Ventilator management for most thoracic surgery patients involves two distinct phases: (1) support in the operating room while the patient is undergoing surgery and receiving general anesthesia and (2) support in the postoperative recovery room or intensive care unit (ICU) as the patient is recovering from surgery. Issues relating to the intraoperative ventilator management of thoracic surgery patients are largely the responsibility of the anesthesiologist and are discussed in detail in Chapter 5. Issues relating to postoperative ventilator management of thoracic surgery patients generally are the responsibility of the thoracic surgeon and intensivist. The information presented in this chapter focuses primarily on this aspect of care of thoracic surgery patients.
As patients transition from the operating room to the recovery room or ICU, it is important to appreciate that general anesthesia and thoracic surgery adversely affect nearly all aspects of respiratory physiology. These changes must be taken into account when planning postoperative ventilator management.
Inhaled anesthetic agents such as halothane, isoflurane, enflurane, and desflurane depress the respiratory drive to varying extents, altering the response to both hypercarbia and hypoxemia.1 These effects can be magnified by the simultaneous use of narcotics, which may be initiated before the effects of halogenated inhaled anesthetics have completely worn off. Thoracic surgery patients may be specifically prone to this complication because preexisting pulmonary disease can result in prolonged retention of inhaled anesthetics as a consequence of gas trapping and nonhomogeneous emptying of diseased regions of lung.2 The combined effects of general anesthesia and thoracic surgery lead to a marked reduction in lung volumes resulting from the development of dependent atelectasis and loss of chest wall tone. Functional residual capacity (FRC) has been shown to decrease by 20–30% as a consequence of anesthesia alone.3 Lung resection and altered chest wall mechanics resulting from the surgical procedure can leave the patient with a loss of 50–60% of FRC of static lung volume at procedure's end. Dynamic lung mechanics also can be adversely affected, particularly during the recovery phase from anesthesia. Airway resistance increases as lung volume is reduced and airway tethering is diminished. During procedures performed with inhaled anesthetics, increases in airway resistance resulting from this effect tend to be offset by the bronchodilatory effects of the halogenated gas.4 On discontinuation of the inhaled agent, these bronchodilatory effects are lost abruptly, although factors promoting increased airway resistance may not have resolved. Thus patients may experience a rather abrupt increase in respiratory system impedance and work of breathing during the recovery phase from anesthesia that can lead to respiratory failure.
Predictably, gas exchange is also adversely affected by the physiologic alterations associated with general anesthesia and thoracic surgery. Supine or lateral positioning is accompanied by preferential perfusion to dependent lung zones.5 In contrast, gas flow is more uniformly distributed in the anesthetized, mechanically ventilated patient, resulting in ventilation/perfusion (V̇/Q̇) mismatching. In most cases, this is of little physiologic consequence and ...