Vasopressors Aggravate Passive Pulmonary Hypertension Due to Left Heart Disease, from Basic Pathophysiology to Clinical Management

Pulmonary hypertension due to left heart disease (PH-LHD) is the most common form of pulmonary hypertension (PH), accounting for 65–80% of cases, and is associated with significant morbidity and mortality. PH-LHD is traditionally considered a passive condition, primarily driven by elevated left heart pressure, which increases pulmonary venous pressure. However, vasopressors, such as phenylephrine, frequently used in critical care to enhance vascular tone, can induce another form of passive PH. This vasopressor-induced PH shares hemodynamic similarities with PH-LHD, characterized by increased pulmonary blood volume and left atrial pressure, and exerts additive effects on pre-existing PH-LHD, exacerbating pulmonary congestion and worsening clinical outcomes. The interaction between vasopressors and PH-LHD is often overlooked, yet it poses significant risks, particularly in patients with heart failure. This review explores the pathophysiology of passive PH-LHD, the mechanisms of vasopressor-induced PH, and their additive effects. We also highlight the challenges in diagnosing passive PH, which is frequently misclassified as pulmonary arterial hypertension (PAH), leading to inappropriate treatment and potential harm. Current therapeutic strategies, such as diuretics and blood volume management, are discussed as potential approaches to mitigate these effects. Improved understanding of these mechanisms is crucial for optimizing treatment and reducing morbidity and mortality. Future research is needed to develop targeted therapies and improve outcomes for patients with PH-LHD and vasopressor-induced PH.