Cardiopulmonary interactions in acute lung injury: clinical and prognostic importance of pulmonary hypertension.
Development of acute lung injury (ALI) in the critically ill is associated with an array of abnormal interactions between the heart and lungs. Of these abnormalities, increased pulmonary vascular resistance (PVR) is common and seems to indicate a worse prognosis than when PVR is normal. Increased pulmonary artery pressure, which follows ALI in humans, has been attributed to many factors. Early in ALI, pulmonary artery hypertension (PAH) is secondary to an imbalance between the release of vasoactive mediators derived from arachidonic acid, endothelium-derived relaxing factor, and other metabolites. As ALI progresses, the combination of mechanical obstruction and severe regional hypoxic pulmonary artery vasoconstriction probably becomes the main factor responsible for PAH. In addition to these elements, in situ and peripherally derived thromboemboli can be seen in ALI, owing to diverse disturbances in the coagulation and fibrinolytic processes. The result is increased workload of the right ventricle which is caused by increased afterload and may induce hemodynamic disturbances that culminate in overt right ventricular failure. However, epidemiologic studies have demonstrated that death following ALI is more often the result of respiratory failure or sepsis. The absence of effective therapy for PAH in ALI might be explained by the pathophysiological and clinical course of the disease. A reasonable conclusion from the contributing elements cited above is that PAH complicating sepsis and trauma is simply a marker of the gravity of the systemic insult that leads to the development of ALI and probably not a separate process.
Romand
J A
JA
Department of Anesthesiology, University Hospital of Geneva, Switzerland.
Donald
F A
FA
Suter
P M
PM
D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D006976:Hypertension, Pulmonary / Q000209:etiology / Q000503:physiopathology*; D008168:Lung / Q000503:physiopathology*; D011379:Prognosis; D012128:Respiratory Distress Syndrome / Q000150:complications / Q000503:physiopathology*