Pulmonary hypertension (PH) is a threatening condition that can be associated with a great variety of both pulmonary and extrapulmonary diseases. In all forms of severe PH the pulmonary vascular bed looses its physiological features of a “high flow-low pressure system”, putting an increased afterload on the right ventricle (RV). Acute pulmonary hypertension in the intensive care unit often represents a clinical problem secondary to acute respiratory failure, left heart failure, pulmonary embolism, or decompensation of prior PH by concurrent pulmonary or cardiovascular disease. Right ventricular failure (acute cor pulmonale) occurs when relevant increases in pulmonary vascular resistance overwhelm its compensatory mechanisms, both abruptly on a previously normal RV, or gradually on a chronic cor pulmonale. This review addresses the main pathophysiological aspects of severe PH, focusing on the hemodynamic derangements occurring in the setting of acute cor pulmonale, and emphasizing the role of ventricular interdependence (the way right ventricular failure greatly affects diastolic and systolic function of the left ventricle), the risk of RV ischemia (the end stage of RV failure) and systemic organ hypoperfusion (caused by antegrade and retrograde heart failure). The understanding of the peculiar features of this type of cardiovascular insufficiency is necessary to both provide effective monitoring and adequate supportive therapy.

Minerva Anestesiol. 2004 Apr;70(4):233-7

Full text attached: Pathophysiology of severe pulmonary hypertension in the critically ill patient – Minerva 2004