Acute right ventricular failure—from pathophysiology to new treatments

Abstract

The right ventricle (RV) provides sustained low-pressure perfusion of the pulmonary vasculature, but is sensitive to changes in loading conditions and intrinsic contractility. Factors that affect right ventricular preload, afterload or left ventricular function can adversely influence the functioning of the RV, causing ischaemia and right ventricular failure (RVF). As RVF progresses, a pronounced tricuspid regurgitation further decreases cardiac output and worsens organ congestion. This can degenerate into an irreversible vicious cycle. The effective diagnosis of RVF is optimally performed by a combination of techniques including echocardiography and catheterisation, which can also be used to monitor treatment efficacy. Treatment of RVF focuses on alleviating congestion, improving right ventricular contractility and right coronary artery perfusion and reducing right ventricular afterload. As part of the treatment, inhaled nitric oxide or prostacyclin effectively reduces afterload by vasodilating the pulmonary vasculature. Traditional positive inotropic drugs enhance contractility by increasing the intracellular calcium concentration and oxygen consumption of cardiac myocytes, while vasopressors such as norepinephrine increase arterial blood pressure, which improves cardiac perfusion but increases afterload. A new treatment, the calcium sensitiser, levosimendan, increases cardiac contractility without increasing myocardial oxygen demand, while preserving myocardial relaxation. Furthermore, it increases coronary perfusion and decreases afterload. Conversely, traditional treatments of circulatory failure, such as mechanical ventilation and volume loading, could be harmful in the case of RVF. This review outlines the pathophysiology, diagnosis and treatment of RVF, illustrated with clinical case studies.

Distinct loading conditions reveal various patterns of right ventricular adaptation

“…Studies in large animal models of combined volume and pressure overload have shown that during disease progression contractility initially increases, but falls back to pseudonormal levels in a more advanced stage of RV dysfunction (28,40,41). Causal factors for the blunted contractility response may include loss of peristaltic contraction pattern (33), disturbed calcium homeostasis (8,26), and changes in coronary perfusion (46). Failure to increase contractility has also been reported in a model of chronic LV volume overload (25).…”

Temporary percutaneous right ventricular support using a centrifugal pump in patients with postoperative acute refractory right ventricular failure after left ventricular assist device implantation

“…Although some patients recover successfully on medical right heart supporting therapies, including inotropes, phosphodiesterase inhibitors, or inhaled nitric oxide, others require mechanical circulatory support [3,7]. The most effective therapy for these patients is an upgrade to biventricular mechanical support.…”

Hemodynamic collapse under anesthesia in a patient with pulmonary artery sarcoma

“…Contractility can be optimized through inotropic agents and prevention of ischemia. 19 The importance of maintaining adequate RV perfusion pressure has been highlighted in animal studies showing reversibility of acute RV failure with improvement in coronary perfusion pressure. These studies suggest that maintaining systemic pressure may be a key factor in managing RV failure.…”