|Year : 2014 | Volume
| Issue : 2 | Page : 232-237
Low tidal volume lung ventilation during cardiopulmonary bypass decreases the potential of postoperative lung injury
Ahmed M. Salama, Magdy H.H. Eldegwy, Hany Othman, Aymen S. Abdelaziz
Department of Anesthesiology and ICU, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
|Date of Submission||29-Jul-2013|
|Date of Acceptance||28-Oct-2013|
|Date of Web Publication||31-May-2014|
Ahmed M. Salama
Department of Anesthesiology and ICU, Faculty of Medicine, Al-Azhar University, Cairo 3050
Source of Support: None, Conflict of Interest: None
Postoperative pulmonary dysfunction is one of the common complications after cardiac surgery that may lead to serious morbidity and mortality. In this study, we investigated the potential benefit of continued lung ventilation while on cardiopulmonary bypass (CPB) to minimize postoperative lung injury whether resulting from CPB alone or from non-CPB causes.
Patients and methods
It is a prospective study including 60 patients who were randomized into two groups, each of 30 patients. One group underwent modified CPB (the MB group) where the lungs were ventilated with low tidal volume 3 ml/kg and PEEP of 5 cmH 2 O, whereas the other group underwent the conventional CPB (CB group) with total ventilation arrest and no PEEP. Parameters such as PaO 2 /FiO 2 ratio, alveolar arterial oxygen gradient [D (A-a) O 2 ], extravascular lung water, static and dynamic lung compliance, extubation time, and postoperative chest complications such as pleural effusion, atelectasis, and pulmonary edema were compared in the two groups.
In the MB group, there were significantly higher post-bypass extravascular lung water, lower static and dynamic lung compliance, higher post-bypass PaO 2 /FiO 2 ratio, lower D (A-a) O 2 , and shorter extubation time. However, postoperative complications on first and fourth postoperative days were insignificant in both groups.
Lung ventilation with low tidal volume during CPB can reduce the potential of post-CPB lung injury by improving lung oxygenation, reducing lung ischemia, and decreasing postoperative lung atelectasis, resulting in shorter extubation time and less postoperative pulmonary complications.
Keywords: Cardiac surgery, cardiopulmonary bypass, lung injury, ventilation
|How to cite this article:|
Salama AM, Eldegwy MH, Othman H, Abdelaziz AS. Low tidal volume lung ventilation during cardiopulmonary bypass decreases the potential of postoperative lung injury. Ain-Shams J Anaesthesiol 2014;7:232-7
|How to cite this URL:|
Salama AM, Eldegwy MH, Othman H, Abdelaziz AS. Low tidal volume lung ventilation during cardiopulmonary bypass decreases the potential of postoperative lung injury. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2021 Nov 27];7:232-7. Available from: http://www.asja.eg.net/text.asp?2014/7/2/232/133448
| Introduction|| |
One of the most frequent complications of cardiac surgery is postoperative lung injury that has been believed to be related to the use of cardiopulmonary bypass (CPB). Postoperative pulmonary dysfunction following CPB is a significant clinical problem ranging from subclinical functional changes in most patients to full-blown acute respiratory distress syndrome (ARDS) in less than 2% of patients after CPB. The mortality rate associated with ARDS is 50-90%, not including the morbidity leading to prolonged postoperative recoveries and hospital stays ,.
Pulmonary dysfunction after CPB may be the result of multiple insults, including extra-CPB factors such as general anesthesia, sternotomy, and breach of the pleura and intra-CPB factors such as inflammatory responses (postpump syndrome), vasoactive and cytotoxic mediators, lung ischemia, ischemia-reperfusion injury, increased pulmonary capillary permeability, administration of heparin-protamine, hypothermia, and lung ventilatory arrest ,,.
Ventilation arrest during CPB has been practiced by most of the cardiac surgeons, as blood oxygenation by the lungs is no longer required and the movement from mechanical ventilation may interfere with the surgery. However, this ventilator arrest is associated with regional atelectasis, retained bronchial secretions, increased physiological arteriovenous shunts with reduced systemic arterial PaO 2 , hydrostatic pulmonary edema, poor compliance, and a higher incidence of infection ,,.
Apnea during CPB has also been suggested to promote activation of lysosomal enzymes in the pulmonary circulation, which in turn are correlated with the incidence of postoperative pulmonary dysfunction (Acute Lung Injury (ALI) or ARDS) .
It has been hypothesized that applying some maneuvers, such as the intermittent/continuous ventilation or continuous positive airway pressure and vital capacity maneuver (VCM - i.e. a peak airway pressure of 40 cmH 2 O with a fraction of inspired oxygen of 0.4 for about 15 s), during CPB might limit post-bypass lung dysfunction ,,,.
Moreover, for the lungs that are totally dependent on oxygen supply from the bronchial arteries during the period of cardiac arrest, an additional contribution to lung tissue oxygenation through gas diffusion by continuous ventilation may be considered as a worth measure .
This prospective randomized study will evaluate the effect of continued lung ventilation during CPB on postoperative pulmonary outcome, in which patients are randomized into either ventilation or no ventilation on bypass, and measures of lung injury as well as clinical outcomes will be compared between the two groups.
| Patients and methods|| |
After approval by the local ethical committee and obtaining informed consent, a prospective randomized study was conducted on 60 patients scheduled for elective coronary artery bypass grafting (CABG) in Heart Hospital Doha, Qatar during the period between April 2012 and April 2013. Patients were randomly allocated into two groups: conventional CPB (the CB group, n = 30) and modified CPB (the MB group, n = 30).
- Patient age more than 70 years,
- obesity with BMI of at least 30%,
- poor left ventricular function (left ventricular ejection fraction< 30%),
- valvular heart disease (any disease process involving one or more of the valves of the heart),
- significant pulmonary disease as defined by preoperative forced expiratory volume in the first second (FEV 1 ) or forced vital capacity values less than 40% of the predicted value,
- insulin-dependent diabetes,
- renal impairment (elevated serum creatinine),
- redo surgery, emergency surgery, combined CABG, and carotid endarterectomy.
All patients underwent CABG surgeries by the same surgeon. All patients were anesthetized by the same anesthesia team using a standardized technique.
All patients were premedicated with intramuscular morphine (0.15 mg/kg) and metoclopramide (0.5 mg/kg) 2 h before the induction of anesthesia.
Arterial and central venous cannulation was conducted for all patients. A 4-Fr femoral catheter was also inserted and connected to the catheter of the PiCCO system (Pulsion Medical Systems, Munich, Germany) after induction of anesthesia.
Anesthesia and surgery
Anesthesia was induced with intravenous fentanyl (3-5 μg/kg), etomidate (50 μg/kg), and cisatracurium (0.15-0.2 mg/kg). After endotracheal intubation, patients were ventilated mechanically with an inspired oxygen fraction of 0.6, and lungs were ventilated mechanically in both groups with a tidal volume of 6-8 ml/kg with a respiratory rate of 12, and adjusted to obtain an end-tidal CO 2 (ETCO 2 ) of 35-40 mmHg. Anesthesia was maintained with combined total intravenous anesthesia and inhalational anesthesia during CPB, where the ventilation was stopped; sevoflurane (2-2.5%), fentanyl infusion (0.03-0.1 μg/kg/min), and cisatracurium (1-3 μg/kg/min) and propofol infusion (1-2 mg/kg/h) were maintained during pre-bypass and post-bypass period.
In the CB group, mechanical ventilation was arrested with no positive end-expiratory pressure.
In the MB group, lungs were ventilated mechanically during CPB with low tidal volume [Vt = 3 ml/kg (lean body mass), relative risk = 12, FiO 2 = 0.6, PEEP = 5 cmH 2 O, and I/E ratio = 1 : 2]; the respiratory rate was adjusted to obtain an end-expiratory carbon dioxide tension (ETCO 2 ) of 35-40 mmHg.
The CPB circuit consisted of a roller pump and a membrane oxygenator. The circuit was primed with lactated Ringer's solution, albumin, and mannitol, with packed red cells transfused, if necessary to maintain the lowest accepted hematocrit at 18%. After systemic heparinization, the target-activated clotting time was 480 s, which was neutralized with protamine sulfate at the end of the operation; the systemic flow was adjusted to 2.4 l/min/m 2 to maintain mean arterial pressure at 60 mmHg. The patient was cooled (32°C) in both groups. Cardiac arrest was accomplished by aortic cross-clamp and infusion of cardioplegic solution (10 ml/kg) into the aortic root.
With the conventional and modified techniques, blood gas management during CPB was directed toward maintenance of pH at 7.35-7.40, arterial carbon dioxide tension (PaCO 2 ) at 35-40 mmHg, and arterial oxygen tension (PaO 2 ) to at least 200 mmHg. After termination of bypass, blood remaining in the CPB circuit was retransfused.
The following were measured for all patients in the study:
- PaO 2 /FiO 2 ratio: It was used as the parameter of oxygenation and pulmonary function and was measured at postintubation, 1 h post-bypass, and 4 h postoperatively.
- Alveolar arterial oxygen gradient [D (A-a) O 2 ]: It was measured at postintubation, 1 h post-bypass, and 4 h postoperatively.
- Extravascular lung water (EVLW): It was measured at postinduction but presternotomy, post-bypass before leaving the theaters, and 1 day postoperatively using the PiCCO system (Pulsion Medical Systems).
- Static and dynamic lung compliance (ml/mmHg): It was measured using the ventilator at postintubation before sternotomy and post-bypass following sternal closure.
- Extubation time (h): It was the time from ICU admission until weaning from ventilation and extubation.
- ICU stay length (h): It was the time from ICU admission until discharge from ICU to high-dependent unit.
- Chest complication: for example, pleural effusion, atelectasis, and pulmonary edema were compared in both groups.
- Operative details included number of grafts, bypass time, and aortic cross-clamp time.
The findings of the groups were statistically compared using SPSS version 16 (SPSS Inc., Chicago, Illinois, USA). Data were expressed as mean ± SD, number, and percentage. Nominal nonparametric data were analyzed using the c2 -test. Parametric data were compared using unpaired t-test. Ordinal nonparametric data were analyzed using Mann-Whitney U-test. P-values less than 0.05 were considered statistically significant.
| Results|| |
The demographic data of patients, types of surgeries, CPB time, aortic cross-clamping (AXC) time, and number of grafts of the two studied groups were comparable with no significant difference (P > 0.05) as shown in [Table 1].
PaO 2 /FiO 2 ratio was significantly higher in the MB group at 1 h post-bypass with no significance at postintubation (baseline) and postoperation [Table 2].
Alveolar arterial oxygen gradient [D (A-a) O 2 ] was significantly less in the MB group at 1 h post-bypass with no significance at postintubation (baseline) and postoperation [Table 2]. EVLW was significantly less in the MB group than in the CB group at post-bypass without any significance at postintubation and at 1 day postoperation [Table 2]. Static and dynamic lung compliance was significantly higher in the MB group at post-bypass without any significance at postintubation and at 1 day postoperation [Table 2].
Extubation time was also significantly shorter in the MB group than in the CB group without any significant difference regarding the ICU length stay in both groups [Table 2].
There was no significant difference in both groups regarding postoperative complications on first and fourth postoperative days [Table 3] and [Table 4].
|Table 3: Postoperative pulmonary complications seen on chest radiography on the first day in patients of both groups|
Click here to view
|Table 4 Postoperative pulmonary complications seen on chest radiography on the fourth day in patients of both groups|
Click here to view
| Discussion|| |
Despite the improvement in the CPB techniques as well as the postoperative intensive care, impaired pulmonary function is a well-documented complication of CPB, resulting in increased morbidity and mortality . The systemic inflammatory response to CPB plays a major role for lung injury following bypass . Bypass primes and activates neutrophils both by their exposure to mechanical shear stress and artificial surfaces . In addition, bypass results in the activation of the complement pathways  and is also associated with the release of proinflammatory cytokines that lead to extravasation of the fluid and activated leukocytes, with trapping and sequestration of these leukocytes in the interstitial lung tissues during their pulmonary vascular transit. CPB results in induction of oxygen-free radicals that mediate pulmonary endothelial damage as well .
Lungs are subjected to ischemia during bypass, and postischemic reperfusion of lungs activates the inflammatory pathway as well. Thus, the systemic inflammatory response and ischemia-reperfusion during CPB constitute a vicious cycle in the pathogenesis of post-CPB lung injury.
An additional factor to lung injury is apnea during bypass that has been associated with the development of lung microatelectasis, increased arteriovenous shunts with reduced systemic arterial PaO 2 , hydrostatic pulmonary edema, poor compliance, and a higher incidence of chest infection ,. Apnea during CPB has been suggested to promote activation of lysosomal enzymes in the pulmonary circulation, which in turn are correlated with the incidence of postoperative pulmonary dysfunction (ALI or ARDS) .
A further possibility is that nonventilation may result in ischemic lung 'injury'. The human lung consumes about 5-6 ml/min of oxygen at 27°C and 11 ml/min at 36°C . During bypass, vascular supply to lungs is only through the bronchial arteries and it appears that lung inflation decreases bronchial blood flow probably because of mechanical compression and stretching of the vessels at the bronchopulmonary arterial anastomoses. Cyclic inflation and deflation of lungs at physiological intra-alveolar pressure leads to cyclic compression and relaxation of the vessels that helps to maintain bronchial arterial flow . In that case, cessation of ventilation during bypass would reduce bronchial flow and predispose to ischemic lung injury.
An experimental study on bronchial artery flow during bypass in a porcine model reported a decrease from 42.1 ± 10.4 to 5.6 ± 1.0 ml/min . If this was also the case with human bypass, then it is possible that cessation of ventilation could lead to bronchial hypoperfusion that could significantly contribute to lung ischemia and complications following cardiac surgery.
Many approaches have been performed to decrease the post-bypass lung injury. Of these approaches was the modification of the ventilation protocol used during CPB. These modifications include the VCM, continuous positive airways pressure, and continued ventilation with low tidal volume.
The results of the current study showed that post-bypass EVLW was significantly less in the MB group probably due to less extravasation in the interstitial lung tissue that was reflected as significant higher compliance and better gas exchange in this MB group.The post-bypass PaO 2 /FiO 2 ratio was significantly higher and D (A-a) O 2 was significantly lower in the MB group, when the lungs were continuously ventilated during CPB, reflecting better oxygenation; this appeared clinically in significantly shorter extubation time in the MB group. Probably, this better oxygenation could be explained by recruitment of the lungs and prevention of microatelectasis, improving gas exchange across the alveolocapillary membrane with less extravasated fluid, in addition to maintaining the normal bronchial blood flow to the lung during the bypass time and using the patient's lungs as an additional oxygenator giving contribution to lung tissue oxygenation through gas diffusion. However, the 4 h post-bypass PaO 2 /FiO 2 ratio and D (A-a) O 2 were insignificant and postoperative complications were also insignificant in both groups, probably because the CPB and aortic cross-clamp times were not prolonged in the two groups in the current study, but with prolonged CPB time and aortic cross-clamp time during redo or complicated surgery the ventilation maneuvers may proof a significant benefit.
The effects of ventilation during CPB have been tested in a number of studies. John and Ervine,  who compared continuous lung ventilation on CPB with conventional CPB without ventilation, found that the post-bypass EVLW was significantly smaller and extubation time was also significantly shorter in the ventilated group. The alveolar arterial oxygen gradient and the respiratory index 1 h postoperatively were smaller in the ventilated group than in the nonventilated group, but this did not reach statistical significance, possibly because of the relatively small sample size, 23 patients compared with 60 patients in our current study in which we found a statistically significant difference in the ventilated group . However, a higher number of patients were intended to be included in the study to rule out the statistical difference more, but because of the exclusion criteria of the study and because the rate of cardiac surgeries is not high only 60 patients were enrolled.
Davoudi and colleagues, who ventilated the lung with 3 ml/kg tidal volume and PEEP of 5 cmH 2 O in one group and compared it with other group without ventilation or PEEP, found that post-bypass PaO 2 was significantly higher and the decrease in postoperative FEV 1 and forced vital capacity was significantly lower in the ventilated group. In addition, time to extubation was shorter in the ventilated group .
Massoudy and colleagues, in addition to continued lung ventilation with low tidal volume on bypass, perfused the lungs through an additional cannulation of pulmonary artery and left atrium (Drew technique) and compared that with the conventional bypass without lung ventilation or perfusion; they found that extravascular thermal volume did not change with modified bypass CPB but increased with conventional CPB with earlier extubation time in the modified CPB. Thus, using the patient's lungs as an oxygenator during bypass mitigates the increase in extravascular pulmonary fluid, which in turn decreases the potential of post-bypass lung injury, similar to the results obtained in our study. However, its complexity and potential for complications has not led to its significant application .
In a porcine model, VCM at the end of CPB resulted not only in improved gas exchange, but also reduced the incidence of atelectasis, as determined by a computed tomographic scan soon after CPB. However, repeating the VCM may not produce extra benefits .
A few limitations of the study deserve mention. One was that it did not evaluate the effect of continued lung ventilation on the inflammatory process involved in the pathology of post-bypass lung injury. Probably, it could be performed by estimating the leukocytes count and inflammatory mediators. The low compliance of surgeons to lung movement during bypass should also be considered as a limitation to that procedure. Another limitation is that the significant increase in post-bypass EVLW in the CB group should be cautiously correlated to the pathogenesis of lung injury, as other factors may affect EVLW, such as priming volume and intraoperative fluid balance, which should be considered in future studies.
Finally, other additional methods may contribute to further lung protection during CPB, such as pulmonary perfusion techniques and shift to modified CPB circuits, and more investigative study is required to determine the precise role of different lung-protective strategies during CPB.
| Conclusion|| |
Continuous lung ventilation during CPB can reduce the potential of post-CPB pulmonary dysfunction by reducing lung ischemia through maintenance of arterial bronchial blood flow, decreasing lung microatelectasis, decreasing arteriovenous shunts, and improving lung oxygenation ending to shorter extubation time and less postoperative pulmonary complications. Fortunately, this could be achieved through simple, noninvasive, and noncostly maneuvers.
| Acknowledgements|| |
Conflicts of interest
| References|| |
|1.||Messent M, Sullivan K, Keogh BF. Adult respiratory distress syndrome following cardiopulmonary bypass: incidence and prediction. Anaesthesia 1992; 47:267-268. |
|2.||Asimakopoulos G, Smith PL, Ratnatunga CP, et al. Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass. Ann Thorac Surg 1999; 68:1107-1115. |
|3.||Picone AL, Lutz CJ, Finck C, et al. Multiple sequential insults cause post-pump syndrome. Ann Thorac Surg 1999; 67:978-985. |
|4.||Wan S, LeClerc JL, Vincent JL. Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies. Chest 1997; 112:676-692. |
|5.||Friedman M, Sellke FW, Wang SY, et al. Parameters of pulmonary injury after total or partial cardiopulmonary bypass. Circulation 1994; 90:262-268. |
|6.||Magnusson L, Zemgulis V, Tenling A, et al. Use of a vital capacity maneuver to prevent atelectasis after cardiopulmonary bypass. Anesthesiology 1998; 88:134-142. |
|7.||Loeckinger A, Kleinsasser A, Lindner KH, et al. Continuous positive airway pressure at 10 cm H 2 O during cardiopulmonary bypass improves postoperative gas exchange. Anesth Analg 2000; 91:522-527. |
|8.||Muller H, Hugel W, Reifschneider HJ, Horpacsy G, Hannekum A, Dalichau H. Lysosomal enzyme activity influenced by various types of respiration during extracorporeal circulation. Thorac Cardiovasc Surg 1989; 37:65-71. |
|9.||Speekenbrink R, van Oeveren W, Wildevuur C. Golstein D, Oz M. Pathophysiology of cardiopulmonary bypass. Minimally invasive cardiac surgery. Vol. 2. Totowa, New Jersey: Humana Press; 2004:3-18. |
|10.||1Ng CS, Wan S, Yim AP, Arifi AA. Pulmonary dysfunction after cardiac surgery. Chest 2002; 121:1269-1277. |
|11.||1Apostolakis E, Filos K, Koletsis E, Dougenis D. Lung dysfunction following cardiopulmonary bypass. J Card Surg 2009; 25:47-55. |
|12.||1Gu YJ, Boonstra PW, Graaf R, Rijnsburger AA, Mungroop H, van Oeveren W. Pressure drop, shear stress and activation of leukocytes during cardiopulmonary bypass: a comparison between hollow fibre and flat sheet membrane oxygenators. Artif Organs 2000; 24:43-48. |
|13.||1Tennenberg SD, Clardy CW, Bailey WW, Solomkin JS. Complement activation and lung permeability during cardiopulmonary bypass. Ann Thorac Surg 1990; 50:597-601. |
|14.||1Ascione R, Loys CT, Underwood MJ, Lotto AA, Pitsis AA, Angelini GD. Inflammatory response after coronary revascularization with or without cardiopulmonary bypass. Ann Thorac Surg 2000; 69:1198-1204. |
|15.||1Loer SA, Scheeren TW, Tarnow J. How much oxygen does the human lung consume? Anesthesiology 1997; 86:532-537. |
|16.||1Deffebach ME. Lung mechanical effects on the bronchial circulation. Eur Respir J Suppl 1990; 12:586s-590s. |
|17.||1Schlensak C, Doenst T, Preusser S, Wunderlich M, Kleinschmidt M, Beyersdorf F. Cardiopulmonary bypass reduction of bronchial blood flow: a potential mechanism for lung injury in a neonatal pig model. J Thorac Cariovasc Surg 2002; 123:1199-1205. |
|18.||1LC John, IM Ervine. A study assessing the potential benefit of continued ventilation during cardiopulmonary bypass, Interact CardioVasc Thorac Surg 2008; 7:14-17. |
|19.||1Davoudi M, Farhanchi A, Moradi A, Bakhshaei MH, Safarpour G. The effect of low tidal volume ventilation during cardiopulmonary bypass on postoperative pulmonary function. J Tehran Heart Cent 2010; 3:128-131. |
|20.||2Massoudy P, Piotrowski JA, van de Wal HCJM, Giebler R, Marggraf G, Peters J, Jakob HG. Perfusing and ventilating the patient′s lungs during bypass ameliorates the increase in extravascular thermal volume after coronary bypass grafting. Ann Thorac Surg 2003; 76:516-521. |
[Table 1], [Table 2], [Table 3], [Table 4]