Advances in Anesthesia, Vol. 28, No. 1, ** **
ISSN: 0737-6146
doi: 10.1016/j.aan.2010.07.002
Modern Understanding of Intraoperative Mechanical Ventilation in Normal and Diseased Lungs
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are devastating occurrences in medical and surgical patients. Their prevalence in ventilated patients is around 40% [1] with mortalities approaching 40% to 50% [2]. Mechanical ventilation strategies introduced in the last 2 decades have led to a significant reduction in the associated mortality [3,4]. Applying these strategies during general anesthesia would represent a substantial shift in commonly applied ventilatory management of the intraoperative period. This article provides guidance for mechanical ventilation in the perioperative setting for the healthy patient as well as the patient with diseased lungs.
Pulmonary mechanics and gas exchange during anesthesia
General anesthesia induces significant changes to the basic lung function. The change from the upright position to the supine position reduces functional residual capacity (FRC) by 15% to 20%. Loss of muscle tone induces a change in the balance of elastic recoil and chest compliance leading to reduced lung volumes [5], increased shunting across the lung, and a further reduction in FRC [6]. The change in lung compliance and the reduction in FRC promote airway closure and induce compression atelectasis. Microatelectasis can be detected in up to 90% of patients undergoing general anesthesia and can involve up to 5% to 20% of the total gas exchange area [5]. Also, absorption atelectasis is common when high inspired O2 concentrations (Fio2) are applied [7]. It occurs when less gas enters the alveolus than is removed by uptake into the blood. In the perioperative period, compression and absorption atelectasis are the 2 major mechanisms for the occurrence of atelectasis.
Mechanical ventilation leads to ventilation-perfusion (V/Q) mismatch, more pronounced in the posterodorsal areas, and causes changes in the function of surfactant [8]. In addition, volatile anesthetics reduce hypoxic pulmonary vasoconstriction (HPV), also known as the Euler-Liljestrand reflex. Venous admixture increases and the alveolar-arterial O2 pressure gradient increases. Under 2 minimum alveolar concentrations of isoflurane, HPV is reduced by almost 50% [5].
In summary, the right-to-left shunting increases from 1% to 5% observed in the healthy, upright, spontaneously ventilating adult to 15% to 20% in the patient who is supine, anesthetized, and ventilated. Therefore, oxygenation is moderately compromised during general anesthesia, despite increase in Fio2 [5]. Also, atelectasis occurring during general anesthesia may promote injury to alveoli resulting from recurrent shear stress caused by opening and closing of the atelectatic areas (ie, atelectrauma).
Traditional intraoperative ventilation strategies
In the intraoperative period, the traditional mode of ventilation has been a volume-control mode with moderately high tidal volumes (10–12 mL/kg), low respiratory rates (8–10 breaths/min), I/E ratio (1:2), slightly increased Fio2 (30%–50%), and zero end-expiratory pressure. The reasons for using twice the physiologic tidal volumes stem from the concern that small tidal volumes can lead to loss of lung volume and hypoxemia caused by right-to-left shunting [9,10]. Volume-control ventilation (VCV) modes are preferred, because they provide fixed tidal volume, even during changes in compliance of chest wall and lungs that can occur during surgery (eg, caused by changes in patient’s position, external pressure on the thorax, and changing degrees of muscle relaxation).
The traditional goal of ventilation is to maintain mild hypocapnia (ie, end-tidal CO2 [ETCO2] around 30 to 35 mm Hg). This goal is probably intended to achieve an apneic threshold, defined as the highest arterial CO2 tension at which a subject remains apneic, which is approximately 4 or 5 mm Hg less than resting arterial CO2 tension achieved during spontaneous ventilation. However, the benefits of maintaining mild intraoperative hypocapnia remain controversial. Recent evidence suggests that mild hypercapnia (ie, ETCO2 values around 40–50 mm Hg) can improve tissue oxygenation through improved tissue perfusion and oxygenation resulting from increased cardiac output and vasodilatation as well as increased O2 off-loading from the shift of the oxyhemoglobin dissociation curve to the right [11,13]. In addition, mild hypercapnia and mild respiratory acidosis attenuate or dampen the inflammation caused by ischemia-reperfusion, established bacterial pneumonia [14], and endotoxin-induced lung injury. However, hypercapnia and acidosis may increase intracranial pressure as well as increase pulmonary vascular resistance, and thereby increase right ventricular workload [15]. Therefore, it should be avoided in select patient populations.
Concerns with traditional ventilation strategies
One of the major concerns of mechanical ventilation is development of VILI, which is caused by volutrauma and barotrauma resulting in an enhanced systemic inflammatory response with worsening oxygenation. One hour of mechanical ventilation alone without surgery in healthy patients did not lead to an increase in measured inflammatory parameters [16]. Choi and colleagues [17] compared the use of tidal volumes of 12 mL/kg without positive end-expiratory pressure (PEEP) with tidal volumes of 6 mL/kg with PEEP of 10 cm H2O in patients undergoing major abdominal surgery. Bronchiolar lavage was performed before and after 5 h of mechanical ventilation. Lavage fluid from the high tidal volume group showed a pattern of leakage of plasma into the alveoli consistent with alveolar lung injury. This study suggests that, even in patients with no lung disease, the use of large tidal volumes without PEEP causes systemic inflammation and lung injury. The severity of this injury seems to be directly related to the duration of mechanical ventilation and usually remains subclinical.
An observational study found a 25% incidence of ALI/ARDS within 5 days of mechanical ventilation [18]. The development of lung injury was associated with the initial ventilator settings and correlated with an odds ratio of 1.6 for peak airway pressures greater than 30 cm H2O and an odds ratio of 1.3 for each milliliter of tidal volume exceeding 6 mL/kg predicted body weight. Perioperative ALI becomes clinically important when injurious ventilation patterns are used in patients who have other concomitant lung injuries, such as pulmonary resection, cardiopulmonary bypass, or transfusion related lung injury (see later discussion).
Edema, secretions, and infiltrations all contribute to worsening pulmonary dynamics measured as a decreased static and dynamic compliance, which increase peak airway pressure, regardless of the mode of ventilation. However, peak inspiratory pressure (PIP) reflects the proximal airway pressure and not the alveolar pressure. Therefore, in the setting of reduced compliance or reduced thoracic expansion, high pressures may not induce lung injury [19]. A better approximation of end-tidal alveolar pressure is obtained by using the plateau pressure in a VCV mode. A plateau pressure of greater than 35 cm H2O has also been implicated in the development of VILI [20].
Overall, volume rather than pressure seems to be the culprit, coining the term volutrauma instead of the traditional expression of barotrauma. Taken together, all studies in healthy patients, as well as in patients at risk, show that ventilation with large tidal volumes for a longer time period may represent a primary hit or an additional hit in cases of extrapulmonary injury [17,21–25]. In patients with pulmonary injury, even shorter periods of harmful ventilation can cause exaggerated injuries to the lung, possibly triggering a systemic inflammatory response.
VILI encompasses 3 different entities: overinflation of alveoli, high-permeability type pulmonary edema (presents as a protein-rich expression of lung fluid), and lung inflammation, also called biotrauma. During ALI, regional compliance heterogeneity creates a functional baby lung. Normal or large tidal volumes delivered to a reduced number of ventilated alveoli can lead to further distention of lung areas that are already overdistended. The alveolar endothelial membrane is altered by mechanical distortion, increased transmural pressure, surfactant inactivation, and the immigration of inflammatory cells. Secondary changes include emphysemalike lesions, lung cysts, and bronchiectasis in nondependant and caudal lung regions [26].
Determination of optimal tidal volume
In the intensive care unit (ICU) setting, ventilation with lung volumes of 6 to 8 mL/kg ideal body weight (IBW), as well as peak inspiratory plateau pressures of less than 30 cm H2O, is now considered the standard of care [27,28]. The ARDSnet study has demonstrated a reduction in mortality from 40% to 31% when a population of patients with ARDS/ALI was ventilated with half the tidal volume (6 vs 12 mL/kg, IBW) [29]. This approach reduces volutrauma caused by high tidal volumes and barotrauma secondary to shear stress related to high airway pressures. Furthermore, biotrauma, a combination of lung and distant organ injury caused by systemic inflammatory response, is reduced [30]. Lower intraoperative tidal volumes of 6.7 mL/kg versus 8.3 mL/kg IBW and avoidance of excessive fluid infusion resulted in reduced respiratory failure after pneumonectomy [31]. Similarly, protective ventilation strategies reduce lung injury and time on the ventilator after esophageal cancer surgery [32].
Intraoperative mechanical ventilation should be similar to that in the ICU setting because of the difficulty in diagnosing ALI/ARDS and the potential for multiple hits caused by intraoperative volutrauma [33]. Therefore, lung protective patterns of intraoperative mechanical ventilation using physiologic tidal volumes and appropriate PEEP should be considered.
Role of PEEP and recruitment maneuvers
Concerns of atelectasis from general anesthesia as well as the use of low tidal volumes have generated a considerable interest in maneuvers designed to prevent and recruit atelectatic lung regions. PEEP prevents alveolar collapse and maintains end-expiratory lung volumes recruited during inspiration. However, the appropriate level of PEEP is controversial [34]. Attempts to optimize alveolar recruitment by increasing PEEP may be either poorly effective [35] or deleterious because of overinflation of more compliant lung regions [36]. This overinflation counteracts the beneficial effects from low tidal volumes and limited airway pressure ventilation [37].
A recent meta-analysis concluded that, in patients with ALI/ARDS, lower tidal volumes reduced hospital mortality regardless of low or high levels of PEEP. However, higher PEEP levels required 50% fewer interventions for rescue therapy in patients with severe hypoxemia, and reduced mortality in this population [38,40]. The appropriate PEEP values in patients with noncompliant thoraces or increased abdominal pressure are not known, because this patient population was excluded in most of the studies.
Overall, selection of PEEP level should take into consideration lung morphology and regional distribution [41]. Higher levels of PEEP may be appropriate when the loss of aeration is diffuse and involves all lung regions, commonly referred to as white lung [41]. In addition, higher PEEP levels can be beneficial without adding harm from overdistention, provided plateau pressures were kept to less than 30 cm H2O [34]. Moderate PEEP levels of around 10 cm H2O should maintain a balance between aeration and overinflation when the loss of aeration is localized and focally distributed (in which the lung behaves as several compartments).
Application of PEEP alone may not always reverse atelectasis and improve arterial oxygenation [42]. The application of 5 cm H2O of PEEP without prior recruitment was similar to application of no PEEP [43]. In contrast, PEEP of 10 cm H2O without recruitment consistently reopened some collapsed lung tissue [44]. In 1963, Bendixen and colleagues [45] suggested that periodic deep breaths prevent progressive atelectasis and intrapulmonary shunting. To reexpand the atelectatic lung, it may be necessary to use a vital capacity maneuver with higher inflation pressures, referred to as a recruitment or Lachmann maneuver [46]. Inspiratory pressures of 30 cm H2O are required to reexpand half of the anesthesia-induced atelectatic lung, but PIPs of up to 40 cm H2O may be needed to fully reverse anesthesia-induced collapse of healthy lungs, and even higher pressures may be required if the patient is grossly obese [47]. The duration of recruitment maneuver should generally be at least 7 to 8 seconds [48]. Most of the reexpanded lung tissue should remain inflated for about 40 minutes [49]. During a recruitment maneuver, arterial blood pressure should be closely monitored because of its potential to reduce preload and induce hypotension. In a pig model, recruitment maneuvers, applied every 6 hours, had no negative effect on alveolocapillary membrane integrity as measured by extravascular lung water, pulmonary clearance, and light microscopy [50].
Recruitment maneuvers should not be used routinely, and should be restricted for the rapid reversal of loss of aeration from disconnections from the ventilator, for example, to perform tracheal suctioning [51]. The primary aim of lung recruitment should be to achieve arterial saturation greater than or equal to 90% at Fio2 less than or equal to 0.6. In cases of severe hypoxemia, adjunctive interventions (eg, prone positioning, inhaled nitric oxide, or extracorporeal oxygenation) may be considered.
Ideally, lung recruitability should be assessed by dynamic lung imaging techniques, which would allow the determination of the best physiologic PEEP. In addition, the use of transpulmonary pressure would allow the assessment of the detrimental effects of low tidal volumes. Until this becomes widely available, optimal ventilator settings would include tidal volumes of 6 mL/kg IBW and the maximum PEEP based on the upper limit of airway pressure. In the perioperative setting, maintaining a PEEP of 5 cm H2O from preoxygenation to the tracheal extubation should reduce atelectasis [52]. Intermittent recruitment maneuvers may be necessary, which should be followed by sufficient PEEP to maintain alveolar unit expansion [49]. Vital capacity maneuvers without subsequently applied PEEP proved to be ineffective for increasing lung volumes and increasing gas exchange [53].
Determination of optimal respiratory rate
Optimal respiratory rate implies selecting the best compromise between 2 opposing goals: CO2 elimination and avoidance of the development of intrinsic (auto) PEEP. With the use of lower tidal volumes, higher respiratory rates may be necessary to maintain adequate CO2 levels. Higher respiratory rates shorten expiratory times, which may result in intrinsic PEEP. In general, respiratory rates can be increased to 20 to 30 breaths/min without generating significant intrinsic PEEP in healthy patients. However, if higher respiratory rates are used, it may be necessary to monitor inspiratory and expiratory flows. If the end-expiratory flow remains zero, respiratory rates can be increased without the risk of intrinsic PEEP formation [54].
Setting inspired O2 concentrations
Intraoperative Fio2 is frequently increased to compensate for the gas exchange impairment related to anesthesia. However, use of excessive O2 concentrations is potentially deleterious for the lungs and other organs. Application of 100% O2 for 24 hours has been reported to cause tracheobronchial irritation and pulmonary toxicity leading to irreversible fibrosis [55]. In the intraoperative period, even short-term high Fio2 may result in absorption atelectasis, which can exaggerate the effects of other stressors to the lung such as stretch injury secondary to inappropriately high tidal volumes or airway pressures [56,57]. High Fio2 has been linked to poor regulation of blood glucose levels [58] and increased systemic vascular tone [59].
Fio2 of 0.8 during surgery and until 2 hours after major colorectal surgery correlated with reduced surgical site infection (SSI) rate and postoperative complications [60]. The incidence of postoperative nausea and vomiting (PONV) may also be reduced by higher Fio2 [61]. However, these early results have not been confirmed in subsequent studies involving other surgeries [62,63]. A recent meta-analysis did not support a beneficial effect of higher Fio2 on PONV [64]. Another meta-analysis found that the use of higher Fio2 resulted in an absolute SSI risk reduction of 3% and relative risk reduction of 25% [65]. However, other measures for improving tissue oxygenation, such as temperature control [66], fluid and sympathetic tone management [67], and avoidance of hypocapnia, may prove to be equally important in reducing infections and improving wound healing [68]. When using high Fio2, lung protective ventilation strategies should be implemented to avoid complications of mechanical ventilation and O2 toxicity [57,69]. Therefore, a low-O2 strategy may preserve lung function and improve arterial oxygenation better than high-O2 therapy during elective surgery [70]. The clinical relevance of these observations currently awaits further confirmation.
PCV
In PCV mode, the airway pressure is fixed and the tidal volume changes with resistance and compliance of chest wall and lungs as well as duration of inspiration. During PCV, the peak pressure is achieved rapidly and maintained for the duration of inspiration, which allows delivery of tidal volumes that are similar to VCV, but at lower PIP, assuming similar compliance. In addition, the decelerating gas flow during PCV improves the distribution of gas flow to the lungs [71]. Furthermore, PCV allows delivery of a more homogeneous tidal volume to all areas of the lung, and quicker delivery of tidal volume with greater time for gas exchange, which improves lung compliance and oxygenation.
Unlike VCV, in which the tidal volume is predetermined, inspiratory pressures must be individualized for each patient to ensure adequate ventilation while using PCV. Also, use of PCV requires increased vigilance because the intraoperative lung compliance/resistance can be highly variable (eg, changes in degree of neuromuscular blockade, abdominal packing, surgeons hand on the patient’s chest), which can decrease tidal volumes and contribute to the development of hypercarbia and atelectasis [72]. Volume-guaranteed PCV, as a new ventilatory mode, may prove useful in addressing these limitations in the future.
PSV
Although commonly used in the ICU setting, PSV is a new intraoperative mode of mechanical ventilation. PSV augments the patient’s spontaneous breaths and reduces the work of breathing. PSV improves gas exchange and prevents perioperative atelectasis in patients breathing spontaneously through supralaryngeal devices (eg, laryngeal mask airway) or tracheal tubes [73,75]. In addition, PSV with or without SIMV may reduce the need for neuromuscular blockers and deep levels of anesthesia. Furthermore, PSV may be used at the end of surgery while the patient is recovering from residual anesthesia and muscle relaxants.
However, as in PCV, the ability of PSV to deliver an adequate tidal volume is dependent on patients’ respiratory mechanics, and therefore vigilance is paramount. Volume-guaranteed PSV is designed to address these concerns by adjusting the pressure support to deliver a preset tidal volume [76,77]. Although promising, the literature is mixed regarding clinical validation of intraoperative PSV [78].
Monitoring of pulmonary mechanics
Real-time monitoring of pulmonary mechanics can allow for the individualization of ventilator settings [79]. Modern ICU ventilators display in real time, breath by breath, flow, volume, and pressure at the mouth curves, both as a function of time and as a loop. Data from curve analysis help understand the interaction between patient and ventilator. The pressure-volume loops can be used to characterize pulmonary mechanics and the changes induced by various pulmonary pathologies [80] as well as to identify the onset of alveolar overdistention; presence of large areas of collapsed, but recruitable, lung units; and best PEEP [81]. The flow-volume loops assess resistance and allow identification of pulmonary obstruction, monitoring of the efficacy of therapeutic interventions, [82] as well as detection of leaks and intrinsic PEEP.
Although monitoring of pulmonary mechanics offers the potential to tailor ventilatory strategies based on individual patient needs, there is no consensus on how such information should be interpreted or applied to clinical decision making [80].
Special patient population and situations
Postoperative Ventilation after Tracheal Extubation (Noninvasive Ventilation)
Noninvasive ventilation (NIV) can reduce the need for tracheal intubation and mechanical ventilation in patients with respiratory compromise. NIV compensates for the loss of respiratory function, reduces the work of breathing, and improves gas exchange by improving alveolar recruitment. Most studies evaluating NIV have reported reduced postoperative atelectasis and pneumonia rate [83]. With the use of NIV, the indications for tracheal intubation and mechanical ventilation have become stringent, including severe respiratory failure as indicated by minute ventilation greater than 15 L/min, Pao2/Fio2 ratios less than 120 mm Hg, and diffuse or patchy densities on chest radiograph representing more diffuse and severe lung injury. Additional indications include the presence of marked metabolic derangements, shock states, and impaired ability to protect the airway [84,85].
Before initiating NIV, it is necessary to prepare the patient by adequate positioning and explanation of the procedure. After an initial setting of PEEP at 7 to 10 cm H2O, the inspiratory pressure setting is slowly increased by 2 cm H2O until patient comfort improves, respiratory rate decreases, and tidal volumes of 6 to 8 mL/kg are achieved [86]. Peak pressures of greater than 20 cm H2O should be avoided in an effort to avoid gastric insufflation and abdominal distention. NIV can be used intermittently (eg, for 60–90 minutes) every couple of hours until the respiratory status is improved. Concerns about anastomotic dehiscence after thoracic or abdominal surgery have been expressed, but do not seem to be validated as long as the limitations on PIP are observed [86,87].
Patients with COPD
Small airway collapse may be prevented by the application of external PEEP to stent the airway open [88]. In spontaneously breathing patients, external PEEP can reduce the work of breathing required to trigger the ventilator [89]. The use of inhalation anesthetics, as well as prophylactic postoperative NIV, may prevent postextubation respiratory failure [90]. In addition, broncholytic therapy should be continued throughout the perioperative period.
Patients Who are Obese
Obesity is associated with a reduction in FRC, increased PIP during positive pressure ventilation, and a decrease in lung compliance [91]. The expiratory flow limitation and development of intrinsic PEEP may further increase the work of breathing at rest. These changes increase the risk for perioperative pulmonary complications [92].
Lung protective ventilation strategies in the obese would include the use of PCV [93] with tidal volumes around 8 mL/kg IBW and a PEEP of 10 cm H2O [94]. In addition, acceptance of mild hypercapnia may limit the need for increased PIP. It is important to avoid hyperventilation (and hypocapnia), because this may result in metabolic alkalosis and lead to postoperative hypoventilation.
Preoxygenation with Fio2 of 1.0 and PEEP of 10 cm H2O has been shown to prevent atelectasis while improving oxygenation during induction of anesthesia in patients who are obese [95]. In one study, a PEEP of 10 cm H2O in patients with mean BMI of 51 kg/m2 improved intraoperative compliance and oxygenation [96]. Another study concluded that a PEEP of 15 cm H2O provided the greatest benefit in terms of FRC improvement and gas exchange without hemodynamic compromise [97]. Optimal PEEP level should reduce intrinsic PEEP as detected by flow measurements. Recruitment maneuvers are beneficial in patients who are obese and should be applied in particular during laparoscopic surgery [98]. However, the effects of recruitment maneuvers are short lasting and often limited by hemodynamic instability.
Patients with Pneumoperitoneum
The insufflation of CO2 into the abdomen creates a hypercapnic physiology pattern, with up to 20% more CO2 elimination and a restrictive respiratory pattern similar to the patient who is obese, which is usually limited to the duration of the pneumoperitoneum. In the obese, lung compliance is reduced, resistance is increased, and oxygenation is worsened even before the creation of pneumoperitoneum [99], and the reversal of atelectasis is slower [100]. Also, creation of pneumoperitoneum can lead to mainstem intubation with a brisk reduction in pulmonary function immediately after insufflation.
The increase in alveolar ventilation during CO2 insufflation can be achieved either by increasing tidal volume or increasing respiratory rate. Because VCV increases peak and plateau pressures and puts the patient at risk for VILI, PCV may be beneficial [93,101,102]. Recruitment maneuvers before [103] and after pneumoperitoneum improve lung function in normal patients [104] as well as in patients who are moderately obese [98,105]. The application of PEEP of 10 to 15 cm H2O improves V/Q mismatch and improves oxygenation as well as ventilation [106].
Patients at Risk for Intraoperative Pulmonary Complications (eg, Cardiopulmonary Bypass Exposure)
Cardiopulmonary bypass may cause lung injury that can be aggravated by injurious ventilation patterns. Zupancich and colleagues [25] compared the use of high tidal volumes (10–12 mL/kg) plus low PEEP (2–3 cm H2O) with a lung protective strategy with low tidal volumes (8 mL/kg) plus high PEEP (10 cm H2O) in patients ventilated for 6 hours after coronary artery bypass surgery. Serum and bronchiolar lavage levels of the inflammatory cytokines were significantly increased at 6 hours only in the high tidal volume group. However, another similar study failed to observe any benefits of a lung protective strategy [23]. Nevertheless, there is the suggestion of benefit for lung protective ventilation during cardiac surgery.
Patients in Prone Position
Overall, FRC and oxygenation is improved on assuming a prone position in normal people [107] and patients who are obese [108]. Although ventilation is not affected by posture, perfusion is always dorsally distributed [109], so ventilation-perfusion matching improves along the vertical axis in the prone position [110]. These findings are more pronounced in patients with ALI [111]. The abdomen must be able to move freely and not impede respiratory mechanics and venous return.
Pediatric Patients
Smaller elastic retraction forces and a lower relaxation volume predispose children less than 7 years of age to more airway collapse than adults [112], particularly with the use of high Fio2. As with adults, atelectasis is more pronounced in the caudal and dependent lung regions [43]. The levels of PIPs that are adequate to reopen small airways and alveoli have not been studied in children, but may be lower in healthy children undergoing surgery [113,115].
In a small study (n = 46 children), it was shown that a PEEP of 6 cm H2O prevented changes caused by higher Fio2. Therefore, PEEP levels in children of 5 to 6 cm H2O may be advocated [43,116]. In contrast with adults, no pediatric studies have been conducted to confirm that a lung protective strategy of low tidal volume and pressure limitation is optimal. Nevertheless, based on adult and animal studies, it can be extrapolated that lung protective ventilation might also be beneficial in children [117].
Summary
In recent years there has been significant attention directed toward the detrimental pulmonary, cardiovascular, and inflammatory consequences of mechanical ventilation that may adversely influence perioperative outcome. An evidence-based approach to mechanical ventilation should reduce perioperative lung injury and improve surgical outcome (Table 1). Use of a lung protective strategy including low tidal volumes of 6 to 8 mL/kg with an initial PEEP of 5 to 10 cm H2O and plateau pressures limited to 30 cm H2O seems to be protective against VILI. Optimal strategies vary by clinical situation (ie, healthy vs diseased or injured lung).
Table 1 Summary of recommendations for perioperative mechanical ventilation and degree of evidence
CPAP 6–10 cm H2O during preoxygenation before induction of anesthesia | Reduces atelectasis Improves arterial oxygenation Prolongs nonhypoxic apnea time |
A B B |
Pressure-controlled ventilation | Reduces peak airway pressure Does not improve gas exchange |
B B |
Tidal volumes 6–8 mL/kg | Reduces alveolar inflammation Reduces postoperative pulmonary dysfunction in patients at high risk |
A A |
PEEP 5–10 cm H2O | Reduces alveolar inflammation in association with low tidal volume ventilation Improves arterial oxygenation in the morbidly obese Improves arterial oxygenation during 1-lung ventilation Prevents derecruitment after vital capacity maneuver |
A A A B |
Fio2 0.8 intraoperatively | May reduce wound infection after abdominal surgery May protect cardiovascular system No effect on incidence of PONV May increase absorption atelectasis |
A A B B |
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