Considerations for Inotrope and Vasopressor Use in Critically Ill Patients With Pulmonary Arterial Hypertension

Abstract

Pulmonary arterial hypertension (PAH) is a rare and progressive cardiopulmonary disease, characterized by pulmonary vasculopathy. The disease can lead to increase pulmonary arterial pressures and eventual right ventricle failure due to elevated afterload. The prevalence of PAH in patients admitted to the intensive care unit (ICU) is unknown, and pulmonary hypertension (PH) in the ICU is more commonly the result of left heart disease or hypoxic lung injury (PH due to left heart disease and PH due to lung diseases and/or hypoxia, respectively), as opposed to PAH. Management of patients with PAH in the ICU is complex as it requires a careful balance to maintain perfusion while optimizing right-sided heart function. A comprehensive understanding of the underlying physiology and underlying hemodynamics is crucial for the management of this population. In this review, we summarized the evidence for use of vasopressors and inotropes in the management of PH and extrapolated the data to patients with PAH. We strongly believe that the understanding of the hemodynamic consequences of inotropes and vasopressors, especially from data in the PH population, can lead to better management of this complex patient population.

Approach to the hospitalized patient with pulmonary arterial hypertension

“…Increasing CO by inotropes frequently overcomes their direct systemic vasodilator effect, but in some cases, co-administration of vasopressors may be required [26] (Table 3). Dobutamine has more potential for tachycardia, while milrinone has more impact on systemic vascular resistance and can accumulate in renal dysfunction [27 ▪▪ ]. Therefore, dobutamine remains the inotrope of choice in RHF, and the dose is best limited to 5 mcg/kg/min to avoid side effects [15].…”

“…Low-dose vasopressin has a more selective systemic effect, but there are concerns of negative inotropy with higher doses [28]. Phenylephrine may worsen pulmonary vasoconstriction and is generally avoided, while epinephrine use is limited by tachycardia [27 ▪▪ ].…”