Asian Cardiovasc Thorac Ann 2006;14:20-25
© 2006 Asia Publishing EXchange Ltd
Perioperative Circulating Blood Volume and Cardiac Function in Valve Disease
Nobuo Tsunooka, MD,
Yoshihiro Hamada, MD,
Shinji Takano, MD,
Yuji Watanabe, MD,
Hiroshi Imagawa, MD,
Kanji Kawachi, MD
Second Department of Surgery, Ehime University School of Medicine, Ehime, Japan
For reprint information contact: Nobuo Tsunooka, MD Tel: 81 89 960 5331 Fax: 81 89 960 5335 Email: tsunooka{at}m.ehime-u.ac.jp, Second Department of Surgery, Ehime University School of Medicine, Shitsukawa, Toon, Ehime 791-0295, Japan.
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ABSTRACT
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Circulating blood volume is important in managing fluid balance and cardiac function after surgery under cardiopulmonary bypass. Appropriate management differs among the valve disorders, but perioperative blood volume has not yet been considered. From February 2001 to March 2003, perioperative blood volume, fluid balance, cardiac index, and left ventricular stroke work index were measured in 31 patients: 10 with aortic stenosis, 9 with aortic regurgitation, 3 with mitral stenosis, and 9 with mitral regurgitation. All immediate postoperative blood volume measurements were less than preoperative values, and gradually returned to baseline. At all time points, blood volume in patients with aortic or mitral regurgitation was high, whereas it was low in those with stenosis, especially mitral stenosis. Fluid balance was positive in all patients. Postoperatively, there was a positive correlation between cardiac index and blood volume in all groups. The left ventricular stroke work index in the mitral regurgitation group was significantly higher than other groups, the aortic stenosis group was slightly lower, the mitral stenosis and mitral regurgitation groups were higher than the baseline, and the aortic regurgitation group was essentially unchanged. Thus, it is necessary to consider blood volume perioperatively in different valvular diseases to manage water balance.
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INTRODUCTION
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Fluid management and maintenance of cardiac function are critical issues after cardiac surgery under cardiopulmonary bypass (CPB). Determination and control of adequate blood volume (BV) is crucial because marked imbalances in circulating BV significantly increases perioperative morbidity and mortality.1 Fluid management is based on measuring perioperative fluid balance and central venous pressure (CVP). Despite a fluid gain of several liters during CPB in most patients, the early postoperative BV is significantly reduced.2 Although fluid balance is negative thereafter, BV increases with time.3 Thus, while BV is an important perioperative measurement in cardiac patients, it has not been reported in those undergoing valve operations. Specific perioperative management for each type of valvular disorder is essential. Therefore, we studied the changes in perioperative BV for fluid management in patients undergoing various valve operations.
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PATIENTS AND METHODS
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All 31 patients with valvular disease in this study underwent either elective aortic or mitral valve operations at our hospital from February 2001 to March 2003. They were assigned to 4 groups according to the affected valve and condition as follows: aortic stenosis (AS group, n = 10), aortic regurgitation (AR group, n = 9), mitral stenosis (MS group, n = 3), and mitral regurgitation (MR group, n = 9). Patients in the AR and MR groups were significantly younger than those in the AS and MS groups, and only 2 in the AR group required diuretics (Table 1
). Patients with an ejection fraction (EF) less than 40%, a cardiothoracic ratio over 70%, both severe stenosis and regurgitation, and those requiring combined aortic and mitral valve surgery were excluded from the study. Operative indications for valvular disease were according to the American College of Cardiology/American Heart Association guidelines.4 All subjects gave informed consent for participation in this study. The study protocol was approved by the Institutional Committee on Human Research.
Standard anesthetic agents, neuromuscular blockade (fentanyl, midazolam, pancuronium, and propofol), and monitoring techniques were used in all patients. Monitoring included electrocardiography, continuous arterial pressure, CVP, pulmonary arterial pressure, pulmonary capillary wedge pressure (PCWP), cardiac index (CI), urinary output, and rectal and skin temperature. A pulmonary artery catheter was inserted in all patients. The CI was determined with a continuous cardiac output measuring instrument (Edwards Critical Care Vigilance; Baxter Healthcare Corporation, Irvine, CA, USA). After a median sternotomy, all patients were heparinized to achieve an activated clotting time greater than 400 sec. Cardiopulmonary bypass was undertaken with a non-pulsatile roller pump (Stockert SIII; Stockert-Shiley, Irvine, CA, USA), a membrane oxygenator (HMO-1040; Jostra Bentley Corporation, Irvine, CA, USA), and an arterial line filter (LH-40AH; JMS, Hiroshima, Japan). Cardiopulmonary bypass flow was initiated at 2.4 L·min–1·m–2 and then decreased to keep the mixed venous oxygen saturation (SvO2) at approximately 75%. Blood pressure was maintained between 40 and 60 mm Hg using chlorpromazine as a systemic vasodilator. Mild hypothermia (rectal temperature, 32°C) was instituted immediately after the start of CPB. Myocardial protection consisting of antegrade induction of cardioplegia was performed initially using crystalloid solution 10 mL·kg–1; then blood cardioplegia (5 mL·kg–1) was infused over 30 min. All patients underwent valve replacement and additional procedures if necessary. Rewarming was started 5 min before concluding the procedure. Terminal warm blood cardioplegia (1,000 mL) was followed by aortic declamping. Retrograde cardioplegia was infused continuously during aortic crossclamping. Fifteen minutes after aortic declamping, when the patient’s rectal temperature was at least 34°C, separation from CPB was started and heparin was neutralized with protamine sulfate. Upon successful weaning from CPB, to maintain adequate arterial pressure, the patient was transfused from the reservoir of the pump oxygenator until the PCWP exceeded 8 mm Hg. Approximately 5 min before weaning from CPB, dopamine (5 µg·kg–1·min–1) and nitroglycerin (0.3 µg·kg–1·min–1) were administered as a continuous infusion in all patients.
The technique for measuring BV was based on pulse dye densitometry using a DDG-2001 densitometer (Nihon Koden, Tokyo, Japan) and indocyanine green (Diagnogreen; Dai-ichi Pharmaceutical, Tokyo, Japan).3 Probes were attached to the index finger. Indocyanine green was diluted (10 mg in 2 mL of sterile distilled water) and injected as a bolus via an intravenous catheter placed in the forearm. The catheter was then flushed with 20 mL of saline. The indocyanine green concentration was plotted semi-logarithmically and extrapolated backward to a mean transit time point. The initial concentration was obtained for the calculation of total BV. The BV was determined before the operation, immediately after, and at 4 h and 12 h postoperatively, and it was expressed in terms of preoperative body weight (mL·kg–1). Fluid balance, left ventricular stroke work index (LVSWI), and systemic vascular resistance index (SVRI) at each time point after the start of the operation were calculated as follows:
Fluid balance (mL·kg–1) = (infusion and transfusion volume – blood loss – urine output)/preoperative body weight
LVSWI (g·m·m–2) = (mean arterial pressure – PCWP) x stroke volume x 0.0136/preoperative body surface area
SVRI (dynes·sec·cm–5·m2) = (mean arterial pressure – CVP)/CI x 79.92
All data are expressed as mean ± standard deviation. Data were small-scale, so nonparametric statistical methods were used (StatView 5.0 for Macintosh, SAS Institute, Cary, NC, USA). The Bonferroni-Dunn test was used to determine differences between preoperative values and different time points within each group. Either the Bonferroni-Dunn test or the chi-squared test for independence was performed for different groups at each time point.
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RESULTS
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All patients completed the study protocol, and no patient was excluded. No postoperative complications or mortality occurred. There were no differences between groups in CPB time, aortic crossclamp time, transfusion rate, minimum hemoglobin, and minimum rectal temperature during the operation (Table 2). Blood pressure, CVP, and fluid balance were similar among the groups during the perioperative period. The fluid balance value was always positive in all groups (Table 3).
Immediate postoperative BV measurements in the AR and MR groups were significantly less than the preoperative values, and also tended to be lower in the AS and MS groups. The BV then gradually returned to baseline. At all time points, BV in the AR and MR groups was higher than the other groups, especially the MS group (Figure 1). Postoperative CI in all groups was greater than baseline. As for intergroup differences at each time point, regurgitative valve diseases (AR and MR) had higher CI measurements than stenotic valve diseases (Figure 2). Preoperatively, LVSWI in the MS group was significantly lower than in other groups. Postoperatively, LVSWI in the MR group was significantly higher than the other groups. Compared with baseline, postoperative LVSWI was slightly lower in the AS group, higher in the MS and MR groups, and essentially unchanged in the AR group (Figure 3). Perioperatively, the MS group had a very high SVRI; this measurement decreased subsequently in all groups (Figure 4).
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Figure 1. Circulating blood volume before and after valve surgery. AR = aortic regurgitation, AS = aortic stenosis, MR = mitral regurgitation, MS = mitral stenosis. *p < 0.05 for intergroup differences in the same period. #p < 0.05 vs. baseline in each group.
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Figure 2. Cardiac index before and after valve surgery. AR = aortic regurgitation, AS = aortic stenosis, MR = mitral regurgitation, MS = mitral stenosis. *p < 0.05 for intergroup differences in the same time period. #p < 0.05 vs. baseline in each group.
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Figure 3. Left ventricular stroke work index before and after valve surgery. AR = aortic regurgitation, AS = aortic stenosis, MR = mitral regurgitation, MS = mitral stenosis. *p < 0.05 for intergroup differences in the same period. #p < 0.05 vs. baseline in each group.
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Figure 4. Systemic vascular resistance index before and after valve surgery. AR = aortic regurgitation, AS = aortic stenosis, MR = mitral regurgitation, MS = mitral stenosis. *p < 0.05 for intergroup differences in the same period. #p < 0.05 vs. baseline in each group.
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DISCUSSION
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This study showed that each major valvular disorder has a specific BV. Due to the low preoperative BV in the MS and AS groups and the high BV in the AR and MR groups, the loading volume for the cardiopulmonary circuit may be underestimated in the MS and AS groups, and overestimated in the AR and MR groups. Minimum hemoglobin in the AR group was high, although not significantly, and this was because preoperative BV was significantly higher in this group. After cardiac surgery and CPB, hypervolemia often occurs, which can lead to severe complications.5 Therefore, the measurement of postoperative BV is important, especially with low BP, CVP, and fluid balance measurements.
Hamada and colleagues3 reported that BV decreased immediately postoperatively in patients undergoing coronary artery bypass grafting, gradually returning to preoperative values despite a positive fluid balance. The same was true in our valvular disease patients. Pulmonary edema after CPB was reported to increase in the immediate postoperative period and gradually decrease with time.6,7 The hypothesis is that postoperative hypovolemia is due to transient microvascular damage and extravascular fluid shifts, and the increased BV then reflects return of the extravascular fluid to the intravascular space.3 The technique for measuring BV was based on pulse dye densitometry. This method is noninvasive and reliable.3 Indocyanine green has very low toxicity and is excreted by the liver in the bile.8,9 There are some recent reports that the PiCCO machine (Koninklijke Philips Electronics NV, Eindhoven, Netherlands) can measure cardiac output, intrathoracic blood volume, extravascular lung water, and cardiac function index at the same time.10–12 There may be more possible examinations using this device.
It is unclear why postoperative BV returns closely to the preoperative values (not higher or lower). We measured BV to determine whether at 1 week postoperatively BV approximated the same value in patients who had different preoperative valvular disorders. In all patients, the BV at 1 week postoperatively was lower than the preoperative BV, and the BV pattern among the valvular disease groups was similar to the preoperative pattern. The influence of preoperative valvular disorders on BV may continue during the early postoperative period. Relationships between preoperative BV, age, and preoperative diuretic use were not clear either; further investigation is necessary. Postoperative CI in all groups was higher than preoperative CI, as the left ventricle could then fully eject the BV without valvular interference. Dopamine infusion, however, may have contributed a positive inotropic effect.
The LVSWI also reflected both the BV and the left ventricular pressure. In MS patients, less blood enters the left ventricle, which results in a low LVSWI; postoperatively, the LVSWI increased slightly as all blood can enter and exit easily. In other valvular diseases, the left ventricle can effectively eject all the blood preoperatively as well as postoperatively. In AS patients, however, the postoperative LVSWI decreased somewhat from baseline with the removal of pressure loading. In AR patients, because the preoperative and early postoperative left ventricular volumes are similar, little change in LVSWI may occur. On the other hand, in MR patients, although preoperative and postoperative left ventricular end-diastolic volumes are similar, the postoperative left ventricle must eject all the BV into the aorta where pressure is very high due to higher postoperative LVSWI than preoperative LVSWI. Thus, postoperative left ventricular load must be reduced by preventing anemia and lowering the afterload. We usually use a phosphodiesterase III inhibitor during CPB to reduce SVRI and LVSWI. In addition, the preoperative oral administration of an angiotensin-converting enzyme inhibitor was reported to decrease SVRI after CPB.13
The small numbers of patients in each group lowers the power of this study, and more cases are required to validate these hypotheses. In particular, there were very few MS patients because of the decreasing incidence of rheumatic fever. Further studies are warranted to verify these preliminary results in valve patients.
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REFERENCES
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ABSTRACT
INTRODUCTION
