CLINICAL STUDY
The effects of hypothermia on human left ventricular contractile function during cardiac surgery
Michael E. Lewis, MB, ChB, BSc, FRCS*,
Abdhul-Hakam Al-Khalidi, PhD ,
John N. Townend, MD, FRCP ,
John Coote, BSc, PhD and
Robert S. Bonser, FRCS, FRCP*,*
* Department of Cardiothoracic Surgery, Queen Elizabeth Hospital, Birmingham, United Kingdom
Department of Physiology, University of Birmingham, Birmingham, United Kingdom
Department of Cardiovascular Medicine, Queen Elizabeth Hospital, Birmingham, United Kingdom
Manuscript received March 30, 2001;
revised manuscript received September 10, 2001,
accepted September 20, 2001.
* Reprint requests and correspondence: Dr. Robert S. Bonser, Department of Cardiothoracic Surgery, Queen Elizabeth Hospital, Edgbaston, Birmingham, B15 2TH, United Kingdom.
Robert.Bonser{at}university-b.wmids.nhs.uk
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Abstract
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OBJECTIVES: We investigated the interaction of heart rate (HR), temperature and contractility using a validated load independent method.
BACKGROUND: Temperature manipulation is an integral part of cardiac surgery, and postoperative hypothermia is extremely common. Myocardial contraction is a series of enzymatic and physico-chemical reactions that may be differentially affected by temperature.
METHODS: Ten patients undergoing coronary artery bypass grafting were studied during moderately hypothermic cardiopulmonary bypass. After conduit procurement and heparinization but before grafting, the patient was placed on cardiopulmonary bypass and rewarmed to 37°C, and the left ventricle (LV) was instrumented with a conductance catheter allowing continuous pressure and volume measurement. The LV pressure volume relationship was examined to assess the contractility at 37, 35, 33 and 31°C, with fixed atrial pacing (100 beats/min) in five patients and at 80 and 120 beats/min, at 33 and 37°C in five patients.
RESULTS: At a HR of 100 beats/min, lower temperature resulted in a highly significant decrease in maximal elastance (100% at 37°C, 29 ± 3.5% at 31°C, p < 0.0001). At 37°C, increasing HR increased contractility (80 beats/min 100%, 120 beats/min 205.9%, p = 0.0021); however, at 33°C contractility fell with increasing HR (80 beats/min 100%, 120 beats/min, 53.7%, p = 0.0014).
CONCLUSION: At normothermia LV contractility has a direct relationship with HR. In hypothermic conditions this relationship inverses. Clinical strategies maintaining higher HRs at colder temperatures result in reduced contractility. These factors are important in the management of cardiac surgical patients.
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Abbreviations and Acronyms
| | ANOVA | | analysis of variance | | CPB | | cardiopulmonary bypass | | EDV | | end-diastolic volume | | Ees | | end-systolic elastance | | Emax | | maximal elastance | | ESPVR | | end-systolic pressure-volume relation | | HR | | heart rate | | LV | | left ventricle, left ventricular | | LVPVR | | left ventricular pressure volume relationship | | P-V | | pressure-volume | | tPER | | time to peak ejection rate | | TPT | | time to peak tension | | Tmax | | time to reach maximal elastance |
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Temperature manipulation is an integral part of cardiac surgery. Corporeal hypothermia is utilized to reduce metabolic demand and therefore increase tolerance to ischemia. Cooling has also been used as a therapeutic maneuver in hemodynamically unstable postoperative patients (1,2). Most cardiac surgical procedures are performed under conditions of moderate hypothermia (26 to 31°C) utilizing cardiopulmonary bypass (CPB). After CPB, despite prolonged rewarming using countercurrent heat exchange and restoring nasopharyngeal temperature to 37°C, a persistent temperature "afterdrop" commonly occurs (3). This afterdrop may have important effects on myocardial contractility.
Although the effects of hypothermia on myocardial contractility have been widely studied in animal models both in vitro and in vivo, studies in human subjects remain sparse. Intuitively, as myofibrillar contraction is in part an active energetic process, hypothermia might be expected to reduce the myocardial contractile state. Paradoxically, experiments with rat myofibrils (4), rabbit (5) and guinea pig (6) papillary muscle and cross-circulated canine hearts (7) have shown an increase in contractility with cooling. Furthermore, the interaction of temperature, heart rate (HR) and contractility has recently come under investigation. The increase in contractility seen with cooling of the in vitro rabbit heart is forfeited if HR is not allowed to slow as myocardial temperature falls (5).
Systolic performance can be most accurately described using the left ventricular pressure-volume relationship (LVPVR), which is largely independent of preload and afterload (7). This relationship can be assessed in humans using the conductance catheter. We have recently shown that the data from these catheters are consistent over a range of relevant temperatures (8). The aim of this study was to examine the interactive effects of temperature and HR on human left ventricular (LV) systolic function.
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Materials and methods
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Patient details.
Ten patients undergoing elective coronary artery bypass grafting (CABG) were recruited. All had triple-vessel disease but good LV function (>50% ejection fraction) and no hypertension, diabetes, atrial fibrillation, left main stenosis, unstable angina, recent infarct (<2 months) or previous cardiac surgery.
All patients received identical premedication (temazepam, 10 to 20 mg; ranitidine, 150 mg; and metoclopramide, 10 mg orally) and induction (fentanyl, 15 µg/kg; etomidate, 0.1 mg/kg; and pancuronium, 0.1 mg/kg). A central venous line, right radial arterial line and a urinary catheter were inserted. In addition, a Swan-Ganz catheter was utilized to allow measurement of cardiac output and the measurement of core blood temperature.
Maintenance anesthesia (fentanyl and propofol) and bypass techniques were standardized in all patients. A maximum heat exchanger temperature gradient of 10°C was used for cooling/warming while on cardiopulmonary bypass. After sternotomy and conduit procurement, pericardiotomy was performed and the patient was prepared for CPB.
The conductance catheter.
The conductance method of determining LV volume is based on the measurement of blood conductivity within the LV. The technique has been described in detail elsewhere (9,10). Briefly the Millar conductance catheter (Millar Instruments, Houston, Texas) has 12 electrodes arranged with an interelectrode distance of 1.0 cm. The catheter is inserted into the LV along its long axis. A conditioner/processor applies a current between the most distal and proximal electrodes and quantifies the conductances (reciprocal of resistances) between the electrode pairs. The sum of these signals is used to obtain an expression for the total volume of the LV. The catheter also contains a solid-state pressure transducer. Hence, the Millar conductance catheter allows online assessment of pressure and volume. A Leycom Sigma-5 signal conditioner processor (Cardio-dynamics; Rÿnsburg, Netherlands) was used to process volume signals. Analysis of data was performed using a customized software package. End-systolic elastance (Ees) was evaluated from the end-systolic pressure-volume relation (ESPVR) using an iterative method as described by Sagawa et al. (11). The stroke-work end-diastolic volume relationship (12) is the ratio of stroke work to end-diastolic volume (EDV) at a fixed EDV, where stroke work is calculated from the area bounded by the pressure-volume (P-V) loop. Time to reach peak ejection rate (tPER) is defined as the time between the instant when the aortic valve opens (i.e., at dP/dtmax) and the instant when ejection reaches its peak rate (i.e., dV/dtmin). It is related to the time to peak elastance (Tmax).
Study protocol.
The conductance catheter was inserted via the aortic root, and its position was verified by observing the volume signals from each segment. End-expiratory thermodilution cardiac output was measured at this point to calibrate the catheter for stroke volume. The resistivity of the blood was measured, and a series of steady-state P-V loops were obtained at end expiration. Parallel conductance effect was measured by injection of 10 ml of 5% saline into the pulmonary artery port of the Swan-Ganz catheter. Patients were then assigned to one of two groups of five patients. All measurements were made following the temporary discontinuation of CPB.
In the first group (HR100), right atrial pacing was established at a fixed rate of 100, to minimize variation in HR with temperature and to simulate the postoperative period. A series of loops at differing preloads were then generated by brief occlusion of the inferior vena cava at end-expiration. Following this, CPB was instituted and the patient re-warmed to 37°C. The blood resistivity measurement was then repeated, and a further series of pressure-volume loops were generated. The patient was then core-cooled on CPB. At 35, 33 and 31°C (by Swan-Ganz thermistor and myocardial temperature probe), the data collection was repeated including repeat resistivity estimation at each temperature. Heart rate was maintained at 100 beats/min throughout. In the second group (HR80/120), the relationship between HR and temperature was investigated further. Right atrial pacing was established. Following this, CPB was instituted and the patient was re-warmed to 37°C. After warming, the patient was weaned from CPB, the blood resistivity was measured, and runs of pressure volume loops were generated at this temperature at atrially paced HRs of 80 and 120 beats/min. The patient was then core-cooled on CPB to 33°C. The sequence of measurements was then repeated at the two different HRs.
Following the final measurement in each group, CPB was reinstituted, cooling was continued to 28°C, and CABG was performed. Each patient received three bypass grafts. Mean CPB time was 88 ± 11 mins. All patients survived the study and suffered no complications attributable to the conductance catheter. One patient died after an acute myocardial ischemic event postoperatively.
Ethical committee approval.
Approval was granted for this study by the South Birmingham Local Research Ethics Committee. All patients gave informed, written consent.
Statistical analysis.
Statistical analysis was performed using one-way analysis of variance (ANOVA) with multiple comparison (Tukey-Kramer) with the ARCUS software (Cambridge Software Publishing, Cambridge, UK) package, on a standard personal computer. Statistical significance was assumed when p < 0.05. In group 1 (HR100), p values were calculated by standard ANOVA to compare all results for each index of contractility and by ANOVA with multiple comparison to compare consecutive temperatures (i.e., 37 vs. 35, 35 vs. 33). In group 2 (HR80-120), p values were calculated by using the paired t test.
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Results
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Group 1 (HR100).
In one patient the study was terminated at 33°C due to atrial fibrillation. At a paced HR of 100 beats/min, there was a progressive fall in Ees (Figs. 1 and 2) and stroke work at constant volume (Fig. 3) with cooling. The tPER (Fig. 4) increased progressively as the temperature was reduced.
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Figure 1 Pressure volume loops from a patient demonstrating a fall in contractility at constant paced heart rate (100 beats/min), with cooling (A = 37°C; B = 33°C). Group 1.
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Figure 2 Change in normalized end systolic elastance from baseline at constant paced heart rate (100 beats/min) with cooling. Group 1. **p < 0.0001.
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Figure 3 Change in normalized stroke work (SW) -end diastolic volume (EDV) relationship from baseline at constant paced heart rate (100 beats/min) with cooling. Group 1. **p < 0.05.
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Figure 4 Change in normalized time to peak ejection rate from baseline at constant paced heart rate (100 beats/min) with cooling. Group 1. **p < 0.05.
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Group 2 (HR80/120).
Since Ees appeared the most sensitive indicator of change in contractility in group 1, only this index was assessed in group 2. At 37°C, Ees increased with increasing HR (Fig. 5). Mean contractility at 120 beats/min was 205.9 ± 13.2% of baseline (p = 0.0021). However, at 33°C, this effect was reversed with a significant fall in Ees at an HR of 120 beats/min (mean 53.7 ± 13.2%) compared to an HR of 80 beats/min (100%, p = 0.0014) (Fig. 6). No consistent changes in the volume intercept, V0, were demonstrated in either group.
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Discussion
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This study shows that human LV contractility is profoundly depressed by hypothermia when the HR is maintained at a rate of 100 beats/min. Furthermore, the positive inotropic response to increasing HR seen at normothermia is reversed at 33°C. These facts are highly relevant in the postoperative management of cardiac surgical patients, where optimization of HR, stroke volume and contractility are essential in the maintenance of cardiac output.
This is a new finding in humans, but there are consistent animal data. In pigs, a depression of systolic function occurred during cooling at a constant atrial paced HR of 150 beats/min (13). However, when the HR is allowed to vary, contradictory results have been obtained. In anesthetized, unpaced dogs, subjected to veno-venous cooling, Goldberg (14) showed that systolic function, as measured by a strain gauge to assess contractile force, was augmented as temperature decreased. These results have been confirmed using load independent techniques (15,16). These apparently contradictory results may be reconciled by considering the effects of alterations in HR on the changes in cellular activity induced by hypothermia.
Mechanism.
Myocardial contractility is dependent on myosin and actin crossbridge formation and is sensitive to the concentration of calcium ([Ca2+]) prevailing within the cell. The Ca2+ is dependent on both the duration of the action potential and the activity of adenosine triphosphate–dependent ion exchange pumps within the cell wall and the sarcoplasmic reticulum. Since enzymatic activity is directly related to temperature, the effect of cooling is therefore dependent on the relative thermal sensitivity of each enzymatic reaction step. Consequently the effects of hypothermia on systolic function cannot easily be predicted. If the negative effects of decreasing temperature are relatively greater on myosin/actin crossbridge formation, then contractility will fall. If hypothermia exerts a greater relative inhibitory effect on Ca2+ ion exchange activity and causes a rise in intracellular Ca2+, this may lead to increased contractility. Although Ruf et al. (17) demonstrated that the reduction in actin/myosin crossbridge cycling rate in a human muscle preparation was directly proportional to temperature, Henderson et al. (4) showed that the force of contraction was increased with decreasing temperature down to 29°C in rat myofibrils, suggesting that Ca2+ handling is the more temperature sensitive of the two processes. Variations in Ca2+ handling with temperature, causing an increase in the intracellular level of Ca2+, have been demonstrated in vitro at the level of the Ca2+ channel, in guinea pigs (6) and dogs (18), the Ca2+/Na+ exchange pump in humans (19) and in the sarcoplasmic reticulum Ca2+ pump, Ca2+/Na+ exchanger, sarcolemmal Ca2+ pump and the mitochondrial Ca2+ uniporter in small mammals (20).
In addition, changes in Ca2+ handling are likely to have an effect on the timings of the contractile cycle. This is because the rate of release and sequestration of Ca2+ directly determine the rate of interaction of myosin and actin (21). As a result of this, hypothermia has been shown to cause a prolongation of the time to peak tension (TPT) (4,22).
Implications.
An explanation that unites the effects of hypothermia on myosin/actin and Ca2+ handling and explains the aforementioned apparently contradictory findings is that even if the rate of tension development (dP/dT) is decreased by hypothermia because of myosin/actin effects, then because the duration of contraction is increased (TPT or Tmax), maximum inotropy may well be increased (22,23).
Hence, the increased inotropy seen with hypothermia in these earlier experiments may be due to an alteration in the duration of contraction. This positive inotropic effect is likely to be sensitive to changes in HR. In both load independent experiments (15,16) in which cooling increased contractility, HR was either allowed to vary (15) or the dog was paced at a normal resting HR (16). However, in a study performed in hypothermic (30°C) isolated rabbit hearts, Mattheussen et al. (5) showed that the increased contractility noted at low HR (30 beats/min) was reversed, and reduced contractility was noted when HR was increased to 90 beats/min by pacing.
Our results confirm the findings of these animal studies. The interaction may occur because of an increase in maximal elastance (Emax) and Tmax with cooling. Hence although there may be an increase in Emax, this is at the expense of an increase in the time taken to reach maximal contraction. In the circumstances of a high HR, Emax may not be reached, resulting in a decrease in the amount of available work (13).
Clinical implications.
The postoperative management of hypothermic cardiac surgery patients would appear to represent a compromise between HR and contractility. Care should be taken when increasing a hypothermic patient’s HR either through pacing or the use of chronotropic agents.
Experimental limitations.
Pressure-volume analysis with the conductance catheter does not give a perfect measure of LV kinetics. This is due to, for example, problems with the nonlinearity of P-V relations at the extreme ends of the physiologic range (24,25) and the difficulty in measuring absolute volumes (9,26). However, it does represent the best technique currently available for human in vivo studies, particularly in the situation where patients act as their own controls. A potential limitation of this study was the fact that the patients were cooled on bypass. Although Wood et al. (27) have shown that cooling on bypass does not affect catecholamine levels in children, the period of time on bypass itself may have a detrimental effect on myocardial function. Knowledge of changes in cardiac function in the early stages of bypass is rather limited (28,29). However, data from Pavlides et al. (30) imply that little change occurs in cardiac function during CPB used to support coronary angioplasty. A further potential limitation relates to possible changes in parallel conductance with changing temperature. Although resistivity was checked prior to each contractility assessment, pre-set time constraints to ensure patient safety precluded repeated measurement of parallel conductance, which was assessed only at normothermia. It is therefore possible that the corrected calculation of absolute volume at lower temperature was inaccurate (Fig. 1). Nevertheless, we believe that the conclusions drawn remain valid, as Ees, the main measure of contractility used in this study, is determined by relative changes in volume rather than the absolute volume. The conductance catheter is thought to provide a more accurate determination of relative rather than absolute volume, even at normothermia (31).
In summary, our results confirm that contractility falls with temperature if HR is artificially maintained. Increasing HR at low temperature causes a fall in contractility. These findings are consistent with differential thermal sensitivities of the two prime elements of contractility: actin-myosin crossbridge formation and intracellular Ca2+ handling. These effects may be clinically important in unstable postsurgical patients. Optimization of postoperative cardiac function in hypothermic patients would appear to represent a compromise between contractile status and HR.
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Acknowledgments
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We gratefully acknowledge the help and support of the anesthetic, perfusion, technical and nursing staff of the Queen Elizabeth Hospital.
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Footnotes
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Dr. Lewis was supported by a Junior Research Fellowship from the British Heart Foundation (BHF) during this work and equipment costs are met by the National Heart Research Fund (NHRF). Dr. Al-Khalidi is supported by the NHRF and BHF.
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References
|
|---|
1. Yahagi N, Kumon K, Watanabe Y, et al. Value of mild hypothermia in patients who have severe circulatory insufficiency even after intra-aortic balloon pump. J Clin Anesth. 1998;10:120–125[CrossRef][Medline]
2. Moat NE, Lamb RK, Edwards JC, Manners J, Keeton BR, Monro JL. Induced hypothermia in the management of refractory low cardiac output states following cardiac surgery in infants and children. Eur J Cardiothorac Surg. 1992;6:579–584[Abstract]
3. Davis FM, Parimelazhagan KN, Harris EA. Thermal balance during cardiopulmonary bypass with moderate hypothermia in man. Br J Anaesth. 1977;49:1127–1132[Abstract/Free Full Text]
4. Henderson AH, Brutsaert DL, Parmley WW, Sonnenblick EH. Myocardial mechanics in papillary muscles of the rat and cat. Am J Physiol. 1969;217:1273–1279[Free Full Text]
5. Mattheussen M, Mubagwa K, Van Aken H, Wusten R, Boutros A, Flameng W. Interaction of heart rate and hypothermia on global myocardial contraction of the isolated rabbit heart. Anesthes Analg. 1996;82:975–981[Abstract]
6. Bjornstad H, Tande PM, Refsum H. Mechanisms for hypothermia-induced increase in contractile force studied by mechanical restitution and post-rest contractions in guinea-pig papillary muscle. Acta Physiol Scand. 1993;148:253–264[Medline]
7. Suga H, Sagawa K. Instantaneous pressure-volume relationships and their ratio in the excised, supported canine left ventricle. Circ Res. 1974;35:117–126[Abstract/Free Full Text]
8. Al-Khalidi A, Townend J, Bonser R, Coote J. Validation of the conductance catheter method for measurement of ventricular volumes under varying conditions relevant to cardiac surgery. Am J Cardiol. 1998;82:1248–1252[CrossRef][Medline]
9. Baan J, van der Velde ET, de Bruin HG, et al. Continuous measurement of left ventricular volume in animals and humans by conductance catheter. Circulation. 1984;70:812–823[Abstract/Free Full Text]
10. Kass DA, Midei M, Graves W, Brinker JA, Maughan WL. Use of a conductance (volume) catheter and transient inferior vena caval occlusion for rapid determination of pressure-volume relationships in man. Cathet Cardiovasc Diagn. 1988;15:192–202[Medline]
11. Sagawa KML, Suga H, Sunagawa K. Cardiac Contraction and the Pressure-Volume Relationship. New York, NY: Oxford University Press; 1988.
12. Matsuwaka R, Matsuda H, Nakano S, et al. A new method of assessing left ventricular function under assisted circulation using a conductance catheter. ASAIO Transactions. 1989;35:449–451[Medline]
13. Greene PS, Cameron DE, Mohlala ML, Dinatale JM, Gardner TJ. Systolic and diastolic left ventricular dysfunction due to mild hypothermia. Circulation. 1989;80 Suppl III:III44–48
14. Goldberg LI. Effects of hypothermia on contractility of the intact dog heart. Am J Physiol. 1958;194:92–98[Abstract/Free Full Text]
15. Suga H, Goto Y, Igarashi Y, et al. Cardiac cooling increases Emax without affecting relation between O2 consumption and systolic pressure-volume area in dog left ventricle. Circ Res. 1988;63:61–71[Abstract/Free Full Text]
16. Mikane T, Araki J, Suzuki S, et al. O2 cost of contractility but not of mechanical energy increases with temperature in canine left ventricle. Am J Physiol. 1999;277:H65–73
17. Ruf T, Schulte-Baukloh H, Ludemann J, et al. Alterations of cross-bridge kinetics in human atrial and ventricular myocardium. Cardiovasc Res. 1998;40:580–590[Abstract/Free Full Text]
18. Kasama M, Furukawa Y, Oguchi T, Hoyano Y, Chiba S. Effects of low temperature on the chronotropic and inotropic responses to zatebradine, E-4031 and verapamil in isolated perfused dog atria. Jpn J Pharmacol. 1998;78:493–499[CrossRef][Medline]
19. Gaughan JP, Furukawa S, Jeevanandam V, et al. Sodium/calcium exchange contributes to contraction and relaxation in failed human ventricular myocytes. Am J Physiol. 1999;277:H714–724
20. Puglisi JL, Bassani RA, Bassani JW, Amin JN, Bers DM. Temperature and relative contributions of Ca transport systems in cardiac myocyte relaxation. Am J Physiol. 1996;270:H1772–1778
21. Tregear RT, Marston SB. The crossbridge theory. Annu Rev Physiol. 1979;41:723–736[CrossRef][Medline]
22. Langer GA, Brady AJ. The effects of temperature upon contraction and ionic exchange in rabbit ventricular myocardium: relation to control of active state. J Gen Physiol. 1968;52:682–713[Abstract]
23. Fukunami M, Hearse DJ. The inotropic consequences of cooling: studies in the isolated rat heart. Heart Vessels. 1989;5:1–9[CrossRef][Medline]
24. Little WC, Cheng CP, Peterson T, Vinten-Johansen J. Response of the left ventricular end-systolic pressure-volume relation in conscious dogs to a wide range of contractile states. Circulation. 1988;78:736–745[Abstract/Free Full Text]
25. Kass DA, Beyar R, Lankford E, Heard M, Maughan WL, Sagawa K. Influence of contractile state on curvilinearity of in situ pressure volume relations. Circulation. 1989;79:167–178[Abstract/Free Full Text]
26. Burkhoff D, van der Velde E, Kass D, Baan J, Maughan WL, Sagawa K. Accuracy of volume measurement by conductance catheter in isolated, ejecting canine hearts. Circulation. 1985;72:440–447[Abstract/Free Full Text]
27. Wood M, Shand DG, Wood AJ. The sympathetic response to profound hypothermia and circulatory arrest in infants. Can Anaesth Soc J. 1980;27:125–131[Medline]
28. van der Veen FH, van der Vusse GJ, Kruger RT, van der Nagel T, Willemsen P, Reneman RS. Metabolic and haemodynamic changes in the heart during the early phase of cardiopulmonary bypass: II: Animal experiments. Cardiovasc Res. 1989;23:472–477[Medline]
29. van der Veen FH, van der Vusse GJ, Flameng W, Coumans WA, Reneman RS. Metabolic and haemodynamic changes in the heart during the early phase of cardiopulmonary bypass: I: Clinical observations. Cardiovasc Res. 1989;23:468–471[Medline]
30. Pavlides GS, Hauser AM, Stack RK, et al. Effect of peripheral cardiopulmonary bypass on left ventricular size, afterload and myocardial function during elective supported coronary angioplasty. J Am Coll Cardiol. 1991;18:499–505[Abstract]
31. Boltwood CM Jr, Appleyard RF, Glantz SA. Left ventricular volume measurement by conductance catheter in intact dogs: parallel conductance volume depends on left ventricular size. Circulation. 1989;80:1360–1377[Abstract/Free Full Text]
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Abstract
Materials and methods
