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Heart failure is simply defined as a chronic, progressive disorder in which the heart muscle is unable to pump enough blood to meet the body's needs. Depending on the primary cause, heart failure can manifest itself as either systolic or diastolic dysfunction. In systolic heart failure the heart muscle becomes weak and cannot squeeze as much blood out. In diastolic heart failure the heart squeezes normally, but becomes stiff and cannot adequately relax to allow for normal ventricular filling. In the presence of heart failure, in order to counteract the effect of falling cardiac output and thus reduced perfusion to vital organs, the body will try to compensate via two tightly regulated mechanisms.
The first one involves the increase in sympathetic nervous system activity. The second one involves the activation of the renin-angiotensin-aldosterone system. This pharmacology lecture discusses mechanism of action of various drugs classes used in management of heart failure including beta-blockers, ACE inhibitors, angiotensin II receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors, aldosterone antagonists, loop diuretics, vasodilators, and cardiac glycosides.
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00:00 Heart & Circulatory System
01:40 Types of Heart Failure
02:50 Sympathetic activation
04:05 RAAS activation
06:40 Natriuretic peptides
08:17 Beta-blockers
09:43 ACE inhibitors
10:45 Angiotensin receptor blockers
11:48 ARB/Neprilysin inhibitor
12:56 Aldosterone antagonists
13:43 Loop diuretics
14:45 Vasodilators
16:11 Digoxin