Perioperative respiratory physiology

Perioperative

Respiratory Physiology Charles

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OLLOWING SURGERY and anesthesia, major changes in respiratory function occur. The cause of these alterations is multifactorial; anesthesia, postoperative pain, surgical manipulation, and respiratory depression caused by analgesics all appear to contribute. Atelectasis is the most frequently encountered postoperative complication. Failure to prevent or treat atelectasis can lead to pneumonia. Atelectasis is most often seen following upper abdominal and thoracic surgery, but problems are also observed following surgical procedures involving other body regions. The incidence of respiratory complications has changed little over the past 40 years, likely reflecting the increased complexity of operations and the aging of the population.’ There has been a revival of interest in postoperative respiratory function occasioned by two factors. One is the introduction and wide popularity of new analgesic modalities, such as epidural narcotics and patient-controlled analgesia. The other factor is the introduction of the prospective payment hospital reimbursement (DRG) system with resultant pressure to reduce the length of hospital stay. This has made it important to reduce postoperative complications. This review will examine the changes in pulmonary function that occur in the perioperative period. It will focus mainly on the mechanisms that lead to the development of atelectasis in patients receiving general anesthesia. THE INTRAOPERATIVE

PERIOD

The formation of atelectasis appears to begin during the induction of general anesthesia.

From the Departments of Anesthesiology and Medicine, College of Physicians and Surgeons, Columbia University New York, NY. Received March 23, 1991; acceptedApril 16, 1991. Address reprints to Charles Weissman, MD, Department of Anesthesiology College of Physicians and Surgeons, Columbia University, New York, NY 10032. Copyright Q 1991 by W.B. Saunders Company 0883-9441 I92 /0603-0004$05.00/O 160

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Inhalational agents (eg, enflurane, isoflurane, and halothane) and most intravenous agents (eg, barbiturates) used for general anesthesia are implicated in its development. The use of muscle relaxants and the mechanical manipulations that occur during surgery are associated with further loss of lung airspaces.2-4 General anesthesia results in reductions in lung volumes and compliance. The changes are due not only to the supine posture used during most operations. Normally, functional residual capacity (FRC) decreases approximately 1 L when subjects move from the upright to supine position due to cranial displacement of the diaphragm. Induction of anesthesia decreases FRC another 0.5 L.5 This 20% decrease in FRC is seen during both spontaneous ventilation and controlled ventilation with or without neuromuscular blocking agents.6 The magnitude of the reduction in FRC correlates significantly with patient age. It is interesting to note that anesthesia does not appear to change FRC when the subject is sitting.’ The cause of this reduction in FRC is likely multifactorial. Initial ideas that it was due to absorption atelectasis were not substantiated.“.’ Whether the use of an endotracheal tube contributes to the reduction is FRC is unclear since, in one study, the reduction in FRC was not seen when a face mask was used during methohexital anesthesia.‘” This reduction in FRC can be substantial (decreases to 60% to 70% of preoperative levels following upper abdominal surgery) and prolonged (up to 7 to 10 days postoperatively).” Vital capacity (VC), expiratory reserve volume, and maximum inspiratory and expiratory flow rates are also reduced. The cause of the decreased FRC is not yet completely defined. It is associated with other alterations in respiratory function that may be either causes or consequences. These include increased elastic lung recoil” and small airway closure with resultant gas trapping.‘3,*4 In older patients, the FRC is often less than the closing capacity. This is thought to cause airway cloJournalof

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1991: pp 160-171

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sure, collapse of the dependent portions of the lungs, shunting, and arterial hypoxemia.15 Whether the trapping of gas distal to closed airways is a major mechanism for reduction in FRC is unclear.” Dueck et all’ demonstrated that a decrease in FRC to less than the awake closing capacity resulted in a larger shunt (11%) than when FRC was larger than the awake closing capacity (2% shunt). In a later study,” it was found that the degree of shunting was directly proportional to the body mass index and the amount and duration of cigarette smoking. There is still no confirmatory evidence that there is a direct correlation between the degree of airway closure and the magnitude of gas exchange impairment during anesthesia.5”9 Another change in respiratory function observed with the induction of anesthesia is cephalad displacement of the diaphragm at end expiration.20-‘2 This has been reported by Froese and Bryan”” using cineradiography and by others using computed tomography.*‘.*’ Cephalad displacement has been seen in both the supine and prone positions in most of the studied patients.” Associated with this, and likely a contributing cause, is a loss of end-expiratory diaphragmatic tone, as has been reported during anesthesia with halothane in a supine patient..‘j The loss of FRC is thus ascribed partially to the cephalad displacement of the diaphragm. In addition, a reduction in the transverse crosssectional area of the thorax has been observed.“.2’ There is disagreement as to whether there is movement of the blood in or out of the thorax.” Hedenstierna et al in Sweden reported a reduction in thoracic blood volume,” while the group at the Mayo Clinic observed an increase in blood volume.2232’Drummond et a126 failed to find any shifts in central blood volume following induction of anesthesia. The consequence of these changes in pulmonary volumes is atelectasis,‘7 specifically, “compression atelectasis.” Histologic studies of the lungs of anesthetized sheep revealed completely collapsed lung with only moderate vascular congestion and no interstitial edema.” The atelectatic areas corresponded to intrapulmonary densities seen on computed tomograms. These densities, which occur in the dependent areas of the lungs, have also been seen in spontaneously breathing humans following the

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induction of atelectasis. Further increases in the atelectasis were seen after subsequent neuromuscular blockade.2y The type of anesthetic used, inhalation agent (halothane) or intravenous agent (barbiturate), did not influence the size of the atelectatic areas. However, ketamine failed to produce atelectasis, yet, with subsequent neuromuscular blockade, atelectasis occurred.” Turning anesthetized subjects from the supine to lateral position caused densities to remain in the same anatomic positions, suggesting that the densities were not composed of pleural or interstitial fluid. The application of a positive-end expiratory pressure (PEEP) of 10 cm H,O reduced or eliminated the densities that rapidly returned on discontinuation of PEEP.“’ In a recent study, Gunnarsson et a13’ observed that with enflurane/nitrous oxide/ oxygen anesthesia, shunt increased and there was a parallel decrease in the perfusion of low V/Q areas after 90 minutes of anesthesia. This was not seen when nitrogen was substituted for the nitrous oxide. The increase in atelectasis with nitrous oxide was ascribed to absorption of trapped gas. The investigators speculated that initially there is compression atelectasis followed by absorption atelectasis? In the lateral position, there is a decrease in the transverse and an increase in the sagittal diameters of the lung. The vertical height also decreases. The dimensions of the dependent lung decreases more than those of the nondependent one, a situation that was reversed by applying PEEP to the dependent lung. After induction of anesthesia, atelectasis was found in the dependent, but not in the nondependent, lung. Turning the subject supine did not change the distribution of atelectasis. Induction of anesthesia in the supine position and then turning subjects laterally resulted in atelectasis shifting to the dependent lung. Positive end-expiratory pressure eliminated the atelectasis. During anesthesia, arterial oxygenation is impaired during both spontaneous and controlled ventilation.i3~35 Cigarette smokers, the elderly, and the obese have increased degrees of hypoxemia.‘7.3h Ventilation/perfusion mismatch along with increased shunting contribute to the lowered PaOz. Shunt fractions of 20% are commonplace, caused by areas of atelectasisZx~” In younger and middle-aged patients, the hypox-

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emia can be ascribed to shunting, while in older patients V/Q mismatch may also play a ro1e.38 The degree of density on computed tomography scans is directly correlated with the shunt but not with V/Q inequality.37 The degree of V/Q mismatch may be minimized in atelectatic areas by diversion of blood flow to areas of normal lung. This is due to increased vascular resistance caused by hypoxic pulmonary vasoconstriction and mechanical collapse of blood vessels. Vasodilating anesthetics, such as isoflurane, may abrogate the vasoconstriction. There is a strong positive relationship between the magnitude of the shunt and the area of atelectasis.3y Ketamine that does not cause atelectasis does not increase the shunt fraction. With ketamine anesthesia, the shunt fraction increased only following the administration of a neuromuscular blocking agent that caused atelectasis.30 Positive end-expiratory pressure decreased atelectasis but not hypoxemia. This is likely because of a decrease in cardiac output with a resultant reduction in mixed venous oxygen content. The increase in shunt appears related to anesthesia and not mechanical ventilation or muscle paralysis. In addition to increased shunting there is an increase in dead space, with the physiologic exceeding the anatomic dead space.4o During anesthesia, the physiologic dead space to tidal volume ratio distal to the carina has been reported as averaging 0.32 during both spontaneous and artificial ventilation.41 Endotracheal tubes and masks all increase dead space. Therefore, during anesthesia, tidal volume needs to be increased. The cause of the increased dead space is unclear. One possibility is the establishment of areas with high ventilation to perfusion ratios, another is decreased perfusion of zone 1 lung areas due to decreased cardiac output. The latter is caused by anesthetic agents such as barbiturates and halothane. The increased dead space, along with a reduced ventilatory response to carbon dioxide, contributes to elevated arterial PaCO, in spontaneously breathing anesthetized patients. It is well recognized that almost all anesthetic agents depress the PaCO, minute ventilation response in a dose-dependent fashion. Doses as small as 0.1 minimal alveolar concentration of enflurane or halothane reduce the response to CO, and acidemia. With halogenated inhalation anesthet-

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ics (halothane, enflurane, isoflurane), almost all responses to CO, are abolished at twice minimal alveolar concentration.42’43 Benzodiazepines and narcotics also decrease the response to carbon dioxide. The mechanism of this decreased response is likely due to effects on the central respiratory mechanisms, although Tusiewicz et al4 proposed that inactivation of the intercostal muscles during anesthesia may also play a role in the decreased response to hypercapnia. The increase in PaCO, seen with anesthesia often disappears with the increase in minute ventilation that occurs with surgical stimulation.45’46 The widespread use of muscle relaxants has made it necessary to mechanically ventilate almost all anesthetized patients, thus negating the respiratory depressant effects of the anesthetic agents. Anesthesia coupled with intraoperative manipulations results in many patients showing signs of altered pulmonary function in the immediate postoperative period. Retraction of abdominal organs against the diaphragm during upper abdominal surgery and collapse and manipulation of pulmonary parenchyma during thoracic surgery all contribute to atelectasis. THE POSTOPERATIVE

PERIOD

The postoperative period is marked by significant respiratory problems. The incidence of severe pulmonary complications requiring major interventions range from 13% for elective surgery to 10% for emergency surgery.47 The incidence is higher following upper abdominal and thoracic surgery. Subclinical pulmonary changes are much more frequent. These alterations include radiographic evidence of atelectasis, pleural effusions, coughing, and fever. The incidence of such changes after upper abdominal surgery has been reported to be as high as 75%, with rates of over 80% reported after cardiac surgery.4x Celli et a14” reported that without prophylactic therapy there was a 48% incidence after upper abdominal surgery. The incidence is lower with surgery to the lower abdomen and extremities. Multiple therapeutic and prophylactic modalities have been used to reduce such complications. The respiratory problems in the postoperative period can be caused by the residual effects of general anesthesia and/or respiratory dysfunc-

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tion due to the surgery itself. The former is usually short-lived, while the latter can last for days. Arterial hypoxemia and hypercarbia are observed immediately following anesthesia and surgery. The increased use of pulse oximetry in the operating room, during transport to the recovery room, and in the recovery room has highlighted the rather high incidence of occult hypoxemia.“‘~s’ The cause of this hypoxemia and hypercapnia is often multifactorial. Residual general anesthesia causes alveolar hypoventilation, depressed ventilatory drive, and depressed cardiac output. The emergence from anesthesia causes diffusion hypoxia as anesthetic gases are excreted. This is often short-lived.” As metabolic rate increases during emergence, there is increased carbon dioxide production and oxygen consumption. Such increases are also observed during the shivering seen with emergence from general inhalation anesthetics and during rewarming from intraoperative hypothermia. When this occurs in the face of a fixed or reduced minute ventilation, hypoxemia and hypercapnia may occur. Pain can also cause alveolar hypoventilation. The administration of narcotic analgesics to patients with residual anesthetic agents can cause respiratory depression leading to hypercapnia, bradypnea, and, in extreme cases, apnea. This period lasts only a few hours until patients eliminate and metabolize the anesthetic agents, rewarm to normothermia, and have their pain controlled. Hypoxemia is rather common so that treatment with oxygen is indicated, as is monitoring with a pulse oximeter.” Risk factors for hypoxemia include duration of anesthesia, age, and a history of cigarette smoking. Following superficial or extremity surgery, lung volumes and arterial PaO, return to preoperative levels within approximately 24 hours.54 However, respiratory abnormalities can persist longer following upper abdominal surgery and thoracotomy. These patients often have arterial hypoxemia without hypercarbia. Major abnormalities of respiratory function are also observed. There has been much study of the changes in static lung volumes after upper abdominal surgery. Immediately following surgery, VC is approximately 40% of preoperative values and remains depressed for 10 to 14

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days.5’ Functional residual capacity is similarly depressed and is often only 70% of preoperative values. Functional residual capacity may fall below the closing capacity. In general, postoperative hypoxemia parallels changes in FRC. The magnitude of the percent decrease in FRC is inversely correlated with the degree of hypoxemia.‘5 Lower abdominal surgery causes less of a reduction in FRC and VC.” Factors other than operative site implicated as affecting lung volumes include incision type (eg, subcostal v midline),” age,55 length of surgery,” pain,” and abdominal distension.54 During upper abdominal surgery, a variety of factors cause a decrease in FRC. These include decreased movement and tone of the chest wall, cephalad movement of the diaphragm, pressure placed on the diaphragm by abdominal retractors or packing, and reduced sputum clearance caused by decreased mucocilliary function.‘” The atelectic areas seen on computed tomography scans during surgery are also present in the first postoperative hour.29 In addition to a reduction in lung volumes, forced expiratory volume in 1 second (FEV,) and maximal inspiratory and expiratory pressures are reduced postoperatively. This leads to ineffective coughing. Respiratory patterns following upper abdominal surgery are characterized by increased breathing frequency and often by reduced tidal volume. This shallow breathing pattern, along with an absence of sighs, likely contributes to atelectasis formation. During the first few postoperative hours, there is little or no further change in pulmonary static pressure-volume relationships or dynamic compliance. Functional residual capacity further decreases only minimally in the first few hours immediately following the completion of surgery, but it begins to decrease significantly over the ensuing hours, reaching its nadir approximately 16 to 24 hours after surgery. This progressive decrease in FRC is associated with a further reduction in compliance due to collapse of air spaces. A major contributor to lung volume changes after upper abdominal surgery is thought to be alterations in breathing patterns, specifically, an increase in respiratory rate, a decrease in tidal volume, and an absence of sighs. In the postoperative period following cholecystectomy, there is also a marked reduc-

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tion in the ratio of abdominal to rib cage motion.59@ This decrease in abdominal motion has been ascribed by most investigators to diaphragmatic dysfunction.59’60 This altered respiratory pattern persists for as long as 10 postoperative days and was not reduced by postoperative epidural fentanyhs9 a narcotic, but was attenuated by thoracic epidural blockade with bupivacaine,6’ a local anesthetic. The use of thoracic epidural blockade likely decreased afferent input from the upper abdomen and/or prevented the intercostal muscles from functioning, necessitating abdominal/diaphragmatic motion to survive. This diaphragmatic dysfunction is thought not to be due to alterations of the contractile properties of the muscle, but to reflexes arising from the chest wall, esophagus, or upper abdomen, since no loss of diaphragmatic strength was observed during direct phrenic stimulation.62 Road et aP demonstrated in dogs that lower abdominal surgery, as well as anesthesia alone, does not change diaphragmatic function, while upper abdominal surgery and isolated stimulation of the gallbladder bed had marked effects. Ford et al&l found that in anesthetized (halothane/nitrous oxide), spontaneously breathing dogs, traction or compression of the gallbladder for 30 seconds caused many of the respiratory changes seen in the postoperative period. These included decreases in tidal volume, diaphragmatic electromyographic output, and transdiaphragmatic pressures. Vagotomy did not change these findings. Similar alterations in diaphragmatic function following upper abdominal surgery have been observed in humans. The cause of this dysfunction is thought to be reflex in nature whereby peritoneal and diaphragmatic receptors59’62stimulated during abdominal surgery may provoke the activation of a central neural mechanism that inhibits phrenic nerve output. This reflex can be overcome voluntarily simply by asking a patient to switch from predominant thoracic to abdominal motion, as was recently demonstrated by Chuter et al.65 The degree of impaired diaphragmatic function correlates well with a reduction in VC. In addition to decreased diaphragmatic excursions, the reduction in movement of the abdominal compartment following surgery may be due to alterations in the function of the abdominal muscles. Duggan and

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Drummond66 noted that there was a progressive increase in the electromyographic activity of abdominal external oblique and lower intercostal muscles during expiration 3 and 24 hours after elective gastric or biliary surgery. This was followed by an abrupt decrease in tone with the onset of inspiration. These investigators correlated their findings with simultaneous recordings of intragastric pressure and questioned whether the decreased abdominal motion was actually due to diaphragmatic dysfunction; they instead proposed that it was due to a loss of abdominal tone on inspiration, making the mechanical coupling of diaphragmatic contraction to lower rib cage movement less efficient.(j’ Raimbult et aP found an increase in abdominal tone, 2 hours, but not 4 hours, following surgery. They ascribed this increased tone to the residual effects of fentanyl that were no longer present 4 hours postoperatively. These investigators thus ascribed the reduced abdominal compartmental motion to diaphragmatic problems.” Dureuil et a169 also failed to observe abdominal muscle activity on the first day after upper abdominal surgery. Others have proposed that pain-induced tonic contraction of the abdominal musculature may cause diaphragmatic displacement into the chest, compressing the lower lobes and reducing lung volume further.” Animal studies have demonstrated that besides reduced diaphragmatic excursions, expiration following surgery involves the active use of muscles, which likely contributes to the lowering of FRC.” Surgical division of the abdominal muscles coupled with pain inhibits the proper function of these muscles, which may reduce abdominal motion and reduce lung volumes.” After laparotomy in dogs, Farkas and deTroyer73 observed inhibition of the transversus abdominus and maintained expiratory activation of the external oblique muscles. The inhibition of transverse muscle activity may decrease expiratory muscle strength, thus impairing coughing ability. Diaphragmatic dysfunction, along with reduced coughing ability, may lead to an increase in atelectasis in the dependent areas. The administration of aminophylline 6 hours after surgery further decreased the transdiaphragmatic pressure seen following surgery.74 This is likely due to stimulation of respiratory drive and/or improvement in diaphrag-

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matic muscle activity. It is clear that further study of respiratory patterns and respiratory muscle function following upper abdominal surgery is needed to elucidate the contributions of the abdominal musculature and the diaphragm. It is likely that the reduced abdominal motion may be due to a number of interrelated factors, including diaphragmatic dysfunction, altered rib cage-abdominal coupling, and changes in abdominal muscle function. Although much has been written about the pathologic changes seen in the respiratory pattern following abdominal surgery, less has been written about what occurs following surgery to the chest. This is despite the fact that patients undergoing chest surgery have numbers of incidences of pulmonary complications higher or equal to those seen after abdominal surgery. Following thoracic surgery for parenchymal resection, patients experience much pain and marked changes in respiratory function.“-” There are significant decreases in maximum expiratory force, VC, FEV,, and peak expiratory flow rate.5J.77.X” The decreases in VC exceed the volume of lung removed at surgery. Persistent intrapleural air spaces, pneumothorax, and mechanical compression during surgery contribute to atelectasis. Breathing pattern may be characterized by shallow breathing, increased respiratory rate, and a lack of sighs.“’ Karlson et al” observed decreased compliance immediately following thoracotomy (while the patient was still anesthetized) that resolved in the weeks following surgery. An association between increased work of breathing and postthoracotomy complications has been reported. The increased work of breathing is likely due to increased elastic work, which increases as lung compliance decreases in proportion to the amount of tissue removed,8’ and to increased airway secretions and atelectasis.% Malmkvist et alXc observed that following thoracotomy for localized pulmonary lesions, the compliance of the operated side was significantly reduced at the end of the procedure. Also, on the operated side, CO, elimination was reduced compared to preprocedure values, likely reflecting reduced perfusion to the operated lung. The effect of thoracotomy on respiratory patterns and respiratory muscle function is still not clear. One would expect less motion of the chest wall likely

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caused by pain.‘” Interestingly, with morphine analgesia there is little change in the relative contributions of the chest wall and abdomen.” Maeda et al,” using a mouthpiece, observed an increase in respiratory rate following thoracotomy but no significant change in tidal volume. They also observed no change in transdiaphragmatic pressure during quiet breathing, suggesting preserved diaphragmatic breathing. However, there was an increase in the esophageal pressure and a decrease in APablAPga, suggesting an increase in intercostal/accessory muscle function. Maximal transdiaphragmatic pressures were reduced postoperatively while the maximal inspiratory mouth pressure was not, suggesting that maximal diaphragmatic strength may be reduced. Phrenic nerve function is not altered by 1obectomyXX or pneumonectomy.” Torres et al,” using sonomicrometry crystals in sheep, found that diaphragmatic shortening was depressed for at least 4 weeks following thoracotomy. More study is needed to examine these issues in humans. There has been much interest in pulmonary mechanics after cardiac surgery both because of the high incidence of atelectasis and the occurrence of phrenic nerve problems. Left lower lobe atelectasis with or without elevation of the left diaphragm are the most frequently observed radiologic abnormalities. Cardiac surgery is usually performed using a median sternotomy. Braun et alyl found significant reductions in VC, total lung capacity, inspiratory capacity, and FRC in patients undergoing saphenous vein coronary artery bypass grafting. These changes were observed as long as 4 months after the procedure. Jenkins et aly2 observed that FRC was 61% of preoperative levels on the second postoperative day and had returned to 76% by the fifth day. When saphenous vein grafts were used exclusively, there was less of a decrease in forced VC and FEV, than when an internal mammary artery graft was also used.y1.Y4Why this is so is not immediately apparent, but may be due to the extensive dissection on the interior portion of the anterior chest wall that may include entering the pleural cavity. Zin et al” observed that preoperatively patients with valvular disease had higher lung and respiratory elastances and lung resistance than patients with ischemic heart disease. Postoperatively,

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these differences decreased. Surgery substantially increased the chest wall resistance and the elastance of the respiratory system, both not unexpected findings given the major disruption of the chest cage. Discriminant analysis showed an increase in the severity of atelectasis with a larger number of grafts, longer operative and bypass times, when the pleural space was entered, when a right atria1 drain and phrenic nerve insulating pad were not used, and with a lower body temperature.” Development of atelectasis is also likely related to poor postoperative coughing, lack of deep inspirations, gastric distension, and direct injury to the left lower lobe due to lung retraction during surgery. Increased interstitial lung water may also contribute to the atelectasis. As expected, patients with left lower lobe atelectasis following cardiac surgery have lower arterial oxygenation when placed in the left lateral decubitus position.“’ A major concern in cardiac surgery is phrenic nerve injury. This most affects the left phrenic nerve, causing paralysis or paresis of the left diaphragm with resultant left lower lobe atelectasis.y8,” The cause of this injury is generally thought to be cold injury of the phrenic nerve secondary to topical cooling of the heart with solutions having temperatures close to 0°C. Incidences as high as 55% to 64% have been reported. The use of a shield to protect the phrenic nerve has been found to decrease the incidence.“’ There is a progressive decline in conduction velocity when the nerve is cooled below 17°C with complete blockade of neural conduction below 5°C. Usually there is complete recovery with rewarming. However, at times there is injury to the phrenic nerve characterized histologically by axonal degeneration of the larger myelinated fibers and paranodal demyelination. Phrenic nerve damage does not explain the high incidence of left lower lobe atelectasis observed following cardiac sursince significant collapse is also seen in geryy96.10’ patients without evidence of nerve damage. ANALGESIA

The management of postoperative atelectasis involves the administration of pain medication, breathing maneuvers designed to increase lung volume, and early mobilization. The aim of

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analgesia, besides patient comfort, is to prevent “splinting” of the rib cage secondary to pain. Narcotics are the most commonly used postoperative analgesics. Yet these drugs are themselves respiratory depressants that cause doserelated decreases in minute ventilation (primarily by decreasing breathing frequency), reduced sighing, and depression of the ventilatory response to carbon dioxide. Rigg and Rondi”’ observed that following the administration of intravenous morphine, normal subjects had decreased mean inspiratory duty cycles and decreased rib cage, but not abdominal, motion. When breathing room air and rebreathing CO,, there is an even greater depression in the response to CO, in patients asleep following morphine administration.“’ Mankikian et al”” observed decreases in minute ventilation, tidal volume (but not frequency), and rib cage contribution 60 minutes after 200 kg of epidural fentanyl had been administered to patients following knee surgery. Intrathecal morphine administered after upper abdominal surgery decreased pain, depressed the ventilatory response to CO,, and did not abolish the shallow (depressed tidal volume) breathing pattern.‘“’ Similarly, the administration of epidural fentanyl failed to reverse the decrease in abdominal motion following upper abdominal surgery.5” Most problematic is the observation that postoperative patients receiving narcotics have apneic episodes.‘” Postoperative pain relief with narcotics thus involves titrating pain relief versus respiratory depression in patients with major underlying alterations in respiratory function. Local anesthetics can also be used to reduce postoperative pain. They can be administered into the area of the incision or via the epidural, intrathecal, or intrapleural routes. Spence and Smith’“’ observed better oxygenation and alveolar-arterial differences in patients given continuous extradural thoracic bupivacaine after gastric surgery than in patients given on-demand intravenous morphine. Similar observations have been made after cholecystectomy.‘“* Others have found that excellent pain relief from epidural local anesthetic analgesia resulted in only partial restoration of VC with only minimal improvement in FRC.‘“9 When epidural analgesia was compared with the systemic administration of analgesics, VC was 15% to 20% higher with

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the former; FEV, also increased.“O-“’ Local anesthetics administered through intercostal catheters to patients after cholecystectomy attenuated the postoperative decreases in forced VC, FEV,, and peak expiratory force, unlike patients given intramuscular narcotics.1’3 More study of the effects of analgesia on respiratory function in the postoperative period is needed. Ideally, an analgesic regimen should provide long-term pain relief while causing minimal respiratory compromise. It is unclear whether the apneic episodes observed in the postoperative period in patients receiving narcotic analgesia contribute to the incidence of atelectasis. Alternately, it needs to be determined if analgesics permit the effective use of prophylactic therapies, such as deep breathing exercises and incentive spirometry. There has been some interest in using pharmacologic agents to improve postoperative pulmonary function. Dureuil et a174 observed increased diaphragmatic contractile force after aminophylline administration to patients 4 to 5 hours after upper abdominal surgery. Doxapram has been reported to increase tidal volume and arterial oxygenation following abdominal surgery in some,“4-“h but not all, studies. Whether it reduces postoperative complications is still an area of controversy.‘17~‘2’ Routine care following upper abdominal surgery and thoracotomy includes prophylactic maneuvers aimed at decreasing the severity of atelectasis.“’ These maneuvers aim to expand the lung by increasing intrathoracic lung volume. Segmental and lobar atelectasis respond to such maneuvers because of collateral ventilation and segmental interdependence of the lung. The aim is to have the patients inspire maximally and then hold their breath for as long as possible at the end of inspiration. This end-inspiratory pause is thought to enhance collateral ventilation through the pores of Kahn, the interbronchiolar channels of Martin, and the alveolar-bronchiolar channel of Lambers.‘22 In humans, the time constant for collateral ventilation is approximately 5.7 seconds or greater for a 60% reduction in intersegmental pressure differences during breath holding.123 It appears that the expansion of the lung with adequate time for collateral ventilation permits re-expansion of lobar atelectasis.‘z4 Breath hold-

ing at end-inspiration for 6 seconds results in “stress relaxation” of the lung whereby a lower transpulmonary pressure is needed to maintain the same degree of inflation.“” Sequential deepbreathing maneuvers further enhance stress relaxation. It has been demonstrated that after periods of shallow breathing, a series of deep breaths increase lung compliance and reduce the alveolar-arterial oxygen gradient.1”‘.“h.“7 Recent studies have advocated the use of breath stacking during postoperative incentive spirometry maneuvers to increase the depth and duration of lung expansion.“’ To prevent and treat pulmonary complications of surgery, chest physical therapy, deep breathing exercises, incentive spirometry, and intermittent positive-pressure breathing have all been used. A number of studies’“’ have demonstrated that such therapy, by encouraging lung expansion, can substantially reduce the incidence of such complications. Incentive spirometry and deep breathing exercises are commonly used, while intermittent positivepressure breathing has become less popular because of evidence that it may not be as effective as other treatments and that it results in complications such as abdominal distension,‘2y a fall in PaC02, and hyperventilation. Celli et al”’ found that incentive spirometry decreased clinical and subclinical atelectasis from 48% to 21%. Others’j” have failed to find any advantage to incentive spirometry following elective cholecystectomy. Another modality that has been endeavored is continuous positive airway pressure, administered by mask. It is a passive way of increasing FRC, unlike incentive spirometry, which requires inspiratory effort and large breaths.13’ The disadvantages of mask continuous positive airway pressure is that it requires the use of a tight-fitting mask and that it is only effective in maintaining the increased FRC, if worn continuously.‘“’ Whether intermittent use of a continuous positive airway pressure mask is useful needs further investigation. Continuous positive airway pressure delivered by nasal mask has also been used to decrease atelectasis after coronary artery bypass surgery. 13j The usefulness of these modalities in reducing respiratory complications is the subject of much debate. It needs to be determined whether it is just the encouragement to take

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deep breaths that is important or whether the various maneuvers actually improve regional ventilation, especially to the lower lobes, the area of most atelectasis. CONCLUSION

Upper abdominal and thoracic surgical procedures frequently result in the development of atelectasis. The initiation of general anesthesia along with intraoperative manipulations begins the chain of events causing the collapse of lung parenchyma that continues into the postoperative period. In the postoperative period, shallow breaths, an absence of sighs, and apneic periods secondary to narcotics all work to further increase the extent of collapse. The worst lung function is therefore found on the first postoperative day, not immediately following the comple-

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tion of surgery. It appears that the atelectasis begins to disappear only when the abnormalities of rib cage and abdominal movement begin to abate, the amount of narcotic administered begins to decrease, and the patient gets out of bed to exercise. Prophylactic therapies such as deep breathing exercises and incentive spirometry decrease the incidence of atelectasis but fail to entirely eliminate this problem. Further understanding of the mechanisms that cause these problems may permit the development of a more focused approach to further reducing postoperative respiratory complications. The introduction of analgesic drugs without respiratory depressant activity along with improved and selective regional analgesic techniques may help decrease the incidence of respiratory changes after surgery.

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