Gas exchange

Postoperative hypoxemia is common. Initially it is related to the residual effects of general anesthesia. Hypoxemia may last days to weeks after thoracic or upper abdominal surgery. This correlates with a reduced functional residual capacity and an increased closing capacity. Induction of general anesthesia is associated with an increase of dead-space (ventilation of non-perfused lung), shunt (perfusion of non-ventilated lung), and inhibition of hypoxic pulmonary vasoconstriction. There is more ventilation to non-dependent areas of the lung, leading to areas of high ventilation-to-perfusion ratio. In addition to the redistribution of ventilation, the anesthesia circuit can result in a dead-space of up to 50 per cent of the tidal volume. If total ventilation is not increased, alveolar hypoventilation results in hypoxemia as well as hypercapnia. Observation of hypoxemia and hypercapnia after surgery may be due to hypoventilation caused by painful excursion of an incision, narcotic effects upon ventilatory drive, or upper airway obstruction.

Intrapulmonary shunt increases from 5 to about 8 per cent during anesthesia. The increase is greater in patients who are obese or who have pre-existing pulmonary conditions. The mechanism is primarily that of loss of normal respiratory muscle support of the lung and subsequent atelectasis. An additional mechanism may be the administration of 100 per cent oxygen. If the oxygen is entirely absorbed, the air spaces will collapse without the presence of the slowly diffusing nitrogen (absorption atelectasis). Positive end-expiratory airway pressure (PEEP) intraoperatively may not improve hypoxemia. Even though atelectasis is reduced, the shunt fraction does not improve. It is believed that this is the result of reduced cardiac output as PEEP is applied.

Hypoxic vasoconstriction is a point of some controversy. It is the normal constriction of the pulmonary circulation in response to hypoxemia. Pulmonary circulation is shifted from poorly ventilated areas to well-ventilated areas, attempting to preserve normal ventilation-perfusion relationships. Intravenous anesthetics do not affect hypoxic vasoconstriction. Inhalation anesthetics induce hypoxic vasoconstriction inhibition when tested on tissue preparations. However, when they are tested on intact preparations, including the human lung, there is little effect upon hypoxic vasoconstriction.

Postoperatively there is a linear relationship between atelectasis and hypoxemia. After upper abdominal and thoracic surgery the patient takes rapid shallow breaths. The small tidal volumes do not allow the opening of small airways that have closed due to the increased closing capacity and reduced functional residual capacity. Both atelectasis and low ventilation-to-perfusion relationships are promoted, resulting in arterial hypoxemia. Alveolar hypoventilation can occur as the result of increased dead-space ventilation, and decreased mixed venous oxygenation can be found as the result of increased peripheral muscle activity and reduced cardiac output.

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