Inotropic Flashcards
Diuretics
Class: Diuretics
Mech: Decrease volume and preload (improve symptoms of CONGESTION!!); no direct effect on CO (too much preload reduction can cause decreased CO)
Thera: Improve arterial distensibility; reduce preload
Important SE’s: Causes neurohormonal activation (increased levels of noradrenaline, AII because of decreased volume and decreased perfusion of kidney)
Misc: Contraindication in hypovolemic patients (SE of volume contraction and electrolyte depletion)
Bisoprolol, carvedilol, sustained release metoprolol
Class: β-blockers
Mech: Blocks high circulating levels of catecholamines
Thera: Dramatically decreases mortality in CHF patients
Misc: Should be started at very low dose and slowly ratchet up; do not stop suddenly!!!!
Digoxin (Lanoxin)
Class: Cardiac glycoside
Mech: Inhibits Na/K/ATPase (increases contractility d/t more Ca with NCX); increases vagal activity to heart (reduces SA firing rate, conduction through AV node)
Thera: Improves LV function, decreases neurohormonal activation, increases vagal tone to heart (reduced SA firing rate and AV conduction velocity), normalizes arterial baroreceptors; decreases hospitalizations in CHF (no mortality benefit)
Important SE’s: Very narrow therapeutic-toxic window (mostly arrhythmias like atrial tachy and AV block)
Misc: Eliminated in kidneys, so dose according to renal function;
increased CO, LVEF, decreased LVEDP, increased exercise tolerance and natriuresis; decreased plasma noradrenaline, PNS, RAAS; increased vagal tone
Dobutamine (Dobutrex)
Class: β1 receptor agonist
Mech: Positive inotrope and chronotrope; some beta 2 and alpha receptor effects with vasodilation at lower doses and vasoconstriction at higher doses; NO NE RELEASE!!!
Thera: Acutely decompensated patients (about half will die after 6 months)
Important SE’s: Quick acting, but can develop tachyphylaxis after 48 hours (ie tolerance)
Misc: No NE release; given IV as continous infusion
Milrinone (Primacor)
Class: Phosphodiesterase IIIa inhibitor
Mech: Inhibits cAMP breakdown
Thera: Inotropy, chronotropy, lusitropy, vasodilation
Important SE’s: Increased hypotensive and atrial arrhythmia events acutely. 2 month mortality nearly 50% higher than placebo
Misc: Given IV, depends on renal clearance, no tolerance after 72 hours
Nesiritide (Natrecor)
Class: Synthetic BNP
Thera: Doesn’t really do much
Misc: Given IV
CHF defined as
inability of the heart to pump blood at rate commensurate with the requirements of the metabolizing tissues or caon only do so from ELEVATED filling pressure (if demand greater than what myocardium can keep up with, like in hyperthyroidism with increased metabolism)
Main clinical manifestations of heart failure are:
- dyspnea
- fatigue
- fluid retention
Drug use for heart failure needs to be
continued indefinitely (especially if not a reversible cause)
Heart classifications:
I. cardiac disease but no physical activity limitations
II. “ with slight limitation of physical activity
III. “ with less than ordinary activity causing fatigue, palpitations, dyspnea, anginal pain (FAP with Dick)
IV. “ and can’t do any physical activity
LV dysfunction usually begins with; we see later:
an injury to the myocardium; followed by change in LV geometry and structure (cardiac remodeling);
endogenous neurohormonal system activated with elevated HF levels (NE, AII, aldosterone, endothelin, vasopressin, cytokines, CAVE mAN)
List compensatory mechs in heart failure:
- ANS (heart with increased HR, contractile stim, rate of relaxation), peripheral circulation with arterial and venous vasoconstriction (increased afterload and preload)
- RAA system (vasoconstriction, Na and water retention to increase afterload and preload, increased contractile stim)
- endothelin 1 (increased pre and afterload), vasopressin, natriuretic peptides (decreases afterload)
- Peripheral O2 delivery (increased O2 extraction by tissues), anaerobic metabolism (short term ONLY!!)
How do we treat the different stages of heart failure?
A: think pts with HTN, diabetes, obesity, atherosclerosis; alcoholics; treat: get them to stop this stuff, drugs are ACEi or ARB
B: think structural heart disease with LV remodeling, previous MI, low EF, valvular disease; treat: ACEi or ARB, then do beta blockers
C: treat: salt restriction; do diuretics if fluid retention, along with other drugs; maybe give digoxin or hydralazine/nitrates
D: May need hospice; heart transplant, permanent mechanical support
ACE inhibitors:
- alleviates symptoms, improves clinical status, reduces risk of death and hospitalization;
- see benefits in those with spectrum of symptoms; with and without CAD
- AV vasodilation (decreases PCWP, LVEDP, SVR and BP; increases CO and exercise tolerance); NO CHANGE in HR/contractility; some diuresis and natriuresis
- No neurohormonal activation or reflex tachy; NO TOLERANCE
Big difference b/w ARBs and ACEis?
No increase in bradykinin
