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The recognition of pulmonary vascular complications in acute respiratory distress syndrome (ARDS) spans more than 40 years. Pulmonary hypertension (PH) is defined as a mean pulmonary artery pressure of ≥25 mm Hg at right heart catheterisation. PH is a recognised consequence of ARDS, with a high prevalence in early studies. The pathogenesis of PH in ARDS is likely to be multifactorial and disease stage-dependent. Further to the modifiable effects of positive pressure ventilation,1 potential underlying mechanisms of PH in ARDS include vessel obliteration, microthrombosis and pulmonary vasoconstriction due to hypoxia, hypercapnia and vasoactive mediator imbalance. Pulmonary vascular remodelling occurs later.2 Sepsis-related right-sided and also left-sided ventricular myocardial dysfunction may also contribute. Whatever the cause of PH, the resulting right ventricular (RV) dysfunction is associated with increased morbidity and mortality,3 ,4 although it is not actually proven that RV failure is a mode of death in ARDS. Trials of pulmonary vasodilators, such as inhaled nitric oxide and prostacyclin, have met with disappointment in terms of outcomes, although there is fair criticism of the design of the studies and the heterogeneity of the populations involved. Notably, these studies targeted oxygenation rather than pulmonary haemodynamics; so, any potential contribution of improved RV function to better outcomes is untested. What is clear is that outcome has improved in ARDS with a parallel apparent reduction in prevalence of PH and RV dysfunction. Both may be due to changes in ventilation practice following the landmark protective ventilation studies, as limiting ventilator airway pressures directly reduces RV dysfunction through physiological mechanisms.5 However, even with the use of ‘modern era’ lower airway pressures, RV dysfunction remains in the region of 20%–25%3 ,4 and interestingly appears to be associated with sepsis.3 So, what is the role of sepsis and, …
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