Heart Failure Agents Flashcards
Decreased CO activates production of
NE, AN-II, and endothelial (ET)
Decreased cardiac output activates production of NE, AN-II, and ET, which causes
Vasoconstriction and increased afterload
Result in greater cardiac work for a given level of ventricular filling pressure
Positive inotropic agents
Improve symptoms of HF by moving patients to lower cardiac filling pressures along the same ventricular function curve
Diuretics
Function to decrease ECF volume/preload and curtail remodeling/fibrosis
-Ex: spironolactone
Diuretics
Function to decrease preload and/or afterload
Vasodilators
Function to reduce arrhythmogenesis, curtail remodeling, and reduce undesired sympathetic effects
Beta-adrenergic antagonists
Primarily used to relieve congestive symptoms in patients with CHF
Loop diuretics
Reduce extracellular fluid volume and ventricular filling pressure (preload)
Loop diuretics
Also reduce extracellular fluid volume by correcting Na imbalances
Thiazides
Typically elevated in CHF
-Increases LV remodeling and fibrosis
Aldosterone
When added w/ an ACE inhibitor, ntagonize cardiac remodeling and increase survival
Low doses of aldosterone antagonists
Side effects include hypokalemic, metabolic alkalosis, ototoxicity, and hyperglycemia
Loop diuretics
Can unveil ectopic pacemakers and cause arrhythmias
-Critical to monitor w/ diuretics
Low K+ levels
Induce prostaglandin and NO generation from endothelial cells, which reduce venous return and pulmonary congestion
Loop Diuretics
Indicated for patients allergic to sulfonamides but can cause more ototoxicity than furosemide
Ethacrynic acid
Side effects include hypokalemic, metabolic alkalosis, hypomagnesemia, hyponatremia, and hypercalcemia
Thiazides
Include blockers of ENaC Na+ channel and direct aldosterone antagonists
K+ sparing diuretics
Aldosterone release from the adrenal gland is promoted by
Hyperkalemia and high AN-II
Major side effects are hyperchloremic metabolic acidosis and gynecomastia
K+ sparing diuretics
Prevent myocardial and vascular fibrosis
Aldosterone antagonists
Decrease afterload by lowering peripheral resistance and reduce preload by reducing aldosterone secretion
ACE inhibitors (the -prils)
Function by decreasing the conversion of AN-I to AN-II
ACE inhibitors
ACE inhibitors cause a decrease in synthesis of aldosterone which can increase the risk of
Hyperkalemia
A substance that stimulates prostaglandin formation and NO output
Bradykinin
Cause a decrease in the degradation of bradykinin
ACE inhibitors
Associated w// high bradykinin levels
Cough and angioneurotic edema
Used for grades II-IV CHF and most frequently used in conjunction w/ diuretics and digitalis
ACE inhibitors
In acute failure, decrease left ventricular diastolic volume and prevent further ventricular dilation, and improve exercise tolerance
ACE inhibitors
A major concern when using ACE inhibitors w/ K+ sparing diuretics is
Hyperkalemia
ACE inhibitors are contraindicated with
Bilateral renal artery stenosis
Block the AT1 receptors and function similarly to ACE inhibitors
Angiotensin II Receptor Blockers (ARBs)
-The -sartans
Does not affect bradykinin duration or its production of prostaglandins or NO
ARBs
More selective for inhibition of AN-II
ARBs
May be particularly effective in a subset of black patients who have been reported to be less responsive to ACE inhibitors
Hydralazine + Isosorbide dinitrate
A nonpeptidic drug that inhibits the protease renin
Aliskiren
Functions via dual inhibition of neprylisin and angiotensin receptors which reduces mortality and hospitalization for HF
LCZ696
Dilates both arterial and venous vessels to increase CO
Nitro dilators such as nitroprusside
Recommended in patients w/ symptoms of HF and asymptomatic patients w/ decreased LVEF or a history of MI
Beta-blockers
Have the adverse effects of symptomatic fatigue, hypotension, and bradycardia/heart block
Beta-blockers
Attenuate the adverse effects of high concentrations of catecholamines
-decrease HR and arrhythmogenesis
Beta blockers
Long term, will prevent deterioration of myocardial function and reverse adrenergically mediated myocardial dysfunction
Beta blockers
Cardiac glycosides, beta-1 agonists, Ca2+ sensitizers, and bypyridines are all
Positive inotropic agents
Cardiac glycosides such as digitalis and digoxin block the
Na+/K+ ATPase
The action of digitalis is antagonized by
K+
Fewer deaths from HF are balanced w/ more death from sudden death because of narrow therapeutic index w/
Digoxin
Does seem to support the ability of ACE inhibitors to retard progressive cardiac deterioration in CHF
Cardiac Glycosides
Shortens the action potential of cardiac tissue
Ouabain
What are the three main variants of cardiac glycosides?
Ouabain, Digoxin, and Digitoxin
Has low lipid solubility and is almost never used
Ouabain
Increase CO, decrease heart size, decrease venous pressure, and produce diuresis
Cardiac Glycosides
Cause decreased sympathetic output and increased vagal activity
-also increase renal perfusion
Cardiac Glycosides
Therapeutically, digitalis enhances vagal tone and reduces sympathetic activity
Digitalis
Slows conduction velocity and increases refractoriness in the AV node
Digitalis
At toxic levels, digitalis causes
AV block
Digitalis-induced tachyarrhythmias are treated w/
K+, lidocaine, or digitalis antibody
Phosphodiesterase inhibitors selective for PDE3, which is found in cardiac smooth muscle
Milrinone and Enoximone
In the heart, cause increase cAMP and phosphorylation/activation of L-type calcium channels
Milrinone and Enoximone
Milrinone and Enoximone in vascular smooth muscle cause increased cAMP-mediated deactivation of myosin light chain kinase, causing
Vasodilation
Causes fatal arrhythmias and bone marrow and liver toxicity
Milrinone toxicity
Useful for treatment of HF not accompanied by hypotension
Dobutamine
A synthetic analog of dopamine that stimulates Beta1-Beta2 and alpha receptors
-Increases contractility through Beta-1 effect but does not increase peripheral resistance
Dobutamine
Acts at beta-1 and peripheral alpha receptors to stimulate heart under conditions in which there is a drop in BP
Norepinephrine
Used for “warm” septic shock
NE
Acts at beta-1, beta-2, and peripheral alpha-receptors
- used for increasing contraction an HR
- Used for “cardiac arrest”
Epinephrine
Occurs after MI or cardiogenic shock
Acute HF
