Heart Failure

Question 1

congestive heart failure

Answer 1

inability of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues

Question 2

clinical manifestations of CHF

Answer 2

dyspnea, fatigue, fluid retention.

Question 3

class 1 heart failure

Answer 3

patients with cardiac disease but without resulting limitations of physical activity

Question 4

class II heart failure

Answer 4

patients with cardiac disease that results in slight limitation of physical activity

Question 5

class III heart failure

Answer 5

patients with cardiac disease that results in a marked limitation of physical activity

Question 6

class IV heart failure

Answer 6

patients with cardiac disease resulting in an inability to carry out any physical activity without discomfort

Question 7

is exercise tolerance a good correlation to cardiac function?

Answer 7

no, as other things can cause exercise tolerance to decrease!

Question 8

progression of heart failure

Answer 8

Left ventricular dysfunction usually begins with an injury to the myocardium. then progresses by cardiac remodeling. activation of the endogenous neurohormonal systems play a major role in remodeling.

Question 9

neurohormonal impact of HF

Answer 9

elevated levels of norepi, angiotensin II, aldosterone, endothelin, vasopressin, cytokines. they all adversely affect the heart

Question 10

compensatory mechanisms in heart failure

Answer 10

ANS acts to increase heart rate and contractility. vasoconstriction happens. kidney uses renin-angiotensin-aldosterone system to vasoconstrict and retain water/sodium. hypertrophy. frank starling law. redistribution of cardiac output.

Question 11

ACE inhibitors as therapy

Answer 11

alleviate symptoms, improve clinical status, reduce risk of death and hospitalization. benefits are seen in patients with mild, moderate, and severe symptoms. arteriovenous vasodilation, no change in HR/contractility, increased renal, coronary, and cerebral flow. Diuresis and natriuresis. inhibit LV remodeling post-MI. no tolerance development. no neurohormonal activation or reflex tachycardia

Question 12

Angiotensin receptor blockers

Answer 12

block type 1 angiotensin II receptors on blood vessels. dilates arteries and veins. promotes renal excretion of sodium and water. inhibits cardiac and vascular remodeling. Can be used in place of ACEi. Can be used in tandem. -sartan drugs. Few side effects: decreases GFR, raises potassium, hypotension.

Question 13

diuretics

Answer 13

decrease volume and preload. no direct effect on cardiac output. improves arterial distensibility. neurohormonal activation. dont use if hypovolemic. volume contraction and electrolyte depletion are side effects

Question 14

aldosterone antagonists

Answer 14

reduce risk of death and hospitalization. side effects: hyperkalemia, metabolic acidosis, gynecomastia, gastric disturbances including peptic ulcers.

Question 15

beta blockers

Answer 15

inhibit the adverse effects of the sympathetic nervous system in patients with heart failure. initiated at low dose. increased dose if tolerated.

Question 16

digoxin

Answer 16

first described to benefit in lower extremity edema (dropsy). inhibits cellular Na/K ATPase. increases intracellular Ca, causing contractility. increases vagal efferent activity to the heart, reducing sinoatrial firing rate and conduction velocity through AV node. narrow therapeutic/toxic window. eliminated by the kidneys

Question 17

hemodynamic and neurohormonal effects of digoxin

Answer 17

increased cardiac output, LVEF, exercise tolerance, natriuresis. Decreased LVEDP, neurohormonal activation. Decreased plasma noradrenaline, peripheral nervous system activity, RAAS activity. increased vagal tone. normalizes arterial baroreceptors.

Question 18

dobutamine

Answer 18

stimulates beta-1 receptors of the heart directly. racemic mixture with some beta 2 and alpha receptor effects. doesnt bind to dopamine receptors. given as continuous infusion. tolerance after 24-48 hours of same dose.

Question 19

milrinone

Answer 19

phosphodiesterase IIIa inhibitor. cAMP causes relaxation of vascular smooth muscle aka vasodilation, PDE IIIa breaks it down. so milrinone prevents PDE from breaking it down. no tolerance up to 72 hours.

Question 20

nesiritide

Answer 20

recombinant form of the 32 amino acid human B-natriuretic peptide. given IV. no differences in rates of death or rehospitalization. no significant improvement in symptoms.