Adult Chest Surgery

Chapter 7. Mechanical Ventilation

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 (/) mismatching. In most cases, this is of little physiologic consequence and is easily managed by increasing the inspiratory oxygen content (FIO2). In those instances where more extensive dependent adsorption atelectasis has occurred during surgery or there is significant preexisting lung disease, the adverse consequences of anesthesia and thoracic surgery on gas exchange can be more pronounced, resulting in significant hypoxemia owing to the combined effects of / mismatching and intrapulmonary shunting.

General anesthesia is also accompanied by an increase in overall respiratory dead space despite the decrease in anatomic dead space that accompanies endotracheal tube intubation.6 Physiologic dead space increases by 40–50% as a consequence of the / mismatching that results from general anesthesia but is easily compensated for by increasing the minute ventilation. However, such changes may be associated with increased minute ventilation demands postoperatively, which may delay extubation in the patient with preexisting borderline respiratory function.


The approach to mechanical ventilation in the postoperative thoracic surgery patient is generally similar to that used in the critically ill medical patient. Occasionally, preexisting lung disease, intraoperative complications, or known physiologic alterations associated with a planned surgery require more innovative approaches.

Mechanical ventilator strategies for supporting thoracic surgery patients can be grouped into three basic categories:

1.     Those used to support postoperative patients who are kept intubated after surgery for a specific indication that is expected to resolve within hours, allowing for rapid discontinuation of ventilator support

2.     Those used to support patients who develop hypoxic or hypercarbic respiratory failure as a consequence of a primary process that will resolve over a period of days to weeks and will require longer periods of ventilator support and gradual weaning

3.     Those used to support patients with unique problems or complications that involve unconventional treatment approaches


In most patients, the physiologic alterations caused by anesthesia and thoracic surgery are well-tolerated. These patients generally have minimal to mild preexisting pulmonary disease and are either extubated in the operating room or arrive in the postoperative recovery area or ICU with normal PaO2 and PaCO2 blood gas values on minimal ventilator support, ready for extubation. Successful extubation in this group is associated with the following:

1.     Intact mental status

2.     Reasonable assurance that the patient will have the ability to cough and protect his or her airway

3.     Initiation of an analgesic protocol that optimizes respiratory mechanics without causing undue respiratory depression

While mental status is usually simple to assess, it is often not possible to confirm intact recurrent laryngeal nerve function through the ability to cough and swallow secretions before attempting extubation. The risk of injury to the recurrent laryngeal nerve is increased in the thoracic surgery population because many procedures involve anatomic dissection or traction on the structures near the left main stem bronchus where this nerve branches from the vagus.7 Postextubation evaluation revealing a weak voice and ineffective cough should prompt direct laryngoscopic evaluation of the hypopharynx and vocal cords, followed by vocal cord medialization if indicated.8

Several factors contribute to respiratory muscle dysfunction after thoracic surgery. Pain is a major contributor, and thus selection of an appropriate analgesic regimen is essential for preventing postoperative respiratory failure.9 Studies of respiratory muscle function also have demonstrated that diaphragmatic contractility is compromised by somatic reflex inhibition of the phrenic nerve as a consequence of afferent intercostal stimulation.10Thus analgesic regimens that address both these factors should provide optimal management. Epidural anesthesia with local anesthetic agents (i.e., bupivacaine) accomplishes this objective and can be administered either alone or in combination with opioids. Systemic opioids administered as continuous infusions or using a patient-controlled anesthesia protocol also can be effective but theoretically may be less so because they are associated with a greater degree of respiratory depression and do not suppress reflex phrenic nerve inhibition.11


A substantial number of patients undergoing thoracic surgery will require ventilator support postoperatively. A successful ventilator strategy for longer-term management involves the following general principles:

1.     Selection of a mode of ventilator that prevents high airway pressures and optimizes patient-ventilator synchrony

2.     Early weaning of FIO2 to prevent adsorption atelectasis and limit possible oxygen toxicity, especially in patients receiving medications that have been associated with free-radical lung injury (e.g., amiodarone and bleomycin)

3.     Selection of an appropriate sedation/analgesia regimen to ensure patient comfort while permitting periodic assessments of mental status and respiratory function

4.     Initiation of nutritional support and deep venous thrombosis prophylaxis

5.     Close monitoring of intravascular fluid status to prevent development of pulmonary edema, especially in areas of lung tissue that have been manipulated during surgery

No guidelines exist for selecting a "single best" mode of ventilation for the postoperative thoracic surgery patient. Anecdotal experiences indicate that many surgeons select pressure-control modes of ventilation in which the user-specified independent variable is airway pressure rather than tidal volume. This ensures that airway pressures will not exceed a known value, limiting stress on newly created staple or suture lines. There are no data to indicate that this approach improves respiratory physiology or ICU outcomes in this patient population.12 Furthermore, appropriate selection of ventilator parameters using volume-cycled modes can ensure equivalent limiting of airway pressures. Thus, in most instances, user preference and experience will dictate ventilator settings.

When choosing ventilator settings for a patient, the mode specifically refers to the manner in which ventilator breaths are triggered, cycled, and limited. The trigger, either an inspiratory effort or a time-based signal, defines what the ventilator senses to initiate an assisted breath. Cycle refers to the factors that determine the end of inspiration. For example, in volume-cycled ventilation, inspiration ends when a specific tidal volume is delivered to the patient. Other types of cycling include pressure cycling, time cycling, and flow cycling. Limiting factors are operator-specified values, such as airway pressure, that are monitored by transducers internal to the ventilator circuit throughout the respiratory cycle; if the specified values are exceeded, inspiratory flow is immediately stopped, and the ventilator circuit is vented to atmospheric pressure or the specified positive end-expiratory pressure (PEEP).

Commonly used modes available on most commercial ventilators include assist/control, synchronized intermittent mandatory ventilation, continuous positive airway pressure, pressure-control ventilation (PSV), and pressure-support ventilation. Setup and operation of these modes are described below.


In assist/control mode ventilation (ACMV), an inspiratory cycle is initiated either by the patient's breathing effort or, if no patient effort is detected within a specified time window, by a timer signal within the ventilator based on user-specified parameters. Every breath delivered, whether patient- or timer-triggered, consists of the operator-specified tidal volume. Ventilatory rate is determined either by the patient or by the operator-specified backup rate, whichever is of higher frequency (Fig. 7-1). ACMV is used commonly for initiation of mechanical ventilation because it ensures a backup minute ventilation in the absence of an intact respiratory drive and allows for synchronization of the ventilator cycle with the patient's inspiratory effort.

Figure 7-1.


Assist/control mode ventilation (ACMV) airway pressure and delivered tidal volume profiles. In ACMV ventilation, two types of breaths can occur. Assisted breaths are initiated by the patient and are fully supported by the ventilator, which delivers a user-specified tidal volume. Ventilator-controlled breaths are initiated by the ventilator at the backup rate specified by the user and are triggered by the timer system in the ventilator if the patient fails to initiate a breath after a specified period.


Problems can arise when ACMV is used in patients with tachypnea resulting from nonrespiratory or nonmetabolic factors such as anxiety, pain, or airway irritation. Respiratory alkalemia may develop and trigger myoclonus or seizures. Dynamic hyperinflation may occur if the patient's respiratory mechanics are such that inadequate time is available for complete exhalation between inspiratory cycles. This can limit venous return, decrease cardiac output, and increase airway pressures, predisposing to barotrauma. ACMV is not effective for weaning patients from mechanical ventilation because it provides full ventilator assistance on each patient-initiated breath.

Synchronized intermittent mandatory ventilation (SIMV) is similar to ACMV in many respects except that not every patient effort is assisted. The major difference between SIMV and ACMV is that in the former the patient is allowed to breathe spontaneously, that is, without ventilator assist, between delivered ventilator breaths. However, mandatory breaths are delivered in synchrony with the patient's inspiratory efforts at a frequency determined by the operator. If the patient fails to initiate a breath, the ventilator delivers a fixed-tidal-volume breath and resets the internal timer for the next inspiratory cycle (Fig. 7-2). During SIMV, only the preset number of breaths is ventilator-assisted.

Figure 7-2.


Synchronized intermittent mandatory ventilation (SIMV) airway pressure and delivered tidal volume profiles. In SIMV ventilation, three types of breaths can occur. Spontaneous breaths are initiated by the patient and are not assisted by the ventilator. These occur between mandatory breaths. Ventilator-assisted breaths are initiated by the patient and supported by the ventilator, which synchronizes with the patient's effort to deliver a user-specified tidal volume. Ventilator-controlled breaths are initiated by the ventilator at the backup rate specified by the user and are triggered by the timer system in the ventilator if the patient fails to initiate a breath after a specified period.


SIMV allows patients with an intact respiratory drive to exercise inspiratory muscles between assisted breaths, making it useful for both supporting and weaning intubated patients. SIMV may be difficult to use in patients with tachypnea because asynchrony with the ventilator can occur as patients attempt to exhale during the ventilator-programmed inspiratory cycle. When this occurs, the airway pressure may exceed the inspiratory pressure limit, the ventilator-assisted breath will be aborted, and minute volume may drop below that programmed by the operator. In this setting, if the tachypnea is in response to respiratory or metabolic acidosis, a change to ACMV will increase minute ventilation and help to normalize the pH while the underlying process is further evaluated and definitive therapy instituted.

Continuous positive airway pressure (CPAP) is not a true support mode of ventilation because ventilation occurs through the patient's spontaneous efforts. The ventilator provides fresh gas to the breathing circuit with each inspiration and charges the circuit to a constant operator-specified pressure that can range from 0 to 20 cm H2O (Fig. 7-3). CPAP is used to assess extubation potential in patients who have been weaned effectively and are requiring little ventilator support.

Figure 7-3.


Continuous positive airway pressure (CPAP) charges the ventilator circuit to a user-specified continuous airway pressure but provides ventilator assist with respiratory efforts. All ventilation occurs through the spontaneous efforts of the patient.


Pressure-control ventilation (PCV) can be used to provide ventilator support either with ACMV triggering (PCV-ACM) or SIMV triggering (PCV-SIMV). In contrast to conventional ACMV or SIMV, which are volume-cycled and pressure-limited, PCV-ACM and PCV-SIMV are time-cycled and pressure-limited. During the inspiratory phase, a given pressure is imposed at the airway opening, and the pressure remains at this user-specified level throughout inspiration (Fig. 7-4). Since inspiratory airway pressure is specified by the operator, tidal volume and inspiratory flow rate are dependent rather than independent variables and are not user-specified. PCV is used commonly for patients with documented barotrauma because airway pressures can be limited, as well as for postoperative thoracic surgical patients, in whom the stress across a fresh suture line can be limited. When PCV is used, minute ventilation and tidal volume must be monitored; minute ventilation is varied by the user through changes in rate or in the pressure-control value.

Figure 7-4.


Pressure-control ventilation (PCV) delivers airway inflation pressure using time cycling rather than a user-specified tidal volume using volume cycling. In this figure, all breaths are shown as timer-cycled, although PCV can be programmed to trigger according to an assist/control algorithm or synchronized intermittent mandatory algorithm.


PCV with the use of a prolonged inspiratory time is frequently applied to patients with severe hypoxemic respiratory failure. This approach, called pressure-control inverse inspiratory-to-expiratory ratio ventilation (PCIRV), increases mean distending pressures without increasing peak airway pressures. It is thought to work in conjunction with PEEP to open collapsed alveoli and improve oxygenation. In acute lung injury, PCIRV may be associated with fewer deleterious effects than conventional volume-cycled ventilation, which requires higher peak airway pressures to achieve an equivalent reduction in shunt fraction, but there are no convincing data to show that PCIRV improves outcomes in acute lung injury or adult respiratory distress syndrome.13,14

PSV is a form of ventilation that is patient-triggered, flow-cycled, and pressure-limited; it is designed specifically for use in the weaning process but is also used commonly to ventilate patients with new-onset respiratory failure who are agitated and become asynchronous with other modes of ventilator support. During PSV, the inspiratory phase is terminated when the inspiratory flow rate falls below a certain level; in most ventilators, this flow rate cannot be adjusted by the operator. When PSV is used, patients receive ventilator assist only when the ventilator detects an inspiratory effort (Fig. 7-5). Thus it is mandatory that the patient have an intact respiratory drive to be maintained safely on this mode of ventilation without additional backup ventilator support. PSV also can be used in combination with SIMV to ensure volume-cycled backup for patients whose respiratory drive is depressed.

Figure 7-5.


Pressure-support ventilation (PSV) requires patient triggering for every breath. The ventilator assists every patient effort by applying a user-specified amount of positive pressure throughout the airway circuit. As the lung fills, inspiratory flow slows. When flow falls below a set value, inspiratory assist ceases, and the expiratory valve opens, allowing for exhalation. The size of each breath is dictated by the patient's inspiratory efforts, which augment ventilator assist. Respiratory rate is determined by the frequency of triggering by the patient.

PSV is well tolerated by most patients who are being weaned. PSV parameters can be set to provide full or nearly full ventilator support that can be withdrawn slowly over a period of days in a systematic fashion to gradually load the respiratory muscles and allow the patient to fully resume spontaneous breathing.


Results recently reported by the Acute Respiratory Distress Syndrome network (ARDSnet) trial have provided valuable guidelines for managing patients with hypoxemic respiratory failure.15 Compared with acute lung injury patients treated with conventional high-tidal-volume ventilation (10 mL/kg) plus PEEP, patients treated with low-tidal-volume ventilation (5–6 mL/kg) plus PEEP had reduced mortality.

This approach, known as open lung ventilation, has been confirmed by other investigators and is thought to work by recruiting damaged, collapsed alveoli and improving oxygenation without causing overdistention and ventilator-associated lung injury in less damaged areas of lung.16 Open lung ventilation is not a distinct mode of ventilation. Rather, it is a strategy for applying either volume-cycled or pressure-controlled ventilation to patients with severe respiratory failure. The level of PEEP is selected to help avoid cyclic opening and closing of alveolar units, thereby allowing the majority of alveoli to remain inflated during tidal ventilation. Achievement of eucapnia and normal blood pH through adjustments in ventilator tidal volume and breathing frequency are of lower priority. Hypercapnia and consequent respiratory acidosis tend to be well tolerated physiologically, except in patients with significant hemodynamic compromise, ventricular dysfunction, cardiac dysrhythmias, or increased intracranial pressure. Furthermore, recent data suggest that hypercapnia may have direct beneficial anti-inflammatory effects in the inflamed lung.17 Open lung ventilation has been shown to primarily benefit medical ICU patients with hypoxemic respiratory failure owing to acute lung injury. While open lung ventilation has not been specifically evaluated in the thoracic surgery patient population, it is reasonable to presume that similar benefits will be observed in thoracic surgery patients with this condition.

Other nonconventional strategies that have been used to manage critically ill patients with hypoxemic respiratory failure include airway pressure-release ventilation (APRV), prone-position ventilation, and nitric oxide supplementation. Each approach has been shown to produce physiologic benefit in uncontrolled observational studies. Results from randomized clinical trials, however, have been less convincing. Nevertheless, a trial of one or more of these approaches may be appropriate in the postoperative thoracic surgery patient with refractory hypoxemia.

APRV involves a specific application of bilevel ventilation in which the ventilator is set to alternate between two different levels of CPAP.18 The user specifies the high (inflation) and low (deflation) airway pressures and their duration. High pressure is usually set at 60–70% of peak inspiratory pressure measured during conventional ventilation, and low pressure is set at whatever level of PEEP appears to optimize recruitment without causing hemodynamic compromise. In APRV mode, the high-pressure time is usually specified to be 70–80% of the respiratory period such that the lung is two-thirds to three-quarters inflated for most of the respiratory cycle. Ventilation is achieved by periodic, brief deflations (Fig. 7-6). The patient has the ability to breath spontaneously and unassisted at any time during the respiratory cycle, ensuring patient-ventilator synchrony without the need for heavy sedation or paralysis. Small trials have demonstrated physiologic and hemodynamic improvements in patients with acute lung injury switched from conventional volume-cycled ventilation to APRV, although larger randomized clinical trials confirming these results have not yet been conducted.19,20 Practical limitations regarding the use of APRV also exist. Not all ventilators can provide bilevel ventilation, limiting access to APRV for some clinicians. APRV can, in theory, adversely affect hemodynamics by increasing mean intrathoracic pressure, although clinical experiences to date have not demonstrated such effects.19 APRV is also not appropriate for patients with severe airflow obstruction because the pattern of application of high and low pressures can cause dynamic hyperinflation.

Figure 7-6.


Airway pressure-release ventilation (APRV) cycles between the high and low level of CPAP. Each level is maintained for a user-specified period of time. When used in support of a patient with hypoxemic respiratory failure, high pressure is maintained for the majority of the cycle, with brief intermittent periods of airway pressure release to provide ventilation. Patients can breathe spontaneously at any time throughout the respiratory cycle.

Prone positioning is an alternative therapy for patients with refractory hypoxemia. It is effective, simple to implement, and often produces dramatic and immediate improvements in oxygenation.21 In contrast to its use in the medical ICU patient, prone ventilation will not be appropriate for many postoperative thoracic surgery patients. It may not be safe or practical to prone patients who have recently undergone pneumonectomies or chest wall resections or have multiple anterior chest tubes. Nevertheless, in patients in whom proning is safe, a trial should be considered for the severely hypoxic patient. Prone positioning can be used in combination with any mode of ventilator support. Patients are rotated from the supine position to the prone swimmer's position. Pads are required for bony dependent areas such as the forehead, elbows, ankles, and knees, and frequent turning is required to prevent skin breakdown. Thus institution of this form of support tends to be labor-intensive.

The physiologic basis for improvement in gas exchange after proning appears to result from improved / matching in newly dependent lung zones and recruitment of damaged areas of lung through gravity-assisted redistribution of transpulmonary pressures.22 Several small nonrandomized trials have demonstrated improvements in oxygenation with proning. Results of a recently completed randomized clinical trial confirmed these observations but failed to demonstrate a mortality benefit from an initial 10-day course of prone ventilation.23 Nevertheless, prone ventilation still may improve oxygenation in selected postoperative patients for whom it can be instituted safely and thus should be considered as a supplement to conventional ventilation for the patient with refractory hypoxemia.

Inhaled nitric oxide (NO; 2–40 ppm) also has been combined with mechanical ventilation to treat patients with hypoxemic respiratory failure.24 Benefits in oxygenation and reductions in pulmonary artery pressures have been observed in many patients receiving NO, although physiologic benefit has not been universal, and clinical parameters to identify responders have not yet been identified.25 Two randomized clinical trials conducted in patients with hypoxemic respiratory failure have failed to show mortality benefits or decreased resource utilization from NO therapy.25,26 While not universally effective, inhaled NO still may be effective in selected patients with postoperative hypoxemic respiratory failure.

Anecdotal experience suggests that NO may be useful in treating hypoxemic respiratory failure owing to ischemia-reperfusion injury (implantation response), which occurs in approximately 15% of patients after lung transplantation.27 One small randomized trial failed to demonstrate a beneficial effect of inhaled NO when used prophylactically in patients after transplantation, but it may improve oxygenation and lower pulmonary artery pressures in patients with established ischemia-reperfusion.28

Extracorporeal membrane oxygenation also may be used in the management of the posttransplantation patient with severe hypoxemia secondary to ischemia-reperfusion injury or severe acute rejection. Although randomized trials have failed to demonstrate consistent benefits from use of extracorporeal membrane oxygenation for established acute respiratory distress syndrome, posttransplantation hypoxemic respiratory failure has been managed successfully using this approach.29,30


Endotracheal intubation and positive-pressure mechanical ventilation have direct and indirect effects on several organ systems, including the lung and upper airways, the cardiovascular system, and the gastrointestinal system. Pulmonary complications include barotrauma, nosocomial/ventilator-associated pneumonia, oxygen toxicity, tracheal stenosis, and deconditioning of respiratory muscles. Barotrauma, which occurs when high pressures (i.e., 50 cm H2O) overdistend and disrupt lung tissue, is manifest clinically by interstitial emphysema, pneumomediastinum, subcutaneous emphysema, or pneumothorax. Although the first three conditions may resolve simply through the reduction of airway pressures, clinically significant pneumothorax, as indicated by hypoxemia, decreased lung compliance, and hemodynamic compromise, requires chest tube thoracostomy.

Patients intubated for longer than 72 hours are at increased risk for ventilator-associated pneumonia as a result of aspiration from the upper airways through small leaks around the endotracheal tube cuff. The most common organisms responsible for this condition are enteric gram-negative rods, Staphylococcus aureus, and anaerobic bacteria. Because the endotracheal tube and upper airways of patients on mechanical ventilation are commonly colonized with bacteria, the diagnosis of nosocomial pneumonia requires "protected brush" bronchoscopic sampling of airway secretions coupled with quantitative microbiologic techniques to differentiate colonization from infection. Current recommendations also include starting empirical broad-spectrum antibiotics pending final culture results because early antibiotic therapy appears to reduce mortality in this syndrome.31

Hypotension resulting from elevated intrathoracic pressures with decreased venous return is almost always responsive to intravascular volume repletion. In patients judged to have hypotension together with hypoxemic respiratory failure on the basis of alveolar edema, hemodynamic monitoring with a pulmonary arterial catheter may be of value for differentiating between low- and high-pressure pulmonary edema and for optimizing O2delivery via manipulation of intravascular volume, FIO2, and PEEP levels.

Gastrointestinal effects of positive-pressure ventilation include stress ulceration and mild to moderate cholestasis. It is common practice to provide prophylaxis with H2-receptor antagonists or sucralfate for stress-related ulcers. Mild cholestasis (i.e., total bilirubin values of approximately 4.0 mg/dL) attributable to the effects of increased intrathoracic pressures on portal vein pressures is common and generally self-limited. Cholestasis of a more severe degree should not be attributed to a positive-pressure ventilation response and is more likely due to a primary hepatic process.


A number of criteria must be met before mechanical ventilator support can be removed. Upper airway function must be intact for the patient to remain extubated, but this is difficult to assess in the intubated patient. Therefore, if a patient can breathe on his or her own through an endotracheal tube but develops stridor or signs of aspiration once the tube is removed, upper airway dysfunction or an abnormal swallowing mechanism should be suspected. Such patients benefit from early postextubation laryngoscopic upper airway assessment and vocal cord medialization to facilitate coughing and clearance of secretions if indicated.

Respiratory drive and chest wall function are assessed by the respiratory rate, tidal volume, inspiratory pressure, and vital capacity. The weaning index (also known as the rapid shallow breathing index), defined as the ratio of breathing frequency to tidal volume (breaths per minute per liter), is both sensitive and specific for predicting the likelihood of successful extubation.32 When this ratio is less than 105 and the patient is breathing without mechanical assistance through an endotracheal tube, successful extubation is likely. A negative inspiratory pressure of more than –30 cm H2O and a vital capacity of greater than 10 mL/kg are considered indicators of acceptable chest wall and diaphragm function. Alveolar ventilation generally is adequate when elimination of CO2 is sufficient to maintain an arterial pH in the range of 7.35–7.40, and an SaO2 of 90% can be achieved with an FIO2 of 0.5 and PEEP of 5 cm H2O. Although many patients may not meet all criteria for weaning, the likelihood that a patient will tolerate extubation without difficulty increases as more criteria are met.

Many approaches to weaning patients from ventilator support have been advocated. T-piece weaning is best tolerated by patients who have undergone mechanical ventilation for brief periods and require little respiratory muscle reconditioning, whereas SIMV and PSV are best for patients who have been intubated for extended periods and require gradual respiratory muscle reconditioning.33

T-piece weaning involves brief spontaneous breathing trials with supplemental O2. These trials are usually initiated for 5 min/h, followed by a 1-hour interval of rest. T-piece trials are increased in 5- to 10-minute increments until the patient can remain ventilator-independent for periods of several hours. Extubation then can be attempted.

Weaning by means of SIMV involves gradually tapering the mandatory backup rate in increments of 2–4 breaths/min while monitoring blood gas parameters and respiratory rates. Rates of greater than 25 breaths/min on withdrawal of mandatory ventilator breaths generally indicate respiratory muscle fatigue and the need to combine periods of exercise with periods of rest. Exercise periods are increased gradually until the patient remains stable on SIMV at 4 breaths/min or less without needing rest at higher SIMV rates. A CPAP or T-piece trial then can be attempted before planned extubation.

PSV, described earlier, is an effective mode of ventilation for weaning patients from mechanical ventilation. PSV usually is initiated at a level adequate for full ventilator support (PSVmax); that is, PSV is set slightly below the peak inspiratory pressures required by the patient during volume-cycled ventilation. The level of pressure support is then withdrawn gradually in increments of 1–5 cm H2O until a level is reached at which the respiratory rate increases to 25 breaths/min. At this point, intermittent periods of higher pressure support can be alternated with periods of lower pressure support to provide muscle reconditioning without causing diaphragmatic fatigue. Gradual withdrawal of PSV continues until the level of support is just adequate to overcome the resistance of the endotracheal tube (5–10 cm H2O). Support can be discontinued and the patient extubated.


The guidelines outlined in the preceding section are satisfactory for weaning most thoracic surgery patients from mechanical ventilation. Patients who have undergone a pneumonectomy, however, often present special challenges that can slow weaning and complicate postoperative management. Shift of the mediastinum toward the remaining lung owing to rapid accumulation of fluid within the hemithorax can increase pleural pressures and thus decrease transpulmonary distending pressures in the remaining lung. This imposes an added, severe restrictive physiologic load on the respiratory system postoperatively that can precipitate respiratory failure. Destabilization of the mediastinum can have additional adverse consequences on lung physiology. The loss of transpulmonary distending pressures owing to mediastinal shift can lead to collapse of small airways and can produce wheezing on examination. This pseudo-obstruction pattern tends to be refractory to bronchodilators and compromises breathing by increasing the work of breathing. Therapeutic drainage of fluid from the side of the pneumonectomy, restoration of pressure equilibrium between the hemithoraces, and reestablishment of a midline mediastinal position lead to resolution of this problem.

Hemodynamic instability also may occur after pneumonectomy because of several factors that influence right-sided heart function. Loss of a portion of the functioning pulmonary vascular bed may contribute to increased pulmonary pressures in patients with limited preexisting reserve. Lowering the intrathoracic pressure by removal of excess air or fluid from the pneumonectomized side can acutely increase right ventricular afterload and contribute to right-sided heart failure. Conversely, increased intrathoracic pressures resulting from rapid accumulation of fluid on the pneumonectomized side can decrease preload and cause hypotension and reduced cardiac output. Reinstituting drainage of the chest cavity to atmospheric pressure via a chest tube connected to a water seal represents effective management.


1. Eger E: Isoflurane: A review. Anesthesiology 55:559, 1981.[PubMed: 7027831]

2. Pride NB, Macklem PT: Lung mechanics in disease. In The Handbook of Physiology: The Respiratory System. Bethesda, MD, American Physiological Society, 1986:659–92.

3. Schmid ER, Rehder K: General anesthesia and the chest wall. Anesthesiology 55:668, 1981.[PubMed: 6458223]

4. Heneghan C, Bergman N, Jordan C: Effect of isoflurane on bronchomotor tone in man. Br J Anaesth 58:24, 1986.[PubMed: 3942666]

5. Rehder K: Anaesthesia and the respiratory system. Can Anaesth Soc J 26:451, 1979.[PubMed: 393367]

6. Pansard JL, Cholley B, Devilliers C, et al: Variation in arterial to end-tidal CO2 tension differences during anesthesia in the "kidney rest" lateral decubitus position. Anesth Analg 75:506, 1992.[PubMed: 1530162]

7. Sugarbaker DJ, Jaklitsch MT, Bueno R, et al: Prevention, early detection, and management of complications after 328 consecutive extrapleural pneumonectomies. J Thorac Cardiovasc Surg 128:138, 2004.[PubMed: 15224033]

8. Schneider B, Schickinger-Fischer B, Zumtobel M, et al: Concept for diagnosis and therapy of unilateral recurrent laryngeal nerve paralysis following thoracic surgery. J Thorac Cardiovasc Surg 51:327, 2003.[PubMed: 14669129]

9. Bromage PR, Camporesi E, Chestnut D: Epidural narcotics for postoperative analgesia. Anesth Analg 59:473, 1980.[PubMed: 6105830]

10. Shannon R: Intercostal and abdominal muscle afferent influence on medullary dorsal respiratory group neurons. Respir Physiol 39:73, 1980.[PubMed: 6244609]

11. Keats AS, Girgis KZ: Respiratory depression associated with relief of pain by narcotics. Anesthesiology 29:1006, 1968.[PubMed: 5673128]

12. Campbell RS, Davis BR: Pressure-controlled versus volume-controlled ventilation: Does it matter? Respir Care 47:416, 2002.[PubMed: 11929615]

13. Shanholtz C, Brower R: Should inverse ratio ventilation be used in adult respiratory distress syndrome? Am J Respir Crit Care Med 149:1354, 1994.[PubMed: 8173778]

14. Mercat A, Titiriga M, Anguel N, et al: Inverse ratio ventilation (I/E = 2/1) in acute respiratory distress syndrome: A six-hour controlled study. Am J Respir Crit Care Med 155:1637, 1997.[PubMed: 9154869]

15. Network TARDS: Ventilation with lower tidal volumes as compared to traditional tidal volumes for acute lung injury and acute respiratory distress syndrome. N Engl J Med 342:1301, 2000. 

16. Amato MB, Barbas CS, Medeiros DM, et al: Effect of a protective-ventilation strategy on mortality in the acute respiratory distress syndrome. N Engl J Med 338:347, 1998.[PubMed: 9449727]

17. Laffey J, Tanake M, Engleberts D, et al: Therapeutic hypercapnia reduces pulmonary and systemic injury following in vivo lung reperfusion. Am J Respir Crit Care Med 162:2287, 2000.[PubMed: 11112153]

18. Downs J, Stock M: Airway pressure release ventilation: A new concept in ventilatory support. Crit Care Med 15:459, 1987.[PubMed: 3568710]

19. Kaplan L, Bailey H, Formosa V: Airway pressure release ventilation increases cardiac performance in patients with acute lung injury and acute respiratory distress syndrome. Crit Care 5:221, 2001.[PubMed: 11511336]

20. Putensen C, Mutz NJ, Putensen-Himmer G, et al: Spontaneous breathing during ventilatory support improves ventilation-perfusion distributions in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 159:1241, 1999.[PubMed: 10194172]

21. Albert RK, Leasa D, Sanderson M, et al: The prone position improves arterial oxygenation and reduces shunt in oleic-acid-induced acute lung injury. Am Rev Respir Dis 135:628, 1987.[PubMed: 3030168]

22. Pappert D, Rossaint R, Slama K, et al: Influence of positioning on ventilation-perfusion relationships in severe adult respiratory distress syndrome. Chest 106:1511, 1994.[PubMed: 7956412]

23. Gattinoni L, Tognoni G, Pesenti A, et al: Effect of prone positioning on the survival of patients with acute respiratory failure. N Engl J Med 345:568, 2001.[PubMed: 11529210]

24. Rossaint R, Gerlach H, Schmidt-Ruhnke H, et al: Efficacy of inhaled nitric oxide in patients with severe ARDS. Chest 107:1107, 1995.[PubMed: 7705124]

25. Dellinger RP, Zimmerman JL, Taylor RW, et al: Effects of inhaled nitric oxide in patients with acute respiratory distress syndrome: Results of a randomized phase II trial. Inhaled Nitric Oxide in ARDS Study Group. Crit Care Med 26:15, 1998.[PubMed: 9428538]

26. Taylor RW, Zimmerman JL, Dellinger RP, et al: Low-dose inhaled nitric oxide in patients with acute lung injury: A randomized, controlled trial. JAMA 291:1603, 2004.[PubMed: 15069048]

27. Date H, Triantafollou A, Trulock E, et al: Inhaled nitric oxide reduces human lung allograft dysfunction. J Thorac Cardiovasc Surg 111:913, 1996.[PubMed: 8622313]

28. Meade MO, Granton JT, Matte-Martyn A, et al: A randomized trial of inhaled nitric oxide to prevent ischemia-reperfusion injury after lung transplantation. Am J Respir Crit Care Med 167:1483, 2003.[PubMed: 12770854]

29. Kollef MH: Rescue therapy for the acute respiratory distress syndrome (ARDS). Chest 111:845, 1997.[PubMed: 9106557]

30. Anderson H 3d, Steimle C, Shapiro M, et al: Extracorporeal life support for adult cardiorespiratory failure. Surgery 114:161, 1993.[PubMed: 8342122]

31. Guidelines for the management of adults with hospital acquired, ventilator acquired, and health-care associated pneumonias. Am J Respir Crit Care Med 171:388, 2005. 

32. Tobin M: Advances in mechanical ventilation. N Engl J Med 344:1986, 1996. 

33. Esteban A, Frutos F, Tobin MJ, et al: A comparison of four methods of weaning patients from mechanical ventilation. Spanish Lung Failure Collaborative Group. N Engl J Med 332:345, 1995.[PubMed: 7823995]

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