BJA Advance Access published online on June 4, 2008
British Journal of Anaesthesia, doi:10.1093/bja/aen145
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Evaluation of the right ventricular ejection fraction during orthotopic liver transplantation under propofol anaesthesia
Liver Transplantation Unit, Bonsucesso General Hospital, Londres Av, 616, Bonsucesso, Rio de Janeiro 21041-030, Brazil
* Corresponding author. E-mail: glaubergouvea{at}ibest.com.br
Accepted for publication April 11, 2008.
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Abstract |
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Background: The right ventricular ejection fraction pulmonary artery catheter (RVEF-PAC) has been widely used to monitor the right ventricular (RV) function during orthotopic liver transplantation (OLT). However, the evaluation of the RVEF during this procedure during propofol anaesthesia has not been described.
Methods: Twenty consecutive patients undergoing OLT without veno-venous bypass were studied. Anaesthesia was maintained with propofol, remifentanil and atracurium infusions. All patients were monitored with a modified pulmonary artery catheter (RVEF-PAC), which continuously measures the RVEF. Haemodynamic data were recorded at: baseline (TB), anhepatic stage (TA), and 1, 5, 10, and 30 min post-reperfusion of the graft.
Results: The baseline RVEF was decreased [40% (SD 6)] and remained so throughout the OLT. A biphasic pattern was revealed, with the RVEF reaching its lowest values during TA [34% (7)] and gradually returning toward baseline at T30 [39% (8)]. Clinical significant RV dysfunction did not occur.
Conclusions: Although the baseline RVEF was decreased, it showed only minor alterations throughout the procedure, suggesting that the RV function is not significantly compromised during OLT under propofol anaesthesia.
Keywords: anaesthetics i.v., propofol; anaesthetic techniques, i.v. infusion; liver, transplantation; measurement techniques, thermodilution; monitoring, cardiopulmonary
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Introduction |
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Orthotopic liver transplantation (OLT) may be associated with significant haemodynamic instability, especially in the anhepatic and reperfusion stages, where major fluid shifts and release of vasoactive substances are expected to occur. It has been increasingly recognized that transient cardiac dysfunction might also develop in cirrhotic patients undergoing OLT,1 which may further contribute to haemodynamic impairment. In particular, right ventricular (RV) function may be compromised in these stages, as it is quite sensitive to alterations in loading conditions.2 3 Thus, close monitoring of RV function during OLT should be considered, as early diagnosis of RV dysfunction may allow early intervention to avoid further worsening of function.
Currently, the two most commonly used methods for monitoring the RV in the intraoperative period are trans-oesophageal echocardiography (TOE) and the right ventricular ejection fraction pulmonary artery catheter (RVEF-PAC). Although the intraoperative use of TOE during OLT has been reported,4 few studies have focused on the RV. One study,5 using TOE in a series of 16 patients, reported a high incidence of transient RV dysfunction in the early post-reperfusion stage, mainly because of air embolism.
However, overt RV failure during OLT seems to be rare despite these concerns, with most reports involving patients with porto-pulmonary hypertension.6 Indeed, case series using the RVEF-PAC7–11 have confirmed this by showing that RV function is not significantly altered during otherwise uncomplicated OLT. However, most studies of RV function during OLT, used isoflurane.7–11 Although total i.v. anaesthesia with propofol has been described for OLT,12 the evaluation of the RV function during propofol anaesthesia has not been reported. This raises some concerns, as the negative inotropic effect of propofol may influence RV function, as propofol and isoflurane may have different effects on RV function.13 14
The aim of this study was to evaluate RV function using the RVEF-PAC in 20 consecutive patients undergoing OLT during propofol anaesthesia, with particular emphasis on the RVEF.
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Methods |
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After Institutional Ethics Committee approval and informed consent, 20 consecutive patients scheduled for OLT over 1 yr period (July 2005 to June 2006) were enrolled in the study. Exclusion criteria were paediatric recipient, fulminant hepatitis, and the presence of pulmonary hypertension, cardiac disease or arrhythmia.
In the operating room after standard monitoring had been placed, anaesthesia was induced with a rapid sequence technique using propofol 2 mg kg–1 and succinylcholine 1.5 mg kg–1 to facilitate orotracheal intubation. Anaesthesia was maintained with propofol (50–150 µg kg–1 min–1), remifentanil (0.1–0.5 µg kg–1 min–1), and atracurium (5–12 µg kg–1 min–1) infusions. Propofol was titrated to keep BIS values (Aspect, version 4.0 XP) between 40 and 60. Aprotinin was routinely used, with its infusion regimen at the discretion of the physician. Normothermia was achieved by forced-air warming, to maintain nasopharyngeal and pulmonary artery temperature within 36.5°C (SD 0.5). An arterial line was placed in the left radial artery and central lines were inserted in the right internal jugular vein [7F double-lumen catheter (Arrow® International, PA, USA) and an 8.5F percutaneous introducer (Edwards Lifesciences, Irvine, CA, USA)] to ensure pulmonary artery catheterization. Our fluid regimen consisted of Ringer lactate (475 ml) solutions mixed with 25 ml of albumin 20%, infused at 4 ml kg–1 h–1. Hypovolemia was treated with bolus of colloid 5 ml kg–1 (HAES 130/0.4 – Voluven®, Fresenius, Kabi) as needed (maximum dose: 30 ml kg–1). Arterial and mixed-venous blood samples were collected hourly or at the discretion of the physician for laboratory analysis. Sodium bicarbonate 0.5 mEq kg–1 was given if metabolic acidosis developed (pH<7.1). Ionized hypocalcemia was treated with calcium chloride 15 mg kg–1 as needed. The threshold for blood transfusion was a haemoglobin concentration <8 mg dl–1 with an increased oxygen extraction ratio, as guided by the mixed venous saturation (SVO2).
The modified PAC used (7.5F CEDV Pulmonary Artery Catheter, 774H, Edwards Lifesciences, Irvine, CA, USA) was interfaced with the VigilanceTM CCO/SVo2/CEDV monitor (Edwards Lifesciences, Irvine, CA, USA). This catheter has a fast-response thermistor on its terminal end which measures the RVEF using an algorithm based on thermodilution curve plateaus. The right ventricle end-diastolic volume index (RVEDVI) is then calculated dividing the stroke volume index (SVI) by the RVEF. This method is described in detail elsewhere.15 Cardiac index, RVEDVI, and RVEF were displayed continuously on the monitor.
Haemodynamic data were collected at six stages: TB, baseline (when the patient was haemodynamically stable after the start of surgery); TA, anhepatic phase (30 min after lateral clamping of the vena cava); T1, T5, T10, and T30: 1, 5, 10, and 30 min after reperfusion, respectively. If the patient developed post-reperfusion syndrome,16 a single bolus of epinephrine (50 µg) was given to restore haemodynamic stability. A norepinephrine infusion was initiated in cases of persistent hypotension with decreased systemic vascular resistance. The technical surgical aspects of OLT are described elsewhere.17 Our team did not use venovenous bypass, performing the venous anastomosis with lateral clamping of the recipient venous cava (piggy-back technique).18 All patients had their trachea extubated at the end of the procedure and were then admitted in the intensive care unit (ICU).
Statistical analysis was performed using the Microcal Origin 6.0 software (Microcal Software, Inc., Northampton). Haemodynamic data were expressed as mean (standard deviation, SD) and analysed using the one-way analysis of variance (ANOVA) test followed by the post-hoc Tukey's test. P<0.05 was considered significant.
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Results |
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The mean age of the patients was 48.8 (10.4) yr and 12 were male (Table 1). Fifteen patients (75%) had hepatitis C, two had alcoholic liver disease and one each of amyloidosis, hepatitis B, and cryptogenic cirrhosis. Eleven patients (55%) were classified as Child C, and nine patients (45%), Child B. Mean ischaemia time was 5 (2.3) h. With the exception of three patients, who underwent living donor liver transplantation, all the grafts were from cadaver.
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The mean baseline RVEF was low and slightly decreased during the anhepatic stage (Fig. 1 and Table 2). Both RV preload (CVP, RVEDVI) and afterload (PVRI) indexes also decreased at TA. However, only SVI and PAP at TA were statistically significant, less than TB (P<0.05). After reperfusion, the RVEF and SVI gradually increased, approaching their baseline values only at T30. The RV preload indexes rapidly increased towards baseline (T5). The PVRI reached a peak value at T5 (P<0.05), decreasing thereafter and approaching baseline values at T30.
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P<0.05 when compared with TAAprotinin was infused after the ‘high-dose’ protocol (2x106 KIU bolus followed by a continuous infusion of 5x105 KIU h–1) in 10 patients, while a low-dose regimen (2x105 KIU h–1, no initial bolus) was used in six patients. Two patients developed anaphylaxis at the start of the infusion, requiring the drug to be stopped immediately but both rapidly responded to volume replacement and small bolus doses of epinephrine. Because of the prompt recovery and the TB data of these two patients had already been collected, we did not exclude them from the study. Aprotinin was not used in two patients. Four patients (20%) developed post-reperfusion syndrome, but rapidly recovered haemodynamic stability after a single bolus of epinephrine. One patient required a continuous infusion of norepinephrine, initiated 1 h after reperfusion (maximum dose: 0.2 µg kg–1min–1), but was stopped before the end of the procedure. No plasma or platelets were transfused. Only one patient required blood transfusion (2 units).
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Discussion |
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Our major finding was a decreased baseline RVEF, with only minor alterations throughout the procedure, with a further decrease at TA and recovery after reperfusion. RVEF is an index of RV function which may be influenced by the loading conditions,2 3 19 which frequently occur during OLT. Indeed, the decreased RVEF found in our patients during anhepatic phase and post-reperfusion could be well explained by the decreased preload (as shown by the decreased RVEDVI and CVP) and increased afterload (as shown by the increased PVRI) that occurred at these stages, respectively. However, the decreased baseline RVEF was clearly unrelated to the loading indexes, suggesting that decreased RV contractility may have played a role at this stage. This raised the concern that propofol may impair RV function. Laboratory studies have shown propofol to have negative inotropic effects,20–22 and one clinical study23 of sedation with propofol in the ICU showed decreased RV end-systolic pressure–volume relation – an index of contractility.
However, other studies,7–11 using isoflurane during OLT, also have reported a low baseline RVEF similar to ours. This suggests that factors other than anaesthetic drugs could have contributed to these findings. Some studies have shown that RVEF-PAC may consistently underestimate the RVEF when compared with imaging techniques, such as angiography24 and standard or 3D echocardiography.25 26 This could also explain, at least in part, the decreased baseline RVEF found in our and other studies. It has been reported that the accuracy of RVEF-PAC may be markedly influenced by the presence of tricuspid regurgitation (TR),27 leading to underestimation of RVEF. In our study, clinically significant TR in the intraoperative period could not be excluded, as we did not perform intraoperative TOE. Transient TR may have occurred during acute periods of increased RV afterload or preload.
In contrast, one study7 using isoflurane during OLT reported a higher baseline RVEF (average 50%) than ours, however, in 11 of their 20 patients, a low-dose dopamine infusion was used. The positive inotropic effect of dopamine, even at a renal dose (up to 5 µg kg–1 min–1)28 could have contributed to a higher RVEF.
A study13 comparing propofol and isoflurane anaesthesia, in a different setting, has reported lower RVEF values with propofol. The differences, however, were small, and the clinical relevance of these findings remains unknown. The randomized study29 of isoflurane or propofol for OLT found that SVI was better maintained in the isoflurane group during reperfusion, suggesting better myocardial performance of this group. However, RV function was not addressed in this study.
In conclusion, we have evaluated RVEF during OLT using propofol anaesthesia and found that RV function is not significantly compromised by propofol anaesthesia. The decreased baseline RVEF could be explained either by a decreased RV contractility induced by propofol or by a measurement effect induced by the RVEF-PAC. The pattern of further decrease during anhepatic phase with recovery after reperfusion is in agreement with other studies,7–11 and probably it was mostly related to the alterations on RV loading conditions that typically occur during OLT. We believe further studies directly comparing propofol and isoflurane anaesthesia for OLT may be warranted. However, if propofol has contributed to a decreased RVEF during OLT, it was of minor clinical significance, as overt RV dysfunction did not occur in any of our patients.
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This work was supported only by institutional funding: Bonsucesso General Hospital (HGB/Ministério da Saúde, Brasil).
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This work should be attributed to the Liver Transplantation Unit of the Bonsucesso General Hospital (HGB).
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References |
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