Respiratory effects

Pulmonary microvascular occlusion increases the fraction of lung tissue which is ventilated but not perfused (high VjQ). Consequently, pulmonary dead-space ventilation rises, resulting in impaired CO 2 elimination and hypercapnia. Theoretically, microvascular occlusion should not impair oxygenation, as it increases rather ■

than decreases VjQ. Clinically, however, hypoxemia is often observed for several reasons.

1. Reduced pulmonary blood flow may alter the surface-active properties of the lung and cause postocclusion atelectasis. Reperfusion of these badly ventilated

regions, for example after break-up of microthrombi, reduces Pa02 because of local VjQ mismatch.

2. Pulmonary edema commonly associated with microvascular occlusion may impair alveolar ventilation, lower VjQ, and increase shunt.

3. The release of vasoactive mediators will impair VjQ matching, even in areas unaffected by local vessel occlusion.

4. Pulmonary hypertension may cause paradoxic intracardiac right-to-left shunting through a patent foramen ovale.

5. Low mixed venous PO2 due to a low cardiac output may amplify the negative impact of shunted blood on PaO2.

It is not clear whether reduced pulmonary capillary transit time due to increased blood flow velocity in unobstructed vessels contributes to hypoxemia.

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