Lung Recruitment and Venous Congestion in ARDS

A new article examines the complex physiological effects of positive end-expiratory pressure (PEEP) in patients with acute respiratory distress syndrome (ARDS), arguing that its benefits should be considered beyond improvements in oxygenation alone. While PEEP is a fundamental component of mechanical ventilation because it promotes alveolar recruitment, stabilises collapsed alveoli and enhances oxygenation, clinical trials have consistently failed to demonstrate a survival benefit from higher compared with lower PEEP levels. The authors propose that this apparent discrepancy may result from systemic haemodynamic consequences that offset the respiratory advantages of PEEP, particularly when it is not individualised according to lung recruitability and the patient's mechanical phenotype.

Traditionally, the adverse haemodynamic effects of PEEP have been interpreted mainly in terms of reduced cardiac output and diminished left ventricular preload. However, the authors argue that this explanation is incomplete and overlooks the important contribution of systemic venous congestion. They suggest that venous congestion represents an under-recognised mechanism linking positive pressure ventilation with dysfunction of multiple organs, despite preserved oxygenation. Current approaches to PEEP titration focus largely on respiratory variables and often fail to account for these systemic effects.

The article explains venous congestion using Guyton's model of venous return, whereby venous return depends on the pressure gradient between the mean systemic filling pressure and right atrial pressure, as well as venous resistance. PEEP influences both of these factors. Increased intrathoracic pressure elevates pulmonary vascular resistance, increasing right ventricular afterload and right atrial pressure. Simultaneously, transmission of airway pressure to the pleural cavity and displacement of the diaphragm compress the vena cava, impairing venous return. Together, these changes reduce the effective perfusion gradient while increasing central venous pressure, ultimately compromising venous drainage from abdominal organs despite improvements in systemic oxygenation.

Several organs are particularly susceptible to these haemodynamic disturbances. The kidneys are often affected early because increased renal venous pressure reduces the filtration gradient, potentially leading to declining urine output and acute kidney injury. The liver is also vulnerable, as even modest increases in hepatic venous pressure impair sinusoidal blood flow and oxygen diffusion. Within the gastrointestinal tract, elevated venous pressure decreases mucosal perfusion, increases intestinal permeability and impairs lymphatic drainage. Cerebral circulation may likewise be compromised because elevated intrathoracic pressure can be transmitted to the jugular venous system, reducing cerebral perfusion pressure, particularly in patients with impaired intracranial compliance. Collectively, these effects illustrate how impaired venous drainage may contribute to widespread organ dysfunction.

The authors emphasise that the haemodynamic consequences of PEEP depend not simply on the level of pressure applied but on the interaction between lung recruitability, respiratory system compliance and transmission of pleural pressure. They describe three representative mechanical phenotypes that illustrate these differing physiological responses.

The first phenotype consists of patients with low respiratory system compliance and poor lung recruitability. In these individuals, increased airway pressure mainly raises transpulmonary pressure, causing alveolar overdistension and compression of pulmonary capillaries. This increases pulmonary vascular resistance, elevates right ventricular afterload and right atrial pressure, and promotes systemic venous congestion.

The second phenotype involves patients with relatively compliant lungs but limited recruitability. In this setting, airway pressure is transmitted more readily to the pleural space, leading to thoracic expansion and diaphragmatic displacement that compress the inferior vena cava. The resulting impairment of venous return promotes splanchnic venous congestion primarily through extrapulmonary pressure transmission rather than pulmonary vascular effects.

The third phenotype includes patients with poor lung compliance but preserved recruitability. Here, appropriate PEEP successfully recruits collapsed alveoli, increases end-expiratory lung volume and improves lung homogeneity. Effective recruitment reduces hypoxic pulmonary vasoconstriction and pulmonary vascular resistance, thereby unloading the right ventricle while preserving venous return. If the left ventricle is operating on the ascending portion of the Frank-Starling curve, particularly during relative hypovolaemia, the resulting increase in preload may improve cardiac output and overall organ perfusion. Thus, identical PEEP levels may produce either beneficial or harmful haemodynamic effects depending on the underlying mechanical phenotype.

The authors also note that these physiological interactions differ during spontaneous breathing and non-invasive ventilation. Unlike controlled mechanical ventilation, spontaneous inspiration generates negative pleural pressure, which tends to preserve venous return and facilitate venous and lymphatic drainage. During non-invasive ventilation, positive airway pressure may partially offset these benefits, although improvements in lung recruitment and reduced inspiratory effort may simultaneously lessen haemodynamic stress and reduce patient self-inflicted lung injury. Consequently, the circulatory effects of non-invasive respiratory support depend on the balance between airway pressure, inspiratory effort and lung recruitment.

From a clinical perspective, the article advocates a broader approach to PEEP titration that incorporates both respiratory and circulatory physiology. Rather than focusing solely on oxygenation or respiratory mechanics, clinicians should evaluate whether respiratory compliance has improved, whether the change reflects alveolar recruitment rather than overdistension, how right and left ventricular function and cardiac output have responded, and whether there is evidence of developing venous congestion.

The authors caution that improvements in oxygenation or respiratory mechanics do not necessarily indicate overall physiological benefit. Signs such as declining urine output, increasing central venous pressure, abnormal venous Doppler findings consistent with venous congestion, including Venous Excess Ultrasound (VExUS), and echocardiographic evidence of right ventricular dysfunction should prompt reassessment of ventilator settings rather than further escalation of airway pressure.

The article concludes that PEEP should be regarded as a therapy that influences both the lungs and the circulation. Across different mechanical phenotypes, its effects on venous return and systemic venous pressure may either preserve circulatory homeostasis or contribute to systemic venous congestion and organ dysfunction. The authors therefore advocate a physiology-guided, individualised approach to PEEP titration that balances lung recruitment with preservation of venous return and organ perfusion, recognising the respiratory and circulatory systems as a single integrated physiological unit.

Source: Intensive Care Medicine
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