• P L Klineberg and R J Bagshaw.
• Int Anesthesiol Clin. 1981 Jan 1;19(3):123-67.

AbstractThere is now overwhelming evidence that anesthesia with and without muscle paralysis is associated with an increased inefficiency of gas exchange, with abnormal oxygenation and CO2 elimination. There is great variation in the degree of this change from individual to individual; it results from increased right-to-left intrapulmonary shunting, increased alveolar dead space, increased dispersion of VA/Q ratios, altered cardiac output, and changes of the ODC. In normal subjects the abnormality can be largely explained by mismatch of ventilation and perfusion. Distribution of perfusion is determined by right ventricular output, the distribution of pulmonary vascular impedance, and their mutual interaction. This interaction is specifically influenced by gravity, right heart dynamics, systemic hemodynamics, particularly via the left atrium, and lung inflation. General anesthesia modifies the distribution of perfusion, largely to the extent that the above determinants are changed by: the particular anesthetic agents used; the posture adopted (gravity); the type and extent of ventilation employed; hypoxic pulmonary vasoconstriction; and any accompanying special techniques such as deliberate hypotension. Ventilation distribution is dependent on the posture of the subject and changes of the lung volumes and mechanics, which probably result from altered chest wall and diaphragm mechanics. These changes occur soon after induction of anesthesia and do not appear to be progressive. They can persist, however, well into the postoperative period. Alterations of pulmonary function during anesthesia and surgery are rarely life threatening in the operating room. Awareness of the problems of hypoxemia during general anesthesia and an appropriate response by the anesthesiologist, however, is a prerequisite of good medical practice.

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