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Interact CardioVasc Thorac Surg 2008;7:14-17. doi:10.1510/icvts.2007.158451
© 2008 European Association of Cardio-Thoracic Surgery
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Work in progress report - Cardiopulmonary bypass

A study assessing the potential benefit of continued ventilation during cardiopulmonary bypass

Lindsay C.H. Johna,* and Ian M. Ervineb

a Department of Cardiothoracic Surgery, Kings College Hospital, Denmark Hill, London SE5 9RS, UK
b Department of Intensive Care Medicine, Kings College Hospital, Denmark Hill, London SE5 9RS, UK

Received 26 April 2007; received in revised form 14 September 2007; accepted 17 September 2007

*Corresponding author. Tel.: +44 20 3299 4365; fax: +44 20 3299 3433.

E-mail address: lindsay.john{at}kingsch.nhs.uk (L.C.H. John).


   Abstract
Top
 Abstract
1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 
It has been suggested that maintaining ventilation during bypass might reduce lung injury, which is a common complication of cardiac surgery. In order to assess this, a study is being undertaken to examine the effect upon a number of parameters that may be indicative of lung injury, of continued ventilation compared with discontinued ventilation whilst on bypass. The following parameters have been assessed: extravascular lung water, static and dynamic compliance, ratio of left atrial/right atrial white blood count, alveolar arterial oxygen gradient and the respiratory index together with clinical end points. Provisional results are reported. Twenty-three elective patients for coronary artery surgery have to date been randomised to either ventilation (VB) (n=12) or non-ventilation on bypass (NVB) (n=11). The post-bypass extravascular lung water was significantly smaller in the VB group compared to the NVB group (530±50 ml vs. 672±32 ml; P=0.028). Extubation time was also significantly shorter in the VB group (3.6±0.3 h vs. 4.8±0.4 h; P=0.038). The provisional results of this work in progress are suggestive that continued ventilation during bypass may reduce lung injury.

Key Words: Acute lung injury; Cardiac surgery; Cardiopulmonary bypass; Ventilation; Extravascular lung water


   1. Introduction
Top
 Abstract
 1. Introduction
2. Materials and methods
 3. Results
 4. Discussion
 References
 
Lung injury of varying severity occurs routinely following cardiac surgery [1]. Its significance varies between postoperative hypoxemia [2] with no adverse clinical effect as seen in the majority, to the development of severe pulmonary failure seen in the minority. The incidence of acute respiratory distress syndrome (ARDS) is relatively low (0.5–1.7%) but its mortality is high (50–90%) [3]. Although severe lung injury post-bypass is uncommon, it remains a significant cause of morbidity and mortality.

The inflammatory process has long been implicated in the aetiology of post-bypass lung injury [4] and the concept of ‘post-pump syndrome’ or ‘systemic inflammatory response to cardiopulmonary bypass’ (SIRS) [3] has arisen. However, this is a generalised inflammatory response. For it to cause specific organ damage then there must also be localisation of the inflammatory response to that organ. Localisation would occur following some form of ‘injury’. Therefore, although bypass causes an inflammatory response, this may only become relevant in the aetiology of lung complications following cardiac surgery if there is also an ‘additional’ injury to the lung during surgery. As the lungs are not in the operative field during cardiac surgery there are few possible causes for such an injury. One possibility is that it is related to the cessation of ventilation during bypass and it has been suggested that the maintenance of ventilation might limit postoperative lung injury [5, 6]. A prospective randomised study is currently in progress to assess this. Patients undergoing coronary artery bypass graft surgery on bypass are randomised to either ventilation or no ventilation on bypass. Measures of lung injury as well as clinical outcomes are being compared between the two groups.


   2. Materials and methods
Top
 Abstract
 1. Introduction
 2. Materials and methods
3. Results
 4. Discussion
 References
 
2.1. Patient population

Twenty-three patients on the elective waiting list for coronary artery surgery have so far been recruited into the study. They were all either non-smokers or had given up smoking for more than five years. Smokers were not included so that the population was more homogenous and not so prone to pulmonary complications unrelated to the conduct of bypass. In addition, they all had the following characteristics:
  1. male,
  2. aged between 50–75 years,
  3. normal or mildly impaired left ventricular function and no significant elevation of pulmonary artery pressure on preoperative echocardiogram,
  4. body mass index <30,
  5. no insulin dependant diabetes,
  6. no history of lung disease.

On the day of surgery, they were randomised using the closed envelope method to either the VB group (n=12) or NVB group (n=11). All the patients gave informed consent and the study had institutional ethical approval.

2.2. Operative protocol

All patients had coronary artery bypass graft surgery performed by the same surgeon using the cross-clamp/fibrillation technique. All patients were anaesthetised by the same anaesthetist using his standardised technique. Etomidate was used for induction and pancuronium as a muscle relaxant. Isofluorane was used pre-bypass and propofol used both pre- and post-bypass. The anaesthetic was not supplemented with thoracic epidurals. The patients in the VB group were ventilated throughout bypass with a tidal volume of 5 ml/kg. On bypass a Jostra Quadrox oxygenator and Quart arterial line filter were used which both had ‘safe line’ coated surfaces. The bypass lines themselves were not coated. The prime consisted of: 1 l Hartman's solution, 0.5 l 10% mannitol, 0.5 l 10% Hespan. Bypass flows were maintained at 2.4 l/min/m2 body surface area. The postoperative care and criteria for extubation were standardised and identical for each patient. The decision for extubation was made according to protocol (adequate gas exchange, haemodynamic stability and absence of bleeding) by nursing staff who were ‘blinded’ as to the study group.

2.3. Parameters measured

The following were measured for all the patients in the study:
  1. Extravascular lung water (EVLW) measured by using the PiCCO system (Pulsion Medical Systems, Munich, Germany). This was measured: (i) post-induction but pre-sternotomy, (ii) post-bypass before leaving theatres, (iii) one day postoperatively.
  2. Static and dynamic compliance of the lungs measured using the ventilator: (i) post-intubation prior to sternotomy, (ii) post-bypass following sternal closure.
  3. The ratio of the left atrial/right atrial (LA/RA) white blood cell count (WBC). A difference in the WBC count measured in the right and left atriae is due to WBC ‘trapping’ within the lungs. Such ‘trapped’ WBCs are likely to be involved with any local inflammatory processes within the lung. The ratio of the WBC count in the RA and LA is, therefore, a measure of inflammation within the lung and comparison of these ratios allows a comparison of different levels of lung inflammation. The LA/RA WBC ratio was measured: (i) post-cannulation but pre-bypass, (ii) post-protamine administration.
  4. Pulmonary gas exchange was assessed by alveolar arterial oxygen gradient (PAO2–PaO2) and the respiratory index [(PAO2–PaO2)/(PaO2)] which were measured: (i) post-intubation, (ii) post-bypass (1- and 4-h postoperatively).
  5. Clinical end points. These included: (i) intubation time, (ii) inpatient stay duration, (iii) incidence of chest complications.

2.4. Statistical methods

The ‘a priori’ hypothesis was that continued ventilation on bypass would reduce extravascular lung water and clinical complications following surgery. The power analysis at the start of the study suggested a study population of 60 (30 in each group) would be sufficient to demonstrate relevant differences between the groups if they existed. A statistical comparison was made between the parameters measured for each group using Student's t-test for the study patients enrolled to date. A P-value of <0.05 was considered statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
4. Discussion
 References
 
Results are shown in Table 1. Data are expressed as mean±standard error of the mean (SEM). The post-bypass extravascular lung water was significantly smaller in VB group than in NVB group (530±50 ml vs. 672±32 ml; P=0.028). Extubation time was also significantly shorter in the VB group (3.6±0.3 h vs. 4.8±0.4 h; P=0.038). The alveolar arterial oxygen gradient and the respiratory index one hour postoperatively were smaller in the VB than NVB groups but this did not reach statistical significance, possibly because of the relatively small sample size. There were no significant differences in operative characteristics between the two groups including graft number, cross-clamp time and bypass time.


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  		Table 1 A comparison of the measured parameters in the ‘ventilated on bypass’ (VB) and the ‘non-ventilated on bypass’ (NVB) groups

 

   4. Discussion
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
References
 
One approach for reducing bypass related lung injury is to avoid bypass altogether and perform ‘off-pump’ cardiac surgery instead. However, only a minority of coronary revascularisation currently takes place ‘off-pump’ and no valve surgery. The alternative approach is to modify bypass to reduce lung injury. To achieve this, elements of bypass that are responsible for the complication need to be identified and avoided.

The systemic inflammatory response to cardiopulmonary bypass has been implicated as a cause for lung injury following bypass [3]. Bypass primes and activates neutrophils both by their exposure to mechanical shear stress [7] and artificial surfaces. In addition, bypass results in the activation of the complement pathways [8]. It is also associated with the release of pro-inflammatory cytokines [9]. However, for a generalised activation of the inflammatory system to be involved in post-bypass lung complications then it is likely that there is also an additional lung ‘injury’ to explain its localisation to this site. It is unclear what the source of such an ‘injury’ following cardiac surgery could be but one possibility is the cessation of ventilation during bypass. Non-ventilation has been associated with the development of microatelectasis, hydrostatic pulmonary oedema, poor compliance and a higher incidence of chest infection [5, 6].

A further possibility that remains speculative is that non-ventilation may result in an ischaemic lung ‘injury’. The human lung consumes about 5–6 ml/min of oxygen at 27 °C and 11 ml/min at 36 °C [10]. During bypass there is no blood flow through the pulmonary arteries and the only vascular supply is through the bronchial arteries. Although there has been little experimental work on bronchial artery flow during bypass in humans it has been reported in a porcine bypass model that it decreases from 42.1±10.4 ml/min to 5.6±1.0 ml/min [11]. If this were also the case with human bypass then it is possible that ischaemia caused by bronchial hypo-perfusion could significantly contribute to lung complications following cardiac surgery. It appears that lung inflation decreases bronchial blood flow [12] and that this is probably due to purely mechanical effects on the broncho-pulmonary arterial anastomoses with both compression and stretching of these vessels. This raises the possibility that the repetitive inflation and deflation of lungs at physiological intra-alveolar pressure is necessary for ‘normal’ bronchial arterial flow secondary to the cyclical compression and relaxation of the vessels. In that case, cessation of ventilation during bypass would reduce bronchial flow and predispose to ischaemic lung injury. Although this remains a conjecture it does provide a theoretical basis for the potential benefit of continuing ventilation during bypass in addition to other previously reported advantages.

Although there has not been a previously reported randomised controlled trial looking at the potential benefits of continued ventilation on bypass, modifications to the normal ventilation protocol have been described. These have included the Vital Capacity Manoeuvre, which appears to reduce atelectasis [13] and the use of continuous positive airways pressure (CPAP) during bypass, which appears to improve postoperative gas exchange [6]. In addition, there have been attempts to reduce lung ischaemia and inflammation by maintaining pulmonary artery perfusion during bypass. In infants with congenital heart disease and pulmonary hypertension this has been reported to be beneficial [14]. The only major report of continued pulmonary perfusion during adult bypass surgery has been with the Drew-Anderson technique [15] involving cannulation of the aorta, pulmonary artery, left and right atriae. An earlier extubation time was reported. However, its complexity and potential for complications has not led to its significant application.

The provisional results of this ongoing study are suggestive of a benefit from continued ventilation during bypass. There was a significantly shorter intubation time in the ventilated on bypass group. This was probably related to the smaller postoperative alveolar arterial oxygen gradient and Respiratory Index in this group. Although these did not reach statistical significance, this may be related to the relatively small numbers so far included in this study. The significantly greater postoperative extravascular lung water post-bypass in the not ventilated on bypass group is suggestive that there is a greater degree of lung injury in this group. However, as the extravascular lung water was not significantly different in the two groups on the first postoperative day there must be some caution in interpreting the relevance of these results. This may become clearer when more patients have been included in the study. So far there have been no significant differences in the LA/RA WBC ratios between the two groups. This is suggestive that any difference in the incidence of lung injury is not due to a difference in the inflammatory response. If it were to show any difference between the two groups then it would be appropriate to include the measurement of inflammatory cytokines in order to determine the nature of any such inflammatory response. In the absence of such a difference in the LA/RA WBC ratio such additional measurements are unlikely to be useful.

In conclusion, the provisional results from this ongoing study have suggested that there may be some benefit to continuing ventilation during cardiopulmonary bypass in reducing lung injury and reducing intubation times. It is speculated that these effects are due to a decreased ischaemic injury because of a smaller reduction in bronchial arterial flow whilst on bypass. Continued ventilation is an attractive method for reducing complications as it is simple to perform and does not have any additional cost. The completion of a larger study is necessary to confirm or otherwise any benefits.


   References
Top
 Abstract
 1. Introduction
 2. Materials and methods
 3. Results
 4. Discussion
 References
 

  1. Johnson D, Thomson D, Hurst T, Prasad K, Wilson T, Murphy F, Saxena A, Mayers I. Neutrophil-mediated acute lung injury after extracorporeal perfusion. J Thorac Cardiovasc Surg 1994; 107:1193–1202.[Abstract/Free Full Text]
  2. Weiss YG, Merin G, Koganov E, Ribo A, Oppenheim-Eden A, Medalion B, Peruanski M, Reider E, Bar-Ziv J, Hanson WC, Pizov R. Post cardiopulmonary bypass hypoxemia: a prospective study on incidence, risk factors and clinical significance. J Cardiothorac Vasc Anesth 2000; 14:506–513.[CrossRef][Medline]
  3. Asimakopoulos G, Smith PLC, Ratnatunga CP, Taylor KM. Lung injury and acute respiratory distress syndrome after cardiopulmonary bypass. Ann Thorac Surg 1999; 68:1107–1115.[Abstract/Free Full Text]
  4. Wan S, Le Clerc JL, Vincent JL. Inflammatory response to cardiopulmonary bypass: mechanisms involved and possible therapeutic strategies. Chest 1997; 112:676–692.[CrossRef][Medline]
  5. Magnusson L, Zemgulis V, Tenling A, Wernlund J, Tyden H, Thelin S, Hedenstierna G. Use of a vital capacity manoeuvre to prevent atelectasis after cardiopulmonary bypass. Anesthesiol 1998; 88:134–142.[CrossRef][Medline]
  6. Loeckinger A, Kleinsasser A, Lindner KH, Margreiter J, Keller C, Hoermann C. Continuous positive airway pressure at 10 cm H2O during cardiopulmonary bypass improves postoperative gas exchange. Anesth Analg 2000; 91:522–527.[Abstract/Free Full Text]
  7. Gu 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.[CrossRef][Medline]
  8. Tennenberg SD, Clardy CW, Bailey WW, Solomkin JS. Complement activation and lung permeability during cardiopulmonary bypass. Ann Thorac Surg 1990; 50:597–601.[Abstract]
  9. Haeffner-Cavallion N, Roussellier N, Ponzio O, Carreno MP, Laude M, Carpentier A, Kazatchkine MD. Induction of interleukin-1 production in patients undergoing cardiopulmonary bypass. J Thorac Cardiovasc Surg 1989; 98:1100–1106.[Abstract]
  10. Loer SA, Scheeren TW, Tarnow J. How much oxygen does the human lung consume. Anesthesiolog 1997; 86:532–537.[CrossRef][Medline]
  11. Schlensak 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.[Abstract/Free Full Text]
  12. Deffebach ME. Lung mechanical effects on the bronchial circulation. Eur Respir J Suppl 1990; 12:586s–590s.[Medline]
  13. Magnusson L, Wicky S, Tyden H, Hedenstierna G. Repeated vital capacity manoeuvres after cardiopulmonary bypass effects on lung function in a pig model. Br J Anaesth 1998; 80:682–684.[Abstract/Free Full Text]
  14. Suzuki T, Ito T, Kashima I, Teruya K, Fukuda T. Continuous perfusion of pulmonary arteries during total cardiopulmonary bypass favourably affects levels of circulating adhesion molecules and lung function. J Thorac Cardiovasc Surg 2001; 122:242–248.[Abstract/Free Full Text]
  15. Richter JA, Meisner H, Tassani P, Barankay A, Dietrich W, Braun SL. Drew-Anderson technique attenuates systemic inflammatory response syndrome and improves respiratory function after coronary artery bypass grafting. Ann Thorac Surg 2000; 69:77–83.[Abstract/Free Full Text]

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