The goal in managing a patient with heart failure is to maximize quality of life, minimize symptoms, prevent hospitalizations, slow disease progression, and prolong survival.
Heart Failure Symptoms Include:
Agents: Furosemide, Bumetanide, Torsemide, and Ethacrynic acid
Mechanism of Action: Block sodium and chloride reabsorption in the ascending loop of Henle. Cause decreased renal vascular resistance and increased renal blood flow. Assists in fluid removal.
Therapeutic effects: Provides symptomatic relief of fluid overload, improves exercise tolerance, and prevents hospitalization.
Furosemide is the most commonly used. Bumetanide and torsemide are much more potent than furosemide. Ethacrynic acid is rarely used due to its adverse effects.
Angiotensin-Converting Enzyme Inhibitors (ACE)
Agents: Captopril, Enalapril, Fosinopril, Lisinopril, Perindopril, Quinopril, Ramipril, and Trandolapril
Mechanism of Action: Prevent the conversion of Angiotensin I to Angiotensin II by blocking the enzyme ACE.
Therapeutic Effects: Proven to reduce mortality, slowing progression, preventing hospitalization, and provides symptomatic improvement. Reduces peripheral vascular resistance without reflexively increasing cardiac output, heart rate, or contractility.
Angiotensin Receptor Blockers (ARB)
Agents: Candesartan, Losartan, and Valsartan
Mechanism of Action: Inhibits Angiotensin II receptors.
Therapeutic Effects: Can be considered in patients who are intolerant of ACE inhibitors. Same therapeutic effects as an ACE inhibitor. Produce arteriolar and venous dilation and block aldosterone secretion, lowering blood pressure and decreasing salt and water retention.
Agents: Bisoprolol, Carvedilol, and Metoprolol succinate
Mechanism of Action: Reduce both resting and exercise heart rate, cardiac output, and both systolic and diastolic blood pressure; reduce sympathetic outflow from the CNS and suppress renin release from the kidneys; agents that block alpha-receptors or increase nitric oxide reduce peripheral vascular resistance
Therapeutic Effects: Long-term benefits of inhibiting the effects of the sympathetic nervous system. Reduces blood pressure primarily by decreasing cardiac output.
Agents: Sprinolactone, Eplerenone
Mechanism of Action: Suppression of Aldosterone
Therapeutic Effects: Shown to reduce all-cause mortality in patients with moderate to moderately severe heart failure.
Sprinolactone is a direct antagonist of aldosterone, thereby preventing salt retention, myocardial hypertrophy, and hypokalemia. Eplerenone is a competitive antagonist of aldosterone at mineralcorticoid receptors. Eplerenone has a lower incidence of endocrine-related side effects compared to sprinolactone.
Mechanism of Action: Inotropic action is the result of an increased cytoplasmic calcium concentration that enhances the contractility of cardiac muscle.
Therapeutic Effect: Improve symptoms and reduce hospitalization.
Isosorbide Dinitrate and Hydralazine
Mechanism of Action: ISDN is a venous vasodilator and Hydralazine is an arterial vasodilator. ISDN also delivers nitric oxide. Hydralazine has antioxidant properties while eliminate the need for nitrate free-interval with ISDN.
Therapeutic Effects: Reduces all-cause mortality and is recommended in African Americans with moderate to moderately severe heart failure receiving standard heart failure therapy.