Pharmacotherapy of acute heart failure (AHF) is a set of emergency interventions aimed at supporting cardiac pump function, decompressing the pulmonary and systemic circulation, and preventing fatal complications. Due to rapidly progressing hemodynamic instability, the primary route of drug administration is intravenous.
Route of administrationExclusively intravenous for rapid and controllable onset of action
Danger of AHFAcute left ventricular failure with a high risk of pulmonary edema
Triad of goalsPump support, vascular unloading, and complication prevention
Antifoaming agentInhalation of ethanol for alveolar pulmonary edema
Pathogenesis and General Treatment Strategy
Acute heart failure occurs upon decompensation of chronic heart failure or as a result of acute myocardial injury (e.g., myocardial infarction, cardiac surgery). The most dangerous manifestation is acute left ventricular failure.
Elevated hydrostatic pressure in the pulmonary capillaries leads to the transudation of fluid into the alveoli. Respiratory movements foam the transudate, blocking gas exchange, provoking severe hypoxia, and creating a life-threatening emergency.
The treatment strategy includes 4 main drug groups:
Positive inotropes (to stimulate contractility);
Vasodilators (for vascular unloading);
Diuretics (to reduce circulating blood volume);
Symptomatic therapy agents.
Use of Vasodilators and Inotropes
Vasodilators play a fundamental role in AHF by lowering pulmonary capillary pressure and reducing cardiac preload and afterload. Drugs such as ACE inhibitors are not used in acute settings due to their delayed onset of action.
Rapid-acting non-glycoside inotropes: dobutamine and levosimendan are preferred due to their rapid onset. Cardiac glycosides (digoxin) are administered strictly via the intravenous route.
Nitric oxide donors: nitroglycerin and sodium nitroprusside dilate capacitance and resistance vessels. Disadvantages include tolerance development, risk of severe hypotension, and reflex tachycardia.
Natriuretic peptides: nesiritide (recombinant human B-type natriuretic peptide) increases cGMP production, lowering vascular tone while providing coronary-dilating and natriuretic effects.
Receptor antagonists: endothelin receptor antagonists (tezosentan — blocking $ET_A$ and $ET_B$) and vasopressin receptor antagonists (tolvaptan — selective $V_2$, conivaptan — $V_{1A}$ and $V_2$).
Diuretics and Symptomatic Management
The diuretic of choice in AHF is furosemide. Its therapeutic effect is twofold:
Direct vasodilation: rapid dilation of venous (capacitance) vessels reduces preload and pulmonary capillary pressure even before diuresis begins.
Ethanol: used via inhalation as an antifoaming agent to break up transudate bubbles in the alveoli.
Antiarrhythmic drugs: prescribed for concurrent rhythm disturbances.
Oxygen therapy: administered to correct hypoxemia caused by impaired gas exchange.
Mnemonic
In acute left ventricular failure, remember the "3D" rule: Dilation (nitrates), Diuresis (furosemide), Distress relief (morphine) — unloading preload and afterload to reverse pulmonary edema.
Frequently asked questions
Which non-glycoside inotropes are used in acute heart failure?
Various non-glycoside inotropic agents are used as emergency medications in acute heart failure:
Dobutamine (dobutaminum) — a $\beta_1$-adrenergic agonist stimulating myocardial $\beta_1$-receptors.
Dopamine (dopaminum) — a dopaminergic and $\beta_1$-adrenergic agonist.
Milrinone (milrinonum) — a phosphodiesterase type III inhibitor.
Levosimendan (levosimendan) — a calcium sensitizer that enhances myofilament response to calcium ions.
Which agents are used as antifoaming agents in alveolar pulmonary edema?
Inhalation antifoaming agents are used to reduce transudate foaming in the alveoli during pulmonary edema:
Ethanol (alcohol aethylicus) — a symptomatic agent used via inhalation to disrupt transudate bubbles.
What is the mechanism of action of levosimendan on the myocardium?
Levosimendan acts directly on the contractile apparatus of the cardiomyocyte without increasing intracellular calcium concentration.
Troponin C (troponinum c) — the primary target of the drug, binding to it and altering its conformation.
Calcium ions (calcium) — levosimendan increases the calcium sensitivity of troponin C, facilitating actin-myosin cross-bridge interaction.
What side effects are characteristic of intravenous furosemide administration?
Loop diuretics like furosemide are associated with the following adverse effects:
Fluid and electrolyte imbalance (dis balans) — hypokalemia and hypomagnesemia.
Metabolic disturbances (dis metabolica) — hyperuricemia and hyperlipidemia.
Ototoxicity (ototoxicitas) — potential adverse effects on hearing.
Why are ACE inhibitors not used in emergency AHF treatment?
ACE inhibitors have a prolonged latency period (slow onset of action), making them unsuitable for emergency situations that require immediate reduction of myocardial workload.
How does furosemide rapidly relieve symptoms in pulmonary edema?
Furosemide exhibits a direct vasodilating effect: it dilates veins, instantly reducing preload and pulmonary capillary pressure even before the diuretic effect manifests.
What is the purpose of ethanol inhalation in pulmonary edema?
Ethanol lowers surface tension and destroys transudate bubbles in the alveoli, acting as a physicochemical antifoaming agent to restore airway patency.
What are the main indications and contraindications for cardiac glycosides?
Glycosides (e.g., digoxin) are indicated for chronic or acute heart failure, especially when complicated by tachyarrhythmic atrial fibrillation. The primary contraindication is atrioventricular (AV) block.
Go deeper
Comparative profile of inotropic non-glycosides: dobutamine vs. levosimendan
Molecular mechanism of action of nesiritide and the role of cGMP in vasodilation
Clinical utility of endothelin receptor antagonists (tezosentan) and vasopressin antagonists (tolvaptan, conivaptan)
Causes and mechanisms of nitrate tolerance during continuous intravenous infusion
Effects of cardiac glycosides on ion transport (calcium, sodium) and their inotropic, chronotropic, and dromotropic effects