Physiology-Guided Management of Acute Right Ventricular Failure and Pulmonary Hypertension in Critically Ill Patients: Hemodynamic Phenotypes, Ventilator Interactions, and Rescue Strategies

Patients with acute right heart failure or pulmonary hypertension require cautious resuscitation because the right ventricle is highly preload-sensitive and has a narrow therapeutic window; both hypovolemia and volume overload may worsen hemodynamics. Echocardiographic guidance can help optimize fluid administration. The management of right heart failure also includes increasing contractility and reducing systemic afterload with inodilators such as dobutamine and milrinone. In cases of high pulmonary vascular resistance (PVR) contributing to right heart failure, the use of selective pulmonary dilators can decrease the right ventricular afterload, while largely avoiding the systemic hypotension associated with intravenous vasodilators. Hypoxemia, hypercapnia, and acidosis may increase PVR, while sedation, intubation, and positive-pressure ventilation (PPV) may reduce preload, precipitating hemodynamic collapse. When possible, noninvasive respiratory support may be cautiously used to optimize oxygenation and ventilation and avoid intubation. With either form of PPV, airway pressures should be minimized to reduce the risk of hemodynamic compromise. Additionally, preload should be carefully optimized; hypotension-inducing sedatives, such as propofol, should be minimized; vasopressors should be readily available. In ARDS complicated by acute cor pulmonale, a right ventricular-protective ventilation strategy should be considered alongside conventional lung-protective ventilation. This approach emphasizes limiting excessive plateau and driving pressures, avoiding severe hypercapnia and hypoxemia, and carefully titrating positive end-expiratory pressure (PEEP) to prevent excessive increases in PVR and right ventricular afterload. In patients with right-to-left intracardiac shunting, elevated right-sided pressures may worsen shunt flow and cause refractory hypoxemia that responds poorly to increasing FiO2 and ventilation pressures. Management should therefore focus on reducing PVR, optimizing right ventricular function, and limiting factors that increase right-sided pressures.