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PAEA EMERGENCY MEDICINE EOR TOPICS EXAM QUESTIONS AND VERIFIED 100% SOLUTIONS LATEAST UPDATED

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PAEA EMERGENCY MEDICINE EOR TOPICS EXAM QUESTIONS AND VERIFIED 100% SOLUTIONS LATEAST UPDATED what is the most common cause of heart failure? specifically left sided? right sided? - ANSWER -MC is CAD (coronary artery disease) -L sided: *CAD* & HTN -R sided: *L sided HF* & pulmonary dz decreased ejection fraction, thin ventricular walls, dilated LV chamber, and an S3 gallop (filling of dilated ventricle) is associated with systolic or diastolic heart failure? - ANSWER systolic (MC form of CHF) *(the sound is actually heard in the diastole though) -memory trick: "sys-to-lic" 3 consonants = S3 normal ejection fraction, thick ventricular walls, narrowed LV chamber, and an S4 gallop (atrial contraction into a stiff ventricle) is associated with systolic or diastolic heart failure? - ANSWER diastolic -memory trick: "di-a-sto-lic" 4 consonants = S4 what are the causes of systolic vs diastolic heart failure? - ANSWER -systolic: post *MI*, *dilated cardiomyopathy*, myocarditis -diastolic: *HTN*, *LVH*, *elderly*, valvular heart dz, hypertrophic or restrictive cardiomyopathy, constrictive pericarditis when the metabolic demands of the body exceed normal cardiac function (d/t thyrotoxicosis, wet beriberi, severe anemia, AV shunting, Paget's disease of the bone) this is termed heart failure - ANSWER high-output *fairly uncommon -low-output HF is just d/t problem w/ myocardial contraction, ischemia, or chronic HTN what are some causes of acute vs chronic heart failure? - ANSWER -acute: *largely systolic*; hypertensive crisis, acute MI, papillary muscle rupture -chronic: dilated cardiomyopathy (systolic), valvular dz (diastolic) explain class I-IV New York Heart Association functional classes - ANSWER - class I: *no sx's*, *no limitation* during ordinary physical activity -class II: *mild sx's* (dyspnea or angina), *slight limitation* during ordinary activity -class III: *comfortable only at rest* (sx's caused maked limitation in activity even with minimal exertion -class IV: *sx's even while at rest*, severe limitations, inability to carry out physical activity what compensations does the body make when heart failure (can be due to something that causes either inc pre/afterload or dec contractility) begins? - ANSWER 1. sympathetic nervous system activation 2. myocyte hypertrophy/remodeling 3. RAAS activation: fluid overload the following are signs/sx's of what sided heart failure? inc pulmonary venous pressure, dyspnea, orthopnea, rales/rhonchi, chronic nonproductive cough with pink frothy sputum, HTN, Cheyne-Stokes breathing, S3 or S4, pale skin/cool extremities, sinus tachy, fatigue - ANSWER L-sided HF the following are signs/sx's of what sided heart failure? inc systemic venous pressure, peripheral edema, JVD, anorexia, N/V, hepatosplenomegaly, RUQ tenderness, hepatojugular reflex (inc JVP with liver palpation) - ANSWER R-sided HF -CXR showing Kerley B lines (alternate flow tracts), cardiomegaly, pleural effusion, pulmonary edema -echo with dec EF -inc BNP on labs are all signs of? - ANSWER heart failure *BNP released from atrium with preload too high (volume overload) what drugs have shown to decrease mortality rates in pts with heart failure? - ANSWER *ACE inhibitors* (-prils), ARBs, *beta-blockers* (-lols), hydralazine + nitrates, spironolactone in pts who experience the following common side effects of an ACE inhibitor to treat heart failure, what is the alternative medication? -1st dose hypotension, renal insufficiency, hyperkalemia, cough, angioedema - ANSWER ARBs (-sartans) what vasodilators are often used to treat heart failure? - ANSWER hydralazine + nitrates -good for african americans -safe in pregnancy -acts to dec pre/afterload -used if pt not able to tolerate ACEi/ARBs/BB or if more control needed what is the most effective treatment for symptoms of heart failure? - ANSWER diuretics -loop diuretics (-semides) act on inc excretion of Na, Cl, K, H2O (so can go hypo on these electrolytes), other s/e: hyperglycemia, hyperuricemia -K-sparing diuretics (spironolactone, eplerenone) aldosterone antagonists; s/e: hyperkalemia, gynecomastia with spirono -HCTZ or metolazone (thiazide like diuretic)- s/e: hyponatremia/kalemia, hyperuricemia, hyperglycemia what medications are used to treat acute severe heart failure? - ANSWER *sympathomimetics* (positive inotropes to inc contractility) -*digoxin*: but has a narrow therapeutic index (can cause arrhythmias, seizures, dizziness, GI upset, visual disturbances, gynecomastia); toxicity = downsloping ST segment; antidote: Digoxin Immune Fab -*dobutamine*: inc contractility (B1 agonist), peripheral vasodilation -*dopamine*: inc contractility giving a synthetic BNP, Nesiritide, works by what mechanism to treat heart failure? - ANSWER -dec RAAS activity -inc Na+/H2O excretion why are beta-blockers started after ACE inhibitors/diuretics in heart failure? - ANSWER want to decrease afterload/preload before slowing down the heart rate at what EF do heart failure patients need to receive an implantable cardioverter defibrillator? - ANSWER EF 35% because they tolerate arrhythmias poorly and there is inc mortality rate what medication used to treat *systolic* heart failure is a selective sinus node inhibitor that slows the sinus rate? - ANSWER *ivabradine*: dec mortality rate in pts w/ EF ≤35%, in sinus rhythm, w/ resting pulse ≥70bpm, & already maxed out on BB dose or unable to take BB what medication used to treat *systolic* heart failure works by increasing levels of natriuretic peptides? - ANSWER *sacubitril-valsartan*: decreases mortality rate in class II-IV HF w/ reduced EF what is the treatment for acute pulmonary edema/congestive (aka decompensated) heart failure? - ANSWER *LMNOP* -*L*asix: removes fluids- improves sx's -*M*orphine: reduces preload reducing heart strain -*N*itrates: vasodilator to reduce pre/afterload -*O*xygen -*P*osition: upright to dec venous return if severe may also need inotropic support although primary HTN makes up 95% of cases, when should secondary HTN be considered? what are some causes of secondary HTN? - ANSWER -if refractory to antihypertensives or severely elevated -causes: *renal artery stenosis*, fibromuscular dysplasia, atherosclerosis, 1° hyperaldosteronism, pheochromocytoma, cushing's syndrome, coarctation of the aorta, sleep apnea, EtOH, OCPs, COX-2 inhibitors what are the complications of HTN? - ANSWER -CV (CAD, HF, MI, LVH, aortic dissection, aortic aneurysm, PVD) -neurologic (TIA, CVA, rutured aneurysms, encephalopathy) -nephropathy (renal stenosis & sclerosis leading to ESRD) -optic (retinal hemorrhage, blindness, retinopathy) thiazide type diuretics (HCTZ, chlorthalidone, metolazone) act on what part of the nephron to increase water excretion? what are the side effects? - ANSWER - distal diluting tubule -s/e: hyponatremia/kalemia/calcemia, hyperuricemia/glycemia (use w/ caution in gout and DM pts) *these are 1st line in uncomplicated HTN loop diuretics (furosemide, bumetanide) are the strongest class of diuretics and can cause s/e's of volume depletion, hypokalemia/natremia/calcemia, hyperuricemia/glycemia, hypochloremic metabolic alkalosis, and ototoxicity; what are they contraindicated in? - ANSWER sulfa allergy what are the DHP (dihydropyridine) and non-DHP calcium channel blockers? what are they indicated and contraindicated in? - ANSWER -DHP CCBs: nife*dipine*, amlo*dipine* (potent vasodilators) -non-DHP CCBs: verapamil, diltiazem (vasodilators but also act on heart to dec contractility and conduction/HR) so often used in pts w/ HTN w/ concomitant Afib -indications: HTN, angina, raynauds -contraindications: CHF (esp non-DHPs), 2nd/3rd degree heart block what are the cardioselective and nonselective beta blockers? - ANSWER - cardioselection (B1): atenolol, metoprolol, esmolol -nonselective (B1, B2): propranolol -a, B1, B2: labetalol, carvedilol what are contraindications for using beta-blockers? - ANSWER -2nd/3rd degree heart block, decompensated heart failure -specifically in nonselective agents: asthma/COPD, may worsen PVD or raynauds, hypotension, or pulse 50 what is the pathophysiology behind a hypertensive urgency/emergency? - ANSWER -abrupt rise in BP -increase in SVR (systemic vascular re

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