Cardiac Flashcards
Drugs that are selective vasodilators of coronary vessels (aka coronary steal)?
Adenosine and dipyridamole (coronary perfusion studies therefore pretty precise)
VSD murmur
Holosystolic murmur over L mid-sternal border
Mucosal cyanosis and fingernail clubbing found in what defects?
Cyanotic congenital heart diseases (like Tetralogy) or late features 2/2 Eisenmengers
Fixed, wide splitting of S2?
ASD! L-to-R shunt –> delayed closure of the pulmonary valve all the time.
Pulsus paradoxus
Dec. in systolic pressure of > 10 mmHg w/ inspiration. Conditions that impair expansion of pericardial space (tamponade, constrictive pericarditis, obstructive lung disease, restrictive cardiomyopathy), causes the inter ventricular septum to move into the left and reduce SV during inspiration.
Cardiac tamponade exam?
Beck’s triad - hypotension, JVD, distant/muffled heart sounds; tachycardia
Fick principle?
CO = rate of O2 consumption/arteriovenous O2 difference. Derived from the idea that flow * concentration difference = amount of substance consumed.
Concentric LV hypertrophy associated with?
Chronic HTN, aortic stenosis
Extended consumption of appetite suppressants leading to?
Pulmonary hypertension
Aortic regurgitation murmur
Diastolic decrescendo, heard loudest in early diastole (increased pressure gradient). Left sternal border w/ pt leaning forward at END-expiration.
Perivascular infiltrate with abundant eosinophils in cardiac tissue?
Hypersensitivity myocarditis
Light micro path after MI
Minimal change < 4h. Up to day 5 becomes coagulation necrosis (edema, wave fibers -> band necrosis -> neurophils). Days 5-10 = macrophage. Days 10-14 = granulation tissue and neovasc. 2 wk-2mo = collagen deposition/scar
Selective beta-blockers?
Metoprolol, atenolol, acebutolol, and esmolol. Preferred in patients with COPD or asthma b/c won’t B2 blockade -> bronchoconstriction
How does nitroglycerin relieve angina?
DECREASED cardiac preload (LV diastolic volume) via venodilation leading to retention of blood in venous system. Modest coronary arteriolar dilation, but high doses -> coronary steal
Phase 0 pacemaker?
Upstroke. Opening of L-type (long-lasting dihydropyridine-sensitive Ca2+ channels leading to slow influx
Phase 3 pacemaker?
Repolarization. Opening of K+ channels and efflux. Closure of L-type Ca2+ channels.
Phase 4 pacemaker?
Pacemaker potential. Slow influx of Na+ occurring at end of 3. Also slow decrease in K+ efflux. At -50 mV, T-type (Transient) Ca+ opens leading to depolarization. At -40, L-types open until we get AP.
Effects of adenosine on cardiac pacemakers?
Adenosine activates K+ channels and prolongs K+ efflux leading to longer time NEGative, while also inhibiting L-type Ca+ channels prolonging time to reach threshold -> decreased HR.
Digoxin toxicity treatment
Oral activated charcoal, mgmt of K+ w/ insulin, kayexelate, or dialysis (avoid Ca gluconate), digoxin-specific Ab fragments
Digoxin toxicity
AV nodal block -> brady -> junctional escape -> ventricular tachyarrhythmias. HyperK leads to increased susceptibility. Anorexia, n/v, abdominal pain, fatigue, confusion, weakness, COLOR VISION change
Effects of an arteriovenous shunt on preload and after load?
Decreased after load but increased preload.
ADP-mediated drugs?
Clopidogrel and ticlopidine
Two QT prolongation congenital syndromes?
Romano-Ward (AD, no defaness) and “Jervell and LAnge-Nielsen syndrome” (AR, neurosensory deafness) —> torsades at young age. K+ channel mutations -> delayed rectifier current
Paradoxical embolism
Cerebrovascular event in setting of known thromboembolic disease is suspicious for an intracardiac or intrapulmonary shunt (patent foramen ovale, ASD, VSD, plum AV malformations). Even if L-R shunt, transient reversal during elevated R-sided pressure periods –> embolization