The two major causes of acute right ventricular (RV) failure in ICU patients are acute cor pulmonale (ACP) during acute respiratory distress syndrome (ARDS) and ACP during acute massive pulmonary embolism (PE).
The increase in pulmonary vascular resistance (PVR) in ARDS can be secondary either to « structural » mechanisms related to lung injury per se and to « functional » mechanisms related to the effects of mechanical ventilation with positive end expiratory pressure (PEEP). The latter mechanism is enhanced when PEEP overdistends more than it recruits lung volume and when tidal volume (VT) is high. The recommended protective ventilation with low VT and PEEP adjusted to driving pressure can also reduce the RV afterload. A reduced central blood volume can also play a role in the increase in PVR (extension of the West’s zone 2). In this case, volume administration can reduce the PVR and improve the RV function. Finally, prone positioning also exerts a beneficial effect on RV afterload through a decrease in PVR (lung recruitment, decrease in hypoxic vasoconstriction, increase in central blood volume with decrease in the extent of zone 2).
In acute PE, RV dysfunction is associated with poor outcome. Thrombolytic treatment, which is indicated in cases of severe PE with shock, prevents hemodynamic decompensation in patients with intermediate risk PE, but also results in increased risk of severe hemorrhage and stroke. In the case of PE with low cardiac output and no RV dilatation, fluid administration can be indicated to improve cardiac output. In cases of systemic arterial hypotension, vasopressors such as norepinephrine can be indicated to restore adequate RV perfusion pressure. Indication of inotropic agents such as dobutamine, which improves the RV-pressure artery coupling should be evaluated individually. Surgical pulmonary embolectomy can be indicated when the thrombolytic therapy is contra-indicated in acute PE with shock.
