Pathogenesis and general treatment strategy
Acute heart failure occurs during the decompensation of a chronic form or as a result of acute injuries (myocardial infarction, cardiac surgery). The most dangerous manifestation is acute left ventricular failure.
An increase in hydrostatic pressure in the pulmonary capillaries leads to the transudation of fluid into the alveoli. Respiratory movements cause foaming of the transudate, which blocks gas exchange, provokes severe hypoxia, and creates a life-threatening hazard.
The treatment strategy includes 4 groups of agents:
- Cardiotonic drugs (to stimulate contractility);
- Vasodilators (for vascular unloading);
- Diuretics (to reduce circulating blood volume);
- Symptomatic therapy agents.
Use of vasodilators and cardiotonics
Vasodilators play a fundamental role in AHF by reducing pulmonary capillary pressure and myocardial preload and afterload. Drugs like ACE inhibitors are not used in acute failure due to their prolonged latency period.
- Fast-acting non-glycoside cardiotonics: dobutamine and levosimendan are preferred due to the rapid onset of their effect. Cardiac glycosides (digoxin) are administered strictly intravenously.
- Nitric oxide donors: nitroglycerin and sodium nitroprusside dilate capacitance and resistance vessels. Their disadvantages include the development of tolerance, the risk of severe hypotension, and reflex tachycardia.
- Natriuretic peptides: nesiritide (recombinant human B-type natriuretic peptide) increases cGMP production, lowering vascular wall tone, and exerts coronary vasodilating and natriuretic effects.
- Receptor antagonists: endothelin antagonists (tezosentan — blockade of $ET_A$ and $ET_B$) and vasopressin antagonists (tolvaptan — selective $V_2$, conivaptan — $V_{1A}$ and $V_2$).
Diuretics and symptomatic correction
The drug of choice among diuretics in AHF is furosemide. Its therapeutic effect is dual-component:
- Direct vasodilation: rapid dilation of venous (capacitance) vessels reduces preload and pulmonary capillary pressure even before diuresis begins.
- Diuretic effect: fluid removal reduces circulating blood volume (CBV) and decreases pulmonary parenchymal hydration.
Symptomatic agents for pulmonary edema:
- Morphine: reduces preload, decreases pulmonary capillary pressure, and relieves psychomotor agitation.
- Ethanol: used via inhalation as an antifoaming agent to break up transudate bubbles in the alveoli.
- Antiarrhythmic agents: prescribed for concomitant rhythm disorders.
- Oxygen therapy: performed to eliminate hypoxemia caused by impaired gas exchange.
Briefly: answers to topical questions
Which non-glycoside cardiotonics are used in acute heart failure?
In acute heart failure, various groups of non-glycoside cardiotonics are used as emergency medications.
- Dobutamine (dobutaminum) is a beta1-adrenomimetic that stimulates myocardial beta1-adrenoceptors.
- Dopamine (dopaminum) is a dopaminomimetic from the group of beta1-adrenoceptor agonists.
- Milrinone (milrinonum) is a type III phosphodiesterase inhibitor.
- Levosimendan (levosimendan) is a calcium sensitizer that increases myocardial sensitivity to calcium ions.
Which drugs are used as antifoaming agents in alveolar pulmonary edema?
For defoaming and reducing transudate foaming in the alveoli during pulmonary edema, an inhalation antifoaming agent is used.
- Ethanol (alcohol aethylicus) is a symptomatic therapy agent used via inhalation to reduce transudate foaming.
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) is the primary target of the drug, to which it binds and alters its conformation.
- Calcium ions (calcium) — levosimendan increases the affinity of troponin C for calcium ions, facilitating the interaction of actin and myosin.
What adverse effects are characteristic of intravenous administration of furosemide?
Furosemide, a loop diuretic, is characterized by the following adverse effects:
- Water-electrolyte balance disorders (dis balans) — hypokalemia and hypomagnesemia.
- Metabolic disorders (dis metabolica) — hyperuricemia and hyperlipidemia.
- Ototoxicity (ototoxicitas) — negative impact on hearing.
In acute left ventricular failure, remember the "3D" rule: Dilation (nitrates), Diuresis (furosemide), Depression of pain/dyspnea (morphine) — they unload the preload and afterload and block edema.
Class and exam questions
Why are ACE inhibitors not used in the emergency treatment of AHFS?
ACE inhibitors have a long latency period (slow onset of action), making them unsuitable for situations requiring emergency reduction of myocardial workload.
How does furosemide rapidly relieve symptoms in pulmonary edema?
Furosemide has a direct vasodilating effect: it dilates veins, instantly reducing preload and pulmonary capillary pressure even before the diuretic effect develops.
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, thereby restoring airway patency.
What are the main indications and contraindications for prescribing cardiac glycosides?
Glycosides (e.g., digoxin) are indicated in chronic or acute heart failure, especially in combination with tachyarrhythmic atrial fibrillation. The main contraindication is atrioventricular (AV) block.
What else to study on this topic
- Comparative characteristics of non-glycoside inotropic agents: dobutamine vs levosimendan
- Molecular mechanism of action of nesiritide and the role of cGMP in vasodilation
- Features of the clinical use of endothelin receptor antagonists (tezosentan) and vasopressin antagonists (tolvaptan, conivaptan)
- Causes and mechanisms of development of tolerance to organic nitrates during intravenous administration
- Effect of cardiac glycosides on ion transport (calcium, sodium) and their inotropic, chronotropic, and dromotropic effects
Master the entire topic in the «Pharmacology» course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Pharmacotherapy of Acute Heart Failure" and 5,304 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 116 video lessons on the subject
Other topics in the section "Cardiovascular Drugs"
Free video lessons: pharmacologyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.