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Propaedeutics · Cardiovascular system

Pharmacotherapy of cardiovascular diseases

Pharmacotherapy of cardiovascular diseases is a comprehensive approach aimed at eliminating hypervolemia, modulating the neurohormonal background, and improving myocardial pump function. The foundation of proper therapy consists of drugs that not only relieve symptoms but also target the pathogenesis, improving the patient's long-term prognosis.

FurosemideTaken strictly once in the morning, the working dosage ranges from 40 to 80 mg per day.
ACE inhibitorsRepresent baseline therapy, prescribed for life with mandatory dose titration.
DigoxinDecreases heart rate, thereby prolonging diastole and increasing cardiac output.
SpironolactoneUsed at a dose of 50–150 mg/day for additional neurohormonal blockade.
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Fluid balance management (Diuretics)

The main clinical goal of prescribing this group of drugs is the complete elimination of hypervolemia (excess fluid retention in the body). During diuretic therapy, a critical condition is strict medical monitoring: it is necessary to continuously control changes in the patient's body weight and daily diuresis.

In clinical practice, there are three main subgroups of diuretics:

  • Loop diuretics. Furosemide is considered the most effective drug. It is prescribed at a dose of 40 to 80 mg per day, taken once in the morning.
  • Thiazide diuretics. The classic representative is hydrochlorothiazide. It is important to remember that it is less effective compared to loop diuretics.
  • Potassium-sparing diuretics. This group includes triamterene and amiloride.

Baseline therapy: ACE inhibitors

Angiotensin-converting enzyme (ACE) inhibitors play a central role in treatment. They act as the primary means of pathogenetic impact on the cardiovascular system and are prescribed to patients for life.

The mechanism of action of the drugs is based on the blockade of the conversion of angiotensin I to active angiotensin II. Through this, crucial therapeutic effects are achieved:

  1. Pronounced vasodilation (widening of blood vessels) occurs, leading to a decrease in both preload and afterload on the myocardium.
  2. Correction of neurohormonal imbalance takes place.

The main representatives of the group include captopril, enalapril, perindopril, and ramipril. The key rule for their application strategy is mandatory titration, i.e., prescribing the drug with a gradual increase in dose to the target.

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Additional neurohormonal system blockade

To enhance the pathogenetic effect, drugs are added to the baseline therapy aimed at further modifying the disease prognosis and correcting the neurohormonal profile (by analogy with the effects of ACE inhibitors).

  • Beta-blockers. The main drugs are bisoprolol, carvedilol, and metoprolol. Their main tactical feature is that the initiation of therapy must be carried out with the lowest possible doses.
  • Aldosterone antagonists. The classic drug in this subgroup is spironolactone. The recommended dose to achieve a neurohormonal effect is 50–150 mg per day.

Myocardial inotropic support

When a patient needs to increase myocardial contractility and cardiac output, cardiac glycosides come to the forefront. The main drug of this group is digoxin.

The prescription of digoxin becomes especially important in concomitant atrial tachyarrhythmia. Its hemodynamic effect is realized through a negative chronotropic effect—slowing down the heart rhythm. Due to the deceleration of contractions, the diastolic phase is prolonged. This ensures significantly better filling of the heart chambers with blood, which ultimately logically leads to an improvement in cardiac output.

Briefly: answers to topical questions

What are the absolute contraindications to prescribing ACE inhibitors?

Absolute contraindications to prescribing ACE inhibitors include the following conditions:

  • Pregnancy and lactation.
  • History of angioedema.
  • Hyperkalemia (potassium level ≥ 5.5 mmol/L).
  • Bilateral renal artery stenosis.
  • Renal artery stenosis of a solitary kidney.

What are the clinical signs of glycoside intoxication during digoxin intake?

Clinical signs of glycoside intoxication (digoxin overdose) include nausea and vomiting, as well as cardiac rhythm disturbances (e.g., ventricular paroxysmal tachycardia and AV conduction disorders).

Which drugs belong to cardioselective beta-blockers?

Cardioselective (selective β1-blockers) include the following drugs:

  • Atenolol (Tenormin)
  • Betaxolol (Lokren)
  • Bisoprolol (Concor)
  • Metoprolol (Betaloc, Eгиlok, Vasocardin)
  • Nebivolol (Nebilet)
  • Talinolol (Cordanum)
  • Esmolol (Brevibloc)

How do loop diuretics differ from thiazide diuretics in their site of action in the nephron?

Loop and thiazide diuretics differ in the localization of their action in the nephron:

Diuretic groupSite of action in the nephron
Loop diureticsAct in the thick segment of the ascending limb of the loop of Henle
Thiazide diureticsAct in the initial segment of the distal tubules
How to memorize

Drug groups: DIBIS (Diuretics, ACE inhibitors, Beta-blockers, Aldosterone antagonists, Inotropic agents).

Class and exam questions

What must be monitored when prescribing diuretics?

When treating with any diuretics, strict and regular monitoring of daily diuresis and body weight is mandatory to assess the elimination of hypervolemia.

How does digoxin affect the heart?

Digoxin causes a negative chronotropic effect—slows down the rhythm. This leads to the prolongation of diastole, which ultimately improves heart filling and increases cardiac output.

From what doses should beta-blockers be started?

The main feature of prescribing beta-blockers (bisoprolol, carvedilol, metoprolol) is the mandatory initiation with minimum doses.

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What else to study on this topic

  • Features of ACE inhibitor dose titration
  • Comparative efficacy of loop and thiazide diuretics
  • Pathogenesis of neurohormonal imbalance in cardiovascular pathology
  • Mechanism of hypervolemia development
  • Hemodynamic effects of the negative chronotropic action

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