What’s new: the management of acute right ventricular decompensation of chronic pulmonary hypertension

Excerpt

In healthy individuals, the right ventricular-pulmonary circulation is a low-pressure, high-compliance system. In high afterload states, the right ventricle (RV) adapts by increasing contractility (homeometric autoregulation) and preload (heterometric autoregulation) [1, 2]. Pulmonary hypertension (PH), defined as a mean pulmonary artery pressure >25 mmHg, results from any physiologic process that increases RV afterload, most commonly left ventricular (LV) disease resulting in a high left atrial pressure and post-capillary pulmonary venous congestion [3]. Pre-capillary PH (PAH) results from high RV loading despite normal pulmonary venous pressure.  PAH may present with RV dysfunction, a physiologic state where the RV ventriculo-vascular unit is unable to perform some necessary functions.  However, many patients with PAH present to the intensive care unit (ICU) in overt RV failure. In this condition, regardless of etiology, the RV is unable to meet increased loading demands leading to RV dilation, tricuspid regurgitation, and increased right atrial pressure reducing forward flow, coronary perfusion, and perhaps systemic hypotension [4]. This presents unique problems for hemodynamic optimization, intubation, and ventilator management. This paper offers strategies to address the complicated physiology of PH with RV failure in the ICU. See Fig. 1 for a summary of our recommendations.

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