Acute respiratory failure and sepsis

In acute respiratory failure, several mechanisms promote the development of pulmonary hypertension. The inflammatory character of the disease leads to neutrophil accumulation within the lung and subsequent release of cytokines, free radicals, and other cytotoxic metabolites ( Gossage and Christman 1994). Increased permeability of the pulmonary capillary bed leads to a subsequent fluid shift to the interstitium, eventually resulting in pulmonary permeability edema. The increase in interstitial pressure compromises capillary blood flow, thus promoting ventilation-perfusion mismatch with hypoxia and respiratory acidosis. Because a high shunt fraction and a patchy distribution of atelectasis is characteristic in acute respiratory failure, hypoxic pulmonary vasoconstriction is an important factor in redistribution of blood flow to ventilated parts of the lung in order to reduce shunt perfusion and prevent hypoxic vasoconstriction in non-injured parts of the lung. The high airway pressures produced by mechanical ventilation cause distortion and high shear forces in the capillary bed of the overinflated part of the diseased lung; this hampers blood flow owing to mechanical compression of the capillaries. Alterations in the vascular endothelium, increases in procoagulatory and fibrinolytic activity, and reductions or stasis of blood flow promote deposition of fibrin and microemboli ( ZapoJiiiand Snjderii1977). These pathological features are not unique to acute respiratory failure but occur in other inflammatory states, including sepsis, where respiratory failure is secondary to the disease process. The reduction of the cross-sectional area of the pulmonary vascular bed restricts pulmonary blood flow without further increases in pulmonary artery pressures. The need for an elevated cardiac output to augment oxygen delivery in sepsis further increases the degree of pulmonary hypertension. Acute pulmonary hypertension ameliorates the ongoing healing process, the restitution of endothelial integrity, normoxia, and normalized acid-base status.

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