Dysfunction of the diaphragm contributes to the postoperative reduction of lung volumes. Studies have shown that, during induction of general anesthesia in supine patients, the diaphragm shifts cephalad, accounting for a loss of 340 to 750 ml of thoracic volume on each side. Intravenous anesthetics depress diaphragmatic tonic activity, and volatile anesthetics depress synaptic transmission affecting the intercostal muscles preferentially (although ketamine preserves respiratory muscle tone). Respiratory muscle tone loss results in perioperative atelectasis. Ninety per cent of anesthesia-induced atelectasis is present 1 h after surgery. Fifty per cent of the anesthesia-induced atelectasis is still present 24 h after surgery. In the aftermath of open cholecystectomy through a subcostal incision, the contribution of the diaphragm to tidal breathing is markedly reduced. Transdiaphragmatic pressure measurements during phrenic nerve stimulation indicate that reduced central nervous system efferent signals to the phrenic nerve are the cause of depressed diaphragm activity. Animal studies suggest that phrenic nerve activity is decreased through the transmission of inhibitory signals from somatic or visceral afferents. Epidural anesthesia ablates the inhibitory signals from the visceral sympathetic receptors; phrenic nerve transmission increases and diaphragm function improves. In contrast, the administration of epidural narcotics ameliorates pain but does not affect phrenic diaphragm function, although intrathecal opioids depress ventilation centrally in a dose-dependent fashion. Pain does not seem to account for the diaphragm dysfunction.
In cardiac and thoracic surgery, late postoperative atelectasis is not explained solely by diaphragmatic dysfunction. Phrenic nerve paralysis is found in fewer than 10 per cent of patients undergoing cardiothoracic surgery. Variables associated with severe atelectasis after cardiac surgery include the number of saphenous vein grafts, the use of internal mammary grafts, the length of cardiac bypass time, and entrance to the pleural space. Mechanisms relate to the low temperature and inadequate blood flow to the alveolar epithelium, resulting in decreased surfactant production or function. Routine thoracic surgery does not involve bypass or cardioplegia, but reduced surfactant activity can occur through the mechanical compression of the lung and the accumulation of lung water.
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