeks, recently had a URI, BP 99/55 and pulse 105 Jugular veins distended and lungs CTA and Xray shows cardiomegaly what additional finding

Non-palpable PMI pt with recent URI, dyspnea, elevated JVP clear lung finds and inc. cardiac silhouette, early cardiac tamponade due to large pericardial effusion (most commonly idiopathic due to viral infection) Large pericardial effusions on chest X-ray as enlarged and globular cardiac siloutthe "water bottle heart shape with clear lung fields INABILITY TO PALPATE PMI and distant heart sounds, consistent with large pericardial effusion and pt's with cardiac tamponade can have Beck's triad: hypotension, elevated JVP and muffled heart sounds and pt's with URI can form viral myocarditis- audible S3, pulm vasc congestion

56yo man with exertion dyspnea for past month, (palpitations, cough and LE swelling), hospitalized 6mo for possible MI, htn diabetes, hyperlipidemia, smoker, and does crack, family history of HD, BP is 144/86, and distended JVD, bibasilar crackles heard and ECG shows ST elevations in V1-V5

Pt has LV aneurysm HF due to LV aneurysm late complication of MI, that can occur up to several months following transmural ST elevation , delayed coronary repercussion inc the risk the healing process following MI results in replacement of necroses myocardium with fibrous scar tissue, which can inc. the convexity of a large portion of the wall, the aneurysm is dyskinetic- resulting in impaired EF HF is the most common presentation but also angina can occur b/c of inc. oxygen demand caused by elevated wall stress in the setting of an enlarged ventricle- ventricular arrhythmia aor systemic embolization (due to mural thrombus in the aneurysm) is also possible ECG typically demonstrates persistent ST segment elevation and deep Q waves in the leads corresponding to a previous MI, and the diagnosis is confirmed by echo showing a thinned and dyskinetic myocardial wall

Pt got cardiac cath and then got blue toe, high cr and lived reticular

Pt has atheroembolism (cholesterol emboli)- when atherosclerotic plaque is disrupted, partial/total occlusion of arterioles can be immediate or >30 days after event atherosclerotic plaques in the aortic arch can symbolize to the brain and cause cerebral infarction, emboli into the peripheral circulation can cause- intestinal ischemia, GI bleeding, pancreatitis, and AKI, "blue toe syndrome" and "lidded reticularis", gangrene and ulcers and eye can show Hollenhorst plaque tx is supportive some pts can have renal dysfunction that persists beyond 2 weeks and need statin

young pt with weakness and Sob, and symptoms of HF (lung crackles, edema etc), and uses metamphetamine- she is given a drug to stimulate B 1 adrenergic receptors

Pt has cardiomyopathy, pt with progressive dyspnea, hypoxemia, diffuse pulm crackles and a third heart sound (low pitched early diastolic sound) is consistent with decompensated HF, having hypotension, cool extremities, diminished pulses and evidence of poor organ perfusion (elevated creatinine due to dec. renal blood flow) is consistent with a low cardiac output state dobutamine is an adrenergic agonist with predominant activity on B1 receptors and minimal activity on B2 or alpha 1 receptors- stimulating B 1 receptors- results in production of inc. cAMP in cardiac myocytes- leading to enhanced calcium binding of actin-myosin complex to troponin C and inc. myocardial contractility (positive ionotriphic effect)- HR also inc. via calcium channel activation (positive chronotrophic effect)- inc. in myocardial contractility allows for a forward ejection of a higher vol of blood and results in a dec. in LV end systolic volume and CO is inc. to perfuse organs and less blood back up into pulm circulation improving symptoms

25yo woman with transient vision loss, high BP but not obese, bruit at the right mandibular angle, found to have high plasma renin and aldo/renin ratio of 10, FH of stroke

Pt has fibromuscular dysplasia , women less than 50yo with one of the following: severe or resistant hypertension, onset of hypertension before the age of 35, sudden inc. in bp above baseline, inc. in creatinine after starting ACEi or ARB w/o significant improvement in BP can have symptoms of brain ischemia (amaurogosis fugax, Horner's, TIA, stroke), headache or dizziness from carotid or vertebral artery involvement, dx is CT angiography or duplex ultrasound of abdomen and pts with inconclusive testing require catheter based digital subtraction arteriography for diagnosis noninflammatory and nonathlerosclerotic condition caused by abnormal cell development in the arterial wall that can lead to vessel stenosis, aneurysm or dissection- most commonly involves the renal, carotid and vertebral arteries

Pt with acute limb ischemia

Pt has the classic 6Ps= pain, pallor, parasthesias, pulselessness, poiklothermia (cool extremity), and paralysis (due to nerve ischemia) of acute arterial occlusion of the right lower extremity- can be embolus from cardiac or arterial source, afterial thrombosis iatrogenic or blunt trauma to the artery the sudden development of symptoms in an asymptomatic patient=embolic occlusion, the majority of arterial emboli originate in the heart and LE are often more affected than UE , common sources include LA thrombus due to Afib , LV thrombus, following anterior MI, infection endocarditis and thrombus from prostatic valve

Pt with sharp pain in chest for 2 hours, worse when lying back and better when forward, he had chronic kidney disease and is scheduled for dialysis soon, and ECG shows nonspecific T wave abnormalities, and lab studies show a BUN of 68 with creatinine of 5.3

Pt has uremic pericarditis, elevated levels of BUN can cause inflammation of the visceral and parietal layers of the pleura of the pericardium- pts can have acute or chronic renal failure, and typically present with pleuritic chest pain worse in supine and improves with sitting up- cardiac auscultation reveals pericardial friction rub (high freq grating sound) best heard at the L sternal border when the pt is leaning forward, specifically UREMIC pericarditis does NOT typically cause diffuse ST segment elevation on ECG as the as the inflammation doesn't affect the myocardium tx is initiation of dialysis but more than 50% can develop pericardial effusion, so cardiac tamponade should be r/o before dialysis initiation

Pt with nocturnal substernal chest pain, and pain resolves spontaneously SCG shows transient ST elections in leads I, aVL, and V4-V6 during pain- what is treatment

Pt has vasospastic angina- hyperactivity of intimal coronary smooth muscle, intimal coronary artery vasospasm, usually a young patient <50yo, smoking, recurrent chest discomfort, pain that occurs at rest/during sleep (accompanied by diaphoresis, nausea, palpitations and dyspnea) and spontaneously resolves after 15 mins, will see ST elevation but no blockages and tx is CCB (to dialate coronary a) for preventive and nitrates for abortive, smoking is a strong RF aspirin should be avoided in pts with vasospastic angina- it can inhibit prostaglandin production and worsen vasospasm

Pt with fatigue and LE swelling, and feeling of pulsation in neck when lying down, no chest pain, underwent pacemaker for SSS non smoker no FH, BP 112/70 JVD distended with pt sitting and 3/6 holosystolic murmur over LLSB, lungs CTA, liver enlarger and tender and 3+ pitting edema

Pt having severe tricuspid regurg b/c of adverse effect of permanent pacemaker the RV lead of a transvenous implantable pacemaker or cardioverter- defibrillator passes through SVC into the RA and then to tricuspid valve to terminate in the endocardium of RV, damage to the tricuspid leaflets or inadequate leaflet coaptation can occur chronic severe TR can cause RHF, right ventricular heave and holosystolic murmur at the L sternal border, and murmurs intensifies with things that inc. preload like inspiration/ leg raise. dx of TR is confirmed by echo transvenous lead placement through the tricuspid valve can cause severe TR due to direct valve leaflet damage or inadequate leaf coaptation, and this should be suspected in patients with RHF after getting implantable pacemaker

Pt having symptoms two weeks after an MI

Pt probably has progressive decompensated HF due to left ventricular aneurysm with is a post MI complication (5 days to 3 months post MI)- thin and scarred fibrotic myocardium in remodeled areas affected by ST elevation MI or transmural MI usually ST elevations resolve in a few weeks after an MI ventricular aneurysms present with persistent ST elevation after an MI and deep Q waves in the same leads, large VAs can lead to LV enlargement causing heart failure, refractory angina, ventricular arrhythmias mural thrombus with systemic arterial embolization or annuar dilation causing mitral regurg (MR) dx is confirmed by echo (thinned, dyskinetic LV portion in area of prior MI)

Pt recently just got a stent put in, has crushing midsternal chest pain, dyspnea and diaphoresis, ST segment elevation in the lateral leads (1, aVL) and anterior (V1-V4) precordial leads- acute ST elevation MI due to LAD occlusion

Pt with drug eluting stent with subacute stent thrombosis due to medication noncompliance, stent thrombosis is a fatal complication of coronary artery stunting and long term dual anti platelet therapy (aspirin plus P2y12 receptor blocker like clopdiogrel, ticagrelor) recommended to reduce the risk of stent thromboses after intracoronary drug eluting stent placement, premature discontinuation of anti platelet therapy is the strongest predictor of stent thrombosis within first 12 mo

Pt with pleuritic chest pain, dyspnea, tachypnea, tachycardia in a long distance truck driver

Pulm embolism can also see cough, hemoptysis lower extremity pain/swelling (DVT) chest radiographs can show atelectasis/infiltrates/pleural effusion/westermark's sign (peripheral hyper lucency due to oligemia) Hampton's hump (peripheral wedge of lung opacity due to pulm infarction) and Fleschiner sign (enlarged pulmonary artery) but also chest X-rays can be normal

18yo reporting dyspnea with climbing stairs, during expiration there is an extra high pitched heart sound heard after S1 and grade 3/6 systolic crescendo-decrescendo murmur loudest at the L upper sternal border, S2 is split throughout the respiratory cycle and splitting inc with inspiration what is mechanism of pt murmur?

Pulmonic stenosis often is an isolated congenital defect, pts with mild PS can remain asymptomatic throughout childhood and develop symptoms (dyspnea with exertion) in early adulthood, cardiac auscultation reveals a pulmonic ejection click (best heard in expiration), followed by harsh crescendo-decrescendo systolic murmur heard at L 2nd intercostal space and murmur intensifies with inspiration the stenosis causes the pulmonic valve to close later than usual- resulting in a widened splitting or aortic and pulmonic components and splitting is further increased during inspiration

Systemic arterial P normally called <10mmHg during inspiration, but this pts tracing shows fall in SBP >10mmHg during inspiration- and this exaggerated drop is puses paradoxicus (most commonly seen in patients with cardiac tamponade), during inspiration, the inc. in venous return to the heart causes the IVS to balloon into the LV leaving less space for LV end diastolic volume=reduced systolic BP

Pulsus paradoxicus can be caused by aortic dissection, but also asthma and COPD , in patients with sever asthma ofr COPD there is a exaggerated drop, and the negative P causes pooling of the vasculature dec. LV preload marked expansion of the lungs in asthma or COPD impinges the outward expansion of the heart- which can also cause an excess drop in SBP and pulsus paradoxicus

Pt having a right heart MI- ST elevation in inferior leads (II, III, avF)- acute, inferior wall ST elevation MI, occlusion of RCA with clear lungs

RV MI leads to impaired RV filling and creates a high sensitivity to intravascular vol depletion ,the administrations of nitrates should be avoided as venous dilation causes an abrupt dec. in RV preload and can lead to profound hypotension, in patients with suspected RV MI, hypotension and low or normal jugular venous pressure- strongly suggests cariogenic shock, due to inadequate RV preload, these pts require bolus with isotonic saline to inc. RV preload and improve CO other wise they should undergo management as other MI- dual anti platelet agent, statin, anticoagulation and urgent revascularization (PCI) after giving IV saline, then may need ionotrophic agents like dopamine and dobutamine

Pt with sudden onset chest pain and 2 episodes of vomiting, bp 80/50, diaphoresis, elevated JVP and positive kusmall sign ECG shows 2mm ST elevations in II, III, avF

RV infarction acute inferior STEMI with RV MI occlusion of RCA ST elevations in the inferior leads: II, III, avF, and pts can have JVD and kusmall's sign (inc. in JVD with inspiration) and clear lung fields suggestive of RV failure hypotension could be worse following nitroglycerin therapy RV failure leads to dec. preload and resultant hypotension so in addition to standard MI therapy- patients are tx with IV fluid boluses (isotonic saline) to improve RV preload and facilitate LV filling

Pt with Prinzmetal Angina, what is that best compared to?

Raynaud's vascular smooth muscle hyperactivity- focal or diffuse spasms of the coronary arteries leading to transient MI and and resulting angina recurrent episodes of chest discomfort that occur at rest of during sleep cigarette smoking is a known RF, and vasospasm leads to contigous ST elevation during an episode of chest discomfort and pathologic mechanisms is similar to raynaud's- cold or stress induced hyperactivity of the digital arterial SM- episodic vasospasm CCB are the first line therapy for Raynaud's and vasospastic angina

pt with isolated systolic hypertension pt has BP 167/75

SBP >140 and DBP <90, inc. stiffness or dec. elasticity of the aortic and arterial walls in elderly patients- it reduces the ability of the arteries to dampen the systolic BP and leads to an inc. pulse wave velocity and this explains the inc. in PP and inc. in systolic BP seen in pts with ISH (isolated systolic hypertension)

Management of STEMI

ST elevation in leads I, aVL, and V2-V6 and depression in II, III and aVF- acute anterolateral MI due to occlusion of the LAD- initial stabilization is aspirin, oxygen P2Y12 inhibitior, nitroglycerin for pain control, B blocker and anticoagulation prompt coronary repercussion with primary PCI or fibrinolytic therapy restores blood flow and limits myocardial damage and reduces myocardial mortality within 12 hours of symptom onset, within 90 mins from first medial contact to device time at a PCI capable facility, or within 120 mins from first medical contact to a nonPCI facility so PCI is recommended within 90 mins for acute STEMI

Medications to withhold prior to cardiac testing

Stress testing can detect reversible underlying ischemia or prior MI through electrocardiogram changes, perfusion deficits, B blockers, CCB, and nitrates are antianginas that reduce extent/ severity of ischemia and these meds should be held 48 hours before stress testing

Patient with atrial fibrillation, ECG shows absence P waves and chaotic fibrillary waves, irregularly irregular RR intervals and narrow QRS complexes

The pulmonary veins are most often the location of the ectopic foci that cause AF, cardiac tissue extends into the pulmonary vein and normally functions like a sphincter to reduce reflex of blood into PV during atrial systole, this tissue has different electrical properties than the surrounding atrial myocytes and prone to ectopic electrical foci so A fib is an ectopic foci within the pulm veins Atrial flutter involves a re-entrant circuit around tricuspid annulus AV nodal re-entrant tachycardia- reentrant circuit formed by 2 separate conducting pathways within the AV node and due to reentrant circuit involving accessory AV bypass tract

Screening reccomendations for abdominal aneurysm

USPSTF men aged 65-75 who have smoked-- 1 time abdominal US in these patients (not CT/or Xray)

Pt with lightheadedness and weakness, ECG in ED shows 3rd degree heart block ( regular P wave activity unrelated to QRS, constant R-R interval and independent P wave occurrence)

Untreated complete heart block can lead to ventricular arrhythmias, pts need immediate place maker this pts chest discomfort and T wave inversions are suggestive of MI--he should be assessed with cardiac enzymes and cath

Prevention of long term complication for pt with afib?

Warfarin prevention of systemic embolization can use warfarin or NOAC- helps to reduce risk in patients with moderate to high risk of thrombotic events and CHADs score can help identify who needs anticoagulation

Pt with intermittent claudication and positive ABI- consistent with PAD

a supervised graded exercise program is the most useful intervention to improve functional capacity and reduce claudication in PAD antiplatelet agents like aspirin and clopidogrel do not constantly reduce claudication symptoms but reduce risk of MI/ stroke/ cardiovascular mortality, other measures for treating PAD include smoking cessation, aggressive diabetes control and BP control current guidelines also recommend high intensity statin use to reduce CV risk in patients with clinically significant atherosclerotic cardiovascular disease moderate intensity stain therapy can be considered for all patients >75, and statin therapy also reccomeded for all patients 40-75 w/ diabetes, baseline LDL > 190, or estimated 10 year ASCVD risk >7.5

Pt with pulsatile nontender mass above umbilicus with high BP

abdominal US probably abdominal aortic aneurysm- usually asymptomatic and discovered incidentally

Pt who is taking warfarin and eating lots of leafy greens and tylenol for pain and now having inc. bleeding

acetaminophen taken at nighter doses may significantly inc. the anticoagulant effect of warfarin- possibly via enzyme inhibition of vitamin K metabolism Acetaminophen, NSAIDs, amidarone, and antibiotics may potentiate the anticoagulant effect of warfarin and may inc. the risk of bleeding

What RF involves the highest rate of aneurysm expansion and rupture?

active smoking RF for the development of AAA include: older age >60yo, cigarette smoking, family history of AAA, white race, and atherosclerosis the main RF associated with aneurysm expansion include large diameter, rate of expansion and current cigarette smoking- but current cigarette smoking is associated with the highest rate of aneurysm rupture the current indications for operative or endovascular repair include: aneurysm size >5.5, rapid rate of aneurysm expansion, and presence of symptoms (abd pain, back or flank pain)

Pt who developed afib after CABG- causing hemodynamic instability with signs of cariogenic shock and pulmonary edema

all patients with a pulse who have persistent tachyarrythmia (narrow or wide complex) causing clinical or hemodynamic instability (hypotension, cariogenic shock, signs of ischemia, acute HF) should be managed with immediate and direct cardioversion with cardioversion, energy delivery is synchronized to the QRS complex to minimize the likelihood of the shock occurring during repolarization (which can precipitate v fib) in contrast immediate v fib provides high energy shock at a random point in the cardiac cycle (unsynchronized shock) and is indicated in patients with v fib or pulseless ventricular tachycardia

Pt with several runs of v tachycardia, and pt has persistent a fib, and pt put on new medication but gets PFTs done

amiodarone- class I antiarrythmic used for management of ventricular arrhythmias in patients with CAD and ischemic cardiomyopathy, amiodarone can cause several potential adverse effects- so they undergo pulm function tests and thyroid tests, lung effects would be chronic interstitial pneumonitis but also can cause acute respiratory distress syndrome, baseline PFT and X-rays are usually done before starting drug

Pt with new onset dyspnea and ankle leg swelling, proteinuria and easy bruising, smoking and drinking history, JVD and scattered bibasilar crackles, echo shows small pericardial effusion, concentric thickining of ventricular walls and diastolic dysfunction

amyloidosis amyloidosis can present with waxy skin, macroglossina, hepatomegaly and peripheral (carpel tunnel syndrome) and /or autonomic neuropathy (orthostatic hypotension) cardiac amyloidosis should be suspected in patients with unexplained CHF, (with predominated diastolic dysfunction), low voltage on echo, and echo should inc. ventricular wall thickness and normal LV cavity dimensions (in a pt w/o hypertension)- tissue biopsy can confirm diagnosis, concentric thickening of ventricular walls

Pt who came in after a MVA bruises noted Pt gets foley catheter and IV fluid, 30 mins after arrival he is getting difficulty breathing and lightheadedness, low BP, high HR and erythematous rash over chest and abdomen

anaphylaxis due to latex allergy, IgE mediated type I HS- urticarial skin rash, rhino conjunctivitis and anaphylaxis, in individuals with previous or repeated exposure "sentization" by repeated exposure creating IgE antibodies, and this is a widespread reaction to the antigen- massive release of histamine and other substances from mast cells and basophils- vasodilation leading to dec. peripheral resistance, leakage of intravascular fluid leading to hypotension, tachycardia and poor oxygen perfusion, bronchoconstriction leads to dyspnea and wheezing and upper airway edema- tx. is rapid epi

Pt with SOB and nonproductive cough, told to inc. furesomide dose and 6 mo ago went into v fib and got antiarrythmic therapy, bilateral lung infiltrations seen on middle lung fields

antiarrythmic tocicity- amidarone pt with progressive dyspnea, nonproductive cough, bilateral inspiratory crackles- amidarone induced interstitial pneumonitis, localized or diffuse reticular or ground glass opacities- pulm tests show a restrictive pattern with reduced diffusion capacity of CO amidarone is a class III antiarrythmiic- for management of ventricular arrythmias, it can cause chronic interstitial pneumonitis within months of use, organizing pneumonia, ARDs, diffuse alveolar hemorrhage, pulm nodules and solidity masses interstitial pneumonitis due to amidarone use can occur months to several years after the initiation of therapy , progressive dyspnea, nonproductive cough and new reticular or ground glass opacities on chest radiograph

Pt having aortic dissection, and while being prepped for surgery chest auscultation reveals bibasilar crackles- what is the cause for this patients SOB?

aortic valve insufficiency aortic dissection involving the ascending aorta (type A) has high mortality, retrograde extension of the intimal tear can cause acute aortic regurgitation and pts can have worsening of chest pain, hypotension and pulmonary edema with early decrescendo diastolic murmur of AR Hypertension is the most common factor for aortic dissection

Pt brought to ER after passing out at home, he had several muscle jerks while unconscious, when measuring BP, notice frequent ectopic beats, he had a prior MI 5 yrs ago, PE shows 2/6 holosystolic apical murmur radiating to the axilla- what is the cause of this event

arrhythmia syncope is a transient loss of consciousness accompanied by loss of postural or motor tone w/ a spontaneous return to baseline in neurological function pt with structural heart disease (prior MI, murmur of mitral regurg) along with frequent ectopic beats-arhythmic cause of syncope, pts with cardiac arrythmias usually have underlying cardiac disorders (coronary artery disease, cardiomyopathy valvular heart disease) and may not have prodromal symptoms prior to this syncopal episode those with vasovagal or neurocardiogenic syncope frequently experience a prodrome w/ nausea, pallor, diaphoresis and a generalized sense of warmth prior to syncopal episode

Pt with early onset hypertension and relative who died early too with bilateral upper abdominal masses

autosomal dominant PKD, hypertension, hematuria, proteinuria, palpable renal masses, and progressive renal insufficiency, extra renal complications include cerebral aneurysms, hepatic or pancreatic cysts, cardiac valvular abnormalities (MVP or aortic regurg), colonic diverticula,, ventral and/or inguinal hernias, the diagnosis of ADPKD is mainly on abdominal US- showing enlarged kidneys with numerous cysts ACEinhibitors are the preferred medication They may have flank pain due to renal calculi, cyst rupture or hemorrhage or urinary tract infections

Pt having occasional palpitations, maternal uncle suddenly died at 40, and one of cousins had heart surgery, when pt sits up leans forward and holds breath in expiration, the stethoscope diaphragm is placed at the sternal border left side and decrescendo early diastolic murmur

bicuspid aortic valve aortic regurgitation EARLY descrescedo diastolic murmur= aortic Regurgitation best heard along the L sternal border at the 3rd of 4th intercostal space while pt wis sitting up , leaning forward in full expiration in young patients BAV can cause AR b/c of aortic root dilation, in older pts it can cause aortic stenosis Bicuspid aortic valve is the most common cause of isolated aortic regurg in young adults in developed countries

48 yo pt with progressive exertional dyspnea, has become progressively more short of breath, harsh systolic murmur heart at right second intercostal space with radiation to the carotids and S4 heard at apex

bicuspid aortic valve pt suffering from CHF as a consqeuence of AS, S4 as a result of L atrial kick against a stiff ventricle, high resistance generated by stenosed aortic valve causes concentric hypertrophy causing an S4- 3 most common causes are 1) calcified aortic stenosis 2) bicuspid aortic valve 3) rheumatic heart disease pt is of young age, bicuspid aortic valve is the primary cause of AS in pts <70yo

Pt with diarrhea, nausea, and dec. appetite with fatigue and palpitations- she takes furesomide, metoprolol, digoxin and warfarin and lung auscultation reveals scattered wheezes, what is most appropriative initial test

blood drug level digoxin level digoxin is a cardiac glycoside used to treat a fib and HF- digoxin toxicity can include N/V/ dec. appetite/ confusion and weakness patients can also have blurry vision and changes in color an event like a viral illness or diuretic can cause the levels to increase hypokalemic which is often associated with diuretic use- can inc. pts susceptibility to toxic effects of digoxin

Pt most likely has peri-infarction pericarditis, occurs b/c of local inflammation and usually <4 days following MI-pts experience pleuritic chest pain, that improves with sitting up and radiates posteriorly to the trapezius ridges

cardiac auscultation indicates a pericardial friction rub, and ECG reveals diffuse ST segment elevation, treatmentt is usually supportive anti-inflammatory agents like NSAIDS and corticosteroids are avoided b/c of impairment of collagen patients with peri infarction pericarditis typically has pleuritic chest pain, pericardial friction rub and diffuse ST elevation on ecg <4 days post MI NSAIDS/colchcine would be for idiopathic or viral

55 yo man brough in for sudden onset palpitations and chest tightness- cardiac monitoring shows A fib with high rate and as nurse attempts to get IV access, patient becomes unresponsive, pt has no palpable pulses and has agonal breathing and cardiac monitoring shows afib at the same rate

chest compressions pulseless electrical activity- organized rhythm on cardiac monitor w/o measurable BP or palpable pulse management of pulseless electrical activity should be with CPR and vasopressor therapy (epi) to achieve adequate cerebral and coronary perfusion no synchronized cardio version or v fib in patients with pulseless electrical activity BUT pulseless ventricular tacycardia does require defibrillation reversible causes of pulseless EA: hypovolemia/ hypoxemia/ Hydrogen ions/ Hypokalemia/ Hypothermia Tension Pneumothorax/ Tamponade/ Toxins/ Thromboss/ Trauma

Management for GERD

chest pain that occurs at rest or after meals and associated laryngopharyngeal irritation (cough, hoarseness) appropriate tx is lifestyle changes w/ H2 receptor antagonist or PPI (omeprazole)

Pt has NSTEMI and gets a drug eluting stent, what meds does he need?

chest pain, ST seg depression, troponin elevation, pt needs 1) dual anti platelet therapy-aspirin and P2y12 receptor blockers [for at least 12mo] 2) B blockers 3) ACEi or ARBs 4) Statins 5) Aldosterone antagonists

Pt with coronary angiogram and stent placement for chest pain 5 days ago he also have hypertension, hypercholesterolemia and PAD and physical exam shows painless purple motting of the skin of both feet labs show low Hbg, high BUN/Cr and low C3 levels

cholesterol emboli systemic artheroemborism- from disruption of athersclerottic aortic plaques (cholesterol crystal embolization) this dx should be suspected in individuals with acute/subacute RF, typical skin manifestations, and/or GI symptoms after a recent vascular procedure Lived reticulis- reticular, erythematous purple discoloration of the skin that blanches, labs can show eosinophilia and eosinophiluria and hypocomplementemia

33 yo with exertional dyspnea, pounding heart sensation, and widened pulse pressure BP= 150/45 noticed pounding most when laying on left side

chronic aortic regurg a portion of LV output leads back into LV- causing an inc. in LVEDV, myocardial hypertrophy and chamber enlargement this inc. the LV size and brings apex closer to chest wall so lying on left makes pounding aware most common cause of AR in underdeveloped countries is rhumatic disease and in developed countries aortic root dilation or congenital bicuspid aortic valve widened PP "water hammer" pulse- rapid upstroke with rapid collapse of peripheral pulse early diastolic murmur that is high pitched

Pt with severe substernal chest pain and ST elevations in leads V1-V4 consistent with acute anterior ST elevation MI with psychomotor agitation, dilated pupils tachycardia and hypertension with multiple ER visits for chest pain

cocaine abuse- cocaine is a sympathomimetic agent- that promotes thrombus formation and inc. risk of myocardial ischemia and infarction by inc. myocardial oxygen demand patients with acute cocaine intoxication are treated with IV benzos to alleviate psychomotor agitation and sympathomimetic effects (tachycardia, hypertension) those with ACS are managed with anti platelet therapy, nitrates and PCI, but B blockers should be avoided due to risk of unopposed cocaine induced alpha agonist activity and worsening vasoconstriction

Pt with crescendo-decrescendo systolic murmur along the L sternal border w/o carotid radiation present in HOCM- inter ventricular septal hypertrophy

common symptoms include dyspnea, syncope and chest pain and syncope in HCOM is multifactorial, in large part due to outflow obstruction from hypertrophied myocardium but syncope can also be due to arrhythmia, ischemia, and ventricular baroreceptor response- inappropriately causes vasodilation

Pt with substernal discomfort, left sided neck pain, diaphoresis and dyspnea

consistent with acute coronary syndrome an abnormal 4th heart sound (atrial gallop) can be heard during the acute phase of MI, due to LV stiffening and dysfunction induced by MI S4 is also heard in patients with dec. LV compliance, including those with hypertensive heart disease aortic stenosis and hypertrophic cardiomyopathy

Pt with dyspnea, orthopnea, PND, bibasilar crackles and hypoxemia

consistent with acute pulmonary edema- due to acute decompensated HF- most commonly due to LV systolic or diastolic dysfunction without additional cardiac disease but pulmonary edema can occur in the setting of normal LV function like uncontrolled htn acute management of acute decompensated HF is oxygen and IV diuretics, IV nitroglycerin (vasodilator) can be given to people with mitral regurg or symptomatic myocardial ischemia

Pt with presentation of RHF, previously tx for hodgkin's lymphoma

constrictive pericarditis from radiation therapy potential cardiac complications of hodgkin's lymphoma include acute or delayed pericardial disease, myocardial ischemia, restrictive cardiomyopathy, CHF, valvular anomalies and conduction defects constrictive pericarditis occurs as a result of scarring and subsequent loss of normal elasciticty of the pericardial sec- and the inelastic pericardium prevents venous return to the right heart during inspiration and causes right heart failure- peripheral edema, ascites, hepatic congestion, elevated JVP, with prominent X and Y descents, hepatojugular reflux, kussmall sign (lack of inc. of JVP on inspiration) and pericardial knock patients may have pericardial calcifications on chest radiograph, echo shows increased pericardial thickness, abnormal septum motion and biatrial enlargement- per careteidectomy is the definitive treatment

22 yo pt with recurrent syncopal episodes can be brought on by emotional distress, episodes preceded by lightheadedness, blurred vision and rapid recovery of consciousness, cardiac work up is normal

counter pressure maneuver education Neurocardiogenic (vasovagal) syncope can be triggered by emotional stimuli associated with prodromal symptoms patients with recurrent episodes are advised to avoid triggers and assume a supine position w/ leg raising and physical counter pressure maneuvers [leg crossing, tensing of muscles] during prodromal phase can inc. venous return and sometimes aborting syncopal episodes

Pt taking niacin for hypertriglyceredemia and gets flushing

cutaneous flushing and generalized prutitis, these effects are explained by niacin induced peripheral vasodilation--drug induced release of histamines and prostaglandins, not hypersensitivity reaction low dose aspirin can prevent cutaneous flushing if taken 30 mins before niacin

Pt with inc. BP and admitted to hospital on IV furesomide and nitroprusside with improvement of symptoms and the next day the nurse finds him confused and agitated with generalized tonic-clonic seizures-normal breath sounds bilaterally and no foci of muscle weakness

cyanide toxicity pt with severe hypertension and associated acute end organ damage (renal failure and signs of CHF)- these findings are suggestive of hypertensive emergency, and nitroprusside if a parenteral vasodialator- metabolism of nitroprusside released NO and cyanide ions (nitric oxide induces arteriolar and venous vasodilation), cyanide toxicity is most common in patients with renal insufficiency- altered mental status, lactic acidosis and seizures, and coma so pt has acute improvement in symptoms followed by decline- most likely due to cyanide toxicity alcohol withdrawal usually peaks after 2nd day of cessation

pt with weakness and dyspnea over the past 2 days, upper respiratory illness 3 weeks ago but symptoms never resolved completely, BP is 87/60, pulse is 109, high internal jugular pressure 11cm H2O, LCA, but heard sounds muffled what is cause of pt's complaints

dec. LV preload pt presentation suggests pericardial effusion and cardiac tamponade most likely infectious etiology (viral) due to upper respiratory viral illness Beck's triad: hypotension, distended neck veins, muffled heart sounds and can have pulsus paradoxicus >10mmHg drop in SBP during inspiration, and abdominal exam can have positive hepatojugular reflux fluid accumulation in pericardiac cavity, restricts venous return to the heart and lowers right and left ventricular filling--dec. preload, SV, and CO Lungs are CTA inspiration worsens b/c of inc. preload to RA and RV and then shifts septum into LV and impaired filling so >10mmHg difference (pulsus paradoxicus)

Pt with dyspnea, third heart sound, bibasilar crackles and low ejection fraction on echo

decompensated CHF due to LV systolic dysfunction, this pt has no evidence of CAD on angiopathy- most likely dialed cardiomyopathy due to heavy alcohol consumption (microcytic anemia, thrombocytopenia and 2>1 ratio of AST to ALT) alcoholic cardiomyopathy is a diagnosis of exclusion in its with dilated cardiomyopathy and h/o alcohol abuse in whom no other potential causes of cardiomyopathy (CAD, valvular HD) are suspected or identified the degrees of LV dysfunction in alcoholic cardiomyopathy is correlated to duration of alcohol intake- and the primary therapy for these pts is alcohol abstinence and intervention is associated with improvement of normalization of LV function over time

Pt with severe heart failure- dyspnea, orthopnea, LE edema, displaced apical impulse, and bilateral lung crackles,

decompensated CHF, due to LV systolic dysfunction hyponatremia in CHF usually parallels the severity of the HF and is an independent predictor of advise clinical outcomes in pts with CHF, low CO, with dec. peripheral perfusion at the baroreceptors and renal afferent arterioles, leads to neurohumoral activation (with release of renin and norepinephrine) and secretion of ADH- which binds to V2 receptor in the renal collecting tubules and promotes water reabsorption, while renin and noepi inc. proximal sodium and water reabsorption= promotes free water retention and causes dilution hyponatremia

Pt with ECG that shows NSR and 1st deg AV block even though he has chest pain that is worse with moving his arm

delayed impulse transmission from atria to ventricles can occur in-atria, AV node, bundle of his, bundle branches/fassicles,, most first degree AV blocks with normal QRS- are due to conduction delay in AV node unless there is syncope and the chest pain is musculoskeletal (Pr interval >5boxes) most first degree AV block with prolonged QRS duration- likely has conduction delay below the AV node and should undergo electrophysiology testing

64 yo with palpitations and SOB, pt has choking sensation w/ dry cough every time he tries to lie down, high BP (180s systolic), high HR, and bibasilar crackles 2+ pitting edema in LE echo shows normal size LV with LV hypertrophy, LV EF 55% what is most likely responsible for symptoms?

diastolic dysfunction HF with preserved left EF= diastolic dysfunction pt with extensional dyspnea, orthopnea, bibasilar rales, LE edema and normal EF on echo, HF, and this is due to hypertensive Heart Dis, pt BP (182/105) w/ LV hypertrophy on echo, but LV size can be normal or inc., can see abnormal LV filling by echo--impaired myocardial relaxation and inc. LV wall stiffness (Dec. compliance)--> inc. LV EDP which is transmitted to the LA and pulm veins-- causing pulm congestion, dyspnea and ex intolerance, and further exacerbated by loss of "atrial kick" and short diastolic filling times in patients who develop a fib

30yo with symptoms of CHF had a cold two weeks ago

dilated ventricles with diffuse hypokinesea h/o recent URI followed by sudden onset cardiac failure--suggestive of dilated cardiomyopathy (secondary to acute viral myocarditis) dilated cardiomyopathy is the end result of myocardial damaged produced by toxic, metabolic and infectious agents cocksackie B viral infection (other viruses include parvovirus B 19, HHV6, adenovirus, enterovirus) viral myocariditis can cause dilated cardiomyopathy as a result of humoral or cellular immune responses diagnosis is made by echocardiogram which shows dilated ventricles with diffuse hypokinesia--resulting in low EF tx is management of CHF symptoms

Pt given antihypertensive medication- enhances naturesis, dec. and II levels and dec. aldo production?

direct renin inhibitor renin is produced by JG cells- cleaves angiotensinogen II to angiotensin 1- which is converted to angiotensin 2 by ACE, and angiotensin 2 is a vasoconstrictor and promotes aldo production in the adrenal cortex, and aldo acts on collecting tubules to inc. Na and Water reabsorption would also be ACE i but this wasn't an answer choice

Pt with Pulm Htn but dilated LV w/ EF 30% best tx

diuretics and ace-i pt with progressive SOB, tricuspid regurg (systolic murmur at the sternal border, inc with inspiration) peripheral edema, and echo findings suggestive of pulm htn PH=mean pulm art pressure >25 at rest PH can be idiopathic or due to LV heart, chronic lung disease, thromboembolism This patient's PH is likely due to LV systolic dysfunction (reduced EF and signs of pulm edema)- and management in this case would be loop diuretics and Ace-i often with B blockers sometimes with aldo-antagonists

Pt taking digoxin for nonischemic cardiomyopathy and then amiodarone was added for afib and then he got anorexia, nausea, weakness

drug interaction digoxin toxicity b/c amiadorone was added on acute digoxin toxicity- GI symptoms (anorexia, nausea, vomiting, abd pain) along with weakness and confusion chronic digoxin toxicity- less Gi symptoms, more neurologic (lethargy, fatigue, confusion) and visual changes amiadarone can inc. digoxin level- it is recommended digoxin dose be decreased 25-50% when initiating amiadarone

Pt developing hemodynamic complications just days after an MI

during this point in the healing process the infrared myocardium is the softest and most prone to rupture the 3 major mechanical complications of MI include MR due to papillary muscle rupture, LV free wall rupture and IV septum rupture the patient who has an inferior wall MI with delayed presentation, sudden onset hypotension dyspnea, and tachycardia pulmonary edema and a soft systolic murmur- consistent with acute MR from posteromedial papillary muscle rupture- acute onset pulmonary edema, mid to late systolic murmur consistent with MR and possible cariogenic shock, diagnosis is confirmed by echo

Pt with continuous early diastolic murmur heard best at the L sternal border best heard with expiration what is the best step in management of this patient?

echocardiogram diastolic and continuous murmurs are usually due to an underlying pathologic cause their further eval should be with a trans thoracic echo- which can identify valvular regurg and evaluate for any associated structural abnormalities or hemodynamic consequences aortic regurg leads to a early and gradually decreasing decrescendo diastolic murmur that begins immediatly after A2, the murmur is high pitched and blowing in quality and best heard along the L sternal border at the third and fourth intercostal space with patient sitting up and leaning forward while holding breath in full expiration

Pt comes to ER after episode of syncope he had upper respiratory infection 1 week ago, his neck veins are distended and his heart sounds are distant, lungs clear to auscultation bilaterally, chest X-ray shows small bilateral pleural effusions and an enlarged cardiac siloutthe what EKG finding is specific for this condition?

electrical alterans -QRS complexes that vary from beat to beat pt has pericardial effusion JVD, muffled heart sound and and borderline BP can indicate cardiac tamponade echo will very definitely demonstrate pericardial effusion

Pt found dead after an MI years before and autoposy showed anterior scar with large LV ventricle and thinned walls what would have prevented the pathological findings

enalapril after MI, ventricular remodeling occurs, and gradually causes dilation of LV w/ thinning of LV walls- this can result in CHF ventricular remodeling weeks-months following an MI therefore not seen on discharge echocardiogram ACE i- limit ventricular remodeling

34 yo man with frequent headaches, very high BP, and 4th heart sound, murmur throughout thorax in multiple areas what will be see on chest X-ray

erosions of the inferior costal surfaces coarctation of the aorta, narrowing of the descending aorta, creates a proximal arterial pressure load affecting the upper body, pts can have asymptomatic hypertension with epistaxis and headaches, PE shows brachial-femoral delay pulse and there may be a systolic murmur. the murmur may be continuous if the collateral vessels are present and 4th heart sound may also be present chest xray will show notching in posterior 3rd-8th ribs, bony erosions due to enlarged intracoastal arteries

Pt with PAD what is the best initial management? has already been started on aspirin and statin

exercise therapy CAD risk equivalent and the medical therapy should include aggressive RF modification w/ counseling for smoking cessation, lipid lowering therapy and tx for htn and DM pt is started appropriately on low dose aspirin and statin and next step is supervised exercise program and after this if symptoms persist, then use cilostazol and percutaneous/surgurical revascularization

pt suddenly collapsing during conditions drills, temp high, BP low, pulse high, respirations high lung exam has rales at both lung bases skin is hot with diffuse sweating hbg high, leukocytes high BUN high

exertional heat stroke young military recruit with hyperthermia, confusion and multi organ dysfunction, findings suggestive of exertion heat stroke the pt was taking an antihistamine which also has anticholinergic activity and can further impair heat dissipation exertional heat stroke is defined as body temp >104 degrees with CNS dysfunction-seizures, ARDs, DIC, and hepatic or renal failure may occur dehydration is common which causes hypotension, tachycardia, and hemoconcentration (high hbg, elevated leuks, and platelets) and BUN tx is rapid cooling, preferably ice-water immersion, fluid resuscitation and management of end organ complications nonexertional (classic) heat stroke can have similar features it occurs in the absence of strenuous activity and affects elderly patients, management of this is evaporative cooling (leukwarm water as fan blows air)

Pt presentation suggestive of aortic stenosis

exertional symptoms (chest pain, dyspnea,, dizziness, and syncope), Delayed and diminished carotid pulse (pulsus parvus et trades), single and soft S2, audible S3, and harsh ejection (crescendo-decrescendo) systolic murmur in the right 2nd intercostal space with radiation to the carotids a trans thoracic echo should be obtained in all patients with syncope due to suspected structural heart disease (aortic stenosis, hypertrophic cardiomyopathy LV dysfunction) and patients with very severe AS should undergo a valve replacement

Major SE of amidarone

fatigue, memory loss, constipation, weight gain, - amidarone induced hypothyroidism and possible hepatocellular injury from amidarone amidarone is used for serious ventricular arrhythmias and for afib with underlying LV systolic dysfunction- pts should be monitored with periodic thyroid and hepatic function panels and pulm symptoms with chest X-ray and PFT

young pt with hypertension, recurrent headaches, bp b/t both arms is similar and full peripheral pulses and bruit heard near carotid

fibromuscular dysplasia- internal carotid artery stenosis ( headaches, pulsatile tinnitus, TIA, stroke) and renal a stenosis (secondary htn, flank pain), can find subarticular systolic bruit and abdominal bruit and diagnosis is UA or MRA or catheter based angiography and tx is antihypertensive PTA or surgery recurrent headache or carotid artery stenosis or aneurysm is the most common presenting symptom- pulsatile tinnitus, flank pain or neck pain are also common, here the internal carotid artery is involved and this usually isn't in atherosclerosis

Pt with paraxosymal a fib- given medication and 2 weeks after after stress testing see widening of QRS complex

flecanimide- class I antiarrythmic that blocks sodium channels after inhibiting the initial depolarization of the action potential, Flecainide and Propafenone are class IC antiarrythmics occasionally used for a fib, in faster HR the drug has less time to dissociate from sodium channels= high number of blocked channels, causing a progressive decrease in impulse conduction and widening of QRS complex= this is called use dependence

acute stabalization of STEMI pt with ischemic HF secondary to an acute anterior wall MI causing acute pulmonary edema (flash pulm edema)

given furesomide already been given, aspirin, statin and clopodigrel loop dieurtic is needed- dec. pulm edema and dec. preload--dec. PCWP and furesomide causes venodialation which also lowers preload, be careful in hypovolemia can also give nitroglycerin (but avoid if pt is hypotensive) ultimately emergency revasculatization (PC angioplasty or thrombolytics needed) so in this cause---b/c pt has pulmonary Edema--needs loop dieuretic and B blockers are also standard therapy in MI but should be avoided in pt with decompensated HF or bradycardia

Pt with acute arterial occlusion, pt has irregular heart beat and palpitations issues in both limbs pain/ pallor/ poiklothermia (cool extremity), paresthesia, pulselessness, and paralysis next step?

heparin infusion most likely due to thromboembolic occasion from LA from A fib can lead to immediately threatened limb (sensory loss, rest pain, muscle weakness) needs immediate anticoagulation heparin prevents thrombus progression and thrombosis in the distal arterial and venous circulation

64yo man having aortic dissection, worst pain of his life, hasn't seen doc in 20 years and hasn't gotten any tx, diastolic decrescendo murmur along L sternal border and ECG shows sinus tachycardia and nonspecific ST and T wave changes X-ray shows widening of mediastinum, what most likely accounts

hypertension severe sudden chest and back pain and diastolic decrescendo (aortic regurg) and widening of mediastinum on X-ray with nonspecific ST and T wave changes- acute aortic dissection involving ascending aorta, systemic hyptertension is the most important predisposing factor, twice as common as in its with type B (descending aorta) dissection compared to type A (ascending aorta)- a sudden and transient inc. in BP is noted in patients with acute aortic dissection, pts are usually >60yo and may have a prior aortic aneurysm, atherosclerosis alone doesn't inc. predisposition to aortic dissection Marfan is a cause of aortic dissection but not common in older individuals, is is responsible for 50% of aortic dissections in patients less than 40yo

Pt with 3rd trimester vaginal bleeding, abd tenderness and evidence of poor organ/tissue perfusion (altered mental status, weak peripheral pulses)

hypovolemic shock from massive hemorrhage-abbruptio placentae, loss of IV volume dec. LV preload, causing dec. CO, and dec. systemic BP, this in turn stimulates the SNS causing inc. HR and peripheral vasoconstriction (inc. SVR in order to maintain CO)- PCWP is representative of LA pressure and dec. due to intravascular vol loss

Pt with persistent tachyarrythmia that is causing hemodynamic instability

immediate synchronized cardioversion common causes of narrow SVT include- inappropriate sinus tachycardia, a tachycardia a flutter, AV nodal re-entrant tachy all pt's with persistent tachyarrythmia (wide or narrow) causing hemodynamic instability should be managed with immediate synchronized direct current cardioversion

Pt with recurrent hematuria, comes to ER after "passing out", after urinating he passed out from loss of consciousness and EEG shows Mobitz type I second deg block

impaired AV nodal conduction the EEG shows progressive prolongation of the PR interval leading to nonconducted P waves and a "dropped" QRS- consistent with Mobitz type I (constant P-P interval, increasing PR interval, decreasing R-R interval, Group beating [repeating clusters of beats followed by dropped QRS]) in younger patients its asymptomatic and benign but in older its it may cause significant bradycardia with symptoms of inadequate CO (fatigue, lightheadedness, angina, syncope, HF)

Pt with WPW and then develops A fib

in WPW, an accessory pathway conducts depolarization directly from atria to the ventricles without transversing the AV node, A fib occurs in 10-30% of individuals with WPW, WPW can bypass the rate limiting function of the AV node leading to rapid ventricular response rates- and persistent AF with a rapid ventricular response in patients with WPW can ultimately deteriorate into vfib hemodynamically unstable pts require electrical cardioversion or for stable patients rhythm control with meds like IV ibutilide and procainamide AV nodal blocking agents like adenosine , b blockers, CCB and digoxin should not be used in AF in pts with WPW as they may promote conduction across the accessory pathway and lead to degeneration of AF into VF

Pt with asymptomatic bilateral carotid artery stenosis

in setting of multiple atherosclerotic RF (hypertension, prior smoking)- these patients should receive intensive medical therapy anti platelet agent (aspirin) a statin and careful BP control symptomatic carotid stenosis- occurrence of TIA or stroke in the distribution of the affected artery , carotid endarterectomyectomy for symptomatic patients which high grade carotid artery stenosis asymptomatic carotid stenosis- carotid atherosclerosis without recent TIA or stroke, its with lower grade lesions are managed medically

32yo man with 6mo of progressive weakness and exertion dyspnea, previously had a knife injury that healed after suturing, alcohol and crack, and brother died of CF and bp is 160/60 and right leg is warmed and more flushed, PMI is displaced and small systolic murmur that doesn't change with valsalva- what is the cause of the patients symptoms?

inc. in cardiac preload high output HF after a traumatic injury to his right thigh, like a symptomatic AV fistula of the popliteal or iliac artery at the site of injury symptomatic AVF can be congenital or acquired, and abnormal connection b/t the arterial and venous systems that bypasses the capillary beds, shunting a large amount of blood thought he fistula dec. systemic vascular resistance, inc. cardiac preload and inc. CO clinical signs include widened pulse pressure, strong peripheral arterial pulsation (brisk carotid upstroke), systolic flow murmur, tachycardia, and flushed extremities, the LV hypertrophies and the PMI is displaced to the L, and ECG shows LVH in its with AVF the AV shunting causes an compensatory inc. in HR and SV to meet the oxygen requirements of peripheral tissues, cardiac function can decompensated over a period of time and result in cardiac failure doppler US is the preferred test to diagnose AVF in an extremity, and surgical therapy is indicated in a large AVF

aortic stenosis

increased intensity of apical impulse, narrow pulse pressure and typical systolic murmur

64 yo man with malaise and palpitations, echo last year showed mild atrial dilation and LVH, ECG shows A-fib

irregularly irregular rhythm w/ narrow complex tachycardia and no organized P waves, consistent with a fib w/ RVR AF is a supra ventricular tachyarythmia, and ventricular rates can go as high as 150/min hemodynamically unstable-- emergency synchronized cardioversion stable patients-- medical therapy (B blockers, diltiazam, digoxin) and should consider rhythm control if this doesn't work all pt's should undergo CHADs score to determine risk, this pt score is 2 so should be started on warfarin or other anticoagulation (dagibatrin, rivaraxabn, apibixan)- to reduce systemic thromboembolism (for PVST- sudden onset narrow rhythm--can use adenosine or carotid massage)

Pt has symptomatic AF with rapid ventricular response and additional features suggesting hyperthyroidism ( weight loss, lid lag and hand tremor)

it is the most common supra ventricular arrythmia in hyperthyroidism, thyroid hormones cause an increase in B adrenergic receptor expression, leading to an inc. in sympathetic activity B blockers are first line therapy- to control HR and hyperadrenergic symptoms, and propranolol dec. conversion from T4--> T3 in peripheral tissues even though pt has afib the underlying cause in hyperthyroidism so that needs to be addressed

Pt 47 with signs of new onset diabetes, what does he need for cholesterol?

lifestyle modification + Statin 40-75 with diabetes= statin + glucose lowering 10 yr risk of athleroscolerotic dis <7.5%= moderate intensity stain and greater than 7.5%= high intensity statin

AA man with exertion dyspnea and cardiac findings over apex show TEN-es-see sound

long standing hypertension causing an S4 sound, and this is an indicator of a stiff left ventricle- which occurs in the setting of restrictive cardiomyopathy or LV hypertrophy from prolonged hypertension near the end of diastole, S4 corresponds to atrial contraction- the sound of blood striking a stiff ventricle so this patient with exertion dyspnea and S4 likely indicate the presence of diastolic HF (from LVH from prolonged hypertension)

Pretest prob for CAD

low risk is men <40 and women <50 w/ atypical chest pain and no sig cardiac RF like FH patients with high risk features for symptomatic CAD should be evaluated for coronary angiography, stress testing is most helpful for risk stratification in patients with intermediate risk features

62 yo female with episode of syncope progressive exertional dyspnea and over apex holosystolic murmur

mitral regurg ID 4911, listen dec. CO and inc. LA pressure the dry cough may be due to pulm congestion and edema- LV dysfunction MR= holosystolic murmur best heard over apex with radiation to axilla MR could be due to primary disease (RHD, IE or trauma) or other cardiac conditions (ischemic heart disease, cardiomyopathy) can also develop a fib

Pt with mitral stenosis as a consequence of rheumatic heart disease causing atrial fibrillation (irregularly irregular rhythm with the absence of P waves)

mitral stenosis leads to dilation of the LA resulting in a-fib, MS is the most common manifestation from rheumatic heart disease, the auscultation findings of a loud S1 and a mid diastolic rumbling murmur at the apex are classic for mitral stenosis- this dilation of the LA predisposes to development of Afib, Afib causes a lack of an atrial kick- which could cause worsening flow through the stenotic mitral valve and inc congestion in the lungs-leading to the pos acute onset of dyspnea

20 yo with intermittent chest pain, sharp localized and lasts 5-10 seconds, and systolic murmur at the apex that shortens with squatting

mitral valve prolapse a short systolic murmur at the cardiac apex that disappears with squatting= MVP atypical chest pain/ dyspnea/ dizziness/ anxiety and nonspecific electrocardiographic changes= MVP syndrome usually a systolic click and/or mid to late systolic murmur of MR

Pt with peripheral edema, ascites, and elevated JVP w/ clear lung fields suggest right heart failure

most likely due to constrictive pericarditis thickened, calcified pericardium that limits diastolic filling idiopathic pericarditis of pericardial involvement from prior cardiac surgery (CABG or Cardiac valve) or mediastinal irridation, tb, malignancy, and uremia includes hepatic congestion and hepatomegaly until cardiac cirrhosis and pt's can have hypoalbuminemia (protein losing enteropathy) PE shows elevated JVP w/ prominent y descent, hepatojugular reflex, kussmal's sign, pericardial knock (mid distolic sound) and pericardial calcifications on radiograph Constrictive pericarditis is an important cause of RHF and characterized by progressive peripheral edema, ascites, elevated JVP, pericardial knock ( mid-diastolic sound), and pericardial calcifications on chest radiograph

pt with chest pain and severe dyspnea with elevated PCWP and dec cardiac index

most likely in cariogenic shock due to an acute MI disruption of blood flow to the myocardium results in myocardial death causing impaired contractility and acute LV failure dec. myocardial contractility causes dec. CI and resultingg hypotension and reflex tachycardia failure of forward flow causes blood to back up into the lungs- causing resultant pulmonary edema- that manifests as dyspnea, tachypnea and hypoxemia PCWP is elevated- and in an effort to maintain organ perfusion SVR is increased via vasoconstriction resulting in cool extremities

38 yo woman with fast irregular heart beat, apical impulse displaced to the left and third heart sounds and holosystolic murmur at the apex that radiates to the axilla?

myxatmous degeneration of the mitral valve this is consistent with severe mitral regurg and mitral valve prolapse is the most common cause of chronic MR in developed countries myxomatous degeneration of mitral valve cordae=mid systolic click followed by a mid to late systolic murmur the third heart sound is from the LV volume overload and chronic severe MR can lead to atrial dilation and A fib, LV dysfunction and CHF

Pt getting IV furosemide for HF symptoms, and very soon after gets wide complex ventricular tachycardia and PE showing dec leg edema and clear lungs

need to measure serum electrolytes, when a patient experiences recurrent VT, then first thing to do is stabilize and find the underlying cause pt most likely has electrolyte imbalance bc of diuretics- furesomide commonly causes hypokalemia and hypomagnesemia- and hypokalemia and hypomagnesemia can lead to v tachycardia- and hypokalemia potentiates the SE of digoxin- arrhythmias like v tachycardia- so initial approach would be serum electrolytes and serum digoxin level

Mechanism of giving Nitrates for angina

nitrates are vasodilators and dilate the veins, arterioles and coronary arteries, by relaxing vascular SM cells, and although they are veno dilators, their primary anti-ischemic effect is systemic vasodilation (rather can coronary vasodilation)- systemic vasodilation lowers preload and LV end diastolic volume and reduces myocardial oxygen demand by reducing wall stress, nitrates also cause arterial and arteriolar vasodilation to a lesser degree to dec. SVR and dec. BP

pt taken to ICU after being in motor vehicle accident and needed ex lap for possible bowel perf, two days after surgery he is hypotensive and required aggressive IV fluids and vasopressors to maintain BP, and extremities are cold to touch with lesion on fingers

noepi induced vasospasm, noepi has the alpha 1 agonist properties that cause vasoconstriction which can else inc. BP in hypotensive patients but in some patients with dec blood flow vasoconstriction can cause ischemia and necrosis of distal fingers and toes= symmetric duskiness and coolness of all fingertips

common causes of inadequate response to antihypertensive therapy

non adherence to lifestyle changes- diet, medication, and using meds that can reduce the response to antihypertensives (NSAIDs, decongestants, glucocorticoids) Nonpharmalogic therapy includes dietary salt restriction, diet rich in fruits/veggies, low fat dairy products, regular aerobic exercise, weight lifting and limiting alcohol intake excessive alcohol intake >2 drinks/day is associated with inc. hypertension

Pt with ST elevations in leads II, III, and avF

occlusion of RCA inferior and posterior wall MI II, III, avF are inferior wall MI and ST depression in V1 and V2 are posterior wall MI inferior MI is also associated with hypotension, bradycardia and AV block

Pt with 10 year calculated risk for cardiovascular disease 9% what is next best step for dyslipidemia (cholesterol is 292)

oral statin pt has severel RF for atherosclerotic cardiovascular disease- smoking, hyperlipidemia, age and male gender moderate intensity or high intensity statin for pt's 40-75 with estimated risk >7.5% and also for those 40-75% w/ diabetes or LDL >190

73 yo man who has been in bed for 1 week stands up and gets syncope

orthostatic hypotension drop in SBP >20mmHg from lying to standing it is common in patients who are elderly, hypovolemic, or have autonomic neuropathy (like diabetes or parkinson's) also meds like diuretics vasodialators, and adrenergic agents can cause orthostatic hypotension, prolonged recumbence inc. the risk pre syncopal light headed sensation

What helps to diagnose malignant hypertension in this patient

papilledema and retinal hemorrhages severe hypertension >180/120- can lead to auto regulation failure, vascular endothelial disruption, fibrinous deposition and narrowed vascular lumen hypertensive urgency- severe hypertension w/o end organ damage hypertensive emergency- sever hypertension w/ malignant hypertension (retinal hemorrhages/papilledema, or malignant nephrosclerosis) or hypertensive encephalopathy (cerebral edema, headache/n/v, can also get subarachnoid or intracerebral hemorrhage)

pt with peripheral edema on BP medication

peripheral edema is a common SE with the tx with dihydropyridine Ca channel antagonists like amlopidpine- these meds cause sig edema, due to the property to dialate blood vessels and if the edema is significant the drug should be discontinued should also consider HF, renal disease and venous insufficiency

67 yo man with resistant hypertension

persistent htn despite using 3 different antihypertensive meds renovascular hypertension is the most common correctable cause of secondary hypertension , renal artery stenosis can be present and systolic-diastolic abdominal bruit can be heard in 40% of patients (which is very specific for RAS) the diagnosis is confirmed by renal duplex doppler US, CT angiography or magnetic resonance angiography so renovascular hypertension is the ,most common correctable cause of secondary hypertension and should be suspected in all patients with diffuse atherosclerosis and resistant hypertension- and the presence of a systolic-diastolic abdominal bruit is highly specific for presence of renovascular hypertension

Pt with recurrent substernal chest pain elicited by strong emotion-suggesting stable angina

pharmacologic stress testing allows for evaluation of obstructive CAD in patients unable to perform adequate exercise (due to amputation) this pt's coronary artery vasodilator stress test (adenosine) reveals MI consistent with obstructive CAD adenosine stimulates A2A receptors on vascular SM cells, causing coronary vasodilation and inc. myocardial blood flow, there is augmentation in blood flow in the non obstructed vessels and blood flow is increased in the stenosed vessels but to a much lesser extent, the blood flow difference is magnified from rest, causing a reduction in radioisotope uptake by myocardial cells in areas supplied by stenoic vessels

Pt with lower extremity swelling due to chronic venous insufficiency caused by incompetence of venous valves causing venous hypertension in the deep venous systems in the legs

pitting edema is the most common PE finding, in severe cases, redirection of blood from the deep venous system to the superficial venous system may lead to other PE findings: abnormal venous dilation (telangtasias, vericose veins), skin discoloration, lipodermatosclerosis or skin ulceration (esp in medial aspect of lower leg), RF are advancing age, obesity, sedentary lifestyle, initial tx is leg elevation exercise and compression stockings and pts who do not respond to conservative measures should undergo venous duplex US to diagnose CVI by identification of venous reflux (retrograde venous flow) in deep venous system dieuretics would be useful in the management of HF but not in this case

CCB and pedal edema

preferential dilation of pre capillary vessels (arteriolar dilation) which leads to inc. cap hydrostatic pressure and fluid extraction into the interstituim- DHP CCB like amlodipine and nifedipine are potent arteriolar vasodilators and cause more peripheral edema than non-dihydropyridine CCB (diltiazam, verapamil)- other symptoms include headache, flushing, dizziness, RAAS antagonists like Ace/arbs cause post capillary venodialation and can normalize increased capillary hydrostatic pressure- combo of CCB and ACEi can lower chance of peripheral edema

Indications for statin therapy

primary prevention- estimated 10 yr risk > 7.5% secondary prevention- known ASCVD (MI or stroke), LDL >190

Pt with aortic stenosis murmur

progressive fatigue and exertion lightheadedness and pre syncope, delayed carotid pulses and mid systolic murmur over the right sternal border- suggestive of aortic stenosis can see 1. diminished to delayed carotid pulse (pulsus parvus and tardus) due to blood flow obstruction, 2. mid-to late- peaking systolic murmur from turbulence of the stenosis 3. presence of soft and single second heart sound (S2)- thickening and calcification of the aortic leaflets lead to a reduced mobility and cause a soft S2, as a result of reduced mobility A2 is delayed and occurs simultaneously with P2 closure causing a SINGLE S2

Pt with chest pain, diaphoresis, arm numbness and nausea, with ECG findings showing elevations in ST segments in II, III, and aVF, inferior STEMI- abrupt right coronary artery blockage

prompt restoration of coronary blood flow with primary percutaneous intervention (PCI) or fibronilysis limits myocardial damage and improves cardiovascular and overall long term mortality, recommended PCI within 90 mins of STEMI

pt comes form brazil with dyspnea w/o palpitations, dizziness, syncope, PMH sig for megacolon, on PE there was 1+ pitting edema and mild JVD and X-ray shows cardiomegaly

protozoal disease chagas- trapanosomi cruzi megacolon/megaesophagus and cardiac disease destruction of nerves controlling the GI smooth muscle and heart is due to prolonged myocarditis secondary to protozoal infection

Pt brought to ER after brief episode of syncope-h/o hypertension, stable coronary artery disease, type II DM and hyperlipidemia, pt has low BP, pt has cool extremities and capillary refill is 3 seconds and ecg is consistent with sinus bradycardia

pt has HR <60, regular rhythm and constant PR interval, normal resting HR is b/t 60-100, sinus bradycardia can occur in adolescents and younger adults, in well conditioned athletes and in elderly patients esp during sleep- pathologic causes include sick sinus syndrome, MI, OSA, hypothyroidism, inc. intracranial pressure and medications the first step for sinus bradycardia in symptomatic patients is IV atropine- for initial treatment of bradycardia and hypotension- if this response is inadequate, then other options include IV episodes, dopamine or transcutaneous pacing adenosine causes a transient block of rhythm at the AV node and can terminate some supraventricular tachycardias it can worsen bradycardia- so symptomatic patients with sinus bradycardia should be initially tx with IV atropine and if that is inadequate, further response with IV epi, dopamine or transcutaneous pacing

Pt admitted for chest pain (possible unstable angina) and appropriately treated, he has occasional episodes of dyspnea and coughing, he has allergic rhinitis and childhood eczema, he is given appropriate treatment including aspirin and ace inhibitor,

pt initially admitted for chest pain (possible unstable angina) and was appropriately treated, his subsequent acute onset dyspnea with wheezing and prolonged expiration indicated bronchoconstriction- h/o rhinitis and eczema w/ intermittent dyspnea and coughing suggest a possible undiagnosed asthma (now exacerbated by aspirin or a b blocker), aspirin and b blockers can trigger bronchoconstriction, cardioselective B blockers act only on B1 receptors- safe in patients with mild to moderate asthma ACEinhibitors can cause a dry cough (and this effect is seen over a few months)

Infective endocarditis in IV drug users

pt with 3day history of cough, fever, and weakness, BP is 120/80 and pulse is 110/min, PE shows multiple needle tracks in his arm, ECG shows sinus tachycardia and chest X-ray shows scattered lesions in lung there will be a systolic murmur that inc. on inspiration HIV inc. IE risk, S. aureus is most common organism, Tricuspid valve is most commonly involved, Holosystolic murmur inc. with inspiration, septic pulmonary emboli common, splinter hemorrhages, janeway lesions, HF more common if there is aortic valve involvement septc pulm emboli usually causes cough/chest pain/hemoptysis and creates alveolar infiltrates on imaging

Pt with systemic sclerosis, hypertension, and kidney injury, low hbg, low platelets normal leukocytes what will you see on blood smear?

pt with hypertension and acute kidney injury in the setting of systemic sclerosis (scleroderma)- scleroderma renal crisis, which can occur in 20% of patients with diffuse cutaneous systemic sclerosis- the mechanism involves vascular permeability, activation of the coagulation cascade and inc. renin secretion and its develop sudden onset of renal failure (w/o previous kidney disease) and malignant hypertension (headache, blurry vision, nausea), U/A is mild and can show mild proteinuria and blood smear can show MAHA- with fragmented blood cells (eg. schistocytes) and thrombocytopenia

Cardiac findings in marfan syndrome

pt with marfanoid habitus w/ chest and neck pain- acute aortic dissection, AD mutation in fibrillin 1, aortic dissection, mitral valve prolapse all marfan syndrome patients with acute chest pain require eval for acute aortic dissection, >20 SBP variation b/t arms patients with aortic dissection or aortic root dilation can develop aortic regurg- early decrescendo diastolic murmur at left sternal border 3/4 intercostal space with pt sitting up, leaning forward and holding breath after full expiration

Pt with V fib

pt with pressure like chest pain, dyspnea, and T wave inversions in lateral leads, MI or NSTMI , troponin may not be elevated in first 6 hrs when the patient became unresponsive, pt was having v fib on strip, and ventricular arrhythmias are common in patients who have MI in patients with sudden cardiac arrest due to VF, survival depends on early identification CPD and successful defibrillation- according to ACLD protocol, all pts with VF should be managed with immediate defibrillation to perfuse normal heart rhythm IN CONTRAST- patients with hemodynamic instability due to narrow or wide QRS arrhythmic (atrial fib etc) should be managed with synchronized cardio version

65yo with fatigue, poor appetite, and lower leg swelling and PMH is significant for htn, type II DM chronic cough chest infections and LE PAD and has 40yo packing smoking history barrel shaped chest with scattered wheezing, abdomen distended with 2+ pitting edema and dilated tortuous superficial veins and hepatojugular reflux- serum Na is 135 and creatinine is 1.2 what is cause of pt's edema?

pulm artery systolic pressure COPD with cor pulmonate impaired function of the RV caused by pulm hypertension (b/c of underlying disease to lungs (copd, interstitial disease), pulm vasculature (idiopathic PAH) or OSA pt's with cor pulmonale have exertional Symptoms (dyspnea, angina, syncope) anorexia, abdominal pain (due to hepatic congestion) and peripheral edema PE shows loud P2 and RV third ventricular heart sound, new tricuspid regurg murmur, elevated JVP, hepatomegaly and ascietes/pleural effusion the dx of cor pulmonate is clinical features and echocardiographic findings- RVH, tricuspid regurg w/ RAE and more definitive dx can be made with right heart cath showing elevated pulm artery systolic pressure >25

Pt with fatigue and dec exercise tolerance, occasional palpitations for months but no chest pain, ECG shows no clear P waves, and EF is 35%, moderate central mitral regurg, and L atrial and L ventricular dilation with global hyperkinesis- which intervention will restore function?

rate or rhythm control pt with progressive dyspnea, dec. exercise tolerance, a fib w/ rapid ventricular response, and LV systolic dysfunction= tachycardia mediated cardiomyopathy chronic tachycardia can cause structural changes in the heart including LV dilation and myocardial dysfunction most pts have palpitations and signs of CHF, dx requires electrocardiogram, echocardiogram, and assessment for other causes of LV dysfunction like CAD-aggressive rate control and restoration of normal sinus rhythm b/c of reversibility of tachycardia mediated cardiomyopathy and normalization of LV systolic function

Pt with localized chest pain that worsens with inspiration and movement, has pain at rest what to do?

reassurance msk chest pain, costochrondtiris, tenderness of >1 anterior chrondral joints tenderness to palpation of the affected area and reassurance with analgesics (acetaminophen, NSAIDS)

Pt with elevated cholesterol and triglycerides and already on statin what is next recommended step?

reduce alcohol intake elevated triglycerides >150 inc. risk for cardiovascular events and extremely elevated triglycerides >1500 can cause pancreatitis pt with moderate hypertriglyceridemia (150-500) who have a known risk for CAD- initiation of high intensity statin therapy and heavy alcohol intake can raise triglyceride levels, so pt should reduce alcohol intake to no more than 2 drinks/day and inc. exercise and weight loss fibrates and niacin lower triglyceride levels but don't improve cardiac outcomes

Patients ECG shows suptraventricular arrhythmia (narrow QRS complex tachycardia), can have retrograde P waves

regular and narrow complex tachycardia, rate of 160 beats per minute- any tachycardia occurring above the his-purkingje bundle (sinus tachycardia, multifocal atrial tachycardia, atrial flutter, a fib, AVNRT, and junctional tachycardia)- pt can have palpitations and dizziness, lightheadedness, SOB, diaphoresis chest pain, or syncope adenosine or vagal manuvers temporarily slow the conduction via the AV node and can unmask hidden P waves (Sinus tachycardia would have normal P wave morphology and would be triggered by a panic attack) i

Pt with elevated BP while on multiple medications= resistant hypertension

renovascular hypertension (renal artery stenosis) is the most common/correctable--it should be suspected in pt with elevated creatinine after starting ACE, ARB, severe htn with recurrent flash pulmonary edema, severe hypertension in patients with diffuse atherosclerosis, onset hypertension after 55, hypertension in patient with asymmetric kidney size, and presence of abdominal bruit This pt has multiple RF (smoking, diabetes, hyperlipidemia) and clinical evidence of diffuse atherosclerosis w/ CAD, and PAD (intermittent claudication)

80 yo woman with progressive LE edema, impaired mobility from knee osteoarthritis, her stomach feels full and her appetitie has been decreased, high BP, elevated jugular veins, high urine protein excretion, echo shows LA enlargement, marked concentric LV hypertrophy and LV EF of 70%

restrictive cardiomyopathy amyloidosis is a multisystemc disease- fibril deposition in tissues, cardiac amyloidosis is a form of restrictive cardiomyopathy, and should be suspected in those who have manifestations of CHF, (progressive dyspnea, LE edema LVD, ascites) and LV hypertrophy and nondialated LV cavity, esp in the absence of a history of hypertension an imp cause of HF with preserved EF- it may be idiopathic or due to infiltrative diseases (sarcoid, amyloid), storage diseases (hemochromatosis) or endocardial fibrosis can also see asymptomatic proteinuria (as in this pt) or nephrotic syndrome, waxy skin, anemia, easy bruising with echymossis, hepatomegaly, GI bleeding early satiety, sub cut nodules, enlarged tongue and peripheral or autonomic neuropathy so amyloid cardiomyopathy should be considered in unexplained CHF, proteinuria, and LV hypertrophy in the absence of history of hypertension

36yo female who is having chest pain and has RF (smoking, family history, estrogen therapy) suggest acute coronary syndrome

retrosternal chest pain radiating to the L arm with associated diaphoresis nausea and vomiting suggest ACS - stable its should get oxygen IV access and ECG and chest X-ray , and its with possible ACS and low risk for aortic dissection should get aspirin ASAP b/c of it's anti platelet effects, it rules rate of MI stroke and overall mortality in ACS and its with ECG findings of ACS should be treated with heparin and those with non diagnosis chest X-ray should get further work up so patients presenting to the ED with chest pain and suspected ACS should receive Aspirin ASAP and early anti platelet therapy with aspirin reduces risk of MI and overall mortality

Pt with an anterior wall MI, after stent placement, and on 4th day of hospitalization, pt develops acute onset SOB and confusion, BP 72/40, and HR 120, PE shows cold clammy extremities and diaphoresis, JVD and crackles in lungs loud harsh systolic murmur at the left sternal border with a palpable thrill what is cause of pt deterioration

rupture of interventricular septum a delay in coronary perfusion >24 hrs from symptom onset higher risk of complication IV septum rupture 3-5 days after large MI involving LAD or RCA, acute cariogenic shock (PE, Hypotension, confusion due to poor organ perfusion), and JVD or hepatomegaly due to liver congestion and blood flowing from LV to RV creates a harsh holosystolic murmur w/ palpable thrill at the left sternal border pulm artery cath can detect a L to R shunt w/ step up in oxygen from RA to RV w. transthoracic echo

30 yo pt comes to ED with intermittentt dizziness and unsteadiness, had episode of uveitis 6mo ago and tx topically, ECG shows sinus rhythm 2:1 AV block and LBBB and chest X-ray shows midfield lung opacities

sarcoidosis pt with uveitis, mild dyspnea, and 2 wk history of presyncope due to conduction abnormalities given bradycardia with AV block and LBBB she has sarcoidosis with cardiac involvement cardiac noncaseating granulomas, infiltration of nonceasating granulomas leads to surrounding inflammation and can cause conduction defects (complete AV block is most common), restrictive cardiomyopathy, dilated cardiomyopathy, valvular dysfunction and HF cardiac sarcoidosis should be suspected in patients with unexplained 2nd or 3rd degree heart block or when ECG changes occur in a patient with known or suspected systemic sarcoidosis

Pt with supravalvular aortic stenosis

second most common type of aortic stenosis - congenital LV outflow tract obstruction due to discrete or diffuse narrowing of the ascending aorta- this causes a systolic murmur, similar tho that seen with valvular aortic stenosis, the murmur is head best in the 2nd right intercostal space, pts have unequal carotid pulses, differential BP in UE< and palpable thrill in substernal notch patients can develop LV hypertrophy and coronary artery stenosis, these changes along with inc. myocardial oxygen demand during exercise can lead to subendocardial myocardial ischemia- which is most likely responsible for the patients anginal symptoms in exercise

Pt with infected sacral ducibutus ulcer, hypotension, tachycardia, tachypnea and mental status changes

septic shock- dec. SVR ( reduced after load) due to peripheral vasodilation decreased PCWP (LA pressure) b/c of capillary leakage which causes dec. preload and mixed venous oxygen saturation because of hyper dynamic circulation-inability of tissues to adequately extract oxygen, inc. CO initially but later on dec CO

Pt with syncope when urinating

situational (post micturation) syncope- a form of reflex associated with certain triggers (micturition, defacation, cough) the specific triggers for reflex syncope cause an alteration in autonomic response- and can lead to cardioinhibitory, vasodepressor or mixed response- inc. parasympathetic stimulation can manifest as profound bradycardia, varying degrees of AV block or systole, and dec sympathetic output can lead to vasodilation hypotension or syncope and this patients prostatic hyperplasia may have caused inc. strain and exacerbating the cardioinhibitory response so situational syncope is a form of reflex or neurally mediated syncope associated with specific triggers and these triggers cause an alteration in autonomic response and can precipitate predominate cardioinhibitory, vasodepressor or mixed response

Pt with statin induce myopathy- what is the MOA of statins

statins inhibit HMG CoA reductase- rate limiting enzyme in the intracellular biosynthesis of cholesterol that converts HMG CoA to menalonate (intracellular HMG CoA reductase enzyme), dec. hepatic cholesterol activates cellular signals that inc. the num of LDL receptors on liver cell membranes and these receptors remove circulating LDL and deliver it to the cells interior= reduced serum LDL with minimal change in liver LDL stain induced myalgia=symmetrical proximal muscle weakness and statins dec. production of coenzyme Q 10 synthesis- involved in muscle cell energy production

Pt with premature atrial complexes found on ECG, has been smoking and drinking for the last 10 years what is next step in management?

stop alcohol and tobacco premature atrial complexes (PACs)- premature activation of the atria at a site originating other than SA node ECG will show early P wave PACs are a benign arrythemia in asymptomatic patinets- such as this one, precipitating factors like tobacco/alcohol/caffine and stress should be identified and avoided B blockers are helpful in symptomatic patients

Pt with elevated BP and ECG findings associated with LVH (high voltage QRS, lateral ST depression, lateral T wave inversion)

suggesting long standing hypertension coarctation of the aorta and narrowing of the descending aorta (just distal to the origin of the L subclavian artery)- results in proximal inc. in arterial pressure and dec. blood flow to the lower body, patients usually present with asymptomatic hypertension- but epistaxis, headache and LE claudication can occur- pt should be evaluated with simultaneous palpation of the brachial and femoral pulses to assess for brachial-femoral delay also, pt should undergo bilateral upper extremity (supine) and lower extremity (prone) BP measurement to eval for upper and lower extremity BP differential

Pt with intermittent claudication, diminished pulses, and abnormal (<1) ankle brachial index

suggestive of PAD in right lower extremity, and in patients with PAD, intermittent claudication is the strongest predictor of cardiovascular morbidity and mortality,Pts with PAD and intermittent claudication have estimated 20% 5yr risk of nonfatal MI and stroke and a 15-50% 5 year risk of death b/c of cardiovascular causes - and the risk rises exponentially with progression of PAD the presence of PAD is a coronary artery disease risk equivalent and needs aggressive management only 1-2% of patients with PAD will progress to develop critical limb ischemia and risk of amputation

Pt with rhythm strip that shows wide complex tachycardia w/ 2 fushion beats

sustained monomorphic ventricular tachycardia (SMVT) Patients with SMVT who are hemodynamically stable can be monitored on antiarrythmic drugs, IV amariadarone is the preferred agent it can convent SMVT to sinus rhythm and avoid cardioversion synchronized electrical cardioversion is for patients with persistent tachyarrythmia who are symptomatic (AMS, PE, acute HF) or hemodynamically unstable (hypotension, signs of shock)

Pt with paraxosymal A fib that spontaneously converted to normal sinus rhythm

systemic thromboembolism is a major cause of long term morbidity in patients with AF and tx with warfarin or NOAC- reduces the risk of embolization in pts who are at moderate risk of embolization and use CHADSS score in its with nonvalvular AF Lone AF is pts with paraxosymal ,persistent or permanent AF with no cardiopulmonary or structural heart disease , these pos are <60 and have a score of 0- they have very low risk of embolization- and anticoagulant therapy is not indicated for them

Pt with exertion dyspnea, PND, Pulm and peripheral edema, and a h/o MI suggests decompensated systolic congestive HF

the dec. in CO by these patients results in neurohormonal adaptations- including inc. sympathetic nervous system tone, activating the RAAS system and inc. secretion of ADH, and these maintain CO by inc. myocardial contractility, peripheral vasoconstriction, and expansion of extracellular fluid volume dec. renal perfusion seen in CHF, and subsequent RAAS activation leads to inc. ang II levels which- vasoconstriction of afferent and efferent glomerular arterioles- leading to a dec. in renal vascular resistance and a net dec. in renal blood flow preferential vasoconstriction of efferent renal arterioles- inc. intraglomerular pressure to maintain adequate glomerular filtration rate (GFR) and direct stimulation of Na reabsorption in proximal tubules and inc. aldo secretion from adrenals to further promote na reabsorption in the cortical collecting tubule- leading to DEC na delivery to the distal tubule and inc. ECF vol

Pt who likely developed pericarditis due to an upper respiratory tract infection

the patients clinical presentation suggests pericardial effusion and cardiac tamponade, electrical alterns (due to swinging of the heart in the pericardial cavity) is seek on EKG showing a changing amplitude of the QRS complex on EKG pericardial inflammation causes extra fluid in the pericardial cavity leading to pericardial effusion , the inc pericardial fluid compresses cardiac chambers and limits diastolic filling, causes a dec. in preload and dec in CO- causing hypotension and syncope- exam shows compensatory tachycardia, distended neck veins, pulsus paradoxicus, and muffled heart sounds electrical alterans plus sinus tachycardia is highly specific for pericardial effusion echo is used to confirm the pericardial effusion- tx involves emergency pericardiocentesis

pt with fatigue, dyspnea and elevated BNP what finding most related

third heart sound CHF third heart sound, low frequency diastolic heart sound produced by passive ventricular filling during early diastole abnormal C3 (higher pitch, S3 gallop) commonly heard in patients with CHF due to LV systolic dysfunction correlated with elevated LA or LV filling pressures and serum BNP levels

Pt with epigastric pain evoked by exertion over several minutes relieved by rest even with heavy PUD symptoms like family history and taking antacids

this is atypical angina (given lack of chest discomfort) SLE is a known RF for accelerated atherosclerosis or premature CAD MI in patients occurs with stable angina when myocardial oxygen demand exceeds oxygen supply, Exercise ECG is recommended as initial stress test for diagnosis coronary angiography is performed for patients with high risk findings on initial stress testing, and indicated in patients with a high pretest probability of ischemic heart disease

pt emigrated from cambodia and has left sided hemiparesis

this is likely due to thromboembolic stroke from a fib in the setting of mitral stenosis a young pt from a developing country, the clinical picture of progressive dyspnea, nocturnal cough, and hemoptysis is highly suggestive of rheumatic MS long standing MS leads to an increase in LA pressure causing elevated pulm pressures and pulm vascular congestion- that can cause dyspnea, orthopnea, , PND or hemoptysis in additional LA enlargement from inc. LA pressure- predisposes to fib which inc. risk of LA thrombus formation and systemic thromboembolic complications like a stroke

Pt have syncope and has conduction system abnormalities- including prolonged PR interval, and inter ventricular conduction delay (prolonged QRS) on initial EKG

this is suggestive of bradyarrythmia or high grade AV block, AV block can be quite intermittent and likely responsible for prior episodes of lightheaded ness, he should be referred for electrophysiologic testing and eval for pacemaker implant

Pt that has 2 hours of vague chest discomfort and X-ray shows a widened mediastinum

thoracic aortic aneurysm, ascending aortic aneurysms start anywhere from the aortic valve to the inominate artery usually due to cystic medial necrosis (with aging) or CT disorders (marfans, erlos danlos) descending aortic aneurysms arise distal to the l subclavian and descending aortic aneurysms are usually due to atherosclerosis (RF hypertension, hypercholesteremia and smoking) chest X-ray can suggest TAA showing widened mediastinal siloutthe, inc aortic knob and tracheal deviation

Pt who collapsed with no pulse, what is most imp factor for survival in this patient?

time to rhythm analysis and defibrillation the most common cause of out of hospital sudden cardiac arrest is sustained ventricular tachycardia/ fibrillation due to MI or infarction the most critical factor in overall survival is elapsed time to effective resuscitation (bystander CPR, rhythm analysis and early defibrillation) and if defibrillation doesn't work then give epi

70 yo man brough to ED with 3 hours of intense, constant chest pain and chest pain that radiates to the intrascapular area , pt describes this pain as sharp and has never experienced it before like this BP 189/110 and 181/ 112 in the left, pulse 105 and respirations 18 and exam shows early descendo diastolic murmur at at l sternal border 4th intercostal space ECG shows sinus tachycardia and LVH with T wave inversions in V5 and V6 what is next step in management

transesophageal echo decrescendo diastolic murmur was aortic regurgitation (proximal extension of the dissection into the aortic valvular annulus) and elevated cr some pt's have differential UE BP but not all of them Transesophageal echo is best for pt's with renal insufficiency or hemodynamic instability CT angio is best in hemodynamically stable pt (but needs contrast)

pt who is a recent immigrant to the US and signs of right HF and was a farmer and X-ray shows a ring of calcification around the heart and JVP show prominent X and Y descents

tuberculosis pt with constrictive pericarditis- with pericardial fibrosis and obliteration of the pericardial space-it impairs ventricular filling during diastole- causing patients to experience symptoms related to decreased cardiac output (fatigue and dyspnea on exertion) and signs of venous overload (elevated JVP, pedal edema), kusmal's sign (lack of typical inspiratory decline in CVP) and the presence of a pericardial knock (early heart sound after S2), and sharp x and y descents can be seen on central venous tracing- pericardial calcifications can be seen on chest X-ray in developing countries, tb is often the cause of constrictive pericarditis, but in the US the most common causes are idiopathic or viral pericarditis, radiation therapy, cardiac surgery etc.

pt with recurrent episodes of prolonged chest pain over several months not associated with activity- ECG, exercise and stress tests are unremarkable (substernal squeezing type chest pain/ discomfort that radiates to the back)

underlying esophageal disorder GERD and esophageal motility disorders are common causes of non cardiac chest pain- features suggesting esophegeal origin include prolonged pain lasting more than 1 hr, postprandial symptoms and associated heart burn and dysphagia and relief of pain by anti reflex therapy, having nocturnal pain is also important

Pt with sharp and pleuritic chest pain, pericardial friction rub, uremia

uremic pericarditis occurs in renal failure patients who have BUN levels >60, this one does not involve diffuse ST segment elevations dialysis is the most effective treatment for UP heparin can cause hemorrhage into the pericardial space and should be avoided during hemodialysis (Dressler's syndrome occurs 1-6 weeks after an MI)

Pt who has an MI and then gets an arrhythmia and syncope

ventricular arrhythmias including ventricular premature beats, nonsustained or sustained ventricular tachycardia and ventricular fibrillation are common in the immediate post MI period v fib is the most frequent underlying arrhythmia responsible for sudden cardiac death in the setting of an acute MI, more than 50% occur within the first hour of symptom onset, reentry is the predominant mechanism responsible for ventricular arrhythmias arrhythmias occurring in the first 10 minutes of coronary occlusion are "immediate" or phase I a ventricular arrhythmias (acute ischemia causes heterogeneity of conduction slowingg and delayed activation- predisposing to reentrant arrhythmias) and "delayed" or phase Ib arrhythmias occur about 10-60 mins after acute infarction and result from abnormal automaticity reentrant ventricular arrythmias (v fib) are the most common cause of sudden cardiac death in the immediate post MI period

Pt with ant wall MI 5 days ago and now having sudden onset chest pain, agitated and restless and 2 minutes later he is unresponsive, pulse not palpable and electrocardiogram shows sinus tachycardia 130

ventricular free wall rupture hemoperricardium and eventual cardiac tamponade blood in the pericardial sac compresses LV dec. SV- hypotension and compensatory sinus tachycardia and can compress to pulseless electrical activity diagnosis with echocardiogram, supportive care, pericardiocentesis, and possible surgical repair

32 yo with worsening dyspnea 1mo after returning from texas, she has symptoms of HF

viral infection causing dilated cardiomyopathy inadequate immune response to viral infection allowing virus to invade the cardiac myocytes- leading to cardiotoxicity and impaired contractile function, dec. systolic dysfunction and ventricular dilation (eccentric) hypertrophy ensue, usually young adults with signs and symptoms of decompensated HF most patients will describe several weeks of viral prodrome (fever, fatigue myalgia) that precedes the development of cardiac symptoms ECG shows nonspecific ST segment changes and echo shows 4 chamber dilation end-myocardial biopsy aided by viral PCR reaction is the diagnostic gold standard but often made by noninvasive cardiac MRI tx is diuretic B blocker and ACEi and transplant if they don't respond

Pt have syncope after shoveling snow in his house and episode one month ago when carrying heavy bags, has had reduced physical activity level over the last year b/c of progressive exertional dyspnea and fatigue, what physical exam finding would be found

weak and slow rising carotid pulse exertional syncope portrays an underlying pathological cause, v arrhythmia (due to MI) and outflow tract obstruction (AS or hypertrophic cardiomyopathy), progressive dyspnea on exertion, fatigue and exertion syncope suggest an outflow obstruction, and patients with fixed outflow obstruction cannot inc CO in response to ex induced vasodilation, leading to hypotension, transient cerebral hypo perfusion and decreased exercise tolerance and syncope- will see 1) delayed and slow rising and diminished (weak) carotid pulse (pulsus parvus et tardus) 2) presence of a single and soft S2 3) mid to late peaking systolic murmur with maximal intensity at the second right intercostal space radiating to the carotids orthostatic hypotension doesn't cause exertional syncope

Most important factors in lowering BP

weight loss is the most effective intervention in those patients who are obese in order to dec. BP all pts should be encouraged to follow dietary salt restriction, DASH diet, regular aerobic exercise, and limiting alcohol intake, after actual weight loss, the most next effective plan in lowering BP is the DASH diet (then it's exercise, sodium intake, and alcohol intake)

Pt with evidence of IV drug use and aortic regurg ( early diastolic murmur)

when aortic regurg is due to valvular disease it is best heard along the left sternal border (3th and 4th intercostal space) but if AR is due to aortic root disease, it is best heard along the right sternal border, in this pt EG shows conduction abnormality with 2:1 second deg AV block (aortic value endocarditis, complicated by perivalvular abscess, causing AV conduction block and syncope) Perivalvular abscess is seen in 30-40% of its with infective endocarditis- the development of a new conduction abnormality in its with infective endocarditis should raise the suspicion for perivalvular abscess extending into the adjecent cardiac conduction pathways, aside from aortic valve involvement IV drug abuse is also an independent predictor of periannular extension of infection and tricuspid value is most commonly the valve seeded by endocarditis but it usually presents as a systolic murmur (murmur accented with inspiration- and cardiac conduction abnormalities are uncommon in patients with tricuspid valve endocarditis)