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Ann Thorac Surg 1996;61:76-81
© 1996 The Society of Thoracic Surgeons
Departments of Anesthesiology, Cardiovascular Perfusion, and Cardiac Surgery, Cardiovascular Center E. Malan, University Hospital S. Donato, Milan, Italy
Accepted for publication August 11, 1995.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. Sixty patients undergoing myocardial revascularization were randomly assigned to one of three oxygenator groups. All the patients were free from preoperative lung dysfunction. Lung function was studied with repeated measurements of respiratory index, intrapulmonary shunt, alveolar dead space, ventilation/perfusion ratio, and static thoracopulmonary compliance.
Results. Immediately after cardiopulmonary bypass, the intrapulmonary shunt and respiratory index values in the bubble oxygenator and hollow-fiber oxygenator groups increased more than those in the heparin-coated oxygenator group. In the intensive care unit, the between-group difference in intrapulmonary shunt disappeared, but the within-group difference in respiratory index (from baseline) remained for the bubble oxygenator group. The other three variables did not significantly differ between groups. Intubation time and stay in the intensive care unit did not differ between groups.
Conclusions. Heparin-coated circuits exert a protective effect on pulmonary function. However, their use did not modify the postoperative clinical course of patients with normal lung function preoperatively.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The type of oxygenator (bubble versus hollow-fiber membrane) has been considered to be responsible for different degrees of complement activation and lung dysfunction [6–9]. However, there is still disagreement concerning the influence of oxygenator type on the intrapulmonary shunt (Qs/Qt) [10, 11].
During recent years, heparin-coated circuits (HCCs) for CPB have been studied, and their improved biocompatibility has been demonstrated. Cardiopulmonary bypass with HCC is associated with limited complement activation and reduced tumor necrosis factor and elastase production [12]. A lower degree of neutrophil activation has been demonstrated [13] together with reduced production of thrombin-antithrombin complexes and thrombin formation [14]. Nevertheless, much of the available information comes from animal studies or from human clinical studies based on a limited number of patients. Moreover, there is little information regarding pulmonary complications after CPB and HCCs in humans. The aim of this study was to determine if there is a different effect of bubble oxygenators (BOs), conventional hollow-fiber membrane oxygenators (CHFs), and heparin-coated circuits (HCCs) on lung function in the early period after perfusion.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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There were two inclusion criteria: the patient had to be a candidate for elective coronary artery bypass grafting and have a left ventricular end-diastolic pressure of less than 30 mm Hg or an ejection fraction of greater than 0.30. The exclusion criteria were as follows: simultaneous valve operation, aneurysm operation, or other major surgical procedure; redo operations; known preoperative coagulopathy; neurologic disorders, chronic obstructive pulmonary disease; insulin-dependent diabetes mellitus; renal insufficiency; liver disease; and active inflammatory disease or infection. The patients were randomly allocated to one of three groups: the BO group (n = 20); the CHF group (n = 20); or the HCC group (n = 20).
Anesthesia
All patients were premedicated with atropine sulfate (0.01 mg/kg intramuscularly), fentanyl (1 µg/kg intramuscularly), and promethazine hydrochloride (1 mg/kg intramuscularly). Induction was achieved with intravenous administration of diazepam (0.15 mg/kg), fentanyl (7 µg/kg), droperidol (0.1 mg/kg), and pancuronium bromide (0.1 mg/kg). After tracheal intubation, patients were mechanically ventilated to give a tidal volume of 8 mL/kg of body weight with an inspiratory mixture of 50% nitrous oxide and 50% oxygen and a respiratory rate of 16 to 18 cs/min. General anesthesia was maintained with a continuous intravenous infusion of fentanyl (10 µg•kg-1•h-1), droperidol (0.15 mg•kg-1•h-1), and pancuronium bromide (0.07 mg•kg-1•h-1). Further boluses of fentanyl (0.5 mg each) were administered if required at the time of skin incision and sternotomy. During CPB, the lung was kept moderately inflated by a continuous low flow of oxygen.
CPB
Once adequate anticoagulation (bovine lung heparin, 300 IU/kg intravenously) was obtained, patients were connected to the CPB circuit. Activated clotting time was controlled (Hemochron; International Technidyne Corp, Edison, NJ) and maintained at a value higher than 400 seconds throughout the duration of bypass by means of further heparin doses. The activated clotting time values were controlled at 15-minute intervals.
Perfusion was provided by a Stöckert roller pump (Shiley Inc, Irvine, CA). In the CHF and HCC groups, the extracorporeal perfusion circuit consisted of a hollow-fiber oxygenator (Univox; Baxter Healthcare Corp, Bentley Laboratories Division, Irvine, CA), a collapsible venous reservoir (BMR 1900; Bentley Baxter), a hard-shell cardiotomy reservoir (BCR 3500; Bentley Baxter), an arterial cannula (Sarns, 3M Health Care, Ann Arbor, MI), a dual-stage venous cannula (USCI, Bard Cardiopulmonary Division, Tewksbury, MA), two cardiotomy suctions, and polyvinyl chloride tubing. In the HCC group, all the blood-contacting surfaces were treated with immobilized heparin (Duraflo II; Baxter Healthcare Corp, Bentley Division, Irvine, CA). In the BO group, the circuit consisted of a BO (Hiflex-E; Dideco, Mirandola, Italy), the same venous and arterial cannulas, a hard-shell cardiotomy reservoir (Dideco), two cardiotomy suctions, and polyvinyl chloride tubing. The circuit was primed with 700 mL of a gelatin solution (Eufusin; Bieffe Medical, Modena, Italy) and 200 mL of THAM (trihydroxymethylaminomethane) solution.
Cardiopulmonary bypass flow started at a perfusion index of 2.4 L•m-2•min-1. The mean arterial pressure was maintained at about 80 mm Hg. Moderate hypothermia (28°C) was achieved and maintained during perfusion, and pump flow was reduced to and maintained at 1.8 to 2 L•m-2•min-1. The arterial pressure was controlled using a vasodilator (nitroglycerin, 0.5 µg•kg-1•min-1) or a vasoconstrictor (norepinephrine, 0.05 µg•kg-1•min-1) to maintain the mean value in a range of 40 to 100 mm Hg. A diuretic (furosemide, 20 mg) was administered if urine output during CPB was less than 0.5 mL/kg 30 minutes after the beginning of perfusion.
At the end of CPB, heparin was reversed by protamine sulfate in a 1:1 proportion. No patient received donor blood or plasma during the surgical procedure. Aprotinin was administered, following our usual protocol, at a low dose (2,000,000 KIU [280 mg] intravenously before CPB) only to the patients treated with acetylsalicylic acid before operation.
Surgical Procedure
The heart was cannulated with a double-lumen single cannula through the right atrium. The arterial cannula was placed into the ascending aorta. The left ventricle was vented through the aortic root. Cardiac standstill was obtained after aortic cross-clamping by intraaortic injection of 500 mL of cold (4°C) crystalloid cardioplegic solution through a needle into the aortic root. The cardioplegic solution was prepared in 500-mL bottles. Its composition was as follows: sterile distilled water, 457 mL; plus KCl 15%, 6.3 mL; NAHCO3 8.4%, 6 mL; NaCl 11.7%, 27.4 mL; and glucose 33%, 3.3 mL. Surface cooling of the heart was maintained using cold (4°C) 0.9% sodium chloride solution.
Data Collection
For each patient, we collected demographic data, intraoperative data (aortic cross-clamp time, CPB duration), and postoperative data (duration of intubation and stay in intensive care unit (ICU), duration of hospital stay).
Data on pulmonary gas exchange were collected at three times: after the induction of anesthesia but before CPB (T0), immediately after the end of CPB and protamine administration (T1), and at 3 hours in the ICU (T2). Data collection at T0, T1, and T2 was performed during ventilation in room air after a 10-minute washout period of ventilation (inspired oxygen fraction = 0.21). The following data were obtained: arterial oxygen pressure (PaO2); arterial carbon dioxide pressure (PaCO2); end-tidal carbon dioxide pressure (PACO2); central venous oxygen pressure (PvO2); central venous carbon dioxide pressure (PvCO2); arterial oxygen saturation (SaO2); central venous oxygen saturation (SvO2); and hemoglobin (Hb) (g/L). On the basis of these data and applying the following formulas, we calculated respiratory index (RI) (alveolar-arterial oxygen gradient/PaO2) = [(713 x 0.21 - PACO2 ÷ 0.8) - PaO2] ÷ PaO2, Qs/Qt = [1.39 x Hb x (1 - SaO2)] ÷ (1.39 x Hb + 0.003 x PaO2 - 0.003 x PvO2 - 1.39 x Hb x SvO2), alveolar dead space (Vd/Vt) = (PaCO2 - PACO2) ÷ PaCO2, and ventilation/perfusion ratio = 8.63 x (9.68 x PvCO20.438 - 9.68 x PaCO20.438) ÷ PACO2.
Static thoracopulmonary compliance was measured at three slightly different points because of the need to perform the measurements under the same experimental conditions (closed chest). Therefore, for this variable, T0 was after the induction of anesthesia and before the skin incision; T1 was after chest closure and immediately before the patient was taken from the operating theater; and T2 was at 3 hours in the ICU.
Static thoracopulmonary compliance (mL/cm H2O) was determined by inflating the lungs with a macrosyringe charged with an air volume of 10 mL/kg of body weight and measuring the corresponding airway pressure: static thoracopulmonary compliance = volume inflated ÷ pressure at end-inflation.
Statistical Analysis
Data were analyzed with a computerized system SYSTAT 5.0 (SYSTAT, Inc, Evanston, IL) on a Macintosh LC II computer (Apple Computer, Inc, Cupertino, CA). Continuous variables are expressed as the mean ± the standard error of the mean in tables and figures. Categoric data are expressed as frequency (%). Data were examined using a multivariate analysis of variance for repeated measures. Differences between groups at various times and differences within each group were examined when the multivariate analysis showed a significant effect of ``group'' or ``time.'' The action of aprotinin on Qs/Qt was investigated by means of a Mann-Whitney U test; correlation between Qs/Qt and RI was explored using a linear regression analysis. A p value less than 0.05 was considered significant.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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).
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). At T2, the increase was significant in all three groups. The RI increased significantly in the BO and CHF groups from T0 to T1, whereas no change was seen in the HCC group (Table 3). The RI values were significantly correlated with the corresponding Qs/Qt values (linear regression analysis) at baseline (r = 0.254, p = 0.05) and T1 (r = 0.387, p = 0.002) but not at T2 (r = 0.226, p = 0.083). The difference between groups was not significant, even though the p value was borderline (0.063). The alveolar dead space data did not demonstrate any significant changes between groups or within groups at the multivariate analysis (Table 4).
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) decreased significantly versus baseline at the end of the operation and at 3 hours in the ICU in all three groups. No significant differences between groups were seen. The ventilation/perfusion ratio values decreased in the BO and CHF groups at T1 and remained stable in the HCC group (Fig 2). At T2, the values were similar for all three groups. However, because of the large deviations from the mean, no significant between-group or within-group differences were seen.
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The action of different CPB materials on this chain of events is still debated. Recently, Reeve and associates [10] demonstrated that bubble versus hollow-fiber oxygenators do not change Qs/Qt deterioration or clinical outcome, even if roentgenographic scoring of atelectasis and lung water content seem to reveal less damage in hollow-fiber oxygenator-treated patients. This observation is confirmed by our data. We could not detect any significant difference between the CHF and BO groups in terms of lung gas exchange, thoracopulmonary compliance, and clinical outcome.
Conversely, we did demonstrate that patients perfused with an HCC exhibited limited lung dysfunction compared with the BO and CHF groups. The maximum increase in Qs/Qt in the HCC group was 29% (at T2) versus 61% and 49% in the CHF and BO groups, respectively (at T1). In 1993, Steinberg and colleagues [11] reported their Qs/Qt data in patients treated with either a traditional circuit or a Duraflo II HCC. Their study revealed no significant differences between groups. One possible explanation is that they primed the circuit with albumin solution, and it is known that during the priming procedure before CPB, albumin can wash off most of the heparin coating.
In our study, the RI values showed a behavior pattern similar to that of Qs/Qt immediately after CPB, but they failed to correlate with Qs/Qt at T2 (3 hours in the ICU). This resulted in limited significance of the statistical analysis on the basis of repeated measures.
The RI is a standardization of the alveolar-arterial oxygen gradient. Its measurement depends on a formula containing the respiratory ratio (carbon dioxide production/oxygen consumption), which is usually arbitrarily set at 0.8. This assumption, which can be accepted for patients in stable metabolic condition, induces an error when these conditions are not normal. During the first hours in the ICU, because of the rewarming of the patient, the presence of cardiac dysfunction, and the use of inotropic agents and vasodilators, the measurement of alveolar-arterial oxygen gradients can be misleading, as demonstrated by their failure to correlate with the Qs/Qt. Therefore, in our patients, this resulted in limited value from a statistical point of view. The Qs/Qt measurement is a little more complicated, but the requirement to evaluate central venous blood enhances its reliability. Central venous oxygen saturation is a well-known index of the efficiency of peripheral perfusion and cardiac output; its evaluation provides essential information regarding how much work will be required for the lung to reoxygenate the venous blood and limits the errors involved in every indirect measurement of Qs/Qt.
Static thoracopulmonary compliance decreased in a similar fashion in the three groups. This index is related to the mechanical properties of the lung-chest wall system. Its decrease is likely due to an increased lung water content, but it is probably not a sensitive index of lung gas exchange.
We are aware of only one study dealing with lung compliance and the HCC. It is an animal study [20] demonstrating that compliance after CPB decreased less in pigs perfused with an HCC than in a control group (standard extracorporeal circuit). This information is not confirmed by our data. However, pigs are a very sensitive model for CPB injury; they do not tolerate CPB well and sustain major pulmonary dysfunction. They are probably similar to patients with preoperative lung dysfunction. The alveolar dead space values failed to demonstrate significant differences between groups or significance as a time-related factor. Alveolar dead space represents the amount of area ventilated but not perfused. In our experiment, this could have been an index of lung damage caused by the presence of microaggregates within the pulmonary circulation. On the basis of our data, the increase in alveolar dead space, even if slight, is trivial and does not demonstrate, at least on a functional basis, a high relevance of this phenomenon.
Finally, the ventilation/perfusion ratio values deserve some consideration, even though the changes were not significant. They represent roughly the ``total lung'' ratio between ventilated and perfused areas. To date, the ventilation/perfusion ratio alone does not help us understand what is happening to the lung, as simultaneous decrease in both ventilation and perfusion results in a normal ratio. However, coupled with the Qs/Qt and alveolar dead space analyses, this index confirms that the main damage in our BO and CHF groups was due to decreased ventilation immediately after CPB and that this effect was limited in the HCC group. The large deviations from the mean of the measurements reflect the rough nature of this index.
Despite its kallikrein-inhibiting properties, aprotinin did not exert any effect on Qs/Qt changes after CPB. This assumption together with the homogeneous distribution of aprotinin treatment between the groups allows us to affirm that at least when used as a low-dose regimen, aprotinin does not play a major role in terms of prevention of postperfusion lung dysfunction and that our experiment is not biased by the administration of this drug.
On the basis of this study, we draw the following conclusions:
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Acknowledgments |
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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