Pulmonary Hypertension in Severe Acute Respiratory Failure

TLDR

Elevated pulmonary vascular resistance increases right‑ventricular workload, potentially limiting survival in severe acute respiratory failure. Pulmonary and systemic hemodynamics were repeatedly measured in 30 patients with severe acute respiratory failure of various etiologies. All patients developed pulmonary‑artery hypertension and elevated pulmonary vascular resistance after systemic hypoxemia correction; altering pulmonary blood flow had little effect on pressure, and although neither elevated resistance nor low cardiac index predicted mortality, survivors showed decreasing resistance over time while nonsurvivors did not, with markedly elevated right‑ventricular stroke‑work index throughout.

Abstract

We repeatedly assessed pulmonary and systemic hemodynamics in 30 patients undergoing therapy for severe acute respiratory failure of diverse causes. Pulmonary-artery hypertension and elevated pulmonar vascular resistance were observed in all patients after correction of systemic hypoxemia. Increasing pulmonary blood flow by isoproterenol infusion or decreasing pulmonary blood flow by partial bypass of the right side of the heart minimally altered pulmonary-artery pressure. Although neither elevated pulmonary vascular resistance nor low cardiac index reliably predicted death, survivors had preogressive decreases of pulmonary vascular resistance with time, whereas nonsurvivors tended to maintain or increase pulmonary vascular resistance. Right ventricular stroke-work index was markedly elevated in all patients. The work load imposed upon the right ventricle by elevation of pulmonary vascular resistance may be a factor limiting survival in severe acute respiratory failure.