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Acute right ventricular failure: causes, symptoms, diagnosis, treatment

 
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Last reviewed: 05.07.2025
 
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Isolated acute right ventricular failure is much less common than left ventricular acute heart failure. This is due to the fact that the right ventricle is more resistant to ischemic damage due to a more favorable relationship between its need for oxygen and the conditions of delivery to it. Therefore, right ventricular failure most often occurs some time after the development of severe left ventricular failure.

In acute right ventricular failure, there is a sudden increase in central venous pressure (swelling of the veins of the neck, increased pulsation of the internal jugular vein), pain and enlargement of the liver, severe dyspnea without orthopnea (patients usually prefer to lie down), tachypnea, hypotension or a clinical picture of shock may be observed.

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What causes acute right ventricular failure?

Acute right ventricular failure is most often observed in the following conditions:

The clinical picture of right ventricular failure can develop with right ventricular infarction, rupture of the interventricular septum, pulmonary embolism, congenital and acquired heart defects.

The development of right ventricular failure with symptoms of congestion may be caused by pathology of the pulmonary artery and right heart (exacerbation of chronic lung disease with pulmonary hypertension, massive pneumonia, pulmonary embolism, dysfunction of the tricuspid valve as a result of injury or infection).

It may develop in acute or subacute pericardial disease, progression of severe left heart failure with involvement of the right heart, as well as decompensation of a long-standing congenital heart defect.

Major non-cardiac causes include nephritis, nephrotic syndrome, end-stage liver disease, and vasoactive peptide-secreting tumors.

As a rule, the development of right ventricular failure is caused by an increase in pressure in the pulmonary artery and the involvement of the myocardium of the right ventricle in the zone of necrosis and peri-infarction myocardial damage.

Symptoms of acute right ventricular failure

The main symptoms of acute right ventricular failure are pronounced venous congestion in the systemic circulation (if there is no hypovolemia) and the absence of congestion in the lungs.

Clinically, right ventricular failure is manifested by an enlarged liver, swelling of the jugular veins, and the appearance of peripheral and cavitary edema. Increasing tachycardia, decreased blood pressure, cyanosis, and dyspnea are noted. A sharp increase in central venous pressure is noted.

On the electrocardiogram, acute right ventricular failure may be manifested by a right ventricular pattern, acute development of right bundle branch block, "Gothic" P in II, III, aVF (P pulmonale), and predominance of the positive phase of the P wave in VI.

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Treatment of acute right ventricular failure

In all these cases, the use of diuretics and vasodilators is contraindicated. After the introduction of diuretics or vasodilators, a decrease in blood pressure always occurs, up to pronounced hypotension or shock. When blood pressure decreases, intravenous fluid administration is indicated (plasma-substituting solutions at a rate that maintains blood pressure at 90-100 mm Hg). If the effect is insufficient, dobutamine infusion is used. Milrinone can be used.

In cases of severe refractory hypotension - infusion of dopamine, norepinephrine, intra-aortic counterpulsation, assisted circulation.

Treatment involves diuretics, including spironolactone, and sometimes a short course of dopamine in a low (“diuretic”) dose.

In the development of right ventricular failure, venous vasodilators are contraindicated, since they reduce venous return and decrease cardiac output.

To correct arterial hypotension in right ventricular failure, the administration of plasma substitutes or plasma is indicated to increase the preload on the right ventricle in combination with dobutamine and arterial vasodilators (hydralazine or phentolamine).

Dobutamine in combination with phentolamine causes vasodilation of peripheral arteries, reduces afterload on the left ventricle, pressure in the left atrium and pulmonary artery. This leads to a decrease in afterload on the right ventricle and an increase in its output.

Stroke output can also be increased by injecting fluid directly into the pulmonary artery.

In cases of pulmonary infection and bacterial endocarditis, the use of antibiotics is indicated.

Treatment of primary pulmonary hypertension is with calcium antagonists, nitric oxide or prostaglandins.

In the event of pulmonary embolism, thrombolytic therapy and, if indicated, thrombectomy are performed.

Acute right ventricular failure is treated based on the therapy of the underlying disease: in case of pulmonary thromboembolism - heparin and thrombolytic therapy, in case of tamponade - pericardiocentesis and drainage of the pericardial cavity, in case of myocardial infarction - thrombolytic therapy or surgical treatment.

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