Aggressive pulmonary toilet, including incentive spirometry, chest physical therapy, and continuous positive airway pressure devices, reduced the risk of perioperative pulmonary complications in patients undergoing upper abdominal surgery, many of which can be instituted preoperatively (237).
Atelectasis accounts for more than 90% of all postoperative pulmonary complications. The pathophysiology involves a collapse of the alveoli, resulting in ventilation-perfusion mismatching, intrapulmonary venous shunting, and a subsequent drop in the PaO2. Collapsed alveoli are susceptible to superimposed infection, and if managed improperly, atelectasis will progress to pneumonia. Patients with atelectasis have a decreased FRC as well as decreased lung compliance, resulting in increased work during breathing. Despite the decrease in PaO2, the partial pressure of carbon dioxide (PCO2) remains unaffected unless atelectatic changes progress to large volumes of the lung or preexisting lung disease is present.
Physical findings associated with atelectasis may include a low-grade fever. Auscultation of the chest may reveal decreased breath sounds at the bases or dry rales upon inspiration. Percussion of the posterior thorax may suggest elevation of the diaphragm. Radiologic findings include the presence of horizontal lines or plates on posteroanterior chest x-rays, occasionally with adjacent areas containing hyperinﬂation. These changes are most pronounced during the first 3 postoperative days.
Therapy for atelectasis should be aimed at expanding the alveoli and increasing the FRC. The most important maneuvers are those that promote maximal inspiratory pressure, which is maintained for as long as possible. This exercise promotes an expansion of the alveoli and secretion of surfactant, which stabilizes alveoli. It can be achieved with aggressive supervised use of incentive spirometry, deep breathing exercises, coughing, and in some cases, the use of positive expiratory pressure with a mask (continuous positive airway pressure). Oversedation should be avoided, and patients should be encouraged to ambulate and change positions frequently. Fiberoptic bronchoscopy for removal of mucopurulent plugs should be reserved for patients who fail to improve with the usual measures.
Cardiogenic pulmonary edema can result from myocardial ischemia, myocardial infarction, or from intravascular volume overload, particularly in patients who have low cardiac reserve or renal failure. The process usually begins with an increase in the ﬂuid in the alveolar septa and bronchial vascular cuffs, ultimately seeping into the alveoli. Complete filling of the alveoli impairs secretion and production of surfactant. Concomitant with alveolar ﬂooding, there is a decrease in lung compliance, impairment of the oxygen diffusion capacity, and an increase in the arteriolar–alveolar oxygen gradient. Ventilation-perfusion mismatching in the lung results in a decrease in the PaO2, resulting eventually in decreased oxygenation of the tissues and impairment of cardiac contractility.
Symptoms may include tachypnea, dyspnea, wheezing, and use of the accessory muscles of respiration. Clinical signs may include distention of the jugular veins, peripheral edema, rales upon auscultation of the lungs, and an enlarged heart. Radiographic findings may include the presence of bronchiolar cuffing and increased interstitial ﬂuid markings extending to the periphery of the lung. The diagnosis can be confirmed with the use of central hemodynamic monitoring, which will denote an elevated central venous pressure and, more specifically, an elevation in the pulmonary capillary wedge pressure.