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903 Cards in this Set
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- Back
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Which mumurs should be investigated further? |
Diastolic and continuous murmurs, as well as loud (>II/VI) systolic murmurs because the probability that an organic cause is present is high.
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Which murmurs don't need further workup?
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Midsystolic soft murmurs (grade I-II/VI) if asymptomatic
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How should you futher evaluate murmurs heard on auscultation?
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Transthoracic Doppler ECHO
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Can you use dihydropyridine CCBs in ACS? What about non-dihydropyridine CCBs?
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No, they are contraindicated in ACS bc they could worsen cardiac ischemia becuase they cause peripheral vasodilation and reflex tachycardia. Ex: Nifedipine. Can use non-dihydropyridines (diltiazem, verapamil) in STEMI and ongoing ischemia, but only after BB - but they don't improve mortality
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When is heparin indicated in ACS?
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All acute MI pts
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What is Captopril and what is its role in ACS?
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ACEI. Improves mortality in STEMI pts, esp pts with diabetes, CKD, and/or poor LV function
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Do BB improve mortality in STEMI pts?
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Yes - ex: Metoprolol. This is likely due to their ability to dec myocardial O2 demand, prolong diastole (thereby increasing coronary perfusion) and reducing ventricular remodeling
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What is the MOA of aspirin and what is its role in STEMI pts? How should it be taken?
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Decreases platelet activity. Improves survival in STEMI pts. Should be chewed so that it can enter the blood stream more quickly.
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What is the murmur of aortic regurgitation? What increases/decreases it?
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Diastolic decrescendo murmur at L 3rd intercostal space. Increases with handgrip (bc inc PVR and AL --> inc regurg). Pts also have a widened pulse pressure (systolic - diastolic BP) due to inc SV
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How do you treat AR murmur?
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Afterload reduction with CCB or ACEI
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What murmur do you see a widened pulse pressure?
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AR
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What can you see in CXR in aortic regurg?
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Cardiomegaly due to dilation of LV bc of regurgitation
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What is quinidine?
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anti-arrhythmic
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Why should you not use BB in CHF secondary to AR (whereas you would use it for other CHFers?
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BB slow down the heart --> inc diastole time (when AR regurg takes place) so BB actually worsen AR
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What is the MOA of ephedrine? What is it sometimes used for?
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alpha and beta agonists. sometimes used to treat orthostatic hypotension
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What type of medication is amiodarone?
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Anti-arrhythmic
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What are BP ranges for the different types of hypertension?
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Normal: <120/<80; Pre-HTN 120-139/80-89; Stage 1 HTN 140-159/90-99; Stage 2 HTN >160/>100 (these are all "or")
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What should you do for a patient who has new hypertension and is young and otherwise health (in general)?
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Search for secondary causes, including meds
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What should you do if a pt has new HTN and on OCP?
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Discontinuing OCP can correct the problem in most cases (over 2-12 mo period)
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When is diet and exercise effective in reducing BP and by how much?
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5-20mmHg per 10kg wt loss. Only effective in obese pts, no non-obese pts
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What is the first step in treating essential HTN? What if that fails
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Starting diet and excerise program (if obese). If that fails, next step is low-dose thiazide
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What is the cause of renovascular HTN in young pts?
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Fibromuscular dysplasia
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What is the preferred method of medical management for Afib?
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Rate control + anticoagulation (most pts prefer this over rhythm control + anticoag). Can use Warfarin or dabigatran for anticoagulation. Rate control with AV nodal blockers (diltiazem, verapamil, metoprolol, digoxin), rhythm control is chemical or electrical cardioversion.
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What is the main complication of atrial fib?
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Embolic stroke (up to 5 events per 100 pt life years). This is due to stasis of blood in the atria leading to thrombi.
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What pts are at increased risk for stroke from Afib?
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(CHADS2 score) - older pts (>75), previous stroke (2 pts), HTN, CHF, DM
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How do you know which anticoagulation should use for pts with afib to prevent stroke?
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CHADS 0 ASA, >2 need either warfarin or dabigatran. CHADS 1-2 is intermdiate and can have either
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What is dabigatran?
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New direct thrombin inhibitor
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What is Salmeterol?
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Long acting beta-2 adrenergic agonist
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When is spironolactone beneficial in cardiac disease?
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Most beneficial in treating pts with ascites from cirrhosis and those with NYHA class III and IV heart failure
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What are the changes in CO, PCWP, SVR, BP, and HR in hypovolemic shock?
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Dec CO, Dec PCWP (central venous pressure), Inc SVR, Dec BP, Inc HR. Blood loss represents intravasclar volume loss -> dec CO and PCWP (indirect measure of LA pressure). The dec in CO -> stimulates SNS -> generalized vasoconstriction (inc SVR) and inc HR
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What is PCWP an indirect measure of
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LA pressure
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How should you initially tx pts with cocaine-assoc chest pain?
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IV benzos - they improve the symptoms of psychomotor agitation, reduce myocardial O2 demand, and alleviate cardiovascular symptoms. Can also intially tx with ASA (dec thrombus formation), Nitro, and CCB (vasodilators) but beta blockers are contraindicated
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Which meds are contraindicated in cocaine-assoc CP?
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Beta blockers bc can cause unopposed alpha adrenergic stimulation and worsen coronary vasoconstriction
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What findings on PE are sugestive of acute cocaine intoxication?
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Psychomotor agitation, dilated pupils, atrophic nasal mucosa, HTN, acute myocardial ischemia (CP< EKG changes). Cocaine potentiates SNS by inhibiting NE reuptake -> stimulation of alpha and beta adrenergic receptors -> coronary vasoconstriction and inc in HR, BP, myocardial O2 demand. It also enhances thrombus formation by promoting platelet activation and aggregation.
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Should thrombolytics be considered in pts with cocaine-induced cardiac ischemia?
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Only if having ST-segment elevation MI when timely access to coronary angiography is not available. Also need to rule out aortic dissection, which can happen in a small minority of pts with cocaine-assoc CP (thrombolytics in aortic dissection could be catastrophic and is absolutely contraindicated)
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When are thrombolytics indicated? When is cardiac cath indicated?
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Thrombolytics: only in STEMI when timely access to coronary angiography is not available. Cardiac cath: STEMI or in pts with persistent CP despite aggressive optimal medical therapy
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What is orthostatic hypotension?
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Drop in BP >20mmHg from lying down to standing, typically preceded by lightheaded or presyncopal sensation
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Who is orthostatic hypotension common in?
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Elderly, hypovolemic, autonomic neuropathy (ex: DM, Parkinsons), as well as meds: diuretics, vasodilators, adrenergic-blocking agents. Also, prolonged recumbence increases the risk
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Who is at risk for syncope due to cardiac arrhythmia?
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Pts with conduction disorders (ex: AV block), tachyarrhythmias (ex: ventricular or supraventricular tachy), or disorders of automaticity (ex: sick sinus syndrome). Pts with cardiogenic syncope usually have a history of underlying cardiac disease, such as CAD or CM
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Who gets syncope from valvular obstruction?
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Pts with critical AS - most often during activity. They usually have preceding history of exertional dyspnea, CP, or fatigue
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What is the mechanism of vasovagal syncope. What are the signs and symptoms and when does it often occur? Which pt population is it most common in?
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Excessive vagal tone. S/S: nausea, diaphoresis, pallor prior to syncope. Frequently occurs in response to stress, pain, certain actions (ex: urination). Particularly common in young women.
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How does hyperventilation cause syncope? Is it common?
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Mech: overbreathing -> dec concentration of CO2 in the blood -> vasoconstriction. Rare. Usually preceded by a psychological stressor or sensation of anxiety
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What must occur for a TIA to cause syncope? Is it common?
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TIA causing syncope is rare. The TIA must affect the posterior circulation and brainstem in order for syncope to occur
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What etiology is most likely in chest pain that is reproducible with palpation?
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Musculoskeletal
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How does costochondritis present?
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Tenderness of the costochondral or costosternal junctions. Pain is sharp, focal, lasts for hours, and worsens with inspiration (means likely MSK). Tenderness is reproducible
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What is the murmur of AR?
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Early diastolic murmur. The murmur varies considerably with the degree of regurgitation - mild has only early diastolic murmur while severe can result in a holodiastolic murmur.
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What are the important PE findings of AR?
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Hyperdynamic pulse, including Bounding/"water hammer" peripheral pulses (bc AR assoc with inc SV which produces an abrupt rise in systolic BP and rapid distension of the peripheral arteries, then during diastolic there is a regurgitation of blood back into the LV resulting in low diastolic pressure and collapse of peripheral arteries.
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What is the murmur of ASD?
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Fixed splitted of S2 classically, but may also be assoc with a midsystolic pulmonary flow murmur
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What is pulsus paradoxus and what does it suggest?
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Fall in systemic arterial pressure by more than 10mmHg during inspration; often assoc with cardiac tamponade
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What is pulsus parvus et tardus and what does it suggest?
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Pulsus parvus = dec pulse amplitude and pulsus tardus = delayed pulse upstroke - assoc with aortic stenosis
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What are common blood test findings of alcoholism?
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Dec platelets, macrocytosis, elevated LFTs
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What is the mainstay of management of alcoholic CM?
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Total absinence from alcohol (it may reverse if early in the course of disease).
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When is digitalis most useful in heart failure?
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In pts who have systolic dysfunction and have rapid ventricular rates due to Aflutter or Afib. It is useful in these cases by its positive inotropic effect and negative dromotropic (slowing AV conduction). However, digitalis has not shown to provide any survival advantage in pts with CHF and has not been shown to reverse the disease process
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Which cardiac pts should be given ACEI?
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All heart failure pts who have systolic dysunfction unless they are contraindicated or pts can't tolerate them
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What are the vascular and immunologic phenomena of infective endocarditis?
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Vascular: systemic arterial emboli (focal neuro deficits, renal or splenic infarcts), septic pulmonary infarcts, mycotic aneurysm, conjunctival hemorrhages, janeway lesions (macular, erythematous, nontender lesions on palms and soles). Immunologic: Osler's nodes (painful, violaceous nodules seen on fingertips and toes), Roth spots (Edematous & hemorrhagic lesions of the retina), glomerulonephritis, arthritis or positive RF
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What criteria can be used to dx infective endocarditis?
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Duke Criteria (blood cultures, UA, CXR, ECHO)
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What joints does RA usually affect?
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Wrist, MCP, PIP but not DIP joints.
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What are the s/s of post-strep GN?
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Preced by sore throat or skin infection. Presents with generalized edema, dark urine, HTN
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What is Adult Still's disease?
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Inflammatory disorder characterized by recurrent high fevers (>39C), rash, arthritis. Rash is often maculopapular and nonpruritic, affecting the trunk and extremities during febrile episodes.
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What are the s/s of adrenal insufficiency?
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Hypotension, hyperpigmentation, hypoNa. Can also have fatigue, weakness, anorexia, GI disurbances, and wt loss
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What is the inheritance pattern of HOCM?
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Autosomal dominant
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What is the murmur of HOCM?
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Murmur at lower L sternal border that decreases with increases in preload (bc inc PL distends the myocardium and decreases the outflow obstruction from the hypertrophied heart) - most murmurs inc with inc PL
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Who is HOCM more common in?
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Younger pts, lack of coronary artery disease, blacks>whites
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When does RV failure occur after MI, which vessel most commonly, what are the clinical findings and what does ECHO show?
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Acute time course, RCA, hypotension & clear lungs, Kussmaul sign, ECHO: hypokinetic RV
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When does papillary muscle rupture occur after MI, which vessel most commonly, what are the clinical findings and what does ECHO show?
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Acute and within 3-5d, RCA, acute and severe pulmonary edema, new holosystolic murmur. ECHO: severe MR with flail leaflet
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When does interventricular septum rupture/defect occur after MI, which vessel most commonly, what are the clinical findings and what does ECHO show?
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Acute and within 3-5d, LAD (apical septal rupture) and RCA (basal septal rupture), shock & CP, new holosystolic murmur, biventricular failure. ECHO: L->R shunt at level of ventricle, step-up O2 level between R atrium and ventricle
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When does free wall rupture occur after MI, what vessel most commonly, what are the clinical findings and what does ECHO show?
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Within first 5d-2wks, LAD, shock & CP, JVD, distant heart sounds. ECHO: pericardial effusion with tamponade
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What ventricular free wall rupture after acute MI? How does the pt present?
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Increased use of early reperfusion therapy and medical management. Abrupt LV rupture often leads ot hemopericardium and eventual cardiac taomponade. Blood in the piercardial sac compresses the LV and decreases SV, resulting in hypotension and compensatory sinus tachycardia. The severe mechanical compromise can rapidly progress to PEA with EKG showing low voltage from the ensuing cardiac tamponade. Therefore, LV free wall rupture should be suspected in pts with PEA after recent first MI and no signs of heart failure. Rapid dx with ECHO, supportive care, pericardiocentesis, and possible surgical repair are all required to save the pts life
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When does acute peri-infarct pericarditis occur after MI and how does it present. How is it different from Dressler's syndrome and how do tx?
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Acute peri-infarct pericarditis: 1-3d after MI vs Dressler's is post-MI pericarditis weeks-months after MI. Present with pericardial friction rub with or without CP in acute and with pleuritic CP in Dressler's. Tx: pts usually improve with NSAIDs (ex: Aspirin, which pts are usually on after MI anyway)
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How do interventricular wall rupture and LV free wall rupture after MI differ?
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Similar bc both peak around 5d after MI. But, IV wall rupture causes VSD whereas free wall rupture causes pericardial tamponade. IV wall rupture presents with sudden onset hypotension, CHF (mostly R), and loud holosystolic murmur best heard at lower L sternal border whereas free wall rupture can present as sudden onset CP with PEA with low voltage and hypotension.
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How does recurrent cardiac ischemia (ie post-infarction angina) present?
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Recurrent CP and new or worsening EKG changes of ischemia. It can cause VT/VF which can degenerate further to asystole
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What leads show ST elevation in inferior MI?
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V4R-V6R
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When does ventricular aneurysm occur and what are its characteristic features?
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Late (weeks-months). Scarred or fibrotic myocardial wall due to healed transmural MI. May present with heart failure, refractory angina, ventricular arrhythmias, or systic arterial embolism due to mural thormbus formed within the aneurysm
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What is the most common paroxysmal tachycardia in ppl without structural heart disease?
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PSVT (paroxysmal supraventricular tachy)
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How does PSVT present? What is the most common mechanism?
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Presents as abrupt attacks/palpitations with HR between 160-220bpm. Most common mechanism is re-entry into the AV node
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What is the tx for PSVT?
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Dec AV node conductivity via vagal maneuvers (Valsalva, carotic sinus massage, immersion in cold water to inc vagal tone and dec AV node conduction) - slowing the heart rate often breaks the rhythm. Adensoine is a very short acting AV nodal blocker that is often used as well
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What node do vagal maneuvers act on?
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Both AV and SA node (dec conductivity)
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What will see on angiogram in acute artery occlusion?
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Contrast will be seen filling the superior portion of the artery before the contrast abruptly ends - this is a pattern suggestive of embolic occlusion
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What are the 5 P's that point to the diagnosis of acute artery occlusion?
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Pain, Pulselessness, Paresthesia, Poikilothermia (coldness), and Pallor
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If suspect acute artery occlusion, what should you do?
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IV heparin immediately when suspect (based on History and PE). Angiography confirms dx. Definitive treatment is surgical embolectomy or intra-arterial fibrinolysis (not IV) /mechanical embolectomy via IR. If limb is non-viable, surgery is mangatory
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Why is recent MI a risk factor for acute artery occlusion?
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MI can result in ventricular embolus
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What is clopidogrel?
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Anti-platelet agent - promotes anticoagulation but does not rapidly break up already existing clots
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What is Cilostazol and what is it used for?
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Inhibits platelet aggregation and causes vasodialtion. Sometimes used to treat chronic (but not acute) claudication.
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How does edema occur in COPD?
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Chronic hypoxia -> constriction of pulmonary artery system which, with time, leads to pulmonary hypertension, RVH, and RVF. RVF causes JVD, HSM, hepatojugular reflux, and lower extremity edema
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How does low serum albumin cause anasarca? What are the leading causes of low albumin?
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Fluid moves from vascular system into intersititum to equalize osmotic pressures. Leading causes: nephrotic syndrome and poor albumin synthesis due to cirrhosis or malnutrition
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What does pulmonary capillary wedge pressure reflect? When is it elevated?
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LA pressure. Elevated in LVF but not in RVF with PHTN bc the pathologic lesion is before the pulmonary capillary bed.
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What is the hallmark finding of cirrhosis?
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Portal HTN
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What is nephrotic range proteinuria?
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>3g per day
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What are the causes of situational syncope?
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Micturition (ex: BPH), coughing fits
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What does Mobitz type I heart block (Wenckenbach) show on EKG?
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narrow QRS, progressive PR prolongation untl a ventricular beat is dropped, and then the sequence is repeated
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When can see Mobitz type I heart block? What is the treatment?
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May be seen after digitalis toxicity, inc vagal tone, inferior wall MI and can occur normally in athletes and older adults. It is also assoc with structural heart disease afected the AV node. Tx: if asymptomatic, observe. If symptomatic, correct reversible causes (hold meds that affect AV node pacing) and uncommonly cardiac pacing (more for 3rd deg and Mobitz type II)
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What does Mobitz type II heart block look like on EKG?
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PR interval remains unchanged prior to P wave and it suddenly fails to conduct to ventricles . Will see a dropped QRS with a normal PR interval.
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What does 3rd degree heart blook look like on EKG?
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P waves and QRS waves are independent bc no atrial impulses are travelling to ventricles
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What does 1st degree heart block look like on EKG?
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Prolonged PR interval (>0.2s) without any dropped beats
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What should you suspect in a pt with poorly controlled HTN despite medical therapy and evidence of atherosclerosis?
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Renal artery stenosis
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What PE finding is helpful in diagnosing renal artery stenosis?
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Continuous periumbilical or flank murmur (systolic and diastolic)
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What is asymmetric BP in L arm suggestive of? R arm?
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L arm - subclavian artery stenosis. R arm - Coarctation (more rare, but if coarc is just proximal to L subclavian (usually coarc is distal))
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Where does subclavian artery atherosclerosis usually occur and what are other things it can present with?
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L artery. May also present with vertebrovasilar insufficency secondary to subclavian steal phenomenon
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What is the PE findings of coarctation of aorta?
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Intercostal arteries become enlarged, which manifests as notching along the undersurfaces of multiple ribs on CXR. Most of the time, BP higher in lower extremiteis bc coarctation is distal to origin of L subclavian but rarely can inc in R arm vs L if coarc is just proximal to L subclavian.
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When should consider aortic dissection?
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Acute HTN, CP, asymmetric BP in extremities
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What is urine test for pheochromocytoma?
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Urinary excretion of vanillylmandelic acid.
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When should suspect pheochromocytoma?
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BP elevations are paroxysmal and assoc with HA, sweating, palpitations
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What is high aldosterone/renin ratio assoc with?
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HTN, hypoK (primary hyperaldosteronism)
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When is inc 240hr urinal free cortisol excretion seen?
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Cushing's syndrome
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What is flecainide? What is a special feature of this med?
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anti-arrhythmic typically used to treat ventricular arrhythmias or supraventricular tachys such as afib. It is a class IC med that blocks Na channels. This results in slowed conduction thru the AV node and His-Purkinje system. Of all the Class IC meds, it has the slowest binding and dissociation from the sodium channels. Flecainide demonstrates a use-dependent phenomenon where its effect on Na channels increases as the HR increases since there is less time between action potentials for the medication to dissociate from its receptors. Therefore, has HR increases, prolongatino of QRS can occur.
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What is the effect of Verapamil on EKG intervals?
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it does exhibit use-dependence phenom, but it prolongs the PR interval not QRS
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Which anti-arrhythmics have use-dependence property (more effective at higher HR because there is not as much time between heartbeats for the medication to dissociate from its receptor)?
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Class I (esp IC) such as flecainide and class IV meds. Class I meds prolong QRS whereas class IV do not
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In a pt with recent MI and cold leg, what diagnostic test should you consider?
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ECHO to look for embolus in LV. WHen MI is large, a thrombus can form and embolize, generally to the legs. MI results in blood stasis in the akinetic part of the herat with resultant thrombus formation. When thrombus is in LV, it is treated with heparin and ECHO follow-up.
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Which is the prognosis better for - Mobitz type I or II?
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Type I (result of AV node dysfunction)
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What does ventricular preexcitation usually result in?
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PVCs
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What is impaired SA node automaticity and what does it result from and how does it present? What does EKG look like?
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Aka sick sinus syndrome. Most often results from fibrosis of the SA node or disease of the SA nodal artery. Can present with bradycardia, lightheadedness, or syncope. On EKG, appears as tachy-brady syndrome
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What does atrial reentry lead to?
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Atrial tachy of abrupt onset and termination
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When does papillary muscle dysfunction occur after MI (which MIs)?
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Classically after posteroseptal (due to solitary blood supply of hte posterior medial papillary muscle) but can also occur with anterolateral MIs
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What does MR murmur sound like? What are common sequelae that you can find on PE?
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Blowing systolic murmur at cardiac apex. Common sequelae - orthopnea, bibasilar crackles (signs of pulmonary edema). If measured PCWP would reveal inc pressure in LA
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What do you think of in pt with recent MI and MR?
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Papillary muscle ischemia or rupture which can casue secondary MR
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What kind of MR does increased L atrial size occur in?
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Chronic MR, not acute. But, acute MR can have inc LA pressure (PCWP)
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How does chronic MR cause LV dilation?
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Due to persistently elevated preloads. Eventually, LVEF decreases as LV weakens and its compliance increases
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What affects RV preload?
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Systemic venous return
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What is cardiac index?
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A measure of cardiac output
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What are the changes in systolic HF in terms of CI, TPR, and LVEDV?
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CI decreased (always in systolic HF). LVEDV should be elevated in systolic pressure but may be normal in pure diastolic HF. TPR is increased in systolic HF due to neurohumoral activation that includes sympathetic hyperactivity and activation of renin-AT-aldo system
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When would you have suboptimal LV filling that may relatively reduce LVEDV?
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Blood redistribution with low TPR (ex: anaphylaxis) or hypovolemia with high TPR (ex: hemorrhage)
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When can you see normal CI, elevated LVEDV and LVEDP and dec TPR?
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Can sometimes see in high-output HF
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What does Afib look like on EKG?
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Irregularly irregular, narrow QRS complex tachy that lacks P waves.
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What is the most common chronic arrhythmia and how does it typically present?
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Afib - usually asymptomatic
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What are the symptoms of afib?
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usually asymp but can have chest discomfort, palpitations, weakness, SOB
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What are the causes of acute Afib? (By category)
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Cardiac: HTN, acute ischemia, HF, myopericardial inflammation, valve disease, surgery. Pulmonary: Acute lung disease (ex: PNA), PE, hypoxia. Metabolic: catecholamine surges or hyperthyroid. Drugs: alcohol, cocaine, amphetamiens, theophylline
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What is the underlying problem in Cushings and what are typical changes?
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Chronically elevated systemic corticosteroids. Changes: central obesity, DM, proximal muscle weakness, psychosis, thin skin, osteoporosis
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How can a proximal aortic dissection potentially cause afib?
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But interfering with coronary blood flow and aortic valve function
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What is high frequency hearing loss associated with?
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Aging and certain congenital long QT syndromes
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What is the most common cause of mitral regurg in developed countries?
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MVP - usually causes mild MR
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What does mild and severe MR sound like
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Mild - mid systolic click and mid-to-late systolic murmur. Severe leaflet dysfunction/severe MR - holosystolic murmur.
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Whare is the sequelae of chronic severe MR?
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LA and LV enlargement leading to Afib, LV dysfunction, and CHF
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What are the PE findings of chronic severe MR?
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Displaced apical impulse, holosystolic murmur, S3
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Why does MVP occur?
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Due to myxomatous degeneration of mitral valve leaflets and chordae
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Why does MR cause S3?
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LV volume overload (doesn't necessarily represent CHF)
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What valvular problem can infective endocarditis cause?
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MR due to inadequate leaflet copation or rarely, leaflet perforation. Would have s/s of infective endocarditis (fever, embolic findings, etc)
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What is mitral annular calcification? WHen does it occur?
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A degenerative process involving the fibrous annulus of the mitral valve. Common incidental finding in older adults, usually associated with mild-to-moderate MR.
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What are presenting s/s of MR due to MI with papillary muscle rupture?
|
Chest discomfort, dyspnea, sudden onset pulmonary edema
|
|
|
What valvular problems can rheumatic heart disease cause?
|
MS, MR, AR. MR is less commonly caused by RF
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What murmurs can you hear at the aortic area? R sternal border
|
Aortic stenosis (systolic ejection murmur)
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What murmurs can you hear at the pulmonic area? L upper sternal border
|
Systolic ejection murmurs: PS, flow murmur, ASD (pulmonic and tricuspid vlaves). Systolic ejection click: PS
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What murmurs can you hear at the L sternal border?
|
Systolic ejection murmur: HOCM. Early diastolic murmur: AR, PR
|
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What murmurs can you hear at the tricuspid area? L lower sternal border
|
Holosystolic murmurs: TR, VSD. Mid/late diastolic murmur: TS, ASD (pulmonic and tricuspid valves)
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What murmurs can you hear at the mitral area? apical
|
Holosystolic murmur: MR. Mid/last systolic click: MVP. Mid/late diastolic murmur: MS
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What are the PE findings of constrictive pericarditis?
|
Hepatomegaly, ascites, inc JVP due to dec diastolic filling and impairment of CO
|
|
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What is constrictive pericarditis and why does it cause the PE findings?
|
Pericardium thickened or scarred resulting in restriction of diastolic filling. Bc the heart is unable to fill properly during diastole, CO is compromised and venous pressures become chronically elevated resulting in inc JVP, severe ascites, hepatic congestion, dyspnea, and weakness. On PE: Kussmaul's sign (failure of JVP to dec on inspiration) is often present but not specific
|
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|
What ar the most common causes of constrictive pericarditis?
|
Cardiac surgery, viral pericarditis, radiation therapy. Many cases are idiopathic.
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How do you diagnose constrictive pericarditis?
|
Calcified pericardium on CXR, thickened pericardium on CT or MRI, or by measuring pressures during cardiac cath
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How do you treat constrictive pericarditis?
|
Diuretics or pericardiectomy
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Why does urinary protein loss cause generalized edema?
|
Dec oncotic pressure in capillary beds
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|
What is lymphedema?
|
Firm, non-pitting edema without skin changes assoc with venous stasis such as ulceration and dermatitis
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|
What is the definition of orthostatic hypotension?
|
Postural dec in BP by 20mmHg systolic or 10mmHg diastolic (sometimes accompanied by an inc in HR) that occurs on standing
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What is the cause/pathophys from orthostatic hypotension?
|
Insufficienc constriction of resistance and capacitance BV in the lower extremities on standing, which may be due to a defect in autonomic reflexes, decreased intravascular volume, or meds. Some baroreceptor sensitivity is lost as a normal part of aging. Arterial stiffness, dec NE content in SNS nerve endings and reduced sensitivity of myocardium to SNS all contribute to a tendency toward orthostatic hypotension with age
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What are normal changes to an aging heart?
|
Dec resting and max CO, dec max HR, inc contraction and relaxation time of heart muscle, inc myocardial stiffness during diastole, decmyocyte number, and pigment accumulation in myocardial cells
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|
What does the adrenal medulla have to do during response to stress (fight or flight)?
|
Releases catecholamines. Doesn't change with aging
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|
What is the change in GFR with aging
|
Decreases which promotes Na retention and expasion of intravascular volume
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|
What is the mechanism of the organ dysfunction in amyloidosis?
|
Extracellular deposition of exces proteins
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|
What are common causes of amyloidosis?
|
Multiple myeloma (AL amyloidosis), chronic inflammatory diseases such as RA (AA amyloidosis)
|
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|
What are the organ function manifestastions of amyloidosis?
|
Deposition of amyloid fibrils in kidneys -> proteinuria, binding of amyloid fibrils in liver -> inhibit coag factor synthesis -> easy bruising, amyloid deposition in heart -> restrictive cardiomyopathy with thickened ventricular walls and diastolic dysfunction (systolic dysfunction well preserved and ventricular dimensions remain unchanged)
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|
What type of CM does alcoholic CM cause?
|
Dilated CM (expended entricular dimensions)
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|
What are the findings of hemochromatosis?
|
Restrictive cardiomyopathy, pancreatic dysfunction, bronzed skin, hepatomegaly
|
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|
What does sarcoidosis cause? Who is it most common in?
|
Restrictive CM, bilateral hilar adenopathy, erythema nodosum. MC in Blacks and usually presents in pts at 20s-30s
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How can distinguish constrictive pericarditis from restrictive pericarditis?
|
Restrictive has inc wall thickness and extracardiac manifestations, which points away from constrictive pericarditis
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|
What are the common SE of digoxin?
|
D, N, fatigue, vision changes (scotomata, bleurry vision with changes in color, or blindness), arrhythmias, weakness, confusion. An inciting event, such as a viral illness or excessive diuretic use can lead to volume depletion or renal injury that acutely elevates digoxin level.
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What is digoxin used for and how is it cleared?
|
Afib, heart failure. It is a cardiac glycoside. It is cleared by the kidneys with narrow therapeutic index
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|
How is hypokalemia assoc with toxic digoxin levels?
|
Hypokalemia (often assoc with loop diuretic use) increases the pts suseptibility to toxic effects of digoxin
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|
When is ECHO helpful?
|
In evaluating systolic and diastolic function, EF, wall motion abnormalities, and valve disorders
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|
What are PFTs used for?
|
To diagnosed restrictive and obstructive pulmonary processes
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|
What are the s/s of hyperthyroid?
|
Diarrhea, palpitations, changes in appetitie
|
|
|
What is the most dangerous complication of Marfan's?
|
Aortic dissection - presents with CP radiating to back and neck
|
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|
What is a common PE finding of pt with aortic dissection?
|
Early diastolic murmur (due to aortic regurg)
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|
|
What are common clinical findings of Marfan's?
|
Defects in fibrillin --> ligamentous laxity of joints, long thin digits and limbs, BV fragility, spontaneous PTX, pectus excavatum, MVP and MR, and retinal detachment
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|
What will find on CXR of aortic dissection?
|
Widened mediastinum
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|
When do you hear an S4?
|
May hear in normal, young pts and in people with LVH.
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|
When is an opening snap heard?
|
Mitral stenosis
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|
What are the sequelae of MS?
|
LA enlargement, pulmonary HTN, eventually RV failure
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|
What is fixed splitting of S2 associated with?
|
ASD
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|
What is Kussmaul's sign and what is it assoc with?
|
Inc in JVP that occurs in response to deep inspiration. It occurs in situations that cause RVF like constrictive pericarditis and RV infarct
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What is pulsus parvus et tardus and when do you see it?
|
Carotid pulse that is slow and late. Classically seen in AS
|
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|
What is a classic heart sound associated with MI?
|
S4 bc MI can lead to diastolic dysfunction and stiffened LV resulting in atrial gallop (S4)
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|
When do you see ejection type murmurs?
|
Ejection type murmurs reflect turbulent blood flow through the aortic or pulmonic valves
|
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|
What is pulsus paradoxus and when do you see it?
|
Pulsus paradoxus - refers to a significant drop in systolic BP with inspiration - it occurs in pts with cardiac tamponade
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|
|
What is the pathway of the renin-AT-aldosterone system?
|
Produced in juxtaglomerular cells of kidney in response to hypoperfusion. Renin cleaves ATinogen to ATI. ATI then converted to ATII by ACE in the lung. ATII is a potent vasoconstrictor and also promotes ADH release from pituitary and aldosterone production in adrenal cortex. Aldosterone acts on distal convoluted tubules and CD to promote Na and water resorption from kidneys. Net result of system is inc in BP, total body Na, total bdy water, and BVV
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|
How do ARBs work?
|
Prevent ATII from acting on angiotensin receptors. They don't dec ATII levels but do dec aldosterone production --> natriuresis
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|
How are alpha-adrenergic blockers used to treat HTN?
|
Direct vasodilators
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|
|
What is the most common primary intracardiac tumor and where is it usually located?
|
Atrial myxoma - usually located in L atrium (80%)
|
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|
What are the s/s of atrial myxoma tumors?
|
Fever, wt loss, neuro symptoms due to tumor embolization, mass on ECHO
|
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|
What is a mid-diastolic rumbling murmur best heard at apex suggestive of?
|
MS but can be due to an intracardiac tumor obstructing the mitral valve as well.
|
|
|
What does endocarditis usually produce?
|
regurgitation murmur and fever. Vegetations can be seen on ECHO
|
|
|
What is myxomatous valve degeneration?
|
myxomatmous valve degeneration is the pathologic cause of MVP, which causes a midsystolic click
|
|
|
Can MS result in Afib?
|
Yes
|
|
|
Why does S3 occur?
|
Inflow from LA strikes blood that is already in LV causing reverberation of blood between the LV walls. Can be normal in young ppl and well-trained athletes, but when it occurs later in life, it is often a sign of LV failure.
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|
What is the tx for decompensated HF with s/s of SOB, tachypnea, and hypoxemia?
|
IV diuretics. Don't use diltiazem in decompensated heart failure due to its negative inotropic effects
|
|
|
What is the initial tx of Afib with RVR?
|
rate control with BB or CCB. If hemodynamically usntable, immediate synchronized electrical cardioversion is indicated. Symptoms in RVR are usually due to fast ventricular rate rather than the arrhythmia itself.
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|
When is digoxin preferred over BB or CCB in afib?
|
pts with AF due to HF or those unable to tolerate BB or CCB
|
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|
When is synchronized electrical cardioversion appropriate in afib?
|
If pt is hemodynamically unstable or if stable and known AF duration <48hrs. If >48hrs or unknown, should get 3-4wks of anticoagulation before cardioversion is attempted or do TEE to rule out LA thrombus first
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|
|
When is anticoagulation indicated for stroke prevention in afib?
|
Based on CHADS2 score
|
|
|
What is lidocaine used for in cardiology?
|
Antiarrhythmic used primarily for treating ventricular arrhythmias
|
|
|
How do PSVTs usually present?
|
suden onset, REGULAR, narrow-complex tachy. Treated with adenosine to slow down AV nodal conduction to interrupt the reentry pathway and terminate PSVT. Can also do carotid masage to slow down SA and AV node (vagal maneuver)
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|
In pts who is young with pleuritic CP, tachycardia, dyspnea, and esp if on OCPs, what should be high on differential?
|
PEricardium thickened or scarred resulting in restriction of diastolic filling. Bc the heart is unable to fill properly during diastole, CO is compromised and venous pressures become chronically elevated resulting in inc JVP, severe ascites, hepatic congestion, dyspnea, and weakness. On PE: Kussmaul's sign (failure of JVP to dec on inspiration) is often present but not specific
|
|
|
What are causes of pleuritic CP?
|
PE, PNA, PTX, collagen vascular disease, viral pleuritis, radiation pneumonitis
|
|
|
What is the diagnostic test of choise for PE?
|
Helical CT of chest with IV contrast
|
|
|
Why can you get pulmonary artery distention in PE?
|
Due to rapid increase in pulmonary artery prssure.
|
|
|
What is the typical pain of myocardial ischemia?
|
Substernal squeezing or pressure
|
|
|
Is hemoptysis common in PE?
|
Yes
|
|
|
What do pts with pericardial inflammation look like on exam?
|
Leaning forwrad to dec their discomfort
|
|
|
How should treat WPW pts who develop Afib with RVR?
|
Cardioversion or antiarrhythmics like procainamide - avoid AV nodal blockers like BB, CCB, digoxin and adenosine bc they can cause increased conductance through the accessory pathway
|
|
|
What type of CM occurs with viral myocarditis?
|
Dilated CM (ex: Coxsackie B)
|
|
|
How diagnose viral myocarditis?
|
ECHO - shows dilated ventricles and diffuse hypokinesia resulting in systolic dysfunction (ie low EF)
|
|
|
How to treat viral myocarditis?
|
Supportive - mainly managem CHF symptoms
|
|
|
What viruses can cause viral myocarditis?
|
coxsackie B, parvovirus B19, HHV6, adenovirus, enterovrius
|
|
|
When do you see asymmetric septal hypertrophy?
|
HOCM
|
|
|
When is concentric hypertrophy of heart seen?
|
Following chronic pressure overload, as with valvular AS or untreated HTN. Develops only in chronic conditions and does not present as acute HF
|
|
|
When is eccentric hypertrophy of heart seen?
|
Following chronic volume overload, as seen in valvular regurgitation. Not seen in acute HF bc develops slowly over time
|
|
|
What is the murmur of MS?
|
Mid-diastolic murmur with opening snap. EKG may show LA hypertrophy.
|
|
|
What are the sequelae of MS?
|
LA hypertrophy, LVH and RV heave in chronic MS secondary to pulmonary HTN
|
|
|
What will be the s/s of primary PHTN that has progressed to cor pulmonale?
|
Dyspnea, elevated JVP, lower extremity eema. Gradual onset over months to years
|
|
|
What do aortic valve vegitations cause?
|
Acute AR (usually without dilated heart) and chronic AR (with eccentric hypertrophy). These pts with infective endocarditis appear sick with low-to-high grade fevers, chills, or night sweats
|
|
|
What to do with PVCs in post-MI pt?
|
They are common and even though they may indicated a worse prognosis, treatment is not indciated unless they are symptomatic. If they are symptomatic, BB are first line. Amiodarone second line
|
|
|
What are indications for aortic valve replacement?
|
1. All symptomatic pts with AS (classic symptoms are SAD: syncope, angina, dyspnea). 2. Pts with severe AS undergoing CABG or other valvular surgery 3. Asympt pts with severe AS and either poor LV systolic function, LV hypertrophy >15mm, valve area <0.6cm2, or abnormal response to exercise
|
|
|
What is the murmur of AS?
|
Harsh systolic murmur over R sternal edge, radiates to carotids, pulsus tardus et parvus (a slowly rising pulse that is sustained)
|
|
|
Which murmurs increase on expiration?
|
Only L sided murmurs
|
|
|
What does AS cause in ventricles?
|
LVH, S4 due to foreful atrial contraction against thick, noncompliant ventricle
|
|
|
What are the classic symptoms of Aortic Stenosis?
|
SAD: syncope, angina, dyspnea. Dyspnea occurs from CHF
|
|
|
Why not do an aortic valvotomy instead of aortic valve replacement for AS?
|
Not nearly as effective. Only consider as a bridge to surgery in a hemodynamically unstable pt or poor surgical candidate
|
|
|
Can you do exercise testing in AS?
|
Generally avoided and performed extremely carefully
|
|
|
When does spontaneous rupture of esophagus (Boerhaave syndrome) occur?
|
After severe retching and vomiting
|
|
|
What does CXR of esophageal rupture look like?
|
Unilateral pleural effusion with or without PTX, subcutaneous or mediastinal emphysema, and widened mediastinum.
|
|
|
What will pleural fluid in esophageal rupture look like?
|
Low pH and very high amylase (>2500 IU) and may contain food particles
|
|
|
What is dx test for esophageal rupture?
|
CT or constrast esophagography with Gastrografin
|
|
|
What is the etiology, clinical presentation, lab/imaging, and treatment for mallory weiss tear?
|
Upper GI mucosal tear (vs esoph rupture which is transmural tear) caused by forceful wretching (inc pressure), submucosal arterial or venule plexus bleeding. Clinical presentation: vomiting, retching, hematemesis, epigatric pain. Dx: EGD confirms. Tx: Most tears heal spontaneously, EGD thearpy for continual bleed
|
|
|
What is the etiology, clinical presentation, lab/imaging, and treatment for esophageal rupture/Boerhaave syndrome?
|
Esophageal transmural tear (vs mallory weiss which is mucosal tear), caused by forceful retching (inc pressure), esophageal air/fluid leakage into nearby areas (ex: pleura). Clinical presentation: vomiting, retching, chest and upper abd pain, odynophagia, fever, dyspnea, septic shock can ensue, may see subcutaneous emphysema. Dx is by CT or contrast esophagograophy with Gastrografin. CXR will show pneumomediastium, pleural effusions, and widened mediastinum. Pleural fluid shows exudative, low pH, very high amylase. Tx: surgery for thoracic perforations, conservative measures for cervical perfs (ex: abx)
|
|
|
How does pain of pancreatitis classically present?
|
Epigastric pain radiating to the back (not the chest)
|
|
|
How does aortic dissection pain present? What will CXR show?
|
Severe tearing CP radiating to the back. CXR can show widened mediastinum and unilateral pleural effusion (hemothorax) - these CXR findings are also seen in esophageal perf so need more info
|
|
|
When does aspiration PNA typically occur? Where in lungs and what will pleural fluid show?
|
pts with altered mental status who are unable to protect their airway. Most commonly in RLL and can present with unilateral pleural effusion due to parapneumonic effusion or empyema. Pleural fluid: many WBC, inc protein, inc LDH
|
|
|
What does peptic ulcer disease present like?
|
Epigastric pain, N/V, hematemesis, or melena due to bleeding from the ulcer
|
|
|
What are the 4 primary mechanisms of peripheral edema and clinical examples of each of them?
|
1. Inc capillary hydrostatic pressure (HF - LV and cor pulmonale; primary renal Na retention - renal disases and drugs; venous obstruction - cirrhosis and venous insufficiency) 2. Dec capillary oncotic pressure (hypoalbuminemia) (protein loss - nehprotic syndrome and protein-losing enteropathy; dec albumin synthesis - cirrhosis and malnutrition) 3. Inc capillary permeability (burns, trauma, sepsis, allergic reactions, ARDS, malignant ascites) 4. Lymphatic obstruction/inc interstitial oncotic pressure (malignant ascites, hypothyroidism, LN dissection)
|
|
|
What are the s/s of acute nephrotic syndrome with fluid overload?
|
Anasarcoa, pulmonary and facial edema, HTN, abnormal UA with proteinuria and microscopic hematuria. Serum Cr can be elevated.
|
|
|
What are causes of acute nephritic syndrome?
|
post-strep GN, IgA nephropathy, lupus nephritis, membranoproliferative GN, RPGN
|
|
|
How does nephritic syndrome lead to its fluid overload s/s?
|
Primary glomerular damage -> inc GFR with eventual development of significant volume overload (pulmonary edema, distended neck veins, anasarca, HTN). Dec GFR is also the cause of edema in pts with ESRD
|
|
|
What is pretibial myxedema?
|
Localized nonpitting thickening and induration fo the skin over the lower legs, pretibial area, or dorsum of the feet in pts with Graves disease
|
|
|
Why doesn't low albumin cause pulmonary edema?
|
Alveolar capillaries have a higher permeability to albumin at baseline -> reduces oncotic pressure difference. Also, alveolar caps have greater lymphatic flow than skeletal muscle, thus protecting the lungs from edema
|
|
|
Why does JVP inc and pulmonary edema not occur in cirrohsis?
|
Venous pressures above the hepatic veins (ex: jugular venous pressure) is usually reduced or normal
|
|
|
When does renal hypoperfusion occur and what does it lead to?
|
Heart failure (dec CO). leads to renal Na and water retention and edema
|
|
|
What is the MCC of RVF?
|
LVF. less common is severe pulmonary disease
|
|
|
What is the perferred diagnostic tool for aortic dissection?
|
Transesophageal ECHO - but must control BP before then. Aortography is an old test
|
|
|
What mumur can you hear with aortic dissection?
|
acute AR (early decrescendo diastolic murmur at L sternal border)
|
|
|
What is a crescendo-decrescendo murmur at L lower sternal border most likely due to?
|
HOCM
|
|
|
What increases HOCM murmur?
|
Valsalva (bc dec PL and dec filling of LV) - most murmurs inc onstrast decrease with dec PL
|
|
|
What is the outflow obstruction of HOCM due to?
|
Both a hypertrophied IV septum and an abnormality in the motion of the mitral valve leaflets referred to as systolic anteiror motion (SAM) which results in inc outflow obstruction
|
|
|
When does dilation of MV annulus occur and what does it result in? What does it sound like?
|
Dilated CM or ischemic CM. Leads to MR. typically heard as a holosystolic murmur at apex with radiation to axilla
|
|
|
What can cause rupture of chordae tendinae?
|
Secondary to MVP, endocarditis, trauma, or MI. Result is MR
|
|
|
When is mitral annulus calcificaiton most common? what does it result in?
|
MC in pts >40yo. Results in MR
|
|
|
What race is HOCM most common in?
|
Blacks
|
|
|
What is the murmur of MVP?
|
Midsystolic click at the apex
|
|
|
What is regular narrow complex tachy represent?
|
SVT (supraventricular tachy) - any tach originating His-bundle and includes sinus tachy, MAT, Aflutter, Afib, AVNRT, AVRT, and junctional tachy.
|
|
|
What are the symptoms of SVT?
|
dizziness, lightheaded, SOB, diaphoretic, CP, presyncope, syncope
|
|
|
What are PSVTs?
|
SVTS with abrupt onset and offset. They include AVNRT, AVRT, atrial tachy and junctional tachy
|
|
|
What to do in pts with PSVT?
|
if hemodynamically stable, next step is to identify the type of SVT with the sue of vagal maneuvers (carotid sinus massage, valsalva, eyeball pressure) or IV adenosine - these measures will temporarily slow conduction via the AV node and can aid in diagnosis by unmasking "hidden" p waves in pts with Aflutter or atrial tachy. They can also cause a transient AV nodal blcok and terminate AV node dependent arrhyhmias including AVNRT and orthodromic AVRT
|
|
|
How can you tell the difference between sinus tachy from panic attacks and PSVT?
|
Panic attacks sinus tachy will have normal P wave morphology wrt QRS whereas in PSVT p-waves are "buried" within or seen just afer QRS complex
|
|
|
What is amiodarone used for?
|
Afib or wide QRS complex tachys (VT)
|
|
|
What does hyponatremia mean for pts with HF?
|
Bad prognosis for heart failure pts bc it indicates the presence of severe HF and a high level of neurohumoral activation. Low serum Na levels is assoc with high renin, aldo, ADH, and NE levels. As a result, pts survival significantly reduced if serum Na <137. Decreasing intake of water, not increasing Na intake, can help control
|
|
|
What does furosemide do to K?
|
decreases it
|
|
|
Why want to avoid digoxin in dec renal fnc?
|
Excreted by kidneys
|
|
|
What is the most common cause of isolated AS in elderly pts?
|
Age-dependent idiopathic sclerocalcific changes
|
|
|
What is the murmur of AS?
|
Inc intensity of apical impulse, narrow pulse pressure, typical systolic murmur
|
|
|
What murmur is caused by bacterial endocarditis?
|
Aortic insufficiency
|
|
|
What do pericardial effusions look like on CXR?
|
Enlarged "water bottle" shaped cardiac silhouette
|
|
|
What s/s of pericardial effusion without tamponade?
|
recent URI, SOB, weakness, water bottle shape on CXR. Lungs are clear, no inc JVP. PE may show distant heart sounds and a diffuse PMI that makes it difficult to palpate apex. Once pericardial space cant' stretch to accomodate the effusion, this is known as tamponade with dec VR to RA and dec CO form LV --> hypotension, RHF (JVD), pulmonary edema, tachy, pulsus paradoxus
|
|
|
What are casues of pericardial effusion
|
most commonly idiopathic (including viral) but can also be due to malignancy, post-MI, uremia, autoimmune disease, and hypothryoid.
|
|
|
When do you hear an S4?
|
LVH
|
|
|
What is pulsus bisferiens (biphasic pulse)
|
2 strong systolic peaks of the aortic pulse from LV ejection separated by a midsystolic dip that acn be seen in AR with or without AS and in HOCM
|
|
|
When is an opening snap heard?
|
MS. Significant MS will cause LA enlargement which on CXR shows straightening of the L part of the cardiac silhouette (as opposd to the normal mid concavity visible below the pulmonary artery shadow)
|
|
|
When is intermittent ptosis seen?
|
MG in assoc with thymoma - which appears as anterior mediastinal mass on CXR with preserved cardiac size
|
|
|
What is 1st line medical therapy for HOCM?
|
Either BB bc they slow the heart and prolong diastole -> more time to fill the heart --> less outflow obstruction or cardiac acting CCB (like diltiazem) bc they promote diastolic relaxation if unable to tolerate BB. Avoid meds that decrase PL. Don't use digoxin bc it is a postitive ainotrope and therefore would worsen diastolic relaxation
|
|
|
What are symptoms of HOCM?
|
syncope (15-25%), presyncope, CP with exertion
|
|
|
What is the murmur of HOCM?
|
systolic murmur at L sternal border, worsens with maneuvers that dec PL
|
|
|
What is the murmur of AS?
|
R upper sternal systolic murmur
|
|
|
What type of heart dysfunction does HOCM lead to?
|
Diastolic heart failure
|
|
|
What is disopyramide?
|
anti-arrhythmic with neg inotropic properties as well. Effective in HOCM bc redues pressure gradient along obstructing hypertrophied myocardium, but not 1st line bc of potential to be pro-arrhythmogenic
|
|
|
What is DOC in pts with hyperthyroid-related tachysystolic afib?
|
BB - not only helps to control the rhythm, but also decreases other symptoms of hyperthyroidism
|
|
|
What are these symptoms suggestive of: insomnia, fatiguability, wt loss, lid lag, tremor
|
Graves disease
|
|
|
When is emergent cardioversion for afib indicated?
|
If the arrhythmia precipitates dangerous complications (like hypotension, angina, or heart failure) or in hemodynamically unstable pts
|
|
|
What are the clinical features of cardiac tamponade?
|
Beck's triad: hypotension, distended neck veins, muffled heart sounds. These symptoms are due to an exaggerated shift of the interventricular septum toward the LV cavity, which reduces LV PL, SV, and CO. Pulsus paradoxus (>10mmHg drop in systolic BP during inspiration) is also a common finding. Abd exam can also show a positive hepatojugular reflux
|
|
|
What is cardiac tamponade?
|
Due to fluid accumulation in the pericardial cavity that increases the intrapericardial pressure above the diastolic ventricular pressure. This resricts VR to teh heart and lowers RV and LV filling. The net rsult is dec PL, SV, and CO. Lungs are clear due to dec ventricular filling (PL) rather than volume overload. Inspiration worsens this condition by lowering intrathoracic prssure and increasing VR to the RV. Under normal conditions, the RV is able to accomodate this inc VR by expanding the RV free wall. Tampnade decreases RV compliance and shifts the IV septum toward the LV cavity to further reduce LV filling - this is what causes pulsus paradoxus (>10mmHg drop in systolic BP during inspiration) in tamponade
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What are the typical signs of LHF and RHF?
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LHF: crackles on lung exam, S3. RHF: JVD, peripheral edema
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What happens to cardiac contractility and HR during cardiac tamponade?
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They increase due to sympathetic stimulation as a compensatory mechanism to maintain adequate CO
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What is LV outflow obstruction usually do to?
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Either critical AS or HCOM
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What can PHTN be due to?
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Inc pulm arterial pressure (ex: primary PHTN) or inc pulmonary venous pressure (ex: LVF).
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What will cardiac exam show on PHTN?
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Loud S2
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What is the time course of pulmonary HTN?
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Typically indolent and does not present as RHF until later in the disease
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What EKG findings suggest arrhythmias as cause of syncope?
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inappropriate sinus brady, sinoatrial block, sinus pauses, AV block, non-sustained ventricular arrhythmias, and short or prolonged QTc interval
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What are the causes of syncope and clinical clues to diagnosis?
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1. Vasovagal/neurally mediated syncope: triggers are prolongd standing or emostional distress, painful stimul. Prodromal symptoms: nausea, warmth, diaphoresis. 2. Situational: triggers: cough, micurition, defecation 3. Orthostatic hypotension: postural changes in HR/BP after standing. 4. AS, HOCM, anomalous coronary arteries:syncope with exertion or during exercise 5. Ventricular arrhythmias: prior history of coronary artery disease, MI, CM, or reduced EF. 6. Sick sinus syndrome, brady arrhythmias, AV block: sinus pauses on monitor, prolonged PR interval or QRS duration. 7. Torsades (acquired long QT): hypoK, hypoMg, meds causing prolonged QT 8. Congenital long QT: FHx of sudden death, prolonged QT on EKG, syncope with triggers (exercise, swimming, sudden noise, suring sleep)
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What is syncope?
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Abrupt and transient loss of consciousness with loss of postural tone, followed by a spontaneous and complete recovery. Usually benign and self-limiting, but can be the inital presentation of a life-threatening disease process. Cause often determined by H & PE, EKG, simple lab tests
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Does normal HR exclude bradyarrhythmia?
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no bc AV block can be intermittent
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Are PVCs assoc with syncope?
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no - they are usually asymptomatic or can cause palpitations in some pts. Isolated PVCs with normal EF not assoc with syncope
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What are symptoms that would suggest seizure?
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tonic-clonic movements, loss of bladder and bowel control, postictal phase
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What is Torsades
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Due to polymorphic ventricular tach in the setting of prolonged QT. Mg, K can be low
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Unstable pt with Afib - what to do?
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Immediate DC cardioversion - preferable to pharmacologic conversion (ex: amiodarone, quinidine) bc of higher success rates and less likely to induce an arrhythmia. Succes of cardioversion approx 90%
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What is a common arrhythmia complication after CABG?
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Afib (up to 40% and if CABG combined with AS repair, up to 50%)
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When is transcutanous pacing most often used?
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Management of symptomatic bradycardia
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What is the algorithm for treating wide-complex tachy?
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1. Is there AV dissocation or fusion/capture beats? If yes -> dx of VT. If stable, give IV amiodarone (preferred, but can also use lidocaoine, procainamide). If unstable (hypotension, AMS, resp distress, do synchronized cardioversion. If there is no AV dissociation or fusion/fapture beats, consider SVT with aberrancy. If unstable, same as VT (synchronized cardioversion). If stable, to maneuvers to determine rhythm (ex: carotid massage, rate control) and then treat
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What does monomorphic VT look like on EKG?
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QRS complexes are wide and all match eachother. Fusion beats - capture of electrical signal through both atrium and ventricle briefly -> a hybrid of normal and wide QRS complex - indicative of VT rather than SVT with abberancy
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When does sustained monomorphic CT occur during MI and what is progonsis?
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Early (6-48hrs), assoc with inc risk of in-hospital mortality
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When is esmolol used?
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rapid rate control in aflutter or afib (ultra short-acting beta blocker)
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When is digoxin used?
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Rate control in supraventricular arrhythmias (aflutter, afib, atachy) esp in pts wth hypotension and/or heart failure who are unable to tolerate BB or CCB
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What is SVT with abberancy?
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wide complex SVT - can look like VT but will not have AV dissociation or capture/fusion beats
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What is DOC for pt with benign essential tremor?
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Propranolol - non-selective beta blcker
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What is an essential tremor?
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Postural tremor (not resting tremor like Parkinsons), usually disturbs performance of fine motor tasks. Sometimes runs in families - AD inheritance. Inhibition of tremor by small amts of alcohol is typical
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In an otherwise healthy young pt who develops CHF, what should you consider high on your differential?
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Myocarditis. Viral infection, esp coxsackie B, is most common cause - pts often, though not always, have preceding viral type symptoms
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What are some signs of CHF?
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PND, DOE, peripheral edema, hepatomegaly, cardiomegaly, bilateral pleural effusions, S3
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Where does Lyme disease often occur and can it cause myocarditis?
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NE states. Yes but will have other symptoms of Lyme
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What fungus do you think of in Texas?
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Coccidiodes
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What murmur has widened pulse pressure?
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AR
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What murmur has "water hammer"/bounding pulses?
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AR
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What positional changes are assoc with AR?
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lying flat and turning to the L brings the heart closer to the chest wall and can make pts more aware of the bounding pulse of AR
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What are common causes of AR in the US?
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Aortic root dilation and bicuspid AV. In other countries where abx not as available, RF is most common cause
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What pulmonary symptoms occur in MS?
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Pulmonary edema and hemoptysis
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What are the s/s of tricupsid stenosis?
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RHF symptoms with clear lungs
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What is the change in pulse in AS?
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pulsus parvus et tardus - weak pulse
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What is the murmur of MR?
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Holosystolic murmur heard best at apex with radiation to axilla.
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What are common clinical features of MR?
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exertional dyspnea, fatigue, afib, signs of herat failure, dry cough. Although clinical manifestations of MR vary significantly with degree of regurg, exertional dyspnea and fatigue are the most common symptoms, which occur secondary to combo of dec CO and inc LA pressure. Dry cough may be related to pulmonary congestion and edema, which is an indicator of more severe disease that has result in LV dysfunction
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When does MR occur?
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As a result of primary MV disease (RF, infective endocarditis, trauma) or assoc with other cardiac conditions (ischemic heart disease, HOCM)
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Which murmur can be assoc with a AAA?
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AR
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What are s/s of constrictive pericarditis?
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Exertional dyspnea, elevated JVP, pulsatile hepatomegaly, signs of fluid overload
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What is the MCC of tricuspid stenosis?
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Rheumatic fever
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Can hyperPTH cause secondary hypertension?
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Yes, but uncommon. Suspect in pts with HTN, hyperCa, renal stones, neuropsych symptoms. If there is significant HTN with primary hyperPTH, think MEN type 2 with pheo and further eval
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What are causes of secondary HTN and clues/features?
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1. Renal parenchymal disease - inc serum Cr, abnL UA (proteinuria, RBC casts) 2. Renovascular disease - severe HTN (>180/120) after age 55, possible recurrent flash pulmonary edema or resistant heart failure, unexplained rise in serum Cr, abd bruit 3. Primary aldosteronism - easily provoked hypoK, slight hyperNa, HTN with adrenal incidentaloma 4. Pheochromocytoma - paroxysmal elevated BP with tachy, pounding HA, palpitations, diaphoresis, HTN with adnreal incidentaloma 5. Cushings - central obesity, facial plethora, proximal muscle weakness abdominal striae, ecchymosis, amenorrhea/erectile dysf, HTN with adrenal incidentaloma. 6. Hypothyroid - fatigue, dry skin, cold intolerance, constipation, weight gain, bradycardia 7. Primary hyperPTH - hyperCa (polyuria, polydipsia), kidney stones, neuropsych (confusion, depression, psychosis) 8. Coarctation of aorta - differential HTN with brachial-femoral pulse delay
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What are s/s of hyperPTH?
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HyperCa: stones, bones, groans, psych undertones - muscle weakness, recurrent nephrolithiasis, neuropsych, hyperCa, constipation, back pain.
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How does hyperCa of primary hyperPTH occur?
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excess PTH causes hyperCa due to inc renal Ca reabsorption, GI Ca absorption, and bone resorption
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What is MCC of primary hyperPTH?
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80% due to parathyroid adenoma
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What are other sequelae of hyperPTH besides the hyperCa symptoms?
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HTN, arrhythmias, ventricular hypertrophy, and vascular and valvular calcification. Mechanism for HTN is unclear
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In pts with primary hyperPTH and significant HTN, what should you consider?
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MEN type 2 with pheo
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What are the 3 types of MEN syndromes and their features?
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Type I: primary hyperPTH (90%), pituitary tumors (10-20%), enteropancreatic tumors (60-70%). Type 2A: medullary thyroid cancer (90%), pheo (40-50%), parathyroid hyperplasia (10-20%). TYpe 2B: medullary thyroid cancer, pheo, other (mucosal and intestinal neuromas, marfanoid habitus)
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How do pts with renal artery stensosi present?
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Severe HTN (>180/120) after age 55yo, abd bruit, recurrent flash pulmonary edema or resistant heart failure, inc serum Ca (esp after starting an ACEI or ARB)
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How do pts with coarc of aorta present?
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HA, epistaxis, blurred vision, elevated BP in upper extremities, possible "to-and-fro machinery murmur" from the aorta over the posterior chest, and brachial-femoral pulse delay on exam
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What are signs of hypothyroid?
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wt gain, fatigue, bradycardia, dry skin. Can cause HTN
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What are lab findings of cushings?
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hyperglycemia, leukocytosis, lymphocytopenia, hypoK
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What does amphetamine abuse present as?
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s/s of sympathetic stimulation (ex: tachy, HTN, diaphoresis, hyperthermia, confusion)
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What is the MCC of lower extremity edema?
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Chronic venous insufficiency - it is thought to result from incompetence fo the valves of the LE veins
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What are the manifestations of chronic venous insufficiency?
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mild varicosities to leg pain, severe edema, stasis dermatitis, skin fibrosis, ulceration, immobility
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What are risk factors for chronic venous insuffiiency?
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Age (older), female, obese, hx of lower extremity surgery, hx of lower extremity DVT
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How can help dec edema in chronic venous insufficiency?
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Leg elevation, compression stockings, intermittent pneumatic compression dressings. Skin fibrosis and ulcerastion require more intense medical management
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How do smoking cessation and O2 therapy improve edema?
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if the edema is secondary to RHF (evidence of cor pulmonale - elevated JVP, ascites)
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How do BP control and salt restriction improve edema?
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if the edema is secondary to LHF (crackles on lung exam, JVD)
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How do AV fistulas cause high-output HF?
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They shunt blood from the arterial to venous side, which increases cardiac PL. The pt develops HF despite maintaining normal or high CO bc the circulation is unable to meet the O2 demands of the peripheral tissues
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How can get acquired symptomatic AV fistulas?
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Trauma, Iatrogenic (ex: femoral cath), Atherosclerosis (ex: aortocaval fistula), cancer
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What are congenital causes of AV fistulas?
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PDA, angiomas, pulmonary AVF, CNS ACF
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What are clinical signs of AV fistulas?
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widened pulse pressure, strong peripheral arery pulsation (ex: brisk carotid upstroke), systolic flow murmur, tachycardia, flushed extremities. As the LV hypertrophies, the PMI is displaced to the L. EKG usually shows LVH
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What are causes of high-output HF?
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AV fistulas, thyrotoxicosis, Paget disease, anemia, thiamine deficiency
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What is the preferred test to dx AV fistula in the extremity? What is the tx?
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Doppler US for dx. If AV fistula is large, will need surgery
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What are the clinical features of dec CO (ex: ischemic HD, HTN, CM)?
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Normal/dec pulse pressure, weak carotid upstroke, cold/pale extremities
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What murmur does papillary muscle rupture cause?
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MR, TR
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What are the s/s of pulmonary HTN?
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weakness, angina, scope/presyncope, dyspnea. PE: JVD, reduced carotid upstroke, RV lift, loud P2, TR
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What is electrical alternans and what is it a sign of?
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Electrical alternans with sinus tachy is Highly specific for large pericardial effusion - it is due to swinging motion of the heart in the pericardial cavity causing a beat-to-beat variation in QRS axis and amplitude.
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What is the tx of cardiac tamponade or pericardial effusion with hemodynamic compromise?
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Emergency pericardiocentesis
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In a pt with electrical alternans and recent URI, what do you think?
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Pericarditis due to URI with inflammaiton that caused extra fluid within pericardial cavity leading to pericardial effusion. The inc pericardial fluid compresses the cardiac chambers and limits diastolic filling of the R-sided chambers --> dec in PL and reduces CO, resulting in hypotension and syncope (due to dec cranial blood flow)
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What is used to confirm dx of pericardial effusion in stable pt?
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ECHO
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What is procainamide and when is it used?
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Class IA antiarrhythmic. Used to treat supraventricular and ventricular arrhythmias, esp WPW
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When is syncronized direct current cardioversion used?
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To convert Aflutter, Afib, and stable monomorphic VT
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When are thrombolytics indicated in cardiac pts?
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Acute ST segment elevation MI when PCI not available.
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When is a transcutaneous pacemaker indicated?
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Sick sinus syndrome or symptomatic second-deg or third-deg HB
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What are the causes of pericarditis?
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Infection (viral is MC, bacterial), Iatrogenic (surgery, trauma, radiation, drug-related), CT disease (RA, SLE), Cardiac (Dressler's syndrome (post-MI pericarditis) usually 1-6wks after MI), Uremic (BUN usually >60 but degree of pericarditis does not always correlate with degree of elevation), malignancy (can be due to cancer (ex: lung, breast, Hodgkins) or treatment (radiation, chemo).
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What is the presentation of uremic pericarditis? How often does it occur?
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sharp and pleuritic CP, pericardial friction rub, uremia. Occurs in 6-10% of renal failure pts, esp in those with BUN >60. But, the degree of pericarditis does not always correlate with degree of serum BUN or creatinine elevation.
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What does the EKG of uremic pericarditis look like?
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Doesn't present like classic findings of pericarditis (diffuse ST seg elevations) bc the inflammatory cells don't penetrate the myocardium
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What is the treatment for uremic pericarditis?
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Dialysis - can resolve symptoms and decrease the size of any pericardial effusion. Should avoid anticoagulation in hemodialysis bc can cause hemorrhage into pericardial space. Steroids if unresponsive - have low success rate and assoc with higher risk of recurrance
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What is the treatment for idiopathic or acute viral pericaridtis?
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NSAIDs or colchicine
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Which meds should be held for 48hrs before cardiac stress testing?
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BB, CCB, nitrates (but should be continued in pts with known CAD undergoing stress testing to assess the efficiacy of antianginal therapy)
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WHich meds should be held for 48hrs perior to vasodilator stress test?
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dipyridamole
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Which meds should be held for 12hrs prior to vasodilator stress test?
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Caffeine-containing food or drink
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Which meds can you continue prior to cardiac stress testing?
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ACEI, ARBs, digoxin, statins, diuretics (but note that diuretic-induced hypoK can cause ST seg depression and have false positive results so should delay testing until K normal)
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What is the time frame of the common complications of acute MI?
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Reinfarction: hours-2days. Free wall rupture hours-5days. Ventricular septal rupture hours-1wk. Post-infarct angina hours-1mo. Papillary muscle rupture 2d-1wk. Pericarditis 1d-3mo. LV aneurysm 5d-3mo
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What does EKG show in ventricular anuerysm from MI? ie what is the hallmark
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Persistent ST-seg elvation along with deep Q waves in the same leads as the recent MI
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What can large ventricular aneurysms after MI lead to?
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Progressive LV enlargement causing heart failure, refractory angina, ventricular arrhythmias, or mural thrombus with systemic arterial embolization. Progressive LV enlargement and remodeling can also lead to mitral annular dilation with MR
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How dx ventricular aneurysms?
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ECHO - dyskinetic wall motion of that portion
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Do pts with Dressler syndrome have the typical clinical features of pericarditis?
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no - don't have pleuritic CP, fever, leukocytosis, or pericardial friction rub
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When aortic dissection is extended, what vessel does it usually involve?
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RCA -> acute inferior MI with ST seg elevation in leads II, III, aVF.
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When does papillary muscle rupture occur after MI and what can happen as a result?
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2-7d post-MI. Life-threatening complication usually due to necrosis of the surrounding tissues. Usually causes acute severe MR leading to hypotension and pulmonaryedema. It does NOT typically cause persistent ST-segment elevation on EKG.
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Can pericardial effusion occur after MI?
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Yes - like acute pericarditis, occurs early in course of MI. A large pericardial effusion should raise suspicion for LV free wall rupture. Usually presents with signs of cardiac tamponade, but the most common EKG sign is LOW-voltage QRS complexes. Electrical alternans can be seen with large effusions
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What do pts with inferior wall MI usually present with?
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Hypotension, elevated JVP, clear lungs
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When does LV free wall rupture occur after MI? What can it lead to?
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Several hours to 2 weeks. Typically leads to hemopericardium and cardiac tamponade and can rapidly progress to PEA
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When do you defibrillate?
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VF and pulseless VT. Time to defibrillation is strongly correlated with survival
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When can VF occur?
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As a feared complication of MI, but also in electrolyte imbalances, myocarditis, CM, and as a drug side effect
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When is upright tilt table testing indicated?
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Vasovagal syncope to confirm the diagnosis if the syncope is recurrant. Can be used with or without pharmacologic provocation (isoproterenol)
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What is the typical prodrome of vasovagal syncope?
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lightheadedness, weakness, blurred vision. Rapid recovery of consciousness
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What meds have mortality benefit in HF?
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ACEI, BB, ARBs, spironolactone
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How do ACEI work?
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dec both PL and AL and also effect local renin-AT systemic in heart
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When is dobutamine used in CHF?
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Can be used temporarily in pts with severe decompensated CHF to improve cardiac contractility, but it increases the likelihood of arrhythmias and may actually increase mortality if used long term
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How can differentiate between heart and liver disease related causes of lower extremity edema?
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Hepatojugular reflex is neg in liver disease and positive in heart disease. RHF can cause LLE, ascites, hepatomgealy and spelnomegaly. Liver disease can cause all of these as well excet HJR
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What are the SE of amiodarone?
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Pulmonary fibrosis, hepatotoxicity, thyroid dysfunction.
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What are the SE of digoxin?
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N/V/D, blurry yellow vision, arrhythmias
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What are the SE of hydralazine?
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salt retention, reflex tachy, lupus-like syndrome
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What are the SE of metoprolol?
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Impotence, bradycardia, AV node blockage
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What are the SE of verapamil?
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constipation, dizziness, flushing
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What are the SE of enalapril?
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hyperK, cough, dec GFR, rash, angioedema
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What is the most important intervention in acute aortic dissection?
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BB
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What are type A and B aortic dissections and how are they treated?
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Type A: involve the ascending aorta and are treated with medical therapy and surgery. Type B: involve only the descending aorta and are usually treated with medical therapy alone
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What is the leading risk factor for aortic dissection?
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HTN
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What will chest CT show in aortic dissection?
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Aorta with both a true and a "false" lumen separated by an intimal flap
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When should vasodilators such as Nifedipine be used in aortic dissection?
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They should only be considered in the treatment of aortic dissection if further BP lowering is needed after BB. Vasodilation can induce a reflex tachy which would inc aortic shear stress
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What meds to avoid in aortic dissection
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Vasodilators, anticoagulants, fibrinolytics, etc
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What 3 clinical findings are characteristic of aortic dissection?
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Abrupt onset of "tearing" pain in the chest or back, variation in pulse or BP between R and L arms, and widened mediastinum on CXR. When 2 or more of these are present, the incidence of dissection exceeds 80%
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What are risk factors for aortic dissection?
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HTN, smoking, Fhx of coronary artery disease
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Where can dissection of ascending aorta extend into?
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Pericardium, coronary arteries or carotids, leading to cardiac tamponade, myocardial infarction, or stroke.
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How does subarachnoid hemorrhage present?
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Sudden onset severe HA, stiff neck, vomiting, impaired consciousness.
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How do hemorrhagic stroke pts present?
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HA, focal neuro deficits
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What is a paradoxical PE?
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Develops in venous system and travels to arterial system thru abnormal communication between R and L sides of heart. THis can result in stroke.
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What should you think of in pt with pupillary dilation and blood at the external nares in pt with CP?
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Cocaine-induced vasospams. Can result in ST elevation MI
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How do you treat cocaine-induced STEMIs?
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Same as classic STEMIs - with PTCA or thrombolysis. Can also give ASA and nitrates but don't give BB! (unopposed alpha agonist can worsen vasospasm). CCB and alpha blockers like phentolamine can also help reduce vasospasm in these pts
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What does acute pericarditis look like on EKG?
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ST elevations with PR depressions
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What is pleurodynia?
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Chest pain typically of pulmonary etiology that is worse with deep breathing.
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What should do if pt on statin presents with myalgias?
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Check CPK - if high, first step is to discontinue statin - the muscle injury can progress to rhabdo with renal failure.
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What are common SE of ARBs?
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hyperK, hypotension, renal failure
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What are the 3 primary uses of N-acetylcysteine?
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dissolution of mucus, protection against contrast induced renal failure, and therapy for acetaminophen overdose
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What can pressors such as NE cause in fingers?
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Ischemia of distal fingertips and toes secondary to vasospasm. PE: symmetric duskiness and coolness of all fingertips (NE has alpha-1 agonist properties which cause vasoconstriction - which is why it is useful in trying to inc BP in hypotensive pts, but in some pts can get ischemia/necrosis). Similar phenomena in intestines (mesenteric ischemia) or kidneys (renal failure)
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Where can endocarditis spread septic emboli?
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Throughout the entire body. But won't affect all fingers at same time
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What is Raynaud's phenom?
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Finger ischemia that typically progresses from pallor to cyanosis to erythema. It can be accompanied by pain and is usually due to cold exposure or stress
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When do cholesterol emboli occur and what do they look like in the digits?
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Pts with atherosclerosis. Can affect the distal portions of the digits -> "blue toe syndrome". But won't affect all digits
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When does SVC syndrome occur and what is PE?
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Pts with lung cancer, thrombi, or fibrosing mediastinits. Causes upper extremity edema.
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What are the common causes of constrictive pericarditis?
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Can follow idiopathic or viral pericarditis (40% in US). Cardiac surgery (10% in US) and radation therapy (30% in US). TB pericarditis (MCC in endemic areas)
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What is the clinical presentation of constrictive pericarditis?
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Fatigue and DOE, peripheral edema and ascites, inc JVP, pericardial knock may be heard
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What are the diagnostic findings of constrictive pericarditis?
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Imaging shows inc pericardial thickening and calcification. Jugular venous pulse tracing shows prominent x and y descents
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What is constrictive pericarditis?
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Pericardial fibrosis and obliteration of pericardial space. It impairs ventricular filling during diastole, causing pts to experience symptoms related to dec CO (fatigue and DOE), signs of venous overload (elevated JVP, ascites, peda edema), Kussmaul's sign, and presence of pericardial knock.
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What is Kussmaul's sign?
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Lack of typical inspiratory decline in central venous pressure
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What is a pericardial knock?
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Early heart sound after S2
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What are the most common causes of cor pulmonale?
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COPD and PE. Cor pulmonale develops due to pulmonary HTN
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What are signs of pulmonary HTN on PE?
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Widely split S2 and inc intensity of P2
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What are the pneumoconioses? S/S, Imaging show what?
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Occupational lung diseases cuased by inhalation of inorganic dust. Examples: asbestosis and silicosis. S/S: DOE, PHTN, cor pulmonale after years of exposure. CXR: parenchymal nodules (silicosis) and pleural plaques (asbetsosis)
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What is Psittacosis?
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DIsease transmitted to humans by birds. Presents with fever, dry cough, HA. PE: pulmonary findings most prominent. Cardiac involvement is rare
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What is Trypanosoma cruzi - what does it cause and where is it found?
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It is the cause of Chagas disease. It is endemic in South America and may cuase megacolon, megaesophagus, and cardiac diseaes. Causes both systolic and diastolic heart failure. May also cause arrhythmias and MR or TR.
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What are the 3 most common causes of aortic stenosis and how can differentiate?
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Senile calcific AS, bicuspid aortic valve, and rheumatic heart disease. Think bicuspid in AS in pt <70yo
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What is the PE of AS?
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Harsh systolic murmur at R upper sternal border with radaition to carotids. Can als ohave S4 as a result of L atrial kick against stiff LV (high resistance generated by stenosed aortic valve causes concentric hypertrophy and stiffening of the LV causing S4)
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Where is rheumatic fever more common?
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Developing countries
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Why does mitral stenosis cause pulmonary congestion symptoms? What are these symptoms?
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Stenotic MV -> inc in LA pressure which is transmitted to the pulmonary vascular bed. This increase in pulmonary vascular pressure causes pulmonary congestion -> symptoms such as DOE, noctural cough, hemoptysis (hemoptysis in particular should raise suspicion for MS)
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What arrhythmia are pts with MS at high risk for?
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Afib due to LA dilation
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What are the typical symptoms of HOCM?
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Syncope, angina, palpitations
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What diseases that are common in developing countries can cause aortic insufficiency?
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Syphilis or rheumatic fever
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Is WPW transient or constant tachy?
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Transient
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What is affected in primary PHTN?
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Pulmonary arteries
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What is the demographic that is most common for primary PHTN?
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females in 4th-5th decade
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What is the inheritance pattern of PCKD?
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Autosomal dominant
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How does PCKD typically present?
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hematuria and hypertension, but can also cause abdominal masses and pain. It is assoc with intracerebral aneurysms. PE: can have flank or abd masses, pain, secondary erythrocytosis due to inc EPO production, and renal failure.
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How dx PCKD?
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Abdominal US
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What is PCKD?
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autosomal dominant condition characterized by bilateral cystic dilation of the renal tubules. HTN is one of the earliest manifestations of the disease. Often also have Hematuria.
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How do pts with PCKD often due?
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Stroke - cerebral aneurysms
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How do you diagnose pheochromocytoma?
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Urine metanephrines
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What does an elevated aldo:renin level suggestion?
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Primary hyperald (a common cause of secondary HTN)
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What is a 24-hr urine cortisol measurement used for?
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Cushing's
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Are adrenal masses palpable?
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Almost ever
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What is a captopril renal scan used for?
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To diagnose renal artery stenosis
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What is a catastrophic complication of acute aortic dissection?
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Cardiac tamponade - suspect in pt with HTN, tachy, distended neck veins, and pulsus paradoxus who have sudden onset of severe tearing CP radiating to the back. Tampoade occurs after aortic dissection bc ofrupture of the aorta and rapid accumulation of blood in pericardial space. An abrupt accumulation of even small amts of blood can significantly raise the pressure inside the pericardial cavity. Inc pericardial presure causes compression of the cardiac chambers and limits diastolic filling of the R-sided chambers which causes dec in PL and dec CO, resulting in hypotension and syncope
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How can you tell if syncope is related to hypovolemia or another problem by PE?
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Hypovolemia/intravascular volume depletion typically occurs in te seting of acute blood loss and protracted vomiting and/or diarrhea. These pts will have dec jugular venous pressure with flat neck veins (vs for example, tamponade which has distended neck veins)
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When does syncope occur with AS?
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During activity.
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What is the chest pain of AS like?
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Typically exertional, not as severe as dissection and doesn't radiate to the back
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What are the pulse findings of AS?
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Pulsus parvus et tardus - slow rising, low amplitude pulse
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Can cardiac tachyarrhythmias cause syncope?
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Yes - ex: afib, aflutter, VT, VF
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How does papillary muscle rupture after MI present?
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Acute MR with sudden onset of pulmonary edema, hypotension, and progression to cardiogenic shock.
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What is the underlying mechanism of vasovagal syncope?
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Vagal hyperactivity. Will have prodromal symptoms including dizziness, nausea, diaphoresis, pallor, and visual disturbances prior to syncope
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What is special in the management of RV infarct?
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Need to fluid resuscitate and avoid nitrates/nitroglycerin. When fluid resuscitation doesn't improve hemodynamics, dobutamine can be used to inc CO thru inotropic and chronotropic sitmulation - but hypotensive pts should also get dopamine bc dobutamine can worsen hypotenion if given alone
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WHat are signs of inferior wall infarct/RV infarct?
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Clear lungs, hypotension, JVD.
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What is the typical acute management of STEMI?
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reperfusion (thrombolysis or percutaneous angioplasty), antiplatelet therapy, morphine, heparin, nitrates, and beta blockers
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When are nitrates contraindicated in STEMI?
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Aortic stenosis, recent PDEI use, or RV infarct (which occurs in more than 30% of cases of inferior wall MI - when RV SV dec, CO impaired --> any med that reduces PL (nitrates or diuretics) will exacerbate rather than improve symptoms)
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When can temporary pacing in RV MI be used?
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If complicated by bradycardia
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What are the s/s of primary hyperaldo (Conn's syndrome)?
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HTN, mild hyperNa, hypoK, metabolic alkalosis - this combo is a result of excess aldo which promotes distal tubular reabsorption of Na, volume expansion, and secretion of K and H ions
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How can confirm dx of Conn's syndrome?
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Low renin and high aldo levels
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What is MCC of primary hyperaldo and what will see on CT?
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adrenal mass which will see on CT
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What are the renin, aldo, and bicarb levels in primary hyperaldo?
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Aldo high -> neg feedback causes renin to be low. Bicarb high -> metabolic alkalosis
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What are symptoms of hypoK?
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Muscle weakness and exercise intolerance
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What is the caue of cardiogenic pulmonary edema? How does it present and what can you do to treat it?
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LHF. Characterized by crackles on pulmonary exam. Tx: Nitro (IV, sublingual, or topical) is the most rapidly acting med to relieve symptoms of pulmonary edema - works more quickly than morphine or loop diuretics
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What should you be concerned about in a pt with long-standed hypertension and signs of pulmonary edema?
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Cardiogenic pulmonary edema from diastolic dysfunction (due to HTN) which causes impaired ventricular relaxation
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Is nitro part of the long term management of pts with HF?
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No, but can be used acutely to alleviate symptoms. Should be used cautiously in pts with hypotension
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What med is the mainstay of therapy in pts with decompensated HF?
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Loop diuretics - works by reducing total body volume
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Why not use BB acutely in decompensated HF?
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They are negative inotropes and may actualy worsen HF symptoms
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When use hydralazine in HF?
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Use in combo with oral nitrate in African American men
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WHat is salmeterol and when is it used?
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Long-acting beta-2 adrenergic agonist. Used in the chronic tx of asthma and bronchodilator-responsive COPD. Bc of its slow onset, it is not beneficial in the treatment of asthma or COPD exacerbations
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When does dopamine inc cardiac contractility?
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At small doses dopamine stimulates myocardial beta receptors to inc myocardial contractility but at these doses it is also arrhythmogenic and may worsen heart failure
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When is amiodarone used?
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To treat Afib or VT
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When is verapamil used?
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To rate control Afib and to improve diastolic relaxation in HOCM. Remember, it is a negative inotrope and may worsen HF symptoms
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What is aminophylline and when is it used?
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Bronchodilator. Used to tx asthma and COPD
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In ischemic CP, how does it change with exercise
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Worsened with exertion, relieved by rest
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What is the most reasonable first step in CP suspicious for ischemia with resting EKG normal?
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Exercise stress test - EKG or ECHO. If positive, go to angiography
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Is lupus a risk factor for CAD?
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Yes, as are steroids which are commonly used to treat SLE
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When are esophageal motility studies helpful?
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Pts with dysphagia or suspected diffuse esophageal spasm or nutcracker esophagus
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What is the main mechanism responsible for pain relief in pts with anginal pain treated with nitro?
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Dilation of veins (capacitance vessels) and dec in ventricular preload. Inc venous capacitance and venous pooling of blood lead to significant dec in ventricular PL and dec in heart size --> O2 requirement of the heart greatly reduces. Nitro also cause arterial dilation and therefore dec ventricular AL, but this effect is less significant in relieving anginal pain. Secondary effects provoked by nitro such as inc heart contractility and reflex tachy are due to change in activity of baroreceptors in response to dec in BP - these effects inc myocardial O2 demand
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What type of CCB can cause peripheral edema?
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Dihydropridine (~dipines). These meds can cause significant edema due to dilation of peripheral BV - this is not an allergic reaction! If edema is significant, d/c drug. Labs should be normal, exclude more serious causes of edema
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If edema is due to CHF, what else will see on exam?
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Dyspnea, orthopnea, elevated neck veins, liver enlargement
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If edema is due to renal disease, what else will see?
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massive proteinuria (as with nephrotic syndrome) or fluid retention (as with acute nephritic syndrome), hypoalbuminemia, inc Cr
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If edema is due to venous insufficiency, what will see on exam?
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Skin changes and varicosities
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What is the basic underlying pathophys in septic shock?
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Dec in systemic vascular resistance due to overall peripheral vasodilation.
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What are the changes in PCWP, SVR, CO, and mixed venous O2 sat in septic shock, cardiogenic shock, and hypovolemic shock?
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Septic shock: normal/sl low RA P (PL), normal/sl low PCWP (PL), high CO, low SVR, high mixed venous O2 sat. Cardiogenic shock: high RA P (PL), high PCWP (PL), low low CO, high SVR, low mixed O2 sat. Hypovolemic shock: low RA P (PL), low PCWP (PL), low CO, high SVR, low mixed O2 sat
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How can tell the difference between hypovolemic, cardiogenic, and septic shock in terms of measurements?
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RA pressure and PCWP will be high in Cardiogenic and nl/low in the others. CO high in septic shock, low in hypovolemic, and very low in cardiogenic. SVR low only in septic shock. Mixed venous O2 sat only high in septic shock
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Why is mixed venous O2 sat high in septic shock?
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Due to hyperdynamic circulation, improper distribultion of cardiac output, and inability of the tissues to adequately extract oxygen
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What are the PE findings of septic shock? Lactate?
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Hypotension, warm (early)/cool (late) extremities, elevated lactate
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What is cardiogenic shock usually due to?
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Significant LV dysfunction and reduced pump function. Often CO is low, PCEP is high, and SVR is high
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What changes does cardiac tamponade have on heart pressures?
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Inc RA, RV pressures. Equalization of RA, RVED, and PCWP
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What is the treatment of 1st deg heart block?
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Nothing - it is a completely benign arrhythmia
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What is the normal PR interval?
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<.2s
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What med can cause 1st deg HB?
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Digoxin
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What med is used to treat symptomatic bradycardia from type II and III heart block?
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atropine. But never for type I
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What meds have proven survival benefit in CHF?
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ACEI, ARBs, BB, spironolactone. Digoxin and Lasix dec symptoms and hospitalizations, but don't inc survival. ASA also have survival benefit bc prevent MI
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What is the MOA of digoxin?
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Cardiac glycoside - helps inc the heart's contractility -> good for improving CHF symptoms like dyspnea and fatigue
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when does spironolactone inc survival in CHF?
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30% dec in mortality at 24 mo in pts with NYHA class III to IV heart failure who were recieving ACEI and loop diuretic
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Where is the most common site for ectopic foci that cause afib?
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Pulmonary veins.
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What is the most common side for ectopic foci that cause atrial flutter?
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Reentrant circuit that rotates around the tricupsid annulus
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Where is PSVT usually located in the atrium?
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reentrant circuit most commonly within the AV node or via an accessory bypass tract
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What do these symptoms suggest: fever, malaise, new systolic murmur, painful skin lesions?
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Subacute bacterial endocarditis. The painful skin lesions are Osler nodes.
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Who is at risk for endocarditis?
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Those with valvular lesions
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What are the most common causes of subacute bacterial endocarditis?
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Viridans strep (upper respiratory), enterococci (GU/GI), coag neg staph (ex: staph epidermidis - usually from the skin). Also, staph aureus but the usual presentation is an acute, severe illness with normal heart valves
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What is the risk of bacteremia with GU procedures?
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generally low, but inc in pts with preexisting urinary infections
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What is Coxiella burnetii?
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A rickettsial bacteria that causes Q fever. Seen in pts with exposure to livestock or unpasteurized milk
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What does a systolic-diastolic abd bruit in a pt with HTN and atherosclerosis suggest?
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Renal artery stenosis
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What is the leading cause of secondary HTN?
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Renal artery stenosis
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What are bruits?
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Turbulent flow within a vessel. Often reflect luminal irregularites
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What is a common PE finding of renal artery stenosis?
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Abd/periumbilical bruits. Systolic-diastolic are seen in 40% of pts with renal artery stenosis
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When are AAA seen?
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Older men with atherosclerosis and smoking hx. Can have pulsatile abd mass. May have systolic bruit but not systolic-diastolic like in renal artery stenosis
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What are aortic coarctations, what can they cause, what is PE, and when are they most often diagnosed?
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Aortic coarctations are congenital strictures along the aorta. They can cause HTN and differences in BP between the upper and lower extremities. In some instances, there may be a higher BP in R arm compared to L if the coarctation is proxmal to the L subclavian artery origin. Most often dx in infancy or childhood
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What are 2 signs of inc cardiac filling pressures? (one is on PE, one is a lab)
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Elevated BNP and audible S3
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What is BNP and when is it secreted?
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Brain natriuretic peptide. Secreted in response to ventricular stretch and wall tension when cardiac filling pressures are elevated. Cardiac myocytes secrete BNP precursor (proBNP) which is then cleaved into biologically active c-terminal BNP and inactive n-terminal proBNP. It is common practice in the ED to measure the BNP level to differentiate dyspnea from heart failure from dyspnea from non-cardiac etiology. The level of circulating BNP correlates both with the severity of LV filling pressure elevation as well as with mortality. A low BNP argues against acute heart failure with a very high NPV
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What is an S3 and when is it elevated?
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A soft, diastolic sound produced by tensing of the papillary chordal apparatus when there is rapid influx of blood into the ventricle in early diastole. S3 is assoc with CHF and elevated ventricular filling pressures
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How can pts with heart failure develop wheezing?
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DUe to bronchial wall edema (generally, wheezing is a sign of respiratory disease)
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In pts with CP in ED and suspect ACS, what should you give first?
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ASA to all pts - early antiplatelet therapy with aspirin reduces the rate of MI and overall mortality in pts with ACS
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What is the evaluation of CP in the ED algorithm?
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First - focused H &PE, vitals. If pt is unstable, stabilize and check for underlying causes. If pt stable, get EKG and CXR and give ASA if risk for aortic dissection is low. If EKG consistent with ACS: if STEMI, tx with emergent cath or thrombolysis. If NSTEMI: treat with anticoagulation. If EKG not consistent with ACS: look at CXR - if diagonstic, treat cause. If not, assess for PE, check CE and risk stratify for ACS, assess for pericarditis and aortic dissection
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What is the MOA of Aspirin?
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Inhibits thromboxane A2 production -> antiplatelet
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What meds can be given for musculoskeletal CP?
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Acetaminophen, oxycodone
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When is Heparin used in ACS?
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for MI (positive CE or STEMI on EKG) or for high suspicion and/or confirmation of PE.
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How do you treat pericarditis medically?
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Ibuprofen
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What is the most likely cause of post-op pt with JVD and new onset RBBB?
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Massive PE
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What is the definition of a massive PE?
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PE complicated by hypotension and/or acute R heart strain. Syncope tends to only occur in massive PE. Pts have JVD and RBBB bc of R heart strain
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How do pts with massive PE get bradycardia?
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R heart strain -> RV dysfunction -> dec flow to L side of heart -> dec CO -> L pump failure -> bradycardia. This results in cardiogenic shock -> CNS effects such as AMS, dilated pupils, etc
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What is the indicated treatment for massive PE?
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Respiratory and hemodynamic support + Fibrinolysis
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What are the classic cardiovascular changes in the setting of sepsis?
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Hypotension, dec PVR, inc CO, dec PCWP. May have fever and warm extremities
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What test is diagnostic for AS?
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ECHO
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What is the treatment for symptomatic AS?
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Valve replacement
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What is the MCC of LV outflow obstruction in adults?
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AS
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How does AS cause symptoms?
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As aortic valve shiffens, teh resulting high pressure gradient between LV and aorta strains the LV and causes hypertrophy.
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What are teh age ranges for calcification of trileaflet AS and bicupsid AS?
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calcification: 60+yo. Bicuspid: teens and early 20s
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What are the symptoms of AS?
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SAD: syncope, exertional angina, dyspnea (on exertion)
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What is the PE of AS?
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Crescendo-decrescendo systolic ejection murmur on the R 2nd intercostal space that radiates to the carotids. Pulsus parvus et tardus, weak S2, present S4. In later stages, LV may dilate causing displaced PMI and overt symptoms of heart failure.
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What is EKG of AS?
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non-specific, suggests LVH
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What will ECHO show in AS?
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aortic valve abnormalities, LV hypertrophy, inc LV-aortic gradient
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What signs after syncope point away from stroke?
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Alter right after, no signs of bowel/bladder incontience, no signs that bit tongue
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What should tell pts with AS regarding exercise?
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Avoid strenuous exercise. Should avoid stress test in severe symptomatic as well
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When does acute pericarditis occur after MI?
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during first seeveral days after MI.
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What are s/s of pericarditis?
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sharp, pleuritic CP that is worse in supine position and improved by sitting up and leaning forward. May hear pericardial friction rub on exam
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What is EKG of acute pericarditis?
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Diffuse ST elevations, esp with PR depressions
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When does interventricular free wall rupture and papillary muscle rupture occur after MI?
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3-7d. Will present with new murmur
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when does ventricular free wall rupture occur after MI and how does it present?
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3-7d after anterior wall MI. Presents with rapid deterioration secondary to pericardial tamponade. PEA is common
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How can tell difference on PE between PE and pericarditis?
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Both are pleuritic but pericarditis improves with leaning forward, whereas PE does not
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WHen does ventricular aneurysm occur after MI? How does it present?
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days to months after. Presents wth akinesis of the involved portion of the LV wall, ventricualr arrhythmias, and systemic embolization
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What is the treatment for 3rd deg HB?
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Expeditious pacemaker placement bc rhythm can degenerate into VT or Vfib
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What are the common rates of p waves and QRS in complete heart block?
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P waves: 90-100bpm. QRS: 30bpm
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When QRS complexes are going at 30bpm and QRS is wide (>120ms), what does that suggest?
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ventricular escape rhythm
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Can an MI cause a 3rd degree heart blcok?
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yes
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If a 3rd degree heart block is caused by an MI, what should be treated first, the heart block (pacemaker) or the cath for the MI?
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heart block
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What is adenosine used for in cardiology?
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Delays conduction thru AV node (atrial tachys)
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What are some AV nodal blockers?
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BB, CCB, digoxin, adenosine
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What is hereditary hemochromatosis and what organs can it affect?
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Causes abnormal iron deposition in various organs, leading to multisystem end-organ damage. Iron deposition within: 1. Cardiac: myocardium deposition leads to dilated or restrictive CM, heart failure, or conduction abnormalities (ex: sick sinus syndrome). 2. Constitutional: lethargy, fatigue, malaise 3. Integumentary: skin pigmentation or discoloration (bronze DM). 4. MSK: arthralgia, arthropathy (assoc with pseudogout), chondrocalcinosis 5. GI: elevated LFTs with hepatomegaly (early), fibrosis and cirrhosis (later) and inc risk of HCC. 6. Endocrine: DM, hypogonadotropic hypogonadism (impotence, dec libido, premature amenorrhea), hypothyroid. 7. Infections - inc susceptibility to infections with Listeria, Vibrio, Yersinia
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What is the inheritance of hereditary hemochromatosis?
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AR. Due to HFE gene mutation causing inc intestinal iron deposition.
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What is the classic triad of hemochromatosis and is it common?
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Cirrhosis, DM, skin pigmentation. But the triad is not that common
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How is hemochromatosis affecting heart often diagnosed?
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Cardiac MRI to detect myocardial iron overload
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What genetic syndromes can ASD bc assoc with?
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Eisenmenger syndrome, Holt-Oram (heart-hand) syndrome. Can also be seen alone
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What is endocardial fibroelastosis?
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Idiopathic, diffuse fibroelastic thickening of the LV endocardiu. Usually occurs in 1st 2 yeras of life and is a cause of restrictive CM
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What is the gene defect in HOCM?
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Mutations of one of several sarcomere genes encoding cardiac sarcomere proteins
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What is the MOA of statins?
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Inhibit intracellular HMG-CoA reductase enzyme - RLS in intracellular biosyn of cholesterol(thus prevents conversion of HMG-CoA to mevalonic acid, which increases the number of cell membrane LDL receptors - these LDL-R remove circulating LDL and deliver it to the cell's interior, where it is digested. Net effect is dec serum LDL with minimal change in liver LDL - but some pts can develop hepatic dysfunction as well). Statins also dec coenzyme Q10 synthesis which is involved in muscle cell energy production and possibly contributes to statin-induced myopathy
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How do myaglias of statins present?
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Symmetrical proximal muscle weakness or tenderness. Myalgias occur in 2-10% of pts but significant myositis with eelvated CK is uncommon
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What SE does captopril potentially have on kidneys?
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drug-induced membranous glomerulonephritis
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What type of enzyme blocker is ACEI?
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Extracellular.
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How does ACEI cause cough and angioedema?
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ACEI also increases levels of bradykinin, which causes cough and angioedema
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Which cardiac drugs work by cell surface receptor blockage?
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BB, alpha blockers, CCB
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What is the strongest influence on long-term prognosis following an ST-elevation MI?
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Duration of time that pases before coronary blood flow is restored (via PTCA or fibrinolysis)
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What are the door to balloon/needle time goals for PCI and fibrinolysis?
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Door to ballon for PCI: 90min. Door to needle for fibrinolysis: 30min
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What is myocardial O2 demand determined by? What are meds that afefct these?
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HR, PL, contractility, AL. Nitrates and BB reduce myocardial O2 demand (among others)
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Should you prophylax against arrhythmias following MI?
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No - no proven benefit
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When can reperfusion injury occur after MI?
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After either PCI or fibrinolysis, taht can cause continued myocyte death. But no meds to inhibit thus far
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What are clues for the diagnosis of arrhythmia as a cause of syncope?
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suden onset of syncope without warning signs, presence of structural heart disease (ex: murmur), and frequent ectopic beats. Also, meds - ex: thiazides can cause electrolyte disturbances predisposing to ventricular arrhythmias)
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What are the s/s of vasovagal syncope?
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(common fainting spell) - usually precipitated by emotional reaction, preceded by presyncopal dizziness, weakness, nausea
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Can you have clonic jerks during syncopal episode?
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Yes - any syncope that is prolonged can cause jerks due to brain hypoxia
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When do pts with Dressler's syndrome present and how do they present? What is the treatment of choice?
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Dressler's syndrome - pericarditis that can occur weeks after an MI - it is believed to be due to immunologic phenomena. Presentation: CP that is worse with inspriation, improved on leaning forward, can have malaise and fever. EKG: classic for pericarditis (diffuse ST elevation with the exception of reciprocal depression in aVR), SED rate is typically elevated. TOC: NSAIDS; can use corticosteroids when NSAIDs are contraindicated. Avoid anticoagulation to prevent development of hemorrhagic pericardial effusion
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What meds should you avoid in pericarditis?
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Anticoagulants to avoid hemorrhagic pericardial effusion
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Should you give abx for Dressler's syndrome?
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No - not indicated bc it is caused by an immunologic abnormality and not an infection
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What are the SE of high-dose niacin and what is the mechanism of the SE? How can you get rid of it?
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Cutaneous flushing and pruritis. This is due to prostaglandin-induced vasodilation and can be reduced by low-dose aspirin (take 30min before niacin; relieves fluishing and pruritis after 2-4 wks)
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What are premature atrial beats - how can you see them on EKG? What are they caused by? How do you treat?
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Premature atrial beats = p waves that are premature relative to sinus cycle length and which differ in morphology from sinus p waves. They frequently reset the sinus node, producing pauses, which are only partially compensatory. QRS width is normal. Causes: normal or due to anxiety, CHF, hypoxia, caffeine, or electrolyte abnormalities. Don't treat, they are completely benign
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Can electrolyte abnormalities cause premature atrial beats?
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Yes but it is rare and unlikely without comorbid diseases. Mg, K, Ca should be checked and replaced/causitive agent removed if that is the cause
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How does HOCM lead to sudden death?
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Can lead to ventricular arrhythmias (VT, VF). Most have no prior symptoms. The generation of the arrhythmias is multifactorial, but all derive from the underlying abnormality of abnormal myocytes and myocardial scarring. Can also ahve death from heart failure and stroke, but unlikely to cause a sudden death
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What is the MCC of aortic aneurysms?
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Atherosclerosis
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What are ascending and descending aortic aneurysms most often due to?
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Ascending (arise anywhere from aortic valve to innominate artery): cystic medial necrosis (usually occurs with aging) or CT disorders (Marfan's, Ehlers-Danlos). Descending (arise distal to the L subclavian artery): atherosclerosis
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What does CXR look like for aortic aneurysm?
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Widened mediastinal silhouette, inc aortic knob, tracheal deviation. Howevere, CXR can not always distinguish aortic aneurysm from tortuous aortha --> need CT with contrast to confirm
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How can thoracic aortic aneurysms present?
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Chest, back, flank or abd pain depending on location
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What are the causes of reflux disease?
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Acid hypersecretion, inc gastric pressure, obseity, pregnancy, loss of LES pressure, smoing, hiatal hernia.
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How can dx hiatal hernia with imaging?
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CXR - shows round retrocardiac mediastinal density with air fluid levels
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How does achalasia present and how can dx it?
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Presents with dysphagia to both solids and liquids. CXR may show absence of gastric air bubble. Barium swallow: dilated esophagus with distal narrowing. EGD, manometry required to confirm dx
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What is usually the cause of unilateral mass near hilum?
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Usually malignant but can be infectious. Most symptomatic. Don't appear well circumscribed on CR
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What is PEA?
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Presence of an organized rhythm on cardiac monitoring without a measurable BP or palpable pulse in a cardiac arrest pt
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What are the reversible causes of PEA?
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H's: Hypovolemia, Hypoxia, Hydrogen ions (acidosis), Hypo or Hyperkalemia, Hypothermia. T;s: Tension PTX, Tamponade, Toxins (narcotics, benzos), Thrombosis (pulmonary/cardiac), Trauma
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What is the approach to an adult pt in cardiac arrest?
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Start CPR, give O2, attach monitor/defibrillator. If in VF or pulseless VT: shock with CPR between and giving Epi every 3-5min. If PEA/Asystole - CPR with rhythm checks every 2 min and epi every 3-5min and shock if it is a shockable rhythm (CPR + vasopressor therapy (epi) to achieve adequate cerebral and coronary perfusion). Can give single dose vasopressin instead of epi
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When can you defibrillate a pt?
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VF or pulseless VT
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When is IV lidocaine indicated in pts?
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It is a second line antiarrhythmic agent used for hemodynamically stable monomorphic VT
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When is immediate synchronized electrical cardioversion indicated?
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Symptomatic or sustained monomorphic VT (unresponsivel to antiarrhythmics) and hemodynamically unstable Afib with RVR. Note: once the pt develops PEA or aystole, need to initiate ACLS
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What are common causes of inadeuqate response to antihypertensive therapy?
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Non-adherence to lifestyle changes and diet, med noncompliance, use of meds that raise BP or reduce the response to antihypertensive agents (NSAIDs, decongestants glucocorticoids)
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What are nonpharmacologic therapy (lifestyle modification) in the management of HTN?
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Dietary salt restriction, diet rich in fruits, veggies, and low-fat dairy products, regular aerobic exercise, wt loss, lmiting alcohol intake
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How much alcohol intake is assoc with inc incidence of HTN?
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>2 drinks per day or >5 drinks in a row. In these people, should have counseling for alcohol intake to reduce BP. (note: in contrast, moderate alcohol intake (1-2 drinks per day for men, 1 drink per day for women) is assoc with dec incidence of CAD and CV mortality
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In a pt already on 2 HTN meds who drinks a lot, should you add another med or get alcohol counseling?
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Alcohol counseling
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If need to add another BP med, should add CCB or BB?
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CCB unless there is a compelling indication for BB use (ex: heart failure, asymptomatic LV dysfunction, post-MI, hyperthyroid, rate control in afib)
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When should screening for secondary causes of HTN take place?
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Resistant HTN (requiring >3 anti-HTN meds from different classes) and in the young (<30yo), nonobese, non-African American pts. Routine testing of every hypertensive pt is not cost effective
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When determining COPD vs CHF - what are things that make it lean towards CHF?
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Orthopnea, lower extremity edema, S3, bibasilar crackles, JVD, hepatomegaly, BNP.
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What is the difference between BNP and ANP?
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ANP is released from atria, BNP is released from the cardiac ventricles in response to volume overload.
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What is the cutoff for BNP for when it predicts CHF?
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>100
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In cases of CHF secondary to CAD what would you expect in ECHO to indicated systolic dysfunction?
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Reduced EF
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What happens to MCV in pts with history of alcohol use?
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MCV slightly elevated
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In a pt with CHF, what happens to sodium balance?
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In CHF, Na is reabsorbed via the kidneys in response to a stimulated renin-angiogensin-aldosterone system. Urine Na levels are usually low
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How do have to treat subacute bacterial endocarditis?
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With IV abx. Don't use IV aminoglycosides as monotherapy for pts with endocarditis!
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How do abnormal vavles predispose to endocarditis?
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Turbulent flow denudes the valve endocardium, inviting bacterial colonization
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What i the most common infection of native heart valves for subacute bacterial endocarditis?
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Strep viridans
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What is the difference between hypertensive urgency and emergency?
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hypertensive urgency: severe hypertension (usually >180/120) with no symptoms or acute end-organ damage. hypertensive emergency: severe HTN with acute, lifethreatening end organ complications: 1. Malignant hypertension: sever HTN with retinal hemorrhages, exudates, or papilledema. 2. Hypertensive encephalopathy: severe HTN with cerebral edema and non-localizing neurologic symptoms and signs
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What is malignant hypertension?
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Usually seen in pts with long-standing and uncontrolled HTN. It is assoc with retinal hemorrhages, exudates, and/or papilledema. Pts can also develop maligant nephrosclerosis (acute renal failure, hematuria, and proteinuria), however renal findings are not always present and are not required for the diagnosis of malignant HTN
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What is hypertensive encephalopathy?
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Assoc with cerebral edema due to breakthrough vasodilation from failure of autoregulation. Pts usually develop insidious onset of HA, N/V followed by non-localizing neurologic symptoms (ex: restlessness, confusion, seizures/coma if untreated). Pts can also develop SAH or intracerebral hemorrhage
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How can sudden inc in BP cause pulmonary edema?
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Sudden inc BP can abruptly cause inc in LV afterload, leading to LVF and acute pulmonary edema
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What are the s/s of PACs?
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Usually asymptomatic but can cause papitations in some. Occasionally they can be assoc with supraventricular arrhythmias or less commonly ventricular arrhythmias. EKG will show early p wave
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When do you treat PACs and what can precipitate them?
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Don't treat unless symptoms cau distress or when there is supraventricular tachy - in the case of symptomatic PACs, the standard treatment of choice is BB. Even in asymptomatic pts, precipitating factors like tobacco, alcohol, caffeien, and stress hsould be identified and avoided
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What is Holter monitor used for?
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Outpatient setting to identify intermittent arrhythmias in pts with symptoms like syncope or palpitations (if can't capture on EKG)
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Inferior MI - what can it cause?
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RV infarction (1/3 of infarcts), leading to R-sided heart failure. Will see hypotension, JVD, and clear lung fiends.
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How should manage pts with inferior MI?
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PL dependent -> treat with IVF and avoid PL reducing meds like nitrates and diuretics
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What EKG changs are found in inferior MI?
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RCA occlusion - ST elevation in II, III, aVF with ST depression in I and AVL (most left-sided leads). R-sided EKG confirms the diagnosis
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What PE findings point to RV failure?
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JVD and Kussmaul's sign (inc in JVD with inspiration) along with clear lungs
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What does relatively low HR with hypotension suggest in inferior MI?
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possible SA node ischemia (supplied by RCA)
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How does PE and RV infarct present similarly and differently?
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Both show R-sided heart fialure and hypotension (if PE is massive). ST elevation in MI, PE more likely to have sinus tachy with new onset RBBB or S1Q3T3
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How can an IV septum rupture lead to RV failure?
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can lead to L->R shutn. Would hear pansystolic murmur
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How does variant/prinzmetal's angina present on EKG?
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Transient ST elevations
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Both intravascular volume depletion and inferior MI can cause hypotension - but how can differentiate between the 2?
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volume depletion will have flattened jugular veins, inferior MI (and tamponade) will have elevated JVP
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What is Chagas disease? What are the 2 primary manifestations?
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A chronic protozoal disease caused by Trypanosoma cruzi - it is common thorughout Latin America. The 2 primary manifestions are megacolon/megaesophagus and cardiac disease. Mega colon/esoph are secondary to destruction of the nerves controlled the GI smooth muscle. Cardiac - prolonged myocarditis.
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What is the main symptom of diphtheria?
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URT symptoms
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What is the pathophys of giant cell myocarditis?
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Likely autoimmune
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Can rickettsial infection cause myocarditis?
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Yes
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What is a sensitive indictor of hydration status in a pt?
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BUN/Cr ratio
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What does dehydration usually due to hematocrit?
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Increases it, due to hemoconcentration
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What vessel is blocked in anterior MI and what EKG leads involved?
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LAD. Some/all of leads V1-V6
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What vessel is blocked in inferior MI and what EKG leads involved?
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RCA > LCX. ST elevation in II, III, aVF
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What vessel is blocked in posterior MI and what EKG leads involved?
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LCX or RCA. ST depression in V1-V3, ST elevation in I, aVL (LCX), ST depression in I and aVL (RCA)
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What vessel is blocked in lateral MI and what EKG leads involved?
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LCX, diagonal. ST elevation in I, aVL, V5 and V6. ST depression in II, III, aVF
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What vessle is blocked in RV MI (occurs in 1/2 of inferior MI) and what EKG leads involved?
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RCA. ST elevation in V4-6R
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What vesslel supplies the AV node?
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RCA in 90% of pts thru AV nodal artery -> can be blocked in inferior MI and cause heart block
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What MI is most commonly assoc with sinus brady?
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Inferior MI due to inc vagal tone in first 24hrs after infarction and dec RCA blood supply to SA ndoe
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What EKG changes can see in left main MI?
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Occlusion of both LCX and LAD -> ST elevation in anterior and lateral leads (I, aVL, V1-V6). Can lead to sudden death
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What is the pathophys of edema in CHF?
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Most important contributor is inc renal sodium retention, which is a result of the activation of the renin-AT-aldosteorne system. This activation is a result of renal hypoperfusion secondary to dec CO. Renal hypoperfersion activates R-A-A system causing inc in ATII and aldo. ATIi dec renal blood flow by constricting efferent arteriole more than afferent. Aldo enahnces Na reabsorption -> water retention, inc total body water
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What happens to Na delivery to distal tubule in CHF?
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Decreases due to both dec renal perfusion and inc Na retention proximally in kidney
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What changes in renal perfusion in CHF?
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Lowers due to dec CO
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What is "cardiac cirrhosis"
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Prolonged CHF -> retrograde transmission of elevated pressure via hepatic veins and IVC to liver -> liver congestion. Prolonged congestion combined with ischemia from poor perfusion associated with CHF leads to necrosis with fibrosis of the liver.
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What is the leading cuase of dec plasma colloid pressure?
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Hypoalbuminemia due to either nephrotic-range proteinuria or poor albumin synthesis. Can have chronic congestion of liver assoc with dec albumin
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What is 1st line for controlled symptoms and improving exercise tolerance in pts with stable angina?
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BB. CCB or long-acting nitrates are used if BB contraindicated, poorly tolerated due to SE, or in combo with BB when BB not effective alone. BB relieve angina by dec myocardial contractility and HR and improve survival in those with MI. CCB improves angina by causing periphreal and coronary vasodilation.
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When are short and long acting nitrates used?
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Short - acute setting. Long (isosorbide dinitreat, isosorbide mononitrate) - add-on therapy for persistent angina
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What is stable angina?
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Chest discomfort occurring predictably with exertion or activity and relieved with rest. Can have abnL stress test and stress ECHO.
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When are ACEI used for HTN?
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DM, CKD, CHF with reduced LV systolic function.
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What is ranolazine?
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late Na channel blocker used occasionally in stable angina pts with recurrent symptoms who are taking combo of BB, CCB, or nitrates. Not initial therapy for stable angina.
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What arrhythmia can pts with mitral stensis develop?
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Afib (in up to 70%) bc of LA dilation.
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What is the most common valve problem due to rheumatic fever?
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MS
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What can hear on heart auscultation in MS?
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Loud S1 and mid-diastolic rumble
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What is the result of the loss of atrial kick in afib?
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worsening flow thru stenotic mitral valve and inc congestion in lungs -> dyspnea
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What is the murmur of TS?
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most prominent at left lower sternal border and symptoms of R-sided HF (peripheral edema, hepatomegaly, JVD)
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Can MS result in secondary pulmonary venous HTN?
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?
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What are the effects of cushings?
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hTN, high systemic cortisol causing hyperglycemia, hypokalemia, prox muscle weakness, central adiposity, thinning skin, wt gain, psych problem (sleep disturbances, depression, psychosis)
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What causes CUshings?
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adrenal CORTICAL hyperplasia, ACTH-producing pituitary adenoma (cushings disease), ectopic ACTH production, exogenous steroids
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What are the effects of hypothyroid?
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wt gain, fatigue, bradycardia, depression, skin and hair changes
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What disease is in the adrenal medulla?
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pheo (inc catecholamines)
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What are the s/s of pheo?
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wt loss, tachy, HTN, diaphoresis, anxiety
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What are the risk factors of aortic dissection?
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HTN (most common), marfans, cocaine use
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What are the clinical features of aortic dissection?
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severe, sharp, tearing chest/back pain. >20mmHg variation in systolic BP between arms.
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What are the complications (involved structures) of aortic dissetion?
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Stroke (carotid arteries -> neurologic signs), acute AR (aortic valves), Horner's syndrome (superior cervical sympathetic ganglion), acute MI/ischemia (coronary artery), pericardial effusion/tamponade (pericardial cavity; can look like pleural effusion on CXR), hemothorax (pleural cavity), lower extremity weakness/ischemia (spinal or common iliac arteries), abd pain (mesenteric artery)
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How make dx of aortic dissection?
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Suggested by mediastinal widening on CXR, but not always present. Dx confirmed with CT chest with contrast or TEE
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What are s/s of mediastinal tumors?
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50% asymp, others have slow onset of retrosternal CP, dysphagia, dyspnea. CXR will show mass
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What can cause restrictive CM?
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infiltrative diseases (Sarcoidosis, amyloidosis), storage diseases (hemochormatosis - the only reversible cause of these), endomyocardial fibrosis, or idiopathic
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HOw do pts with restrictive CM present?
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primary diastolic dysfunction, normal LV volume, normal/sl thickened LV wall. Signs of RHF often predominate -> JVD, bilateral ankle edema, tender hepatomegaly. Can also show signs of LHF (bibasilar rales, pleural effusion)
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How can you tell the difference between restrictive and HOCM?
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HOCM has very thick interventricular septum
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What is the primary treatment of hemochromatosis?
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Phlebotomy (removes Fe from bloodstream)
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How can you treat restrictive CM from sarcoidosos or scleroderma?
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Corticosteroids (slows progress but doesn't reverse it)
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What is electrical alternans on EKG specific for?
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Pericardial efusion (it is thoght to result from the heart's swinging back and forth within an inc quantity of pericardial fluid.
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What will see on x-ray in pericardial effusion?
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Enlargement of cardiac silhouette
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What is often the cause of pericardial effusions?
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Secondary to viral pericarditis
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What is a delta wave and when is it seen?
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upsloping just before QRS complex that occurs in pts with accessorry conduction pathway, like WPW
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what are F waves?
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flutter waves - diagnostic of atrial flutter.
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Can RHF cause ascites?
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Yes, it can raise the portal venous pressure - but would likely also see other signs of RHF like JVD and hepatojugular reflux and lung findings
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What is the most common cause of ascites?
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Portal HTN, usually due to cirrhosis from chronic liver disease (alcoholic or viral)
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What is protein C deficiency?
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Predisposes to venous thromboembolism. Can be inherited or acquired in pts with liver disease
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What is the nephrotic syndrome triad?
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Proteinuria, edema, hyperlipidemia. Can cause ascites, but this condition also typically causes anasarca as well due to severe hypoalbuminemia
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What is the first thing to do when a pt experiences recurrent VT?
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First stabilize if unstable, then search for underlying cause - ex: diuretics - Lasix commonly causes hypoK and hypoMg, which if uncorrected can lead to VT.
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What effect does hypoK have on digoxin
|
Potentiates SE (ex: inc risk of arrhythmias like VT)
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What is the effect of spironolactone on K?
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Spares K
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What is Metolazone?
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Thiazide diuretic
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What can result from latex allergy? Who has a higher risk for allergy?
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Anaphylactic shock. Inc risk: pre-existing atopic dermatitis (pts with atopic disease), healthcare workers, surgical pts
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What hormonal problem should be on the differential in a pt who becomes suddenly hypotensive during a stressful condition such as surgery?
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Primary adrenal insufficiency (Addison's)
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What are common PE findings in DIC?
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Bleeding from operative/venopuncture sites, petechiae, ecchymoses
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How can distinguish seizure from syncopal event?
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Seizure - LOC often followed by post-ictal state of clouded sensorium, may have biten tongue, sore muscles. Syncopy: arouse rapidly to baseline mental status
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Are stress/poor sleep common seizure triggers?
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Yes
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What is the workup for new onset seizures?
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CBC, CMP, drug screen, EEG, brain MRI
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When does syncope with HOCM occur?
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During activity
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When do you see pulsus paradoxus?
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Cardiac tamponade
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Is hypotension required for diagnosis of cardiac tamponade?
|
Yes
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How can PE cause syncope?
|
increases pulmonary arterial BP and decreases CO
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What is the murmur of MVP?
|
mid-systolic click over cardiac apex with a short, systolic murmur at the apex after the click if MR is present.
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What changes the murmur of MVP?
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Squatting decreaes it - squatting increaes cardiac PL
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What symptoms can be assoc with MVP?
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chest pain (easily distinguishable from angina, lasting 5-10 sec), anxiety, palpitations, hyperventilation
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What does VSD cause?
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L->R shunt, holosystolic murmur which increases with squatting
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What is the most common murmur of rheumatic heart disease?
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MS
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What is the murmur of AS? What are other PE findings?
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Systolic ejection murmur loudest at R upper sternal border and radiates to the carotids. The murmur begins after S1 and terminates before S2, with an intensity dependent upon the degree of turbulence across the valve. Palpation of peripheral pulse reveals pulsus parvus et tardus (pulse that rises gradually and has a delayed peak). May also have a prolonged cardiac impulse palpated ad the apex
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What are the typical symptoms of Aortic Stenosis?
|
SAD: syncope, angina, exertional dyspnea
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What are common causes of exertional dyspnea?
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VT, LV outflow obstruction (AS, HOCM).
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When does AS generally become symptomatic (what is the valve area)?
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<1.0cm2
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WHat is pulsus paradoxus?
|
Exaggerated dec (>10mmHg) in the systemic arterial BP with inspiration. SEen in cardiac tamponade
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When can see capillary pulsations in fingers and lips?
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Aortic regurg (presents with CHF)
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When are late diastolic murmurs most commonly heard?
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MS
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How do pts with mitral stenosis present?
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Pulmonary edema and Afib
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What is the most common EKG change in digoxin toxicity?
|
Atrial tachycardia with AV block. Digoxin toicity causes increased ectopy in atria or ventricles. and incrased vagal tone. Atrial tachy with AV block occurs from a combo of these 2 effects and is relatively specific for digoxin toxicity
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How distinguish Atrial tachy from Aflutter?
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Atrial tachy has a slower rate (150-250 vs 250-350 for aflutter).
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What does atrial tachy with AV block look like on EKG?
|
P-waves present but may appear differntly from normal p-waves seen when conduction originates from SA node. THe closer the ectopic focus is to the SA node, the closer the resemblance of its p-waves are to normal SA node p-waves.
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What is MAT arrhythmias assoc with?
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Pulmonary disease
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What does GERD chest pain feel like?
|
Retrosternal burning sensation after eating and with lying down. May be accompanied by chronic cough and hoarseness, esp when recumbent. Classically, pt may report symptoms 30-60min after eating and describe relief with antacids. Cough is due ot reflux of gastric secretions in lungs. Hoarseness is due to reflux-induced laryngitis
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How treat MSK CP?
|
NSAIDs
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What distinguishes reflux CP from cardiac CP?
|
Reflux - not assoc with activity, pain is burning not squeezing/pressure. Both are retrosternal though
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What is the cutoff for abnormal ST depressions?
|
1mm, but 10-30% of ppl with 1mm depression don't have ACS
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When are BB used?
|
Acute MI, heart failure, chornic angina
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What is the classic CP of anxiety?
|
Sense of impending doom, tachypnea, numbness of lips and digits
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When is amitriptyline used?
|
Tricyclic antidepressant - used to treat depression, insomnia, neuropathic pain
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What are the changes in CI, PCWP, and SVR as a result of cardiogenic shock?
|
Dec CI, inc PCWP both due to ventricular pump failure. SVR inc to maintain adequate tissue perfusion - the lower tissue perfusion signals the tissue ot extract more O2 from the blood, which decreases mixed venous O2 sat. Failure of the L or R ventricles to pump adequate amt of blood in acute MI accounts for most cases. Once pump failure occurs in cardiogenic shock, blood backs into the lungs causing inc PCWP.
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How can you tell the difference btwn hypovolemic shock, cardiogenic shock, and septic shock with different tests?
|
Hypovolemic shock will have dec PCWP, Cardiogenic shock will have inc PCWP and both will have inc SVR and dec mixed venous O2 sat. Septic shock is the weird one and has inc CI, dec SCR, and inc mixed venous O2 sat
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What are the changes in numbers of neurogenic shock?
|
Like septic shock - inc CI, peripheral vasodilation, PCWP and SVR dec
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WHat does noncardiogenic pulmonary eema do to CO and PCWP?
|
Causes backflow of fluids into the lungs -> compensatory inc in CO and low to normla PCWP
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What are the effects on PCWP and CI due to RV infarction?
|
RV infarction -> RV pump failure, which leads to increased RA and RV pressures. Both PCWP and CI are generally low due to the reduced PL
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What are the cahnges in PCWP and CI and SVR in pts with intravascular volume depletion?
|
Low PCWP, CI sl reduced, and SVR increased
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What are the changes in PCWP and CI and SVR in pts with systemic volume overload?
|
Inc PCWP and CI. SVR usually not affected
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What should do when suspect thrombosis of prolonged central lines?
|
Remove the catheter (most impt bc the longer the catheter stays in, the higher the changes of irreversible injury) and order duplex (to document thrombus and need for anticoagulation). Don't need long term anticoagulation, but can be continued if the symptoms don't resolve
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How does thrombosis of the subclavian line or SVC after TPN lines present and why does it happen?
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Thrombosis is insidious and usually presents after a couple of weeks. TPN lines should be placed in the RA. The irritating and hyperosmolar fluid can traumatize the veins and lead to thrombosis. Pts will usually present with swollen arm (which is pale) and present pulses. The swelling may extend from the hand to the neck and engorged veins in the upper neck and face may be visible. Most pts have minimal symptoms bc the process is gradual. Once the line is removed, swelling may take a few weeks to resolve . Don't start new IV lines in affected arm in the future.
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Who should amiodarone be avoided in?
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Pts with liver, pulmonary, thyroid problems. Lung toxicity is cumulative.
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What are the first and second line choices for rate control in Afib with RVR?
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BB, CCB 1st line. Digoxin 22nd line
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What is quinidine and what is it used for?
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Antiarrhythmics, can be used to convert pts back to sinus rhythm
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When are BB relatively contraindicated?
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pts with COPD or asthma
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How should treat symptomatic sinus bradycardia?
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IV atropine followed by transcutaneous pacing. Avoid meds that slow HR. If the bradycardia doens't resolve, may need a permanent pacemaker. Atropine provides an immediate increase in HR by decreasing vagal input)
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What is sinus bradycardia assoc with?
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Excellent physical conditioning, exaggerated vagal activity, sick sinus syndrome, hypoglycemia, meds (digoxin, BB, CCB)
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When is adenosine used for?
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SVTs bc it causes temporary AV block - helpful in identifying SVTs and sometimes terminating
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When are pts with sinus brady indicated for epi?
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When they are hemodynamically unstable
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When is amiodarone used?
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SVT, VT. It slows both the SA and AV nodes.
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When are premanent pacemakers indicated in sinus brady?
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Those who have chronic symptomatic sinus brady after meds and reversal of underlying etiology
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What does valsalva do to HOCM?
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Increases it bc increases PL (as does standing). Contrary to most murmurs, increases as PL decreases since this lessens the size of the ventricular cavity and causes inc outflow obstruction.
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What is the PE of HOCM?
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Carotid pulse with dual upstroke from midsystolic obstruction that develops as heart contracts. Systolic ejection-type murmur along L sternal border, often has a strong apical impulse
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What does squatting do in terms of murmurs?
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Decreases vertical height of the column -> increases VR to the heart
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What does sustained handgrip do to murmurs? What murmurs does it help to differentiate?
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Leads to inc SVR and inc AL. It is typically used to differentiate between murmurs of AS and MR where it will decrease and increase, respectively, in the severity of the murmur
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What does recumbency do to murmurs?
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Increases venous return
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What does leg raising do to murmurs?
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Increases venous return
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What is pulsus paradoxus and when do you see it?
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Exaggerated fall in systemic BP >10mmHg during inspiration (normal is 2-5mmHg drop). It is classically found in cardiac tamponade but can also occur in conditions without pericardial effusion such as asthma and COPD
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How does significant AR prevent pulsus paradoxus even in pericardial effusion/tamponade?
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Significant AR causes a large increase in LVEDP that precludes the IV septum from shifting toward the LV cavity during inspiration
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What is the diagnostic criteria for ARDS?
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Acute onset, bilateral patchy airspace disease on CXR, PCWP <18 or no clinical evidence of inc LVEDP, and PaO2/FiO2 <200
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What are the 2 most common causes of acute pancreatitis?
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Alcohol and gallstones
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What is the pathophysiology of ARDS?
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Results from endothelial injuyr and leakage of fluid from capillaries. Fluid then fills intersitial spaces and alveoli. ARDS results in intrapulmonary shunting and therefore the hypoxia is typically refractory to O2 admin - the alveoli are so full of fluid that they are unable to participate in gas exchange.
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How to distinguish ARDS from CHF (cardiogenic pulmonary edema)
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Low PCWP and absence of JVD in ARDS
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What is the definition (time frame) for hospital acquired PNA?
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Onset >48hrs after admission
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What will see on CXR of alcohol-induced dilated cardiomyopathy?
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Cardiomegaly
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How do pts with vasovagal/neurocardiogenic syncope present?
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Syncopal episode preceded by nausea, diaphoresis, tachycardia, pallor. Pain, stress, situations with medical needles, and urination can precipitate. Occurs due to excessive vagal tone. Esp common in young women.
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How can dx vasovagal syncope?
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Tilt table test
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What is the presentation of syncope caused by arrhythmias?
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No preceding signs or symptoms. Usually have underlying cardiac disease
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WHen does syncope assoc with AS occur?
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With activity. Syncope is a later finding than dyspnea, CP, and fatigue
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What is orthostatic hypotension? (def) and who is it common in and how do pts with syncope present?
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Drop in systolic BP >20mmHg after pt rises to standing positon. MC in elderly, DM, autonomic neuropathy (ex: parkinsons), hypovolemia, pts taking diuretics, vasodilators, or adrenergic-blocking agents. Prolonged recumbence is an inc risk. Usually present with pre-syncopal lightheadedness
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What part of the brain must a TIA affect for syncope to occur?
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Posterior circulation and brainstem
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What must be added to treatment plan in pts with MI and pulmonary edema?
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Diuretics, bc acute HF can cause pulmonary edema ("flash pulmonary edema") which can be secondary to acute MI. Lasix are treatment of choice. BB are contraindicated in presence of pulmonary edema even though they improve mortality in acute MI
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When is digoxin used for CHF?
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to improve symptoms in chronic CHF - not used for acute CHF secondary to MI
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How is the treatment different for SVT in pts that are hemodynamically stable vs unstable?
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Stable: vagal maneuvers followed by adenosine and AV nodal blockers. Unstable: should undergo DC cardioversion
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What is the first line med for paroxysmal SVT if stable?
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Adenosine, but should try vagal maneuvers first. Can use digoxin if adenosine fails
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What is procainamide and can it be used for SVT?
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Class Ia anti-arrhythmic that can be used to treat supraventricular tachy when AV nodal blockers and/or DC cardioversion have failed or are contraindicated
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Can hypovolemia precipitate paroxysmal SVT?
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Yes
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What is the most effective way to reduce the risk of systemic embolization in pts with nonvalvular Afib?
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Antithrombotic therapy with warfarin (or other anticoagulants such as dabigatran, rivoaroxaban, and apixaban). Risk stratify with CHAD2 scoring system to assess need for long-term anticoagulation
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Why is amiodarone used in Afib?
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conversion and maintenance of sinus rhythm
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Is combo of ASA + clopidogrel bettern than warfarin?
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No - it is better than aspirin alone, but inferior to warfarin
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What is the definition of heat stroke?
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Temp >40.5 (105F)
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What are the common and systemic s/s of heat stroke?
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Common: Dehydration, hot and dry skin, hypotension, tachycardia, tachypnea, hemoconcentration. Systemic: seizures, ARDS, DIC, hepatic/renal failure
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Who is at risk for heat stroke?
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In healthy pts: those exposed to hot, humid weather (ex: >75% humidity -> sweating ineffective). Meds with anticholinergic properties (ex: antihistamines) prevent sweating
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Can you have meningitis without nuchal rigidity or photosensitivity?
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Unlikely
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How does anticholinergic toxicity present?
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Hot dry skin, tachycardia, hyperthermia, absent bowel sounds
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What is the BP and muscular tone of serotonin syndrome and NMS?
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High BP, neuromuscular hyperactivity
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How does thyroid storm present?
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Tachycardia, hyperthermia, AMS
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What are the s/s of sympathomimetic toxicity?
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Hyperthermia, HTN, mydriasis
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What is the study of choice for diagnosis and follow-up of AAA?
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Abdominal ultrasound - nearly 100% sens and specific. Reasons we don't use CT: higher $, requirement for contrast (contraindicated if Cr elevated), poor visualization of aortic branch origin
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Is MRI ok in pts with renal insufficiency?
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no bc of assoc with nephrogenic dermatopathology with gadolininum administration
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When should suspect AAA rupture?
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Pulsatile abd mass, hypotension, abd pain.
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When you suspect AAA rupture, what is your next step?
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Forego imaging and send directly to OR
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What is the common story for variant/Prinzmetal's angina?
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Coronary vasospasm. Typical in young females, greatest risk factor is smoking. Classicaly occurs at night (midnight to 8am) and can be assoc with transient ST elevations on EKG.
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What is the treatment for variant/Prinzmetal's angina?
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CCB or nitrates (promotes vasodilation and prevents vasoconstriction), elimination of risk factors such as smoking. Avoid nonselective BB (ex: propranolol) bc B2 receptor inhibition can lead to worsened coronary vasospasm. Avoid ASA bc causes prostacyclin inhibiton which may promote coronary vasospasm
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What is a risk factor for Prinzmetal's angina?
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Smoking, young females
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What is the test of choice for acute aortic dissection?
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TEE or CT chest (TEE, CT chest, MRI more sensitive than TTE bc can't visualize many parts of aorta with TTE)
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What are the s/s of acute aortic dissection?
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Tearing pain radiating to the back, difference in BP of >30mmHg between 2 arms
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What 2 cardiac conditions does marfan's inc risk for?
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Aortic dissection, MVP
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What is order of most effective lifestyle changes for decrasing BP?
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Wt loss most important, followed by physical activity, salt restriction, moderation of alcohol consumption. For every 10kg reduction in weight, can dec systolic BP by 5-20mmHg. Regular exercise (at least 30min per day most days of week) can dec systolic BP by 4-9mmHg. Limiting alchool to no more than 2/1 drinks per day for men/women can dec 2-4mmHg. Restricting salt to <2.4g/d will dec by 2-8mmHg
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What are the unfavorable metabolic SE of thiazides?***
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***hyperglycemia, inc LDL, inc TG, hypoNa, hypoK, hypoCa. Also inc risk of gout flare. (however, thiazides have dec cardio M/M at least equal to ACEI, dihydropyridine CCB)
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What are s/s of PE? CXR, EKG?
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Dyspnea, tachypnea, pleuritic CP, tachycardia. Can also hav efever, cough, hemoptysis CXR usually normal but can show diation of pulmonary arery proximal to the clot and collapse of teh vessels distal to the clot (Westermark's sign), as well as pleural infiltrates corresponding to the areas of pulmonary infarction (Hampton's hump), pleural effusions, and atalectasis. Most common EKG finding: sinus tachy
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What are the most common PE findings in pt with PE?
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Tachypnea and tachycardia
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What will CXR show for PTX?
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Radiolucency at the apex of the lung. If severe, can cause esophageal and mediastinal deviation
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What do pleural effusions look lke on lateral CXR and lateral decubitus x-ray?
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Blunting of costophrenic angles on lateral CXR, free-flowing effusion layer on lateral decubitus x-ray
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When do CK-MB and troponin levels normalize after MI:
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CK-MB: within 1-2d, Troponin T takes up to 10 days (but more sensitive for cardiac injury).
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Is LDH used for marker of cardiac injury?
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not anymore
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What is alk phos a marker for?
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biliary or bone pathology
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How do nitrates improve cardiac cest pain?
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They cause venodilation -> dec PL -> dec myocardial O2 demand by decreasing ventricular volume and wall stress/stretch. (they also cause some aterial vasodilation -> dec AL - but the dec in PL is more effective).
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What SE of nitrates is caused by significant arterial and venous dilation?
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Rebound tachy, which can inc myocardial O2 demand and worsen CP. BB are used in acute MI to prevent tachycardia
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What is a potential SE of metoprolol in pts with eczema/atopic disease?
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Can block bronchilatory B2 adrenergic receptors at high doses (even tho selective B1 antagonist) -> causes bronchoconstriction in suspectible individuals (ex: asthma pts). Can lead to wheezing, cough, prolonged expiration
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When is post-infarct pericarditis usually seen after MI? What about autoimmune?
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2-5 days for post-infarct, 1-several weeks for autoimmune after MI (Dressler's) or opne heart surgery
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What are the s/s of bronchitis?
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SOB, productive cough, fever
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What s/s assoc with pulmonary symptoms assoc with acute HF?
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Wheezing (cardiac asthma), crackles, elevated JVP
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What do pleural effusions present with on PE?
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Dullness on thoracic percussion, dec breath sonds, dec movement of the ipsilateral chest wall
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What can you do to improve LV function in pts with prolonged tachysystolic Afib?
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Controlling rate/rhythm is the best.
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What does LV dysfunction result from in prolonged tachysystolic atrial fib?
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Tachycardia, neurohumoral activation, absense of an atrial "kick" (accounts for up to 25% of LVEDV), and atrial-ventricular desynchronization
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Where can an aortic dissection extend to and what do these complications lead to?
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Carotid arteries, renal arteries, aortic valve, pericardium -> stroke, ARF, AR, cardiac tamponade (respectively)
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What are s/s on PE of cardiac tamponade?
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hypotension, inc JVD, pulsus paradoxus, muffled heart sounds, pericardial fluid on ECHO
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What does difference in BP in R and L arm in dissection mean?
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It reflects extension of the dissection into the great vessels feeding the L arm
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How does tension PTX present?
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CP, SOB, hypotension, JVD, deviated trachia, absent breath sounds in one hemithorax
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What is the pathophys of prinzmetal angina?
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Temporary vasospasm of the coronary arteries. More common in women, risk factor is smoking (usually no CV risk factors).
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What other disorders is variant angina assoc with?
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Other vasospastic disorders such as Raynaud's and migraine headaches.
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How does variant angina usually present?
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Middle of the night (midnight to 8am), precipitated by exercise, hyperventilation, emotional stress, cold exposure, or cocaine use. ST elevations with return to baesline with resolution of symptoms
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How do you treat variant angina?
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CCB or nitrates
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What are lacunar strokes?
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Occur in the setting of hypertension, affect the small penetrating arteries which supply the basal ganglia, subcortical white matter, and pons - occlusion of these small arteries by microatheroma and lipohylanosis is the mechanism
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What is intermittent claudication leg pain caused by?
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Occurs with exercise, due to atherosclerotic narrowing of the arteries feeding the leg
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What is the MCC of PE?
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Emoblization of blodo clots from the deep veins of the lower extremities
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What is the algorithm for the evaluation of chest pain?
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Pretest probability of CAD (history, RF, clinical variables - exam, EKG, labs) - if low, no further testing. if intermediate - if ekg normal and able to exercise - either exercise ECHO or nuclear stress test and if positive cath. if ekg normal and not able to exercise - do pharm stress test - if positive do cath. if pretest prob high - start pharm therapy for CAD and then go to cath
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WHen is stress testing most useful?
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To risk startify pts in INTERMEDIATE risk of CAD (low risk shouldn't do, high risk should go straight to cath with pharmacologic therapy)
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What does TTE look for?
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Segmental wall motion abnormalities during chest pain episode; also looks at valves
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What is diastolic heart dysfunction?
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aka heart failure with preserved LV EF. Refers to impaired filling of the L or R ventricle - either bc of impaired myocardial relaxation or a stiff, non-compliant ventricle. EF (contractility) may remain normal, but diastolic pressures are elevated -> dec CO -> typical findings of CHF
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What is the classic cause of diastolic dysfunction?
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Systemic hypertension. (chronically elevated LV diastolic pressures -> LA dilation -> afib)
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How to treat diastolic dysfunction?
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Diuretics, BP control
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What is usually the cause of cardiogenic shock?
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Compromised LV function due to acute MI or CHF. Will have signs of shock - low BP; with HF symptoms
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What is high-output HF? What are the causes?
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Supranormal ventricular function that stll can't meet the body's metabolic demands. Causes: anemia, hyperthyroid, BeriBeri, Paget's disease, AV fistulas
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What is the cause of asthma?
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Small airwary bronchosconstriction
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What happens to lung compliance in COPD and pulmonary edema?
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Inc in COPD, dec in pulmonary edema
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What is Lidocaine and what is its role in ACS?
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Class IB anti-arrhythmic that is effecive in a variety of ventricular arrhythmias and has a wide therapeutic-to-toxic artio. Widely used to control complex forms of ventricular arrhythmia (ex: CT) in pts with ACS - at the same time, its use prophylactically to prevent the development of VFib in acute MI is actually DISCOURAGED bc while it decreases the frequency of ventricular premature beats (VPBs) and decreases risk of Vfib, it actually can increase the risk of aystole and doesn't help prognosis.
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What are the basic labs to start with to assess for possible secondary causes of HTN?
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UA (for hematuria and protein/Cr ratio), CMP, lipid proifel (to stratify for CAD), baseline EKG (to evaluation for CAD or LVH)
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What are s/s suggestive of possible secondary HTN?
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Severe/malignant HTN, resistant HTN requiring 3+ drugs, sudden BP rise in pt with previously controlled BP, age of onset <30 without Fhx of HTN
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How can primary hyperaldo present?
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Low plasma renin, hypoK due to renal K wasting, HTN
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How can you screen for renl artery stenosis in pts with severe or resistant HTN? When is it indicated?
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Duplex Doppler US - indicated when inc serum Cr or abnormla UA
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What are common s/s of pheochromocytoma?
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Inc BP, palpitaitons, HA
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What is a crescendo-decresendo systolic murmur along the L sternal border WITHOUT carotid radiation indicitive of?
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HOCM (interventricular septal hypertrophy) - vs AS which would be on 2nd R intercostal space with carotid radiation
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What is AV conduction delay usually due to?
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(occurs when AV node is slowed) - usually due to meds such as BB or ischemic heart disease. Results in bradycardia
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When does syncope occur with aortic dissections?
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When they involve the ascending aorta
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What is syncope in HOCM due to?
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Most often multifactorial but can be due to outflow obstruction, arrhythmia, ischemia, and a ventricular baroreceptor response that inappropriately causes vasodilation
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What are the factors assoc with poor outcome after witnessed out-of-hospital sudden cardiac arrest?
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TIme elapsed prior to effective resuscitation (delayed bystander CPD, delayed defib), initial rhythm of PEA or asystole, Prolonged CPR (>5min), absence of vital signs, advanced age, prior hx of cardiac disease, 2+ chronic diseases, persistent coma after CPR, need for intubation or vasopressors, PNA or renal failure after CPR, sepsis, CVA, or class III-IV heart failure. Most critical factor is elapsed time to effectiv resuscitation
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What is the MCC of out of hospital sudden cardiac arrest in adults?
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sustained VT or VFib due to MI
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What is the most common cause of death in pts with acute MI?
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Complex ventricular arrhythmia - reentrant ventricualr arrhythmia (Vfib). Acute ischemia creates heterogeneity of conduction in the myocardium. Areas of partial block of conduction are frequently formed that predispose pt to reentrant rhythm
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When does full conduction block in pts with acute MI usually occur?
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Inferior MI
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When does electromechanical dissociation of heart often occur?
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PE, pericardial tamponade
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What is commonly the source of increased automaticity arrhythmia?
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Glycoside intoxication
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When does remodeling after MI occur and what can prevent it?
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Weeks to months after MI -> gradual dilation of LV with thinning of ventricular walls -> CHF. ACEI can prevent and should be initiated within 24 hours of MI in all pts without contraindication
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Why is ASA given to pts after MI?
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To inhibit platelet aggregation and prevent recurrence of coronary artery blockage
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What does digoxin do for symptomatic systolic HF pts?
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Doesn't provide mortality benefit - just with symptomatic relief
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What are the 3 major mechanical complications of MI? How do they present/how do you tell them apart?
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MR due to papillary muscle rutupre, LV free wall rupture, IV septum rupture. All 3 can result in hypotension but presence of pansystolic murmur that is loudest at the apex with radiation to axilla is the classic murmur of MR - will also have soft S1 bc S2 is formed by closure of MV and TV - if having pulmonary edema and LV failure as well, will have SOB and bibasilar crackles. LV free wall rupture will classically result in pericardial tampoade - sudden death - hypotension, JVD, distant herat sounds, pericardial rub, pulsus paradoxus. VEntricular septal rupture - pansystolic murmur like papillary muscle rupture, but it is best heart at L sternal border and often accompanied by a thrill.
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What are teh 5 common SE of amiodarone?
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Pulmonary toxicity: total rather than serum drug levels (longer use -> inc risk). Thyroid tox: hypo>hyper; very common. Hepatotox: up to 25% have inc AST, ALT, usually asympt. Corneal deposits - bc amio secreted by lacrimal gland; vision not affected; doesn't mean need to stop drug. Skin changes - some pts - blue/gray skin discoloration, esp on face
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What is procainamide used or and what are its SE?
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Treats atrial and ventricular arrhythmias. SE: nausea, drug-induced lupus, agranulocytosis, QT prolongation
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What is lidocaine, what is it used for, and what are SE?
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Class IB anti-arrhythmic used to treat ventricular arrhythmias. High doses can casue confusion, seizures, resp distress
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What is quinidine and what is it used for and what are its SE?
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Class IA anti-arrhythmics used to treat atrial arrhythmias. SE that are well known: diarrhea, tinnitus, QT prolongation, torsades, hemolytic anemia and thrombocytopenia
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WHat is digoxin used for and what are its SE?
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To treat atrial arrhthymias. SE: nausea, anorexia, AV block, ventricular and supraventricular arrhythmias
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How does dipyridamole work in myocardial perfusion scanning?
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Reveals the areas of restricted myocardial perfusion by causing redistribution fo coronary blood flow to a "non-diseaed" segmented (coronary steal phenom). Dipyridamole and adenosine are coronary vasodilatiors - however, pts with coronary artery disease have already maximally dilated their BV distal to the obstruction - therefore, their ability to inc myocardial perfusion is limited - therefore, redistribution of coronary blood flow to "non-diseased" areas occurs and perfusion to diseased segments diminishes
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What are the 2 actions of dipyridamole?
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Coronary vasodilator (used in perfusion scanning) and a potent antiplatelet aggregate
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What is the order of lifestyle modifications in terms of how much they dec BP?
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Wt loss (if obese) > DASH diet (high fruits and veggies > Dec dietary sodium > Exercise > Alcohol intake. (smoking no effect on HTN, neither does eliminating animal protein)
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What are the HTN stages by BP?
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Normal <120/80, pre-HTN 120-139/80-89, Stage I 140-159/90-99, Stage II >160/100
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For newly dx stage I HTN, what is the first line intervention?
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Lifestyle modificaiton (wt loss is best if obese, then DASH diet)
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What is the most common sustained cardiac arrhythmia? How common is it?
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Afib - >1% of population
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What is the classificiation of Afib and how do you treat?
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1. First detected (initial dx, independent of duration) 2. Paroxysmal (recurrent (2+) epidsodes that terminate spontaneously in <7d, usually within 24 hrs) 3. Persistent (episodes lasting >7d) 4. Longstanding persistent (>1 duration) 5. Permanent (persistent with no further plans for rhythm control). Antiarrhythmics usually reserved for pts with recurrent symptomatic episodes or with LV systolic dysf thought to be secondary to uncontrolled Afib. Anticoagulation: CHADS2 0 - none; 1 - ASA or oral anticoag (preferred); 2+ - oral anticoag (warfarin, rivaroxaban)
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What is lone Afib?
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Paroxysmal, persistent, or permanent Afib with no evidence of cardiopulmonary or structural herat disease. They are generally <60yo and by definition have CHADS2 of 0 - if no recurrent episodes of Afib and no symptoms, don't need therapy
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What should all post-MI pts be given on d/c for secondary prevention? What should be given in addition to pts who are post-PCI or have UA/NSTEMI?
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ASA (75-325), BB, ACEI, lipid-lowering statin for all. If UA/NSTEMI or who are are post-PCI, give Clopidogrel (Plavix) along with ASA - in class of drug called Thienopyridines (which also includes ticlopidine) - have anti-platelet effect and act by antagonizing ADP. Clopidogrel has less SE so is preferred.
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Who whould benefit from Clopidogrel?
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1. Pts who need ASA but can't tolerate it 2. post-UA/NSTEMI --> Clopidogrel (plavix) + ASA more effective than ASA alone. D/C plavix for at least 12mo, ASA should be continued indefinitely 3. Plavix + ASA more effective than ASA alone for first 30d following PCI bc prevents subacute stent thrombosis - pts who recieve drug-eluting stents frequire a longer duration bc epitheliaizaiton occurs slowly.
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When is LMWH given post-MI?
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First 48hrs or until angiography performed, then stopped
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When is warfarin indicated post-MI?
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If pt has evience of ventricular thrombus (usually seen in apical infarcts and dyskinetic wall motion abnormalities)
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Are dihydrop CCB indicated in acute coronary syndrome??
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No, they have inc mortality. They are typically used as anti-anginal therapy (along with long-activing nitrates) in pts with diffuse CAD who are not candidates for eitehr PCI or bypass).
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Which are they dihydropyridine CCB?
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~dipines
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What drugs/things increase the effect of warfarin? What things decrease it?
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Inc warfarin/bleeding effect: tylenol, NSAIDs, abx, amiodarone, cranberry juice, ginkgo biloba, vit E, omeprazole, phenytoin, thyroid hormone. Dec: Rifampin, carbamazepine, OCP, ginseng, st johns wort, green veggies (ex: spinach, brussel sprouts bc they are good source of Vit K)
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What is the MOA of warfarin?
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Inhibits vit K-dependent coag factors (II, VII, IX, X) in the coag cascade
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What is the most common predisopsing factor for aortic dissection? What are less common RF?
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Hypertension (75%). Less common: Marfans, Ehlers-Danlos, bicuspid aortic valve, etc
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What is the murmur of AR?
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Descrendo diastolic murmur
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How do pts with acute aortic dissection present?
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Sudden, tearing pain that radiates to the back. 60% have widened mediastinum on CXR
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What causes Marfan's?
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Mutatin in fibrillin gene -> weakened CT
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What size vessels does giant cell arteritis affect?
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Large vessels - most commonly cranial branches of aortic arch
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What is the main risk factor for aortic aneurysms?
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Atherosclerosis
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Do aortic aneurysms predispose to aortic dissection?
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Yes
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What causes isolated systolic HTN in elderly?
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Dec elasticity of the arterial wall -> inc systolic BP without change in diastolic BP. During systole, heart ejects blood at slightly higher P than peak systolic presure in aorta. The elastic properties of teh aorta and major arteries dampen some of this pressure by converting it into stored elastic energey and the elastic recoil of the arterial walls is then used to maintain diastolic BP when the heart relaxes. As a person ages, the elastic properties of the arterial wall diminish and the arteries become more rigid. This reduction in compliance reduces the ability of the arteries to dampen the systolic P -> systolic HTN with widened pulse pressure (systolic-diastolic). Note: inc systolic BP and widened pulse pressure are important CV risk factors in the elderly
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What is the most appropriate tx of isolated systolic HTN?
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low dose thiazide, ACEI, or long acting CCB
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When does inc intravascular volume cause both systolic and diastolic HTN?
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Various renal disorders where kidneys have dec ability to excrete solutes and/or water
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What are the symptoms, PE, EKG, CXR, diastolic tools, and assoc conditions of coarc of aorta?
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Symptoms: Most pts present with HTN and are asymptomatic. HA, epistaxis, blurred vision, or HF due to severe HTN. PE: "brachial-femoral"delay, different BP in upper and lower extremities, well-developed upper body compared to lower body, continuous cardiac murmur from flow thru large collateral vessels. EKG: LVH with inc voltage of QRS and ST and T wave cahnges in L precordial leads. CXR: notching of 3rd-8th ribs due to erosion by enlarged intercostal arteries, classic "3" sign caused by indentation of aorta at the site of coarc with pre- and post-stenotic dilation. Diagnosis with ECHO; CT or MRA. Assoc conditions: bicuspid aortic valve, PDA, VSD, Turners
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What should all pts (esp young) with systemic HTN be evaluated for and how?
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Coarc of aorta with simultaneous palpation of brachial and femoral pulses to assess for "brachial-femoral" delay. They shoudl also have supine bilateral (brachial) and prone right and/or left leg (popliteal) BP
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What is coarctation of the aorta?
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Narrowing of the descending thoracic aorta, usually just distal to the origin of hte L subclavian artery at the site of the ligamentum arteriosum. Can be congenital or acquired (ex: Takayasu arteritis)
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What disease increases infective endocarditis risk in IVDA?
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HIV infection
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What is most common organism in infective endocarditis in IVDA)?
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Staph aureus
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What is the most common valve involved in infective endocarditis in IVDA?
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Tricupsid valve
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What murmur indicates TR (ex: in infective endocarditis)?
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Holosystolic murmur that increases with inspiration - augmentation of intensity with inspiraiton has 100% sens in differentiating R-sided systolic murmurs from all others
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What is a common pulmonary complication of infective endocarditis (esp in drug users - bc affects tricupsid valve in IVDA most often)?
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Septic pulmonary emboli (scattered round lesions in peripheral lung fields bilaterally that to me, look like multiple cavitary lesions. with cough, CP, hemoptysis)
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What is the difference between infective endocarditis in IVDA and non-IVDA
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Fewer peripheral IE manifestations in IVDA (splinter hemorrhages, Janeway lesions)
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What valve involvement makes heart failure more common in infective endocarditis in IVDA?
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Aortic valve (rare with tricuspid)
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Why do pts with infective endocarditis get proteinuria?
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immune-mediated GN with deposition of IC in glomerular membrane
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When do pts get S4 heard over cardiac apex in L lateral decubitus position?
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pts with reduced ventricular compliance (or inc stiffness) - can be heard in many healthy older adults and in pt with hypertensive heart disease, AS, and HOCM. Can be normal in children and young adults
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What is the murmur of AR?
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Early and decrescendo diastolic murmur that begins immediately after A2. High pitched, blowing quality, best heart along L sternal borer at 3rd and 4th intercostal space when pt is sitting up and leaning forward while holding breath in full expiration
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Where can septic emboli from aortic valve endocarditis go to ?
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Systemic circulation, but not lungs like in tricuspid infective endocarditis
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When does murmur worsen when standing?
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HOCM - bc decreases venous return to the heart
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When does paradoxical splitting of 2nd herat sound occur?
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(A2 follows P2 with max splitting during expiration) - fixed LV outflow obstruction - ex: AV or subaortic stenosis, LBBB, RV paced rhythm
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When can hear normal splitting of 2nd heart sound best?
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During inspiraiton over 2nd intercostal space
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Why do pts with severe AS have anginal CP?
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Due to increased myocardial O2 demand. Accompanying prolonged myocardial contraction (exercise) and impaired diastole, both which reduce blood flow thru coronaries, makes it worse
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How can an anomalous RCA origin lead to angina?
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If it is compressed by other structures
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Can the myocardium increase its extraction of O2?
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No - instead the myocardium usually meets inc O2 demands by dilating its coronary arteries
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What is S4 associated with in terms of cardiac dysfunction?
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LV hypertrophy from prolonged HTN or restrictive CM. It is an indicator of a stiff LV. S4 corresponds with atrial contraction and is believed to result from sound of blood striking stiff LV
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What is the murmur of MVP?
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Mid-systolic click with late systolic murmur heard best over cardiac apex
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What are the strongest predictors of AAA expansion and rupture?
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Large aneurysm diameter, rapid rate of expansion, and current cigarette smoking
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What are the current indications of operative or endovascular repair of AAA?
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Aneurysm size >5.5cm, rapid rate of aneurysm expansion (>0.5cm in 6mo or >1cm per yr), and presence of symptoms regardless of aneurysm size (abd, back or flank pain; limb ischemia)
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What are RF for AAA?
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Older age >60yo, smoking, FHx of AAA, white race, atherosclerosis
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How do most pts with AAA present?
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Initially asymptomatic with dx made during imaging study for unrelated cause
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