Defend the right ventricle with what you know

Right ventricle failure in patients with pulmonary hypertension (PH) has high mortality and is often unrecognised because the syndrome is less evident on exam than left heart failure. PH is an uncommon condition and management of patients with PH during critical illness is largely based on experience, as data from randomised clinical trials in this specific population do not exist. At the academic medical centres where relatively large numbers of PH patients are treated, the specialists and the intensivists who work with them share a common experience. Patients with decompensated right ventricle function and cardiogenic shock can look surprisingly stable, but reversing the shock or managing these brittle PH patients through an elective or emergent surgical procedure involves a delicate balance. Each intervention is determined by a mixture of physician experience, inference from physiology and by local practice norms, not randomised investigations. In the current issue of the European Respiratory Journal , French clinician-scientists provide descriptive results of the largest database collected to date on patients experiencing acute right heart failure requiring admission to an intensive care unit 1 and patients requiring surgical procedures 2 at their internationally recognised centre. There have been few publications regarding the management of and outcomes from acute decompensated right heart failure or the peri-operative management of patients with PH. This prompted investigators in Paris to report their collective experience in these areas. The readers of this journal are familiar with pulmonary arterial hypertension (PAH), a fatal group of diseases characterised by an elevated pulmonary vascular resistance with a normal pulmonary artery wedge pressure in the absence of chronic lung disease/hypoxia, chronic thromboembolic disease (CTEPH), or left heart disease. PAH is characterised by pulmonary vasoconstriction, endothelial dysfunction, excessive smooth muscle cell proliferation and in situ thrombosis 3–6. The consequence of this process …