Pulmonary Function After Cardiac and Thoracic Surgery

Perioperative care is undergoing significant change due to clinical advances and economic pressures. As more emphasis is placed on cost-containment and improved efficiency, current practices should be reviewed and critiqued to determine whether they are actually effective. Common problems, such as postoperative pulmonary complications, should be a focus of these efforts because the "bottom line" is to devise methods to reduce these complications and so decrease the costs of medical care. This requires a multifaceted approach that entails a better understanding of the causes of the complications, devising effective treatments and preventive strategies, and performing outcome studies to determine the success of currently used and new procedures. In this review, I examine the pulmonary changes after surgery involving the thoracic cavity and the consequences of modern pain management techniques. Perioperative Respiratory Function: A Brief Overview Surgery and anesthesia alter ventilatory function beginning with the induction of anesthesia and often lasting well into the convalescent period. The most frequent problem after upper abdominal and thoracic surgery is atelectasis, which reduces lung compliance and functional residual capacity. The natural history of postoperative atelectasis is usually one of spontaneous reinflation. However, failure of atelectatic regions to reinflate may lead to pneumonia. Therefore, much effort is directed at preventing and treating postoperative atelectasis, including incentive spirometry, deep breathing exercises, chest physical therapy, and, most importantly, early mobilization. Preoperative Pulmonary Function Testing Identifying patients at increased risk of developing postoperative pulmonary complications should theoretically aid in overall risk assessment and provide an opportunity to optimize pulmonary function before surgery. A critical review of 22 studies found no evidence that routine preoperative spirometry was useful or had any predictive value [1]. This led to recommendations that routine preoperative pulmonary function testing is no more useful in identifying patients at increased risk than a thorough history and physical examination [2]. It is recommended that spirometry be reserved for characterizing the type and severity of pulmonary dysfunction among patients with a history of pulmonary symptoms or tobacco use [2]. Such tests may help to determine whether any observed pulmonary dysfunction is reversed by bronchodilators. One study found that preoperative pulmonary function tests fail to completely predict which patients require extended postoperative mechanical ventilation after cardiac surgery [3]. This is not unexpected, because a major determinant of poor pulmonary outcome after cardiac surgery is poor cardiac function. The exception to these recommendations are patients undergoing lung resection, in which spirometry and arterial blood gas tension determinations are essential for predicting postresection lung function [4]. When there is doubt about the predicted amount of residual postresection function, patients may require further assessment with diffusing capacity, right heart catheterization with temporary unilateral pulmonary artery occlusion, cardiopulmonary exercise testing, quantitative computed tomographic (CT) scanning, or radionuclide quantitative ventilation-perfusion scanning [5,6]. Cardiac Surgery Cardiac surgery by its very nature-median sternotomy, cardiopulmonary bypass (CPB), depressed cardiac function, and manipulation of the thoracic contents-alters pulmonary and cardiac mechanics. Therefore, the pulmonary problems observed after such surgery include those secondary to cardiac dysfunction, e.g., pulmonary edema and congestive heart failure; those due to intrinsic pulmonary problems, such as atelectasis and pneumonia; and those resulting from CPB, specifically the "postpump" lung syndrome. Clinical manifestations span the spectrum from fever and productive cough to respiratory failure requiring prolonged mechanical ventilation. The major determinant of poor pulmonary outcome after cardiac surgery is poor cardiac function [3]. This is not unanticipated, because a low cardiac output state directly and indirectly contributes to varying pulmonary problems. A low cardiac output with increased pulmonary capillary wedge pressure results in increased lung water. Depending on its severity, a spectrum of problems from mild congestive heart failure to overt cardiogenic pulmonary edema may occur (Figure 1). Moreover, the low cardiac output state results in muscle fatigue, leading to weak coughing, reduced mobility, and lack of deep breathing. These may contribute to and worsen atelectasis and increase the possibility of pneumonia.Figure 1: Pulmonary edema after cardiac surgery may be cardiogenic-caused by decreased cardiac output, leading to increased intrapulmonary hydrostatic pressure-or noncardiogenic-caused by increased capillary permeability.The incidence of pneumonia after coronary artery bypass surgery ranges from 3% to 16% and from 5% to 7% after valvular surgery [7,8]. However, lesser complications, such as atelectasis and pleural effusions, occur more frequently. In a large series, 63% of patients had atelectasis and/or pleural effusion detected on postoperative chest radiographs [9]. Left lower lobe atelectasis, the most frequently observed radiological abnormality after cardiac surgery, occurs in 73% of patients after internal mammary artery grafting and in 54% when only vein grafts were used [10]. CT scans of patients with normal chest radiography but reduced oxygenation reveal crescent-shaped bilateral densities in the dependent portions of the lungs consistent with atelectasis. The causes of atelectasis are many (Table 1). Discriminant analysis shows an increase in the severity of atelectasis with a larger number of grafts, longer operative and bypass times, violation of the pleural space, lack of a phrenic nerve insulating pad during surface myocardial cooling, and a lower body temperature during bypass [11].Table 1: Causes of Postcardiac Surgery AtelectasisAfter cardiac surgery, there are decreases in forced vital capacity (FVC), expiratory volume in the first second of forced expiration (FEV1), peak expiratory flow rate (PEFR), and maximum voluntary ventilation (MVV). These changes may persist for >3 mo after surgery [17]. When saphenous vein grafts are used exclusively, Functional Residual Capacity (FRC) and FEV1 decrease less than when an internal mammary artery graft is also used [13]. Pleural changes on chest radiographs after internal mammary artery grafting are associated with larger decreases in pulmonary function than when no pleural changes are noted and when only saphenous veins are used. This has been ascribed to the extensive dissection of the interior portion of the anterior chest wall and violation of the pleural cavity. As expected, there is a greater restrictive defect after bilateral than after unilateral mammary artery harvesting [13]. Median sternotomy alters the spinocostal angles, thus reducing the mobility of the ribs [14]. These structural changes, along with incisional pain, may contribute to a breathing pattern characterized by small tidal volumes and increased respiratory rates. The degree of postoperative diaphragmatic dysfunction is unclear, although elevated diaphragms are seen on chest radiographs in >or=to13% of patients after surgery. Clergue et al. [15] speculated that these diaphragmatic elevations might be due not only to atelectasis, but also to diaphragmatic dysfunction caused by either phrenic nerve damage or reflex-mediated decreases in diaphragmatic function. Phrenic nerve injury most often occurs on the left side, and it is almost always caused by irrigating the pericardial space with cold solution for myocardial preservation during CPB. Electrophysiological evidence of nerve injury is seen in 32% of patients when ice slush is used and in 2%-6% when cold saline is used [16]. The prevalence of clinically significant diaphragmatic dysfunction is 2.1% when the heart is cooled without an insulation pad protecting the phrenic nerve and approximately 0.5% without any topical cooling [17]. It is rarely seen when only intracoronary cardioplegia is used [18]. Although it is often short-lived, diaphragmatic dysfunction may interfere with discontinuation of mechanical ventilation. Unfortunately, in some patients, the dysfunction may persist for >or=to6 mo and interfere with activities of daily living. Rarely, phrenic injury may occur during internal mammary artery harvesting because the nerve crosses the path of the artery on the left side and the two run in parallel on the right side [19]. Despite the high rate of radiographic atelectasis, the incidence of clinically significant pulmonary complications after cardiac surgery is relatively low [7]. This is likely due to early mobilization and pain control. This low incidence and low morbidity of pulmonary complications are reflected by the inability of a randomized study to identify any advantage of adding single-handed percussions to early mobilization and deep breathing exercises after valvular surgery [7]. Similarly, routine physical therapy does not benefit patients after elective coronary artery surgery [20]. There are less common causes of postcardiac surgery respiratory failure. Noncardiogenic pulmonary edema has long been of concern because early CPB techniques were associated with postoperative hypoxemia and noncardiogenic pulmonary edema-post-pump lung. Yet, the incidence of this complication has decreased likely because of changes in techniques, such as the introduction of membrane oxygenators. This was demonstrated by a recent study, which revealed that adult respiratory distress syndrome occurred in only 1% (38 of 3848) of patients after coronary artery bypass and valve replacement surgery [21]. Changes in clinical management have altered the pattern of postoperative complications so that supraventricular arrhythmias (incidence 17%-20%), not serious pulmonary problems, are now the leading cause of postcardiac surgery morbidity [22]. There are a number of causes of hypoxemia after cardiac surgery. The incidence of severe hypoxemia (PaO2 <or=to150 mm Hg) was found by Rady et al. [23] to be 12% in a group of patients without preexisting pulmonary hypertension or obstructive or restrictive lung disease undergoing coronary bypass and valve replacement. Such patients have a higher mortality rate and longer hospital stay. Risk factors for severe hypoxemia include age >75 yr, body mass index >30 kg/m2, mean pulmonary artery pressure >20 mm Hg, reduced stroke volume, decreased serum albumin, a history of cerebrovascular disease, emergency surgery, and extended bypass time [23]. The amount of bilateral dependent atelectasis seen on CT scans correlates with the degree of venous admixture [24]. The hypoxemia is mainly due to increased shunt fraction, although low mixed venous PO2 secondary to reduced cardiac output also is a contributing factor [24]. As expected, patients with left lower lobe atelectasis have lower arterial oxygen tension when placed in the left lateral decubitus position. In a subsequent study, no differences were found between intra- and postoperative intrapulmonary shunt and ventilation-perfusion relationships when patients undergoing coronary bypass and mitral valve replacement were compared. This does not support the hypothesis that patients with mitral valve disease have more intrapulmonary shunting after surgery due to residual lung water from chronically increased preoperative lung water [25]. Zin et al. [26] observed that, before surgery, patients with valvular heart disease had increased lung and respiratory elastances and lung resistance than patients with ischemic disease, probably because of the higher incidence of left ventricular failure in the former group. These differences decreased postoperatively. Long-term respiratory outcome after valve surgery is favorable, as pulmonary function actually improves after surgery. However, after mitral valve surgery, FVC, FEV1, and MVV are all reduced below preoperative levels on discharge from the hospital, and after 3 mo, all increased above preoperative levels, but remained below predicted values [27]. Fast-Tracking The increasing popularity of early postoperative extubation has confirmed the advantages of allowing patients to cough and ambulate soon after surgery. A retrospective matched cohort study demonstrated that patients tracheally extubated early after surgery have significantly less atelectasis than those extubated later. Additionally, on Postoperative Day 5, vital capacity (VC) and FEV1/FVC were increased after early extubation [28]. Fast-tracking is also associated with significantly lower rates of nosocomial pneumonia. In one study, 3.4% of patients <70 yr old and 4.4% of those >70 yr developed pneumonia [29]. Minimally Invasive Cardiac Surgery Minimally invasive cardiac surgery performed through a limited thoracotomy or thorascopically, at times without CPB, has recently been introduced. In a preliminary report, Chitwood et al. [30] reported no cases of pneumonia after video-assisted mitral valve surgery and three cases after sternotomy. After port-access coronary artery bypass with a left mammary artery graft, 3 of 42 patients had pleural effusions and 2 had left lower lobe atelectasis. No prospective randomized study has compared the incidence of pulmonary complications after minimally invasive cardiac surgery with that after sternotomy. Pain Management After cardiac surgery, patients have significant thoracic pain, and patients who underwent coronary artery bypass also have pain in the area of the venous graft harvest. However, it is not surprising that the pain is less than that after upper abdominal surgery and lateral thoracotomy, because median sternotomy does not entail dividing muscles (Table 2). Once the effects of anesthesia dissipate, IV opioids are used most commonly. Until extubation, this tends to be nurse-administered IV morphine, and after extubation, nurse-administered or patient-controlled analgesia are used. Within a day or two, many patients require only oral analgesics, such as oxycodone plus acetaminophen. Yet, several studies have shown that pain relief is often inadequate, a situation especially problematic when early extubation is planned [31].Table 2: Pain Scores After Thoracic SurgeryThe intrathecal administration of morphine before the induction of anesthesia has been used with some success. However, the dose must be small enough not to interfere with early extubation, while providing adequate pain relief. In a prospective, randomized, double-blinded, placebo-controlled trial, the time from intensive care unit (ICU) arrival to extubation was prolonged among patients who received 10 [micro sign]g/kg subarachnoid morphine [32]. Respiratory depression was observed in 1.9% of those receiving 30 [micro sign]g/kg intrathecal morphine [33]. Swenson et al. [34] used small-dose intrathecal morphine (0.5 mg) combined with 50 [micro sign]g of sufentanil, and 8 of their 10 patients were extubated within 8 h of have reported the use of thoracic anesthesia and analgesia the of and postoperative No complications have been and compared with IV extubation was and there were lesser in FEV1 and on the second and after surgery Despite these and analgesia are not used after cardiac surgery because patients usually be with an Thoracic Surgery and Surgery for the of lung is usually performed in patients with varying of lung disease due to Surgery is usually performed a thoracotomy, which is a associated with changes in respiratory function These changes include significant in expiratory FEV1, and The decrease in the volume of lung during surgery patients receiving postoperative is reduced by and mechanical of lung during surgery contribute to atelectasis Additionally, with the of ventilation to the operative lung may atelectasis characterized by increased respiratory and a lack of further atelectasis et al. observed decreased lung compliance after thoracotomy the was that in the after surgery. compliance was also noted to decrease in to the amount of the amount of and the degree of atelectasis. There was an between complications and increased of the likely due to increased secondary to reduced lung Respiratory muscle and expiratory is also reduced after thoracotomy and, along with pain, reduces the of coughing, which is vital in preventing and atelectasis. The in muscle are greater in patients than and of pulmonary blood flow increase shunt to and ventilation-perfusion leading to hypoxemia The of thoracotomy on respiratory and muscle function of the chest wall is because of muscle injury and as well as However, thoracotomy does not change the of the chest wall and to tidal volume The lack of an on chest wall is not but be due to pain relief a normal respiratory the that most thoracotomy are and by the or diaphragmatic dysfunction caused by chest wall et al. observed an increase in respiratory but not tidal volume, after there were of diaphragmatic function but evidence of increased muscle function likely due to expiratory of the abdominal muscles or resistance to lung there were of reduced diaphragmatic Similarly, after pressure to be in et al. found that diaphragmatic was depressed for at after studies decreased of the portion of the which is by However, the is associated with greater tidal and It that surgery above the reduces diaphragmatic function, although not to the degree as upper abdominal surgery. Pulmonary complications are a major cause of morbidity after In a prospective study, et al. reported that respiratory failure developed in 3 of and 3 of was observed in three and no In a on thoracic performed in there was a mortality rate after after were due to pneumonia and respiratory and were due to and The thoracotomy a long that results in pain and muscle after surgery. have developed such as limited and to decrease this cause less in respiratory muscle and than a thoracotomy with of the anterior causes less of a in FEV1 and after surgery than thoracotomy Despite the differences in pulmonary function, there are no differences in either or pulmonary or morbidity between the two with two or three further reduces postoperative and postoperative in pulmonary function. This is confirmed by the that causes less pain, decreases and results in lesser in respiratory muscle and lung volumes compared with thoracotomy When are compared with those performed through there are no differences in postoperative pulmonary function, although there is less This is not because of lung are these reduce the of the that postoperative pain an in reducing postoperative pulmonary function. Similarly, in the diaphragmatic after but this does not into a functional advantage compared with lateral thoracotomy Long-term consequences of pulmonary include the effects of reduced lung FEV1 and are reduced after surgery due to the of lung pain, and atelectasis. the mo, there is in pulmonary function after but not and lung capacity increase as atelectatic and as ventilation-perfusion capacity mo after is from preoperative capacity in most patients, it is reduced by after are observed mo after pulmonary Pain Management thoracotomy is reported to be among the most of because major muscles are and are (Table 2). Additionally, chest are often very this pain is essential for and to and to atelectasis, such as deep breathing exercises and incentive The effects of postoperative pain management techniques after thoracotomy the of analgesia to decrease the incidence of pulmonary complications must be the respiratory effects of The most frequently used is of opioids and a but not all studies have reported that opioids are to IV opioids in postoperative in lung However, these studies small of patients and on analgesia and side effects with respiratory limited to spirometry and blood gas No large randomized study has whether analgesia reduces complications and improves outcome after A that and patients that, compared with opioids reduce the incidence of atelectasis, pulmonary and pulmonary complications Additionally, patients who received had reduced of pulmonary complications compared with The administration of opioids after thoracotomy a because of the to to the upper thoracic without respiratory studies found significant elevations mm Hg) when and morphine were into the This led to the that the dose of morphine be reduced to with these found that the possibility of respiratory depression with opioids is always but the incidence is of patients receiving analgesia with plus or morphine have respiratory rates have found the incidence to be of and opioids are currently such in less respiratory depression is unclear, although they decrease the incidence of In patients, adding to a thoracic does not alter the degree of in FVC, FEV1, or but it reduces the Similarly, adding morphine to a of thoracic does not FEV1, or FVC, is there a in the of the ventilatory to between and in with However, after the is in the group especially are used to These with opioids and have no respiratory include dysfunction and IV is a better for patient-controlled analgesia than adding is also more effective less than nerve with opioids with or without with Although these provide pain it is whether they reduce pulmonary of the is usually performed to either or an are performed an abdominal with or without an or a lateral of whether the chest is there is to the especially when the or is used to the Therefore, the degree of respiratory may be greater than that from the and of the Postoperative respiratory complications in these patients may be due to a number of There may be to lung during surgery, and the may lung especially it The of upper abdominal surgery with its diaphragmatic dysfunction and the pain and muscle secondary to a lateral thoracotomy the that atelectasis complications, such as and may also cause respiratory In one series, pneumonia occurred in 12% of of patients after In study, of were due to pneumonia are often after The introduction of analgesia has early extubation either or soon after the of surgery. In patients who 2 of morphine at and at at the time of the of a of 3 results in extubation than when solution is extubation after is associated with reduced morbidity and decreased of have analgesia with outcome after either patient-controlled or IV morphine have respiratory complications, hospital and complications, as well as lower mortality than those in hospital have been reported among patients who than IV morphine The is by changes in the and function of the respiratory on the induction of and it may be function has been to preoperative This of postcardiac and thoracic surgery and the consequences of modern pain management that much is and many Pain management has long been of the postoperative atelectasis and pneumonia. the evidence is and because most studies small of patients and focus on analgesia and side a have there is more evidence that and pain may reduce morbidity after than after or cardiac surgery. The on evidence is that when in has only a limited to reduce or the postoperative in pulmonary function and may contribute to pulmonary complications by respiratory this is more that not should be used in this There is limited evidence whether the to pain management are The of hospital of of pain relief has been demonstrated in surgery and studies are in cardiac and thoracotomy It is also currently whether analgesia improves and the and of atelectasis and pneumonia with incentive spirometry and deep breathing The be to the of current practices while devising new methods that reduce complications and