ONE LUNG VENTILATION
Intentional collapse of the lung on the operative side facilitates most thoracic procedures, but greatly complicates anesthetic management. Because the collapsed lung continues to be perfused and is delib-erately no longer ventilated, the patient develops a large right-to-left intrapulmonary shunt (20% to 30%). During one-lung ventilation, the mixing of unoxygenated blood from the collapsedupper lung with oxygenated blood from the still-ventilated dependent lung widens the alveolar-to-arterial (A-a) O2 gradient and often results in hypoxemia. Fortunately, blood flow to the nonventi-lated lung is decreased by hypoxic pulmonary vaso-constriction (HPV) and possibly surgical compression of the upper lung
Factors known to inhibit HPV (increasing venous admixture), and thus worsen the right-to-left shunting, include (1) very high or very low pulmo-nary artery pressures; (2) hypocapnia; (3) high or very low mixed venous Po2; (4) vasodilators such as nitroglycerin, nitroprusside, phosophodiesterase inhibitors (milrinone and inamrinone), β-adrenergic agonists, calcium channel blockers; (5) pulmonary infection; and (6) inhalation anesthetics.
Factors that decrease blood flow to the venti-lated lung can be equally detrimental; they counter-act the effect of HPV by indirectly increasing blood flow to the collapsed lung. Such factors include
high mean airway pressures in the ventilated lung due to high positive end-expiratory pressure (PEEP), hyperventilation, or high peak inspiratory pressures;a low Fio2, which produces hypoxic pulmonary vasoconstriction in the ventilated lung; (3) vasocon-strictors that may have a greater effect on normoxic vessels than hypoxic ones; and (4) intrinsic PEEP that develops due to inadequate expiratory times.Elimination of CO2 is usually unchanged by one-lung ventilation, provided that minute ventila-tion is unchanged and that preexisting CO 2 retention was not present while ventilating both lungs; arterial CO2 tension is usually not appreciably altered.
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