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CARDIOVASCULAR ANESTHESIA

Continuous Positive Airway Pressure at 10 cm H₂O During Cardiopulmonary Bypass Improves Postoperative Gas Exchange

Department of Anesthesiology and Critical Care Medicine, The Leopold-Franzens-University of Innsbruck, Innsbruck, Austria

Address correspondence and reprint requests to Alexander Loeckinger, MD, The Leopold-Franzens-University of Innsbruck, Department of Anesthesiology and Critical Care Medicine, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to alex.loeckinger @uibk.ac.at.

	Abstract

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Postbypass pulmonary dysfunction including atelectasis and increased shunting is a common problem in the intensive care unit. Negative net fluid balance and continuous positive airway pressure (CPAP) have been used to reduce the adverse effects of cardiopulmonary bypass (CPB) on the lung. To determine whether CPAP at 10 cm H₂O during CPB results in improved postoperative gas exchange in comparison with deflated lungs during CPB, we examined 14 patients scheduled for elective cardiac surgery. Seven patients received CPAP at 10 cm H₂O during CPB, and in the other seven patients, the lungs were open to the atmosphere (control). Measurements were taken before and after CPB, after thoracic closure, and 4 h after CPB in the intensive care unit. CPAP at 10 cm H₂O resulted in significantly more perfusion of lung areas with a normal ventilation/perfusion distribution (V_A/Q) and significantly less shunt and low V_A/Q perfusion 4 h after CPB in comparison with the control group. Consequently, arterial oxygen partial pressure was significantly higher and alveolar-arterial oxygen partial pressure difference was significantly smaller. We conclude that CPAP at 10 cm H₂O during CPB is a simple maneuver that improves postoperative gas exchange.

Implications: Inflation of the lungs at a pressure of 10 cm H₂O as compared with leaving the lungs deflated during cardiopulmonary bypass was examined. Lung inflation during bypass resulted in significantly improved postoperative gas exchange.

	Introduction

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Impaired pulmonary function after cardiac surgery with cardiopulmonary bypass (CPB) is a common postoperative problem in the intensive care unit (ICU). This "postbypass lung" is characterized by increased intrapulmonary shunt (1), atelectasis (2), increased alveolar-arterial oxygen partial pressure difference (AaDO₂) (3), increased extravascular lung water (4), and decreased compliance (5). Major causes of postbypass lung are the reduced or absent blood flow during CPB through the lungs (partial CPB) (6) and entry into pleural spaces during surgery (7). One measure to reduce these adverse effects is the use of static inflation of the lungs (CPAP) during CPB (1,3,4,8). In a porcine model, Magnusson et al. (1) compared the use of CPAP with leaving the lungs deflated. Using the multiple inert gas elimination technique (MIGET), they found that CPAP at 5 cm H₂O offered no significant advantage over deflated lungs. Berry et al. (3) found that, in patients, CPAP at 5 cm H₂O decreases the AaDO₂ at 30 min but not at 4 and 8 h after CPB compared with deflated lungs, no matter which gas mixture used. In both Magnusson et al.’s (1) and Berry et al.’s (3) studies, there was a trend toward improved postbypass pulmonary function by using CPAP. Airway closure occurs at a lung volume called the closing capacity. Closing capacity increases with age and becomes equal to the functional residual capacity (FRC) at a mean age of 44 yr (supine position) (9). Moreover, in anesthetized patients, closing capacity exceeds FRC in the supine position (10). Patients scheduled for coronary artery bypass grafting are increasingly older (11). As yet, no information is available on the postbypass gas exchange in patients using the MIGET. This technique offers a very detailed profile of the pulmonary gas exchange (12). The aim of this study was to examine whether CPAP at 10 cm H₂O during CPB improves the postoperative ventilation/perfusion ratio as compared with leaving the lungs deflated.

	Methods

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After obtaining ethics committee approval and written, informed consent, we studied 14 patients with coronary artery disease listed for elective CABG. Patients with valvular cardiac disease or chronic obstructive lung disease were excluded from the study. Patients were randomly assigned to two groups, one group received CPAP at 10 cm H₂O during CPB, whereas in the other group, the lungs were left open to the atmosphere. After preoxygenation for at least 3 min, anesthesia was induced by using midazolam 0.07–0.14 mg/kg, fentanyl 7 µg/kg, and rocuronium-bromide 0.6 mg/kg. This was followed by manual ventilation at a fraction of inspired oxygen (FIO₂) of 1.0 for 60 s and subsequent tracheal intubation. Lungs were ventilated by using 7 mL/kg tidal volume at 15 breaths/min respiratory rate, and the FIO₂ was initially adjusted to 1.0 (SA 2; Dräger, Lübeck, Germany). Positive end-expiratory pressure was set to 5 cm H₂O during the whole procedure. After termination of CPB, a vital capacity maneuver was performed in all patients at FIO₂ = 1.0. An arterial catheter (radial artery, nondominant hand), a central venous catheter (left subclavian vein), and a Swan-Ganz catheter (right internal jugular vein) were inserted. Anesthesia was maintained by a constant infusion of fentanyl and midazolam as required. On average, anesthetic regimen was performed as follows: At induction, boluses of fentanyl (7 µg/kg) and midazolam (70–140 µg/kg) were given. From the induction of anesthesia until the completion of sternotomy, a continuous infusion of fentanyl at 0.3–0.4 µg · kg^-1 · min^-1 and midazolam at 3–4 µg · kg^-1 · min^-1 was administered. From sternotomy until the initiation of CPB, fentanyl was infused at 0.2–0.3 µg · kg^-1 · min^-1 along with midazolam at 2–3 µg · kg^-1 · min^-1. During CPB, the fentanyl infusion was reduced to 0.1 µg · kg^-1 · min^-1, and the midazolam infusion was reduced to 1 µg · kg^-1 · min^-1. After completion of CPB, the midazolam infusion was stopped, while the fentanyl infusion was continued at 0.1 µg · kg^-1 · min^-1 until the end of the procedure. No vasodilator was used in any of the patients observed. Patients of both groups underwent the following measurements: A baseline measurement, performed after the induction of anesthesia immediately before surgical incision at FIO₂ = 0.75, a second measurement 30 min after CPB at FIO₂ = 1.0, a third measurement immediately after thoracic closure at FIO₂ = 0.8, and a final measurement 4 h after CPB in the ICU at FIO₂ = 0.4. At each point of observation, hemodynamic variables, arterial and mixed venous blood gas analysis, and inert gas measurements were performed. In addition, respiratory system compliance was determined by using the loop-technique (12) using an extension of the anesthesia monitor (AS-3; Datex, Helsinki, Finland).

Ventilation and perfusion distributions were determined by using the MIGET as previously described (13–15). The main goal of the MIGET are precise calculations of the amounts of blood flow or ventilation to lung areas with zero ventilation (shunt), limited ventilation (low V_A/Q), and normal ventilation (normal V_A/Q). Ventilation of unperfused lung areas (alveolar dead space) can be calculated equally. To perform the MIGET, a mixture of six inert gases, including sulfur hexafluoride, ethane, cyclopropane, halothane, diethyl ether, and acetone, was dissolved in saline and infused via a peripheral vein at a rate of 2 mL/min. This infusion was started 45 min before the first set of measurements. Ten-milliliter blood samples were collected in heparinized glass syringes from the pulmonary artery and radial artery. Thirty-milliliter mixed expired gas samples were obtained from a heated mixing chamber into warmed gas-tight glass syringes. All samples were kept at a temperature of 38°C and immediately prepared for analysis. Inert gas extraction was performed as described by Wagner et al. (16). Concentrations of inert gases were measured by using gas chromatography.

Ventilation/perfusion distributions were then computed from inert gas data by using the 50-compartment model of Evans and Wagner (15) and West (17). Inert gas shunt (Q_S/Q_T), log standard deviation of the Q (log SD Q), log standard deviation of V_A (log SD V), mean V_A/Q ratios of V_A and Q distributions, and dead space (V_D/V_T) were calculated from this model. For examining the irreducible variability (noise) in the data, the residual sum of squares (RSS) was calculated and used as an indicator of fit of the experimental data in this model (12). Mean arterial, central venous, pulmonary arterial, and pulmonary capillary wedge pressure were measured by using an anesthesia monitor (AS-3; Datex) and standard pressure transducers zeroed to the level of the right atrium. Hemodynamic measurements were taken immediately before each collection of blood and expired samples for inert gas determination. Arterial and mixed venous samples of 2 mL each were collected and instantly analyzed for the partial pressures of oxygen (PO₂) and carbon dioxide (PCO₂), pH, oxyhemoglobin saturation, hemoglobin concentration, and hematocrit by using a Ciba Corning 806 blood gas analyzer (Ciba-Geigy, Basel, Switzerland). Values were corrected to body temperature.

Because the inert gases are exhaled, standard rebreathing systems (semiclosed circle) cannot be used with the MIGET. Consequently, a specially designed Dräger SA 2 ventilator based on a semiopen circle was used. For generating a static inflation of 10 cm H₂O, fresh gas flow (FIO₂ = 0.21) was adjusted to 1 L/min, positive end-expiratory pressure was set to 10 cm H₂O, and the ventilator’s pop-off valve was also set to 10 cm H₂O. The actual pressure in the breathing circuit was monitored by using the ventilator’s built-in manometer and at the proximal tip of the endotracheal tube with a cuff-manometer. CPB management was identical in all patients: The pleural cavity (left hemithorax) was opened because of internal mammary artery dissection before CPB. Anticoagulation was achieved by administration of heparin (300 U/kg) before aortic cannulation and monitored by repeated measurements of the activated clotting time. The CPB circuit included a pump-through membrane oxygenator and a roller pump (550 Bio-Console Pump Speed Controller; Medtronic, Lausanne, Switzerland). The system was primed with a standard solution consisting of crystalloid (1000–1200 mL) and mannitol (400–500 mL). Hypothermic CPB (30°C) was started with a pulsatile flow at a rate of approximately 2 L/min, and perfusion pressure was maintained between 50 and 60 mm Hg. Core temperature was monitored by using a temperature probe placed in the esophagus. Net negative fluid balance was maintained in all patients.

In the (ICU), lungs were ventilated by using an Evita 4 respirator (Dräger) in airway pressure release ventilation mode. In the initial setting, time for inspiration was 2 s, and time for exhalation was 4 s with pressure low set to 8 cm H₂O and pressure high set to 16 cm H₂O. Time for exhalation was then adapted to obtain an arterial PCO₂ between 35 and 40 mm Hg. At the time of the final measurement, FIO₂ was 0.4 using oxygen enriched air. All settings, except time for exhalation, were maintained until final measurements had been taken.

Data were examined by using an analysis of variance for repeated measures. Significant differences were subsequently analyzed by using the Student-Newman-Keuls test. Data were mean ± SD. P values smaller than 0.05 were considered significant.

	Results

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Patient and CPB Characteristics
Demographic data are given in Table 1. The distributions of age, sex, weight, height, and smoking history were comparable, and the number of diseased vessels was equal in both groups. All patients had an ejection fraction between 40% and 55%, estimated by using transesophageal echocardiography during the preparatory phase of the procedure. Mean CPB run time was 91 min in the CPAP group and 88 min in the control group. Mean aortic clamp times were 32 min (CPAP group) and 28 min (control). There was no significant difference in any of the demographic variables between the treatment and control groups.

Arterial PO₂ was higher in the CPAP group 4 h after CPB completion (Table 2). Similarly, the AaDO₂ was significantly smaller in the CPAP group as compared with the control group at 4 h after CPB.

No significant intragroup or intergroup differences in hemodynamic measurements could be found (Table 3).

Discharge from the ICU and Time to Extubation
In the morning after the surgery, 18 h after CPB, all patients in the CPAP group were extubated and scheduled for transfer to the intermediate care unit. Some delays in extubation encountered in the control group should be mentioned. Three patients had a low output syndrome and respiratory dysfunction caused by pulmonary congestion, and they were still in the ICU at 48 h after CPB but could be discharged on the third day after the operation without sequelae. One patient had isolated respiratory dysfunction and needed CPAP therapy via a face mask for 20 h. Another patient of the control group developed a multi-organ dysfunction syndrome during the night after the operation. This patient required intensive care and mechanical ventilation for 6 days and could then be discharged.

	Discussion

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The aim of this study was primarily to determine the effect of CPAP at 10 cm H₂O during CPB on postoperative pulmonary gas exchange. We observed that this maneuver results in significantly improved postoperative gas exchange variables. The potential danger of overdistending a lung that is not encapsulated in an intact thorax during cardiac surgery should be kept in mind: proper setting of the ventilator’s pop-off valve is of fundamental importance to avoid a potentially dangerous barotrauma. The mechanism by which this maneuver works is not definitively established. Previous studies have concluded that CPAP at 5 cm H₂O does not result in significantly better postoperative gas exchange variables (1,3). Magnusson et al. (1) showed that CPAP at 5 cm H₂O does not effectively prevent post-CPB shunt using the MIGET in pigs. In our study, the CPAP level applied was 10 cm H₂O. This pressure resulted in significantly better inert gas exchange variables with respect to blood flow to lung areas with shunt, low, and normal V_A/Q ratios (Table 2). Arterial PO₂ was significantly higher, and AaDO₂ was significantly smaller in the CPAP group four hours after CPB completion (Table 2). At the time of extubation in the ICU, gas exchange was significantly better in patients who had been treated with CPAP at 10 cm H₂O in comparison to patients whose lungs had been opened to the atmosphere. The authors suggest that CPAP at 10 cm H₂O may avoid dispersed alveolar collapse throughout the lungs.

A beneficial effect on postoperative compliance could not be achieved in comparison with control, which may be a result of the negative net fluid balance in both groups. A negative influence of CPAP at 10 cm H₂O during CPB on postoperative hemodynamics could not be found. The improved inert gas exchange after CPB found in our study compared with earlier studies is presumably related to the higher level of CPAP used, which exerts a higher pulmonary inflation than CPAP at 5 cm H₂O. In the lungs of elderly patients, airway closure occurs at increased closing capacities (10), or in other words, at higher lung volumes. In addition, as airway closure happens above FRC in anesthetized patients in the supine position (11), a higher inflation pressure appears to prevent alveolar and airway collapse and its consequences. Prolonged time to extubation secondary to cardiac, pulmonary or other problems cannot be attributed to the different respiratory management used during CPB. Equally, whether CPAP at 10 cm H₂O during CPB leads to a decreased time to extubation cannot be predicted from our data because the number of patients examined is too small. However, in our study, CPAP at 10 cm H₂O proved to be a practical maneuver during CPB to enhance post-CPB pulmonary gas exchange variables when compared with deflated lungs.

	Acknowledgments

 
The authors wish to thank Prof. Dr. W. Seeger and Dr. D. Walmrath for introducing Dr. A. Loeckinger to the multiple inert gas elimination technique during the years 1997 and 1998 in Giessen, Germany.

	References

Top Abstract Introduction Methods Results Discussion References

 

1. Magnusson L, Zemgulis V, Wicky S, et al. Effect of CPAP during cardiopulmonary bypass on postoperative lung function: an experimental study. Acta Anaesthesiol Scand 1998; 42: 1133–8.[ISI][Medline]
2. Tenling A, Hachenberg T, Tyden H, et al. Atelectasis and gas exchange after cardiac surgery. Anesthesiology 1998; 89: 371–8.[ISI][Medline]
3. Berry CB, Butler PJ, Myles PS. Lung management during cardiopulmonary bypass: is continuous positive airway pressure beneficial? Br J Anaesth 1993; 71: 864–8.[Abstract/Free Full Text]
4. Boldt J, King D, Scheld HH, Hempelmann G. Lung management during cardiopulmonary bypass: influence on extravascular lung water. J Cardiothorac Anesth 1990; 4: 73–9.[Medline]
5. Ellis EL, Brown A, Osborn JJ, Gerbode F. Effect of altered ventilation patterns on compliance during cardiopulmonary bypass. Anesth Analg 1969; 48: 947–52.[Free Full Text]
6. Chai PJ, Williamson JA, Lodge AJ, et al. Effects of ischemia on pulmonary dysfunction after cardiopulmonary bypass. Ann Thorac Surg 1999; 67: 731–5.[Abstract/Free Full Text]
7. Ghia J, Andersen NB. Pulmonary function and cardiopulmonary bypass. JAMA 1970; 212: 593–7.[Medline]
8. Hewson JR, Shaw M. Continuous airway pressure with oxygen minimizes the metabolic lesion of "pump lung." Can Anaesth Soc J 1983; 30: 37–47.[ISI][Medline]
9. Nunn JF. Nunn’s applied respiratory physiology. 4th ed. Oxford: Butterworth-Heinemann, 1993; 81–2.
10. Hedenstierna G, Bindslev L, Santesson J, Norlander OP. Airway closure in each lung of anesthetized human subjects. J Appl Physiol 1981; 50: 55–64.[Abstract/Free Full Text]
11. Akins CW, Daggett WM, Vlahakes GJ, et al. Cardiac operations in patients 80 years and older. Ann Thorac Surg 1997; 64: 606–15.[Abstract/Free Full Text]
12. Nunn JF. Nunn’s applied respiratory physiology. 4th ed. Oxford: Butterworth-Heinemann, 1993; 57–9.
13. Roca J, Wagner PD. Contribution of multiple inert gas elimination technique to pulmonary medicine. I. Principles and information content of the multiple inert gas elimination technique. Thorax 1994; 49: 815–24.[Abstract/Free Full Text]
14. Wagner PD, Saltzman HA, West JB. Measurement of continuous distributions of ventilation-perfusion ratios: theory. J Appl Physiol 1974; 36: 588–99.[Free Full Text]
15. Evans JW, Wagner PD. Limits on VA/Q distributions from analysis of experimental inert gas elimination. J Appl Physiol 1977; 42: 889–98.[Abstract/Free Full Text]
16. Wagner PD, Naumann PF, Laravuso RB. Simultaneous measurement of eight foreign gases in blood by gas chromatography. J Appl Physiol 1974; 36: 600–5.[Free Full Text]
17. West JB. Ventilation-perfusion inequality and overall gas exchange in computer models of the lung. Respir Physiol 1969; 7: 88–110.[ISI][Medline]

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999