Pulmonary Circulatory Dysfunction in ARDS: From Pathophysiology to Clinical Practice

By
Antoine Vieillard-Baron
Michelle Chew
Michael R. Pinsky
October 12, 2026

Intensive Care Medicine

Overview

ARDS involves pulmonary vascular dysfunction as well as alveolar injury and impaired lung mechanics. The supplied article describes how altered pulmonary blood flow, pulmonary hypertension, and right ventricular dysfunction can worsen gas exchange and hemodynamics, while mechanical ventilation can modify pulmonary vascular resistance and right ventricular afterload.

Background

The pulmonary circulation normally matches regional perfusion to ventilation while carrying the full cardiac output at low pressure and resistance. In ARDS, alveolar epithelial and capillary endothelial injury can impair hypoxic pulmonary vasoconstriction and alter pulmonary vascular tone. These changes can increase pulmonary vascular resistance and pressure, burden the right ventricle, and disrupt ventilation–perfusion matching. Positive-pressure ventilation also affects pulmonary blood flow through changes in airway pressure and lung volume.

Data Highlights

Measure or condition	Value or reported effect
Pulmonary blood volume at rest in a 70 kg individual	Approximately 300 mL, including about 120 mL in alveolar capillaries
Normal pulmonary arterial systolic pressure	15–25 mmHg
Tidal volume in healthy lungs	6–8 mL/kg
Low-to-moderate lung volumes	Recruitment of extra-alveolar vessels lowers pulmonary vascular resistance
High lung volumes	Compression of intra-alveolar vessels increases pulmonary vascular resistance and right ventricular afterload
Optimal PEEP, as described in the article	Alveolar recruitment and improved oxygenation can decrease hypoxic pulmonary vasoconstriction, pulmonary vascular resistance, and right ventricular afterload

Key Findings

Alveolar epithelial and capillary endothelial injury can cause capillary leak, compromised hypoxic pulmonary vasoconstriction, and altered pulmonary vascular tone.
Pulmonary vascular dysfunction is described as contributing to morbidity and mortality through impaired right ventricular function and reduced cardiac output.
Right ventricular dysfunction can alter pulmonary blood flow and pulmonary vascular resistance, disrupting ventilation–perfusion regulation and potentially sustaining ARDS.
Positive airway pressure can raise alveolar pressure, reduce cardiac output, enlarge West Zones 1 and 2, and worsen ventilation–perfusion matching; blood volume expansion may mitigate this effect, according to the article.
The relationship between lung volume and pulmonary vascular resistance is U-shaped: recruitment of extra-alveolar vessels at low-to-moderate volumes lowers resistance, whereas compression of intra-alveolar vessels at greater volumes raises resistance and right ventricular afterload.
Optimal PEEP is described as recruiting collapsed alveoli, improving oxygenation, and decreasing hypoxic pulmonary vasoconstriction, pulmonary vascular resistance, and right ventricular afterload; overinflation from PEEP or airflow obstruction can have the opposite effect.

Clinical Implications

The article frames ARDS management around the interaction of lung mechanics, pulmonary circulation, and right ventricular function, noting that ventilatory strategies alter pulmonary vascular load. It describes both potential benefits of alveolar recruitment with optimal PEEP and adverse effects associated with excessive lung volume or airway pressure; the supplied excerpt does not provide a specific bedside protocol.

Conclusion

The supplied article presents pulmonary circulatory dysfunction as an integral component of ARDS pathophysiology, with consequences for gas exchange, cardiac output, and right ventricular function. Its heart–lung-centered framework emphasizes that ventilation-related changes in pressure and lung volume can influence these processes.