Volume 17, Issue 1 , Pages 40-44, February 2003
The effect of high-frequency ventilation of the lungs on postbypass oxygenation: A comparison with other ventilation methods applied during cardiopulmonary bypass☆
Article Outline
Abstract
Objective: To compare the effect of high-frequency ventilation versus other ventilation methods applied during cardiopulmonary bypass on postbypass oxygenation. Design: Prospective, randomized study. Setting: University hospital. Participants: Seventy-five patients undergoing coronary artery bypass graft surgery. Interventions: Patients were allocated to 5 equal groups of different ventilation methods during bypass. Groups 1 and 2 received high-frequency, low-volume ventilation with 100% and 21% oxygen, respectively. Groups 3 and 4 received 5 cm H2O of continuous positive airway pressure (CPAP) with either 100% or 21% oxygen. Patients from group 5 were disconnected from the ventilator during the bypass period. Measurements and Main Results: Spirometry data, blood gas analysis, oxygen saturation as measured by pulse oximetry, and end-tidal carbon dioxide were recorded 5 minutes before chest opening, 5 minutes before bypass, 5 minutes after bypass, 5 minutes after chest closure and 6, 12, 18, and 24 hours after surgery. There were no differences in compliance and mean airway pressures. Alveolar-to-arterial oxygen gradients increased, and PaO2 decreased significantly (p < 0.05) in all groups 5 minutes after bypass and this trend continued in the postoperative period. Patients from group 3 had higher PaO2 and lower alveolar-to-arterial oxygen gradients, 5 minutes after weaning from bypass (p < 0.05). Extubation times were similar in all groups. Conclusions: The alveolar-arterial oxygen gradient was lower, and the PaO2 was higher 5 minutes after bypass in patients receiving CPAP (100% O2) as compared with those ventilated with high-frequency ventilation. Copyright 2003, Elsevier Science (USA). All rights reserved.
Keywords: High-frequency ventilation, cardiopulmonary bypass, oxygenation, pulmonary complications
Impaired gas exchange consistent with transient acute lung injury is a well-recognized complication of cardiopulmonary bypass (CPB).1 Accumulation of excessive extrapulmonary lung water may lead to increased shunting and hypoxemia.2 Atelectasis of the lungs is another major cause of hypoxemia after CPB.3 Risk factors such as preoperative pulmonary disease or arterial hypertension have also been implicated.4
It is controversial whether the ventilation mode during bypass and composition of the anesthetic gas mixture during bypass affects postbypass alveolar gas exchange and ventilation. One study5 failed to show any advantage of passive inflation of the lungs over allowing them to remain collapsed during bypass in decreasing postoperative shunting and improving pulmonary compliance. The authors also failed to prove an effect of different types of gas mixtures administered during CPB.5 Others6 showed that ventilation with lower (6 mL/kg) tidal volumes (which the authors called “protective ventilation”) during surgery may attenuate the postoperative pulmonary dysfunction. Pizov et al7 have found that high oxygen concentration exacerbates CPB-induced lung injury by a supposed proinflamatory cytokine-induced mechanism. At the present time, no specific technique of managing the lungs during CPB has been proven to be beneficial.
In this study, the effects of high-frequency ventilation versus other ventilation methods on postbypass oxygenation applied during CPB were compared.
Methods
This prospective, randomized study was approved by the Institutional Human Investigations Committee, and each patient signed an informed consent. Seventy-five patients scheduled for coronary artery bypass grafting were enrolled in the study. Excluded were patients with an ejection fraction <40%, pre-existing pulmonary hypertension (regardless of cause, pulmonary hypertension defined as mean pulmonary arterial pressure is greater than 25 mmHg at rest or 30 mmHg during exercise8), documented chronic lung disease (chronic obstructive pulmonary disease is defined as a disease state characterized by the presence of airflow obstruction because of chronic bronchitis or emphysema; the airflow obstruction is generally progressive, may be accompanied by airway hyperreactivity, and may be partially reversible9), and patients who were mechanically ventilated preoperatively. Patients who had a bypass period longer than 3 hours were subsequently excluded from the study.
Anesthesia was induced with fentanyl, 20 to 30 μg/kg; midazolam, 2 to 5 mg; vecuronium, 0.1 to 0.15 mg/kg; and isoflurane in 100% oxygen. Monitoring consisted of an electrocardiogram, pulse oximetry, capnography, rectal and nasopharyngeal temperature, invasive blood pressure, cardiac output, systemic and pulmonary vascular resistance, pulmonary artery, and pulmonary capillary wedge pressure measurements. Hemodynamic variables were measured and calculated at the same time points as the spirometry variables, with the thermodilution technique, whereas systemic and pulmonary resistances were calculated from the Ohm's equation (Appendix 1).10
Patients were randomly allocated to 5 groups (15 patients per group) of different ventilation methods during bypass. Group 1 received high frequency ventilation (HFV) at a rate of 100 breaths/min, a tidal volume of 2 mL/kg, and fraction of inspired oxygen (FIO2) of 1. Group 2 received the same type of ventilation with FIO2 of 0.21 (oxygen in air). Groups 3 and 4 received 5 cm H2O of continuous positive airway pressure (CPAP) with an FIO2 of 1 or 0.21, respectively, at a total fresh gas flow of 3 L/min. In group 5, patients were completely disconnected from the ventilator during the bypass period (lungs collapsed).
Before and after bypass, patients were ventilated with FIO2 of 1, at a rate of 10-12 breaths/min, and a tidal volume of 10 mL/kg. The inspiration-expiration time ratio was standardized at 1:2. Intraoperative spirometry was performed with the spirometry module of the AS3-Datex monitor (Datex, Helsinki, Finland) and consisted of ventilatory volume, peak inspiratory pressure (PIP) and mean airway pressures, lung compliance, along with pressure/volume and flow/volume loops recording. Data from spirometry were recorded 5 minutes before chest opening, 5 minutes before inducing CPB, 5 minutes after weaning from bypass, and 5 minutes after chest closure. Lung compliance was calculated from 3 consecutive readings at each measurement point, and the final number recorded was the average of these 3 readings. Blood gas analysis was performed at the same stages. End-tidal carbon dioxide and oxygen saturation as measured by pulse oximetry values were recorded at the same time with the parameters from spirometry. Patients received the same maintenance fluid regimen (4 mL/kg/h). The total amount of fluids infused and urinary output during the whole procedure were also recorded.
In the intensive care unit, patients were mechanically ventilated with an FIO2 of 0.5. The FIO2 was increased to 1 and maintained at this level for 15 minutes before each measurement point of the study. Patients were ventilated with the same ventilatory settings along with 5 cm H2O of CPAP for at least 12 hours, whereas spirometry data and blood gas samples were taken 6, 12, 18, and 24 hours after surgery. The alveolar-arterial partial pressure differences (dO2) were calculated with each blood gas sampling according to the alveolar gas equation (Appendix 1).10 Gases were measured at 1 atm (760 mmHg) barometric pressure (sea level). End-tidal carbon dioxide readings were used as alveolar carbon dioxide. The respiratory quotient was considered 0.8. A postoperative chest radiograph was performed in each patient. Weaning from the ventilator was started 12 hours after surgery after confirming that the patient was awake, had gained full motor strength (head lift for at least 5 seconds), was hemodynamically stable, and had no ongoing bleeding. Weaning was performed according to standard criteria.11 The trachea was extubated under the conditions described earlier, along with the patient's ability to develop a negative inspiratory pressure of more than −30 cm H2O and a dO2 of <200 mmHg.
Results are expressed as mean ± SD and percentage. Repeated measure general linear mode analysis was applied to the data set. Differences were considered significant with p ≤ 0.05. Bonferroni technique was used for post hoc comparison between pairs of groups.
Results
Demographic and intraoperative data are presented in Tables 1 and 2. Among the 5 groups, there were no significant differences with regard to preoperative diseases, age, type of grafts, bypass time, the volume of fluids administered, and urinary output. There were more men (57 v 18 women), but sex was evenly distributed among the 5 groups. The number of grafts and aortic cross-clamping times were shorter in groups 1 and 5 (Table 2). Other demographic and intraoperative data were similar (Tables 1-3).
Table 3. Intraoperative hemodynamic data
| Variable | Group 1 | Group 2 | Group 3 | Group 4 | Group 5 |
|---|---|---|---|---|---|
| HR-1 | 72 ± 16 | 68 ± 10 | 70 ± 20 | 69 ± 32 | 72 ± 23 |
| HR-2 | 68 ± 12 | 67 ± 23 | 72 ± 22 | 70 ± 16 | 70 ± 18 |
| HR-3 | 69 ± 12 | 71 ± 19 | 66 ± 17 | 70 ± 9 | 68 ± 11 |
| HR-4 | 95 ± 28 | 98 ± 24 | 97 ± 22 | 101 ± 23 | 103 ± 16 |
| MAP-1 | 87 ± 19 | 90 ± 18 | 88 ± 16 | 88 ± 19 | 91 ± 18 |
| MAP-2 | 90 ± 16 | 91 ± 18 | 87 ± 12 | 88 ± 12 | 87 ± 11 |
| MAP-3 | 86 ± 11 | 91 ± 17 | 90 ± 13 | 88 ± 12 | 89 ± 21 |
| MAP-4 | 88 ± 16 | 87 ± 20 | 88 ± 22 | 91 ± 21 | 88 ± 12 |
| CI-1 | 2.9 ± 0.3 | 2.7 ± 0.2 | 3 ± 0.3 | 2.8 ± 0.2 | 3.1 ± 0.3 |
| CI-2 | 2.6 ± 0.2 | 2.5 ± 0.1 | 2.7 ± 0.3 | 2.5 ± 0.2 | 2.5 ± 0.2 |
| CI-3 | 2.5 ± 0.1 | 2.5 ± 0.2 | 2.6 ± 0.2 | 2.3 ± 0.1 | 2.5 ± 0.2 |
| CI-4 | 2.7 ± 0.2 | 2.6 ± 0.2 | 2.6 ± 0.1 | 2.6 ± 0.3 | 2.7 ± 0.4 |
| MPAP-1 | 18 ± 4 | 19 ± 6 | 20 ± 7 | 19 ± 5 | 20 ± 6 |
| MPAP-2 | 19 ± 4 | 20 ± 7 | 22 ± 7 | 17 ± 3 | 19 ± 4 |
| MPAP-3 | 17 ± 4 | 19 ± 5 | 20 ± 6 | 22 ± 7 | 19 ± 4 |
| MPAP-4 | 21 ± 8 | 22 ± 7 | 19 ± 6 | 23 ± 8 | 20 ± 4 |
| PCWP-1 | 12 ± 2 | 10 ± 1 | 8 ± 1 | 14 ± 3 | 11 ± 2 |
| PCWP-2 | 10 ± 2 | 13 ± 3 | 8 ± 1 | 12 ± 2 | 11 ± 3 |
| PCWP-3 | 15 ± 3 | 13 ± | 9 ± 1 | 13 ± 2 | 10 ± 2 |
| PCWP-4 | 15 ± 4 | 16 ± 54 | 11 ± 3 | 16 ± 4 | 9 ± 1 |
| SVR-1 | 1000 ± 110 | 800 ± 78 | 890 ± 78 | 1100 ± 120 | 980 ± 88 |
| SVR-2 | 880 ± 80 | 880 ± 75 | 980 ± 100 | 1000 ± 78 | 960 ± 100 |
| SVR-3 | 920 ± 78 | 860 ± 90 | 980 ± 76 | 1020 ± 88 | 1000 ± 152 |
| SVR-4 | 1020 ± 100 | 1120 ± 98 | 1210 ± 110 | 1280 ± 200 | 1220 ± 200 |
| PVR-1 | 98 ± 10 | 113 ± 20 | 100 ± 18 | 86 ± 10 | 100 ± 12 |
| PVR-2 | 90 ± 14 | 110 ± 15 | 100 ± 12 | 84 ± 11 | 100 ± 12 |
| PVR-3 | 89 ± 12 | 106 ± 16 | 105 ± 16 | 90 ± 12 | 100 ± 14 |
| PVR-4 | 110 ± 20 | 116 ± 22 | 115 ± 22 | 128 ± 24 | 106 ± 16 |
Table 1. Demographic and intraoperative data
| Group | 1 | 2 | 3 | 4 | 5 |
|---|---|---|---|---|---|
| Previous MI | 4 | 3 | 4 | 5 | 5 |
| Hypertension | 7 | 9 | 7 | 8 | 8 |
| Diabetes mellitus | 6 | 5 | 4 | 6 | 5 |
| Beta-blockers | 4 | 3 | 5 | 4 | 3 |
| Ca channel blockers | 5 | 3 | 3 | 4 | 3 |
| Diuretics | — | 1 | — | — | 1 |
| Total fentanyl (μg/kg) | 38 ± 8 | 40 ± 6 | 38 ± 11 | 39 ± 7 | 40 ± 3 |
| Total vecuronium (mg/kg) | 0.26 ± 0.05 | 0.27 ± 0.03 | 0.26 ± 0.01 | 0.28 ± 0.01 | 0.27 ± 0.01 |
| Intraoperative fluids (mL) | 1,600 ± 300 | 1,800 ± 200 | 2,000 ± 100 | 1,800 ± 200 | 1,700 ± 300 |
| Packed red cells (U) | 0.5 ± 0.5 | 0.6 ± 0.2 | 0.5 ± 0.4 | 0.5 ± 0.4 | 0.6 ± 0.4 |
| Urinary output (mL) | 400 ± 55 | 380 ± 100 | 360 ± 120 | 460 ± 60 | 420 ± 40 |
Table 2. Demographic and intraoperative data
| Group | Age (y) | BSA | Number of Grafts | Aortic Cross-Clamp Time | Bypass Time (min) |
|---|---|---|---|---|---|
| 1 | 66 ± 6 | 1.8 ± 0.3 | 2.7 ± 1 | 79 ± 10 | 107 ± 15 |
| 2 | 66 ± 8 | 1.8 ± 0.2 | 3.3 ± 1 | 81 ± 8 | 123 ± 2 |
| 3 | 68 ± 5 | 1.8 ± 0.4 | 3.1 ± 1 | 83 ± 6 | 119 ± 2 |
| 4 | 67 ± 7 | 1.7 ± 0.3 | 3.0 ± 1 | 90 ± 3 | 117 ± 5 |
| 5 | 65 ± 4 | 1.8 ± 0.6 | 2.8 ± 1 | 79 ± 11 | 105 ± 8 |
No differences were recorded with regard to lung compliance (Table 4).
Table 4. Perioperative lung compliance
| Group | Compliance† 1* | Compliance 2* | Compliance 3* | Compliance 4* | Compliance 5* | Compliance 6* | Compliance 7* | Compliance 8* |
|---|---|---|---|---|---|---|---|---|
| 1 | 49 ± 4 | 54 ± 6 | 56 ± 8 | 49 ± 4 | 49 ± 6 | 54 ± 3 | 56 ± 5 | 48 ± 4 |
| 2 | 48 ± 4 | 54 ± 1 | 51 ± 5 | 48 ± 4 | 48 ± 1 | 52 ± 1 | 51 ± 3 | 47 ± 4 |
| 3 | 46 ± 5 | 52.46 | 48 ± 5 | 47 ± 1 | 47 ± 5 | 50.46 | 48 ± 4 | 48 ± 1 |
| 4 | 52 ± 5 | 56 ± 7 | 55 ± 6 | 50 ± 6 | 51 ± 5 | 56 ± 3 | 55 ± 2 | 51 ± 6 |
| 5 | 49 ± 1 | 55 ± 1 | 56 ± 5 | 49 ± 3 | 48 ± 1 | 53 ± 1 | 54 ± 5 | 49 ± 1 |
| *Timing of measurements: 5 minutes before chest opening (1), 5 minutes before bypass (2), 5 minutes after bypass (3), 5 minutes after chest closure (4), and 6-24 hours after surgery (5-8). †Expressed in mL/cm H2O. | ||||||||
Table 5. Perioperative arterial PaO2
| Group | 1 | 2 | 3 | 4 | 5 |
|---|---|---|---|---|---|
| PaO2-1* | 494 ± 40 | 494 ± 29 | 483 ± 18 | 475 ± 24 | 484 ± 22 |
| PaO2-2* | 493 ± 33 | 494 ± 30 | 447 ± 23 | 488 ± 11 | 488 ± 12 |
| PaO2-3* | 295 ± 44 | 322 ± 38 | 404 ± 38 | 327 ± 33 | 325 ± 18 |
| PaO2-4* | 289 ± 48 | 286 ± 47 | 329 ± 18 | 293 ± 22 | 298 ± 19 |
| PaO2-5* | 189 ± 28 | 166 ± 56 | 180 ± 43 | 191 ± 22 | 178 ± 60 |
| PaO2-6* | 183 ± 13 | 186 ± 43 | 188 ± 26 | 169 ± 18 | 168 ± 22 |
| PaO2-7* | 165 ± 60 | 175 ± 10 | 166 ± 44 | 177 ± 12 | 166 ± 43 |
| PaO2-8* | 172 ± 54 | 163 ± 65 | 176 ± 43 | 176 ± 10 | 165 ± 60 |
| *Timing of measurements: 5 minutes before chest opening (1), 5 minutes before bypass (2), 5 minutes after bypass (3), 5 minutes after chest closure (4), and 6-24 hours after surgery (5-8). All patients received 100% at the time of measurements. | |||||
The patients' tracheas were extubated 16 ± 3 hours postoperatively in group 1, 17 ± 4 hours in group 2, 17 ± 5 hours in group 3, 16 ± 4 hours in group 4, and 17 ± 3 hours in group 5. Three patients required prolonged mechanical ventilation (group 1, one patient who was reoperated 24 hours after surgery for uncontrolled bleeding, and group 3, 2 patients who developed pneumonia). No other patients had radiologic evidence of gross atelectasis or lung infiltrates.
Discussion
Lung injury is a known complication of CPB. However, the linkage between the postbypass lung injury and the method of managing the lungs during bypass has not been fully elucidated. Five different methods of managing the lungs during bypass were chosen because no studies have been undertaken to compare the effect of high-frequency, low-volume ventilation with other ventilation modes with respect to postbypass oxygenation. This study tried to find out whether postbypass oxygenation was affected by the method of ventilation and/or by the composition of the gas mixture used during bypass. The study has shown that the dO2 after bypass was lower in patients receiving CPAP with 100% oxygen. Berry et al12 showed that the dO2 with CPAP either on FIO2 1 or 0.21 was lower during the first 30 minutes after bypass but increased afterward. Loeckinger et al13 have also shown that the application of a CPAP of 10 cm H2O during bypass significantly improved pulmonary gas exchange after cardiac surgery. Similar to Berry's12 observation, the reduced dO2 in the CPAP group was not persistent in the postoperative period and did not influence the postoperative pulmonary morbidity. Furthermore, a high level of lung inflation (ie, CPAP = 15 cm H2O) may lead to increased extravascular lung water after bypass.2
Loer et al14 used differential lung ventilation during bypass, with one lung receiving a tidal volume of 150 mL at a rate of 6 breaths/min. The other lung was allowed to collapse. Not surprisingly, a decrease in oxygenation was detected in the pulmonary veins draining the collapsed lung. However, these changes were reversible and leveled after weaning from bypass and expansion of the collapsed lung. Stanley et al5 estimated the postoperative shunt fraction and lung compliance in animals ventilated with different methods during CPB. They found that ventilation of the lungs during bypass might actually increase the shunt fraction and decrease the lung compliance, whereas the type of gas mixture had no effect at all. Chaney et al6 reported similar results in humans.
The idea behind the use of HFV to improve postbypass oxygenation was based on the presumption that it may decrease the total lung water, hence increasing lung compliance and decreasing the shunt fraction. However, this study could not show such an effect. In this study, high-frequency ventilation did not decrease dO2.
These results revealed no significant changes in lung compliance. The authors cannot explain why a decrease in compliance after CPB was not observed. Presumably, this may be attributed in part to the relatively short bypass time.
The administration of 100% oxygen during bypass may lead not only to absorption atelectasis but also to oxygen toxicity.7 In a study by Pizov et al,7 the improvement of postoperative lung function was delayed in patients ventilated with 100% oxygen during bypass. Three patients in the study required prolonged postoperative ventilation; each received 100% oxygen during CPB. However, these numbers are too small to draw any conclusion.
In contrast to the current belief, Cox et al15 showed that off-pump coronary artery bypass surgery was not associated with less postoperative pulmonary complication than surgeries in which CPB was used. The authors speculated that intraoperative factors other than CPB might be responsible for the transient impairment of the gas exchange.
In conclusion, this study did not show a beneficial effect of ventilating the lungs during bypass with high-frequency ventilation in preventing postoperative pulmonary dysfunction. The alveolar-arterial oxygen gradient was lower, and the PaO2 was higher 5 minutes after bypass in patients maintained with continuous positive airway pressure and FIO2 of 1 compared with those ventilated with high-frequency ventilation or other ventilation methods.
Appendix
Appendix 1.10
| 1. Systemic vascular resistance (SVR): |
| SVR = MAP − RAP (CVP)/CO |
| Where MAP, mean arterial (systemic) blood pressure and RAP, right arterial pressure (CVP = central venous pressure). |
| 2. Alveolar air (gas) equation: |
| PAO2 = FIO2(Pb − 47) − PaCO2/R |
| Where PAO2 = alveolar partial pressure of oxygen in mmHg, |
References
- . Ventilation, cardiopulmonary bypass, and acute, respiratory distress syndrome: Are the lungs the problem?. Crit Care Med. 2001;29:463–465
- . Lung management during cardiopulmonary bypass: influence on extravascular lung water. J Cardiothorac Anesth. 1990;4:73–79
- Atelectasis is a major cause of hypoxemia and shunt after cardiopulmonary bypass: An experimental study. Anesthesiology. 1997;87:1153–1163
- Predictive risk factors for pulmonary oxygen transfer in patients undergoing coronary artery bypass grafting. Jpn Heart J. 2001;42:143–153
- . Effects of ventilatory techniques during cardiopulmonary bypass on postbypass and postoperative pulmonary compliance and shunt. Anesthesiology. 1977;46:391–395
- Protective ventilation attenuates postoperative pulmonary dysfunction in patients undergoing cardiopulmonary bypass. J Cardiothorac Vasc Anesth. 2000;14:514–518
- High oxygen concentration exacerbates cardiopulmonary bypass-induced lung injury. J Cardiothorac Vasc Anesth. 2000;14:519–523
- . Primary Pulmonary hypertension in children. In: Rubin LJ, Lenfant C, Rich S editor. Primary Pulmonary Hypertension. New York, NY: Marcel Dekker; 1997;p. 179–225
- . Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Resp Crit Care Med. 1995;152:S77–S120
- In: Lake C, Hines RL, Blitt C editor. Clinical Monitoring. Philadelphia, PA: Saunders, Philadelphia; 2001;p. 219–339
- . Weaning from mechanical ventilation. In: ed 4. Grenvik A, Ayres SM, Holbrook PR, et al. editor. Textbook of Critical Care. Philadelphia, PA: Saunders; 2000;p. 1140–1141
- . Lung management during cardiopulmonary bypass: Is continuous positive airways pressure beneficial?. Br J Anaesth. 1993;71:864–868
- Continuous positive pressure at 10 cm H2O during cardiopulmonary bypass improves postoperative gas exchange. Anesth. Analg. 2000;91:522–527
- . Effects of ventilation on pulmonary venous blood gases and markers of lung hypoxia in humans undergoing total cardiopulmonary bypass. Crit Care Med. 2000;28:1658–1660
- Effect of cardiopulmonary bypass on pulmonary gas exchange: A prospective randomized study. Ann Thorac Surg. 2000;69:140–145
☆ Address reprint requests to Tiberiu Ezri, MD, Department of Anesthesia, Wolfson Medical Center, Holon, Affiliated with Sackler School of Medicine, Tel Aviv, Israel. E-mail: etb@netvision.net.il
PII: S1053-0770(02)47708-7
doi:10.1053/jcan.2003.8
© 2003 Published by Elsevier Inc.
Volume 17, Issue 1 , Pages 40-44, February 2003
