Heart Failure Flashcards
Symptoms of L-sided HF
dyspnea, fatigue, edema, and specifically for L: PULMONARY CONGESTION
Most common causes of L-sided HF
general: MI, atherosclerotic heart ds, hypertensive changes, valve ds, dilated cardiomyopathy, congenital heart ds. Most common: MYOCARDIAL ISCHEMIA due to coronary artery ds, followed by HTN
Symptoms of R-sided HF
dyspnea, fatigue, edema, and specifically for R: PERIPHERAL EDEMA
Most common causes of R-sided HF
general: MI, atherosclerotic heart ds, hypertensive changes, valve ds, dilated cardiomyopathy, congenital heart ds. Most common: MYOCARDIAL ISCHEMIA due to coronary artery ds, followed by HTN
Compensatory effects of HF
3 major responses: Increase sympathetic activity, activate RAS (renin-angiotensin system), myocardial hypertrophy
Two Pathways of SNS stimulation during HF
Stimulation of B-adrenergic receptors; alpha 1-adrenergic stimulation
Effects of alpha 1-adrenergic stimulation in HF
produces vasoconstriction that enhances venous return, Increase cardiac preload and afterload.
Effects of B-adrenergic stimulation in HF
Stimulation of B-adrenergic receptors in heart Increase HR, Increase force of contraction
Adverse Effects of SNS Stimulation as a Compensatory Measure in HF
Increase work-load of heart (which causes further decline in cardiac function)
Mechanism of Renin-Angiotensin System Activation due to HF
Decrease in CO leads to Decrease renal blood flow that triggers release of renin to both: Increase formation of angiotensin II (vasoconstrictor that Increase peripheral resistance); and release aldosterone
Effects of Renin-Angiotensin System Activation in HF
Release of aldosterone promotes retention of Na & water thus Increase blood vol and amount of blood returned to heart
Adverse Effects of Renin-Angiotensin System Activation in HF
edema because of Increase venous pressure due to inability of heart to pump extra vol
Effects of Myocardial Hypertrophy in HF
Myocardial Hypertrophy: heart Increase size via: chambers dilate; initial stretching leads to more forceful, stronger contraction, but excessive elongation of fibers and thus weaker contractions (ultimately Decrease ejection ability - systolic failure); a
Compensated HF
compensatory mechanisms (myocardial hypertrophy, RAS activation, SNS stimulation0 are restoring ADEQUATE CARDIAC OUTPUT
Decompensated HF
mechanisms eventually Increase overall workload on heart and lead to furhter decline in cardiac functio; compensatory mechanisms FAIL TO MAINTAIN ADEQUATE CO
Drug classes used to treat HF
Inhibitors of renin-angiotensin-aldosterone system (RAAS); β-blockers; diuretics; inotropic agents; direct vasodilators; aldosterone antagonists
Types of RAAS Inhibitors
ACE inhibitors; Angiotensin-Receptor Blockers (ARBs)
Indications for ACEIs
MONOTHERAPY (pts with mild DOE and no apparent signs of vol overload); ASYMPTOMATIC PTS WITH EJECTION FRACTION <35% (left ventricular dysfunction); PTS WITH RECENT MI; all stages LEFT VENTRICULAR FAILURE with or w/o symptoms
Indications for ARBs
Angiotensis-Receptor Blockers (ARBs): HTN, SUBSTITUTES FOR ACEI (esp. when ACEI associated with cough &/or angioedema)