Abstract

Acute right ventricular (RV) failure is a devastating syndrome caused by a variety of common diseases and conditions. Acute RV failure is caused by acute alterations in preload, afterload, and/or contractility. Ventricular interdependence and decreases in perfusion pressure make the RV particularly prone to acute failure. Histologic and biochemical correlates of RV failure are inflammation, oxidative stress, mitochondrial dysfunction, and cardiomyocyte death. The most common causes are pulmonary hypertension, pulmonary embolism, left heart failure, acute right-sided myocardial infarction, and sepsis as well as acute respiratory distress syndrome. Invasive hemodynamic assessment and echocardiography remain the most valuable methods to diagnose and manage acute RVF in critically ill patients. In more stable patients, cardiac MRI can be used as an alternative or complementary imaging method. These strategies are complemented by biomarker assessment, radiographic studies, and incorporation of clinical parameters into validated risk scores. The key principle in the management of acute RV failure focuses on treatment of the underlying etiology, complemented by supportive strategies focused on improving RV function via optimization of volume status and oxygenation, enhancing contractility, and reducing afterload. The latter two are achieved through use of vasopressors (e.g., norepinephrine), inotropes (e.g., dobutamine, milrinone), pulmonary vasodilators (e.g., inhaled nitric oxide, parenteral prostacyclins, phosphodiesterase type 5 inhibitors), and interventional or surgical therapies (e.g., extracorporeal membrane oxygenation). This chapter will provide a definition of acute RV failure and review its pathophysiology, etiologies, diagnosis and risk stratification as well as treatment.

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