Acute cor pulmonale and the acute respiratory distress syndrome

Excerpt

Acute respiratory distress syndrome (ARDS) is characterized by arterial hypoxemia secondary to protein-rich pulmonary edema associated with acute inflammation and loss of aerated lung volume [1, 2]. ARDS also involves injury to the pulmonary circulation that is associated with pulmonary hypertension and an elevation in pulmonary dead space [1, 2]. The pulmonary circulation is involved at different stages of ARDS with progression of the clinical syndrome. First, injury to the lung microcirculation causes an increase in lung vascular permeability which initiates the accumulation of pulmonary edema. Second, intravascular microthrombi can develop from an imbalance between procoagulant and fibrinolytic activity in the presence of acute inflammation and endothelial injury. Third, the marked reduction in functional residual capacity (FRC) can increase pulmonary vascular resistance (PVR). Fourth, positive pressure ventilation can induce high lung volume in some lung regions and compress alveolar vessels, resulting in increased PVR. The resulting higher regional FRC can also increase PVR. Fifth, hypoxic pulmonary vasoconstriction can further increase PVR. All these of mechanisms can contribute to an elevation in PVR that can occur within 48 h after the onset of ARDS, as demonstrated many years ago [3] and also more recently [4, 5]. The elevation in PVR may also be exacerbated by hypercapnia and acidosis. These mechanisms are summarized in Fig. 1.

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