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Ann Thorac Surg 1996;61:118-123
© 1996 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Effects of Cardiopulmonary Bypass Temperature on Pulmonary Gas Exchange After Coronary Artery Operations

Bristol Heart Institute and Department of Anesthesia, University of Bristol, Bristol, United Kingdom

Accepted for publication August 30, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. Pulmonary dysfunction is one aspect of the postoperative morbidity associated with cardiopulmonary bypass. Normothermic systemic perfusion can result in shorter intubation times, which have been attributed to improved pulmonary gas exchange, but the influence of perfusion temperature on pulmonary gas exchange itself is not known.

Methods. Pulmonary gas exchange was assessed using alveolar-arterial oxygen pressure gradients in 45 patients undergoing routine coronary revascularization who were randomized to undergo cardiopulmonary bypass at 28°C, 32°C, or 37°C. This was part of a more comprehensive study of the effects of temperature on bodily systems. The gradients were estimated preoperatively with the patients breathing air, again over a period between 2 and 4 hours postoperatively during mechanical ventilation with three different oxygen concentrations (30%, 40%, and 60%), and again 1 hour after extubation while breathing the same three oxygen concentrations.

Results. Preoperative alveolar-arterial oxygen pressure gradients on air were 24.4 ± 8.2 mm Hg (mean ± standard deviation) (28°C), 24.5 ± 20.4 mm Hg (32°C), and 20.5 ± 9.5 mm Hg (37°C). Postoperatively, during ventilation and after rewarming, the gradients increased with the increase in inspired oxygen fraction concentrations (30% to 60%) from 67.1 ± 12.0 mm Hg to 193.1 ± 30.5 mm Hg (28°C), from 76.4 ± 20.6 mm Hg to 246.7 ± 47.7 mm Hg (32°C), and from 79.0 ± 18.0 mm Hg to 222.9 ± 40.5 mm Hg (37°C), respectively. A similar pattern was noted 1 hour after extubation, when the gradients increased from 72.4 ± 12.5 mm Hg to 256.6 ± 26.5 mm Hg (28°C), from 75.7 ± 13.9 mm Hg to 252.7 ± 38.3 mm Hg (32°C), and from 69.1 ± 19.3 mm Hg to 253.1 ± 33.0 mm Hg (37°C). There were no significant differences in alveolar-arterial oxygen pressure gradient between the three groups during ventilation or after extubation.

Conclusions. Cardiopulmonary bypass perfusion temperature does not influence alveolar-arterial oxygen pressure gradients in the first 12 hours after routine coronary artery bypass grafting in patients with uncompromised pulmonary and left ventricular function.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The desirability of systemic hypothermia during cardiopulmonary bypass (CPB) perfusion has recently been challenged by the reintroduction of normothermic systemic perfusion as a theoretically more physiologic means of maintaining normal homeostatic functions [1–4]. However, the higher oxygen consumption [2] and the potential for increased activation of inflammatory mediators [5] have raised concerns about the risk of end-organ injury during normothermic CPB. This study was designed to investigate the effects of CPB perfusion temperature on pulmonary gas exchange after routine coronary artery bypass grafting as part of a more comprehensive randomized study of its effects on a range of bodily functions.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Forty men and 5 women undergoing primary myocardial revascularization were allocated by random number table to undergo CPB at a systemic perfusion temperature of 28°C (hypothermia), 32°C (moderate hypothermia), or 37°C (normothermia). The patients were carefully selected for relatively good health. Patients older than 70 years were prospectively excluded, as were those with impaired left ventricular function (ejection fraction less than 0.40 on angiography), unstable angina, myocardial infarction within the previous 6 months, respiratory disease (bronchitis, emphysema, or asthma), or diabetes mellitus, or those who had smoked in the preceding 6 months. The study protocol was approved by the United Bristol Healthcare Trust Ethics Committee, and informed consent was obtained from all patients.

Anesthesia Technique
A standardized anesthesia technique was used, including sodium thiopental (1 to 3 mg) and fentanyl (3 to 5 µg/kg) at induction, volatile agents in 50% O₂/N₂ for maintenance, and a propofol infusion (3 mg•kg^-1•h^-1) during CPB. Pancuronium bromide (0.1 to 0.15 mg/kg) was used for neuromuscular blockade. The ventilation was adjusted to maintain normocapnia, and alpha-stat acid-base management was used.

Surgical Technique
An initial dose of heparin sodium, 3 mg/kg, was given and was supplemented as required to maintain an activated clotting time of greater than 480 seconds. Preparation for CPB consisted of ascending aortic cannulation and two-stage venous cannulation through the right atrial appendage. A standard CPB circuit was used in all patients: polyvinyl chloride tubing (Sorin Biomedica UK Ltd, Midhurst, UK), a Cobe roller pump (Cobe, Lakewood, CO), a hollow-fiber membrane oxygenator, and a 40-µm arterial line filter (Sorin Biomedica Cardio, Saluggia, Italy). The extracorporeal circuit was primed with 1,000 mL of Hartmann's solution, 500 mL of Gelofusine (B Braun Medical Ltd, Emmenbrücke, Switzerland), 60 mg of heparin, and 0.5 g/kg of mannitol.

In the normothermic group, the patients were actively rewarmed to maintain a nasopharyngeal temperature of 37°C. In the other groups, CPB was conducted with the systemic perfusate cooled so that all patients reached the target nasopharyngeal temperature. A nonpulsatile flow of 2.4 L•m^-2•min^-1 was used throughout CPB for the normothermic group, but it was reduced to 2.0 L•m^-2•min^-1 in the moderately hypothermic group and 1.8 L•m^-2•min^-1 in the hypothermic group once the target nasopharyngeal temperature had been reached. Phenylephrine hydrochloride was used as necessary to maintain systemic perfusion pressures at 50 to 60 mm Hg. Electromechanical arrest was induced for myocardial protection using an initial liter of antegrade cold crystalloid cardioplegic solution (St. Thomas' I) followed by 300 mL every 30 minutes after aortic cross-clamping, or earlier if electric activity returned. Normal saline solution at 4°C was used for additional topical cooling.

Distal anastomoses were completed during a single period of aortic cross-clamping. Rewarming in the hypothermic and moderately hypothermic groups was started once all distal anastomoses had been accomplished, and the proximal anastomoses were completed on the beating heart using an aortic partial occlusion clamp. The patients were actively rewarmed with a temperature difference of 8°C at the level of the heat exchanger between the blood and the rewarming fluid, and CPB was discontinued only after the patients were fully rewarmed to a stable nasopharyngeal temperature of 37°C. None of the patients required inotropic support for weaning from bypass. Autologous blood was predonated after anesthesia induction and was used for volume replacement, and blood remaining in the circuit was reinfused to the patient through a 40-µm filter (SQ40S; Pall Europe Ltd, Portsmouth, UK).

At the end of the operation, patients were transferred to the cardiac intensive care unit and were initially ventilated in a controlled mandatory ventilation mode (Servo Ventilator 900C; Siemens, Sweden) with a tidal volume of 12 mL/kg. The respiratory rate was adjusted to maintain a partial pressure of arterial carbon dioxide between 35 and 40 mm Hg. The inspired oxygen fraction (FiO₂) was initially adjusted in the routine way to maintain a partial pressure of arterial oxygen between 80 and 100 mm Hg, with a positive end-expiratory pressure of 5 mm H₂O. Once the patients had stable hemodynamics and normal nasopharyngeal temperature, the FiO₂ was set at 0.30, 0.40, and 0.60 for a period of 30 minutes each for formal studies of pulmonary gas exchange. Thereafter, when alert, the patients were extubated, and the study was repeated with the patients breathing spontaneously on the same three oxygen concentrations provided by a Venturi system (Kendall Resp Inflo MN, Germany) driven by up to 15 L of oxygen.

Sample Collection
Blood samples of 3 to 5 mL were taken for immediate blood gas analysis (Stat Profile 5 analyzer; Nova Biomedical, Waltham, MA) at three different times: (1) preoperatively by radial artery puncture with the patients breathing air; (2) from a radial artery line between 2 and 4 hours postoperatively when the patients were being artificially ventilated with the three different oxygen concentrations (stage 1); and (3) 1 hour after extubation when the patients were spontaneously breathing the same three oxygen concentrations (stage 2).

Calculation of Alveolar-Arterial Gradient
Because of the well-recognized uncertainties of obtaining a representative sample of alveolar gas, the alveolar-arterial gradient is conventionally referenced ``ideal'' alveolar partial pressures, which for carbon dioxide is taken to be identical to the arterial partial pressure (PaCO<sub>2</sub>). The ``ideal'' partial pressure of alveolar oxygen (PAO₂) is then calculated using the ideal alveolar gas equation [6, 7]: PAO₂ = PiO₂ - PaCO₂/RQ, where PiO₂ is the product of FiO₂ and the dry barometric pressure (the difference between an assumed total of 760 mm Hg and the saturated vapor pressure at 37°C, which is 47 mm Hg) and RQ is the respiratory quotient, which was taken to be 0.77 [8]. The alveolar-arterial oxygen pressure [P(A-a)O₂] gradient was thus estimated as follows: P(A-a)O₂ = PAO₂ - PaO₂, where PaO₂ is the partial pressure of arterial oxygen.

Statistical Analysis
Results are expressed as the mean ± the standard deviation unless otherwise stated. The principal comparison of intergroup differences in partial pressure of arterial oxygen, partial pressure of arterial carbon dioxide, and P(A-a)O₂ and was by six analyses of variance (one for each of the three FiO₂s for each of the two postoperative stages). Six subsidiary stepwise multiple regression analyses were carried out on the P(A-a)O₂ gradients to check that the estimates of P(A-a)O₂ were sensitive enough to detect some of the expected influences on pulmonary gas exchange and to maximize the chance of identifying an effect of CPB temperature by allowing for any confounding effects of those influences. The interval variables offered as potential explanators were age, CPB time, aortic cross-clamp time, intubation time, and preoperative P(A-a)O₂ gradient. Sex, whether or not the patient had ever smoked, and whether or not he or she was placed on the operating list in the morning or afternoon were offered as binary dummy variables. Cardiopulmonary bypass temperature was offered as a pair of binary variables, one to indicate any difference between the hypothermic and moderately hypothermic groups and the other to indicate any difference between the moderately hypothermic and normothermic groups. An additional similar multiple regression analysis was undertaken to identify explanators of intubation time. A p value of 0.05 or less was taken to indicate significance.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The three temperature groups were reasonably well matched for age, sex, and smoking history (Table 1). The Parsonnet score [6] was less than 10 in all patients and less than 5 in 93%. The randomization happened to allocate a disproportionate number of the hypothermic group to a morning rather than an afternoon operation (p < 0.05). The number of grafts was similar in all three groups (see Table 1). In all patients except 1 in each group, the left internal mammary artery was used, with wide opening and drainage of the left pleura. Aortic cross-clamp and CPB times were similar in all three groups, but the intubation time was shorter in the group who underwent CPB at 28°C than in either of the other two groups. It should be recognized that the overall mean intubation time for patients having operation earlier on the list was significantly shorter than for those who underwent operation later in the day (5.1 ± 2.2 hours versus 7.4 ± 4.7 hours; p < 0.05). All patients progressed well postoperatively, with no cardiorespiratory complications.

View larger version (14K): [in this window] [in a new window]   Fig 1. . Alveolar-arterial oxygen pressure gradient in the 28°C (-•-), 32°C (--), and 37°C (--) groups postoperatively during mechanical ventilation (stage 1). (FiO2 = inspired oxygen fraction.)

View larger version (16K): [in this window] [in a new window]   Fig 2. . Alveolar-arterial oxygen pressure gradient in the 28°C (-•-), 32°C (--), and 37°C (--) groups after extubation (stage 2). (FiO2 = inspired oxygen fraction.)

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Pulmonary dysfunction has been a well-documented complication of CPB since the earliest days of cardiac surgery [7, 9] with a reported incidence of up to 30% [10]. In its most severe manifestation, it can progress to a form of the adult respiratory distress syndrome [11]. Factors implicated in the pathogenesis of pulmonary dysfunction include lung trauma, atelectasis, phrenic nerve palsy, and infection. In addition, during the initial phase of CPB, complement is activated primarily through the alternate pathway [12, 13], resulting in release of the anaphylatoxins C3a and C5a, which are known to be associated with pulmonary dysfunction [10]. Activation of leukocytes is followed by deposition in most organs, but the absence of pulmonary blood flow during total CPB may make the lungs a particular target [9], thus promoting an increase in the alveolar-capillary permeability, which leads to transit of fluid and macromolecules into the pulmonary interstitium and ultimately the alveoli [10, 14]. The overall effect is that blood is shunted through the lungs, either perfusing inadequately ventilated alveoli or being inadequately oxygenated because of alveolar-capillary block.

With improvements in CPB techniques, there has been an increasing interest in the use of normothermic CPB perfusion [1–3]. The effect of normothermic perfusion on lung function is not clear. There have been reports of shorter intubation time after normothermic bypass [1, 15, 16], and better pulmonary function has been proposed as an explanation. Nevertheless, the possibility of increased complement activation, with extended humoral and cellular responses, has raised concerns about the damaging potential of normothermic CPB on pulmonary function [5].

The aim of the present study was to conduct a controlled, noninvasive investigation of the effects of perfusion temperature on pulmonary gas exchange using a simple but more sensitive and selective measure of respiratory function than merely the duration of tracheal intubation. Although intubation time has been used commonly in previous studies, it depends on many factors other than pulmonary function alone. A conventional index of deficits in pulmonary gas exchange is ``venous admixture''-the notional proportion of the cardiac output that fails to participate in complete exchange and equilibration with the ``ideal'' alveolar ventilation. Venous admixture cannot be calculated rigorously without measuring mixed venous oxygen content (which is an invasive step), but it is often estimated on the basis of an assumed arteriovenous difference [17].

Alveolar-arterial oxygen gradients are commonly used as a less invasive measure of pulmonary gas exchange [18, 19]. If gas exchange were perfect, so that venous admixture were zero, the P(A-a)O₂ gradient would be zero at all FiO₂s. For any venous admixture that is not zero, there is bound to be a P(A-a)O₂ gradient that is not zero. The shape of the hemoglobin dissociation curve makes the P(A-a)O₂ gradient increase with FiO₂ for a given venous admixture, as observed in this study. Though this study was conducted at sea level, its inclusion of a range of FIO₂s might allow the conclusions to be applied quite reasonably to higher altitudes provided that the main effect of altitude was simply to reduce the product of FiO₂ or PiO₂ for a given FIO₂.

The simplest conclusion from similarity of the P(A-a)O₂ gradients between temperature groups in the six different measurement conditions is that that the CPB perfusion temperature did not affect pulmonary gas exchange. There is, however, a possible counter-argument that, despite all the care that was taken to ensure an appreciable period of stable normality of the nasopharyngeal temperature in all groups, the process of whole-body rewarming might still have been more or less incomplete (respectively) in the groups who underwent CPB at 28°C and 32°C or that metabolism altered by hypothermia during CPB might still not have normalized. If altered ratios of substrate utilization had persisted into the measurement period, they might have altered the respiratory quotient in a systematic temperature-dependent way. A plausible error of ± 0.7 in the assumed respiratory quotient would produce an error of about ± 5 mm Hg in the estimate of ideal partial pressure of alveolar oxygen and thus the P(A-a)O₂ gradients; this small error would not materially affect the conclusions.

If the hypothermic depression of metabolic rate had not been reversed by the time measurements were made, the arteriovenous differences in oxygen content would have been smaller in the groups who underwent hypothermic perfusion [2, 20], unless the cardiac output had also been reduced in proportion. Because the size of the P(A-a)O₂ gradient for any given venous admixture depends on the amount of oxygen remaining in the blood returning to the lungs [21], a given venous admixture after hypothermic CPB would tend to produce the same P(A-a)O₂ gradient as a smaller venous admixture after normothermic CPB (though the tendency would decrease as the venous admixture increased).

Thus the alternative to the simple conclusion that CPB temperature does not affect pulmonary gas exchange is a complex hypothesis that the rewarming or the reversal of metabolic effects of hypothermia was incomplete over the whole period in which the measurements were made and that there was a degree of relative pulmonary dysfunction after more hypothermic conditions that happened to exactly balance the effects of the incomplete reversal of the metabolic effects. The usual principle in science is to accept the simpler of two hypotheses or conclusions, pending support for the more complex. It is also worth noting that the mean P(A-a)O₂ gradients at the three different FiO₂s were practically superimposable (see Fig 2) after the patients had been extubated and had been thermally and hemodynamically stable for the longest time.

Previously reported data have drawn simplistic inferences about pulmonary function from the period of time that patients underwent tracheal intubation. There are reports [7, 15, 16] that intubation time is longer after hypothermic than after normothermic CPB, but the clinical management in these reports included differences between types of myocardial protection as well as differences in the temperature of systemic perfusion during CPB. Nor is it clear whether the observed differences in intubation time were related merely to the improved hemodynamic stability and earlier rewarming that are well-recognized after normothermic techniques. All patients in the present study were actively rewarmed to a normal nasopharyngeal temperature by the time they arrived in the intensive care unit, and this may have eliminated any temperature effects of this sort.

The finding that intubation time was shorter in the hypothermic (28°C) group is explained quite simply by the additional findings that a disproportionate number of patients in that group happened (by an unlikely chance) to have been placed early on the operating list and that patients who were thus placed tended to have a significantly shorter intubation time. It is well recognized in many units that patients who undergo operation late in the day are more likely intubated overnight purely as a precautionary measure, even though their pulmonary function might well warrant earlier extubation.

It should be noted that the patients in this study were selected to be free of pre-existing lung disease and to have left ventricular function uncompromised by the coronary artery disease. The assessment period of the postoperative pulmonary function in this study was also relatively short and early in the recovery period-between about 2 and 8 hours after arrival in the intensive care unit. If more exacting studies are contemplated of the pulmonary effects of the temperature of systemic perfusion during CPB, the selection of patients in more compromised condition and a more prolonged period of assessment might well be needed to repay the effort of the investigation.

In conclusion, in this noninvasive study of patients with no preexisting lung disease and good left ventricular function, CPB temperature did not influence P(A-a)O₂ gradient in the early period after coronary revascularization.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
This study has been supported by the Garfield Weston Trust and the Sir Jules Thorn Trust.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Mr Angelini, Department of Cardiac Surgery, Bristol Royal Infirmary, Bristol BS2 8HW, United Kingdom.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Inderpaul Birdi Mohammad Bashar Izzat Alan J. Bryan Gianni D. Angelini Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Birdi, I. Articles by Angelini, G. D. Search for Related Content PubMed PubMed Citation Articles by Birdi, I. Articles by Angelini, G. D.