|Year : 2008 | Volume
| Issue : 6 | Page : 805
Comparison of Haemodynamic and Cardiovascular Effects of VIMA with Sevoflurane Versus TIVA with Propofol in Patients Undergoing Coronary Artery Bypass Surgery
Neerja Bharti1, Pramila Chari2, Shyam K S Thingnam3, Suman Arora1
1 Associate professor, Department of Anaesthesia and Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh - 160012, India
2 Ex-Professor & Head, Department of Anaesthesia and Intensive Care, Post Graduate Institute of Medical Education and Research, Chandigarh - 160012, India
3 Professor & Head, Department of Cardiovascular & Thoracic Surgery, Post Graduate Institute of Medical Education and Research, Chandigarh - 160012, India
|Date of Acceptance||09-Nov-2008|
|Date of Web Publication||19-Mar-2010|
Department of Anaesthesia and Intensive Care, PGIMER, Chandigarh-160012
Source of Support: None, Conflict of Interest: None
Sevoflurane provides protection against myocardial ischaemia during bypass surgery. This prospective, randomized study was conducted to compare the haemodynamic and cardiovascular effects of sevoflurane induction& maintenance of anaesthesia(VIMA) with a standard total intravenous technique using propofol(TIVA) during coronary artery bypass graft (CABG) surgery.
Thirty adult patients undergoing elective CABG surgery were randomly allocated to receive either sevoflurane (S group) or propofol (P group) for induction and maintenance of anaesthesia. In both groups, analgesia was supplemented with fentanyl and muscle relaxation with vecuronium. Patients' heart rate, systemic and pulmonary pressures, cardiac index and mixed venous oxygen saturation were measured at following time intervals: pre-induction, postinduction, post-intubation, skin incision, post sternotomy, chest closure, and 1 hr after surgery, at spontaneous respiration and post extubation. The type and duration of inotropic support, duration of postoperative ventilation and ICU stay, perioperative complications and outcome were assessed.
Patients' characteristics and demographic data were similar for both groups. Induction of anaesthesia was rapid and smooth in all patients. Compared to sevoflurane group more patients in the propofol group required nitroglycerine(NTG) to control blood pressure during prebypass period. Patients receiving sevoflurane had higher cardiac index (P<0.05) and required less inotropic support during post-operative period as compared to propofol treated patients. Duration of postoperative ventilation and ICU stay was similar in both groups. The incidence of postoperative complications and outcome were comparable between groups.
In conclusion, sevoflurane provided better perioperative haemodynamic control and cardiovascular profile than propofol during elective CABG surgery.
Keywords: Cardiac anaesthesia, Sevoflurane, Propofol, CABG surgery, VIMA, TIVA
|How to cite this article:|
Bharti N, Chari P, Thingnam SK, Arora S. Comparison of Haemodynamic and Cardiovascular Effects of VIMA with Sevoflurane Versus TIVA with Propofol in Patients Undergoing Coronary Artery Bypass Surgery. Indian J Anaesth 2008;52:805
|How to cite this URL:|
Bharti N, Chari P, Thingnam SK, Arora S. Comparison of Haemodynamic and Cardiovascular Effects of VIMA with Sevoflurane Versus TIVA with Propofol in Patients Undergoing Coronary Artery Bypass Surgery. Indian J Anaesth [serial online] 2008 [cited 2019 Dec 16];52:805. Available from: http://www.ijaweb.org/text.asp?2008/52/6/805/60692
| Introduction|| |
The perioperative period imposes physiological burdens on the heart by surgery and anaesthesia for patients with coronary artery disease (CAD), leading to serious complications, like, acute myocardial infarction (AMI) and death  . Not only the adequacy of surgical revascularisation but also the choice of anaesthetic regimen influences postoperative myocardial function and outcome in coronary bypass surgery patients  . Although intravenous induction of anaesthesia is generally favored because of its speed and smoothness, current cardiac anaesthesia practice devotes considerable attention to preserve myocardial function and avoidance of myocardial ischaemia. Volatile anaesthetics have been shown to exert protection against myocardial ischaemia and reperfusion injury during coronary artery bypass graft(CABG) surgery , . Therefore, volatile induction and maintenance of anaesthesia (VIMA) is gaining popularity in cardiac anaesthesia especially with the introduction of low-solubility and non- irritating volatile agents.
Sevoflurane is a non-pungent, non-irritating volatile agent with low blood gas partition coefficient. These properties enable sevoflurane to provide rapid and smooth induction like intravenous agents with minimal induction complications ,  . When used in high concentrations for rapid inhalational induction of anaesthesia in adults, it is well accepted by majority of patients  . Several studies have shown that sevoflurane exerts cardio protective effects against myocardial ischaemia and reperfusion injury during CABG surgery  . However, only few studies have compared the efficacy of sevoflurane induction and maintenance of anaesthesia with total intravenous anaesthesia (using either high doses of opioids  , midazolam  or etomidate , in cardiac surgery. Two of them , have reported higher incidence (>50%) of bradycardia during induction of anaesthesia with sevoflurane in cardiac patients.
The aim of this study was to compare the haemodynamic effects and cardiovascular profile of volatile induction and maintenance of anaesthesia with sevoflurane versus total intravenous anaesthesia (TIVA) with propofol in patients undergoing CABG surgery.
| Methods|| |
After obtaining ethical committee approval, 30 adult patients of ASA grade I-III, scheduled for elective CABG surgery were included in the study. Patients were examined for their cardiac and respiratory functions and associated medical illnesses. All the necessary investigations including complete haemogram, blood sugar, serum electrolytes, renal function test, pulmonary function test, x-ray chest, liver function test, coagulation profile, ECG, echocardiography and angiography were performed before surgery. Patients with severely impaired left ventricular function (EF <30%, LVEDP >18), renal or liver impairment, recent myocardial infarction (<6 weeks), associated valvular lesion or heart block, gross obesity (BMI >30%) and anticipated difficult intubation were excluded. Patients undergoing repeat coronary surgery, concurrent valve repair, or aneurysmal resection were also excluded. An informed consent was taken after explaining the procedure to the patients. All patients received a standard pre-medication consisting of 5 mg diazepam orally at night and 2 hour before surgery. Patient's usual cardiac medications were continued until the morning of surgery. Morphine sulphate 0.15 mg.kg -1 and promethazine 0.5 mg.kg -1 were administered intramuscularly one hour before surgery.
In the operating room, all patients received 5 ml.kg -1 normal saline before induction. Standard basic anaesthesia monitors including ECG of lead II and V 5 with continuous ST-segment analysis, pulse oximeter& non invasive blood pressure were connected to the patient. A 20-G radial artery cannula, a double lumen central venous catheter and thermo-dilution pulmonary artery catheter were placed under local anaesthesia and supplemental intravenous (IV) sedation with 0.02 mg.kg -1 midazolam. Fentanyl (2 µg.kg -1 ) was injected five min before induction. Patients were randomly divided into two groups using a sealed envelope technique. In VIMA group (Group S), anaesthesia was induced using the vital capacity rapid inhalational induction (VCRII) technique with 5% sevoflurane in oxygen via a closed anaesthesia circuit. In this technique the patients were instructed to breathe out to residual volume. The facemask connecting to a close circuit delivering 100% oxygen with sevoflurane was then applied, and the patients were instructed to breathe in deeply and to hold their breath for as long as it was comfortable. They were then asked to take deep breaths until loss of consciousness i.e. absence of response to verbal command and the absence of eyelash reflex. In TIVA group (Group P), anaesthesia was induced with propofol 1.01.5 mg.kg -1 IV while the patients were breathing 100% oxygen. In both groups following loss of consciousness, the patient's lungs were manually ventilated and a bolus of vecuronium bromide 0.1 mg.kg -1 was given IV to facilitate orotracheal intubation. After intubation controlled ventilation was established with 100% oxygen via closed circuit at 10-12 breaths/ min and a tidal volume of 8-10 ml.kg -1 aiming at normocapnia.
Anaesthesia was maintained with sevoflurane 0.52 MAC (Group S) or propofol infusion 40-150 µg.kg1 .hr -1 (Group P) and was adjusted to maintain the bispectral index (BIS) between 40 and 60. Both groups received a continuous infusion of fentanyl at a rate of 0.5 µg.kg -1 .hr -1 until closure of the chest. In addition a bolus of fentanyl (0.5 µg.kg -1 IV) was administered before skin incision and sternotomy. Neuromuscular block was maintained with intermittent boluses of vecuronium 0.02 mg.kg -1 . If anaesthetic adjustments failed in maintaining haemodynamic values within 20% of baseline, the following drugs were administered: phenylephrine and dopamine for hypotension, nitroglycerine (NTG) and/or sodium nitroprusside (SNP) for hypertension, atropine for bradycardia and esmolol for tachycardia. When cardiac index was below 2.5 l.min1 .m -2 , dobutamine was initiated. Intravenous nitroglycerine was administered if myocardial ischaemia was detected by ST-segment analysis. During cardiopulmonary bypass, in the S group, 2% sevoflurane was administered by connecting the vaporizer to the fresh gas flow canalization proximal to the oxygenator.
Standard median sternotomy and pericardiotomy were performed. After administration of 300 U.kg -1 heparin, the aortic cannula was secured in place. Cardiopulmonary bypass (CPB) was performed with a membrane oxygenator and moderate hypothermia (2830 0 C). Activated coagulation time was kept above 450 seconds throughout the CPB. After removal of aortic cannula heparin activity was neutralized with protamine at a ratio of 1 mg protamine/100 U heparin. After completion of surgery, the patients were transferred to the intensive care unit (ICU). Postoperative analgesia was managed with fentanyl 0.5-1.0 µg.kg -1 IV as required. Haemodynamic and respiratory variables were monitored continuously. Patients were weaned from mechanical ventilation when they were haemodynamically stable, completely rewarmed and responding to verbal stimuli.
| Data collection|| |
The time from initiation of induction to loss of consciousness was recorded. Any behavioural or airway incidents like excitation, movement, cough, laryngospasm, etc were noted. Haemodynamic measurements including heart rate (HR), mean arterial pressure (MAP), central venous pressures (CVP), pulmonary artery pressure (PAP), pulmonary capillary wedge pressures (PCWP) and cardiac index (CI) were recorded at pre-induction, post-induction, post-intubation, 5 min post-intubation, at skin incision, at sternotomy, at beginning of chest closure, 1 hr after arrival in ICU, on spontaneous breathing (before extubation) and 1 hr after extubation. At the same time, arterial and mixed venous blood gas analysis was also done. ECG and ST-segment changes, oxygen saturation, end-tidal carbon di-oxide concentration, inspired and expired concentration of volatile agent and nasopharyngeal temperature were monitored continuously. The type and duration of inotropic support needed, time to extubation, length of stay in ICU and major adverse events like myocardial ischaemia, ventricular failure and death were recorded.
| Statistical analysis|| |
Sample size was calculated on the basis of 50% reduction in the incidence of bradycardia based on the previous study for a power of 0.8 and cc = 0.05. Data were analyzed using student's t-test and chi-square test. One way analysis of variance with post hoc analysis was used for continuous variables such as heart rate, systemic and pulmonary pressures. P value of <0.05 was considered as significant.
| Results|| |
The groups were demographically similar with no differences in terms of age, weight, height, body surface area, sex ratio, ASA physical status and New York Heart Association (NYHA) grading [Table 1]. Distribution of patients was comparable with regard to the number of vessels involved, left ventricular ejection fraction, associated medical illness and preoperative cardiac medications [Table 2].
All the patients were rapidly unresponsive to stimulation within one minute of beginning the induction (Gp P: 38±9 s vs Gp S: 46±11 s, P=NS) and remained free of excitation, movement or airway related incident. Mean baseline blood pressure was numerically higher in P group than in S group although not statistically significant. The remaining baseline values were similar [Table 3]. After induction, there was a significant decrease in heart rate, mean arterial pressure and cardiac index compared to base line values in both groups. During the same period there was an increase in mixed venous oxygen saturation (SvO 2 ). Thereafter, these variables remained stable following tracheal intubation, skin incision, sternotomy and prior to onset of CPB.
Following CPB, heart rate increased significantly (P<0.001, compared to base line) in both groups. There was a reduction in MAP values during post bypass period in propofol group but not in sevoflurane group. MPAP and CVP were kept stable throughout in both groups. The values of HR, MAP, CVP and MPAP pressure were comparable between the groups throughout the data collection [Table 3]. The post bypass values of cardiac index were significantly (P< 0.05) higher in sevoflurane group than propofol group. However, the SvO 2 remained lower than the preoperative values secondary to an increase in oxygen consumption and extraction.
There were no significant inter-group differences with regard to the duration of surgery, cardiopulmonary bypass and aortic cross clamp times and number of vessels grafted [Table 4]. The incidence of hypotension (Gp P: 39% vs Gp S: 26%, P=NS) and bradycardia (Gp P: 13% vs Gp S: 19%, P=NS) was comparable between the groups. No patient presented tachycardia or ischemic changes during induction and tracheal intubation. Hypertension was observed more frequently in P group than in the S group (Gp P: 69% vs Gp S: 26%, P<0.05) during sternotomy. The use of vasoactive drugs was similar during induction. However, during prebypass period, more patients in Propofol group than Sevoflurane group required pharmacological intervention (NTG) to control blood pressure [Table 4]. The duration of postoperative ventilation and ICU stay was comparable between the groups. The incidence of atrial fibrillation and need for pacing after bypass did not differ between the groups. The intra-aortic balloon pump was never needed. The duration of post-CPB inotropic support was significantly (P<0.05) longer in Propofol group than Sevoflurane group. The requirement of vasopressor therapy was also higher in Propofol group during postoperative period [Table 4].
The postoperative complications were comparable among both groups [Table 5]. Two patients in Sevoflurane group and one in Propofol group presented excessive postoperative bleeding and needed re-exploration surgery. No cerebrovascular insult occurred in any group of patients, and none of the patient required postoperative haemofiltration or dialysis. One patient in propofol group developed congestive cardiac failure and expired.
| Discussion|| |
The results of present study indicate that volatile induction and maintenance of anaesthesia with Sevoflurane provided better haemodynamic control than total intravenous technique with propofol during perioperative period in patients undergoing CABG surgery. With vital capacity rapid inhalational technique the induction of anaesthesia was rapid, smooth and well tolerated by all the patients in Sevoflurane group. No episode of coughing, laryngospasm or excitation was observed. A vital capacity breath technique is reported to be both faster& safer than commonly used tidal breath technique  . VCRII technique requires lower concentration of volatile agent with less haemodynamic effects as compared to the conventional technique  . Djaiani et al  demonstrated that vital capacity inhalational induction with 8% sevoflurane produces rapid onset of anaesthesia and a good haemodynamic profile like etomidate. Vidal et al  found that the time to induction of sevoflurane anaesthesia was significantly shorter with vital capacity technique as compared to tidal volume breathing technique in patients undergoing CABG surgery.
In present study, there was a comparable reduction in HR, MAP, CVP, PAP and CI during induction period in both groups. Although, heart rate values were in the lower range (45-65 bpm), only 3/15 patients in Sevoflurane group and 2/15 patients in Propofol group required atropine. Few studies , have reported higher incidence of bradycardia with sevoflurane induction in cardiac patients, which may be related to the high preoperative doses of beta-blockers and combined use of remifentanil/sufentanil, midazolam and cis-atracurium in these studies. The mean value of post-intubation MAP was in clinically acceptable limits and the variance in pre-induction and post-intubation MAP was not statistically significant between the groups. The incidents of hypotension were transient and non consequential. They were easily managed with adjustments of anaesthetic agents and, if required, intravenous fluids and/or vasopressors. There was no hypertension or tachycardia during induction in either group. This may be related to the combined effect of premedication and sedation prior to invasive monitoring. During pre-CPB period significantly more patients in Propofol group required NTG to control blood pressure than Sevoflurane group despite adequate level of anaesthesia. This is consistent with previous report which showed that intraoperative control of blood pressure was better maintained with sevoflurane than propofol during CABG surgery  . Gravel et al  also demonstrated higher incidence of pre CPB hypertension with propofol than sevoflurane in patients undergoing CABG surgery.
The patients who were anaesthetised with sevoflurane had preserved cardiovascular function after weaning from CPB, and needed less inotropic support than the patients anaesthetised with propofol. The post-CPB CI values were also significantly higher in Sevoflurane group than the Propofol group. Many factors are known to determine the effectiveness of myocardium and left ventricular function after CABG surgery. Among these, patient characteristics (age, extent of coronary artery disease and degree of left ventricular dysfunction etc) and surgery related events like number and quality of grafts, type of cardioprotection, duration of aortic cross-clamp and CPB are the most commonly related with postoperative ventricular function. Patient characteristics and surgical events were similar in both groups in our study. This suggests that the differences in cardiac function between both groups are not caused by patients characteristics and intraoperative events but instead seems to be related to the choice of anaesthetic agent. However, opioids were shown to mimic the cardioprotective effect of ischaemic preconditioning  . The dosages of fentanyl were similar in both groups in the present study, suggesting that the observed differences in cardiac function between groups might not be related to fentanyl.
Although, underlying mechanisms responsible for the difference in postoperative cardiac function can not be elucidated from present study, previous observations indicated that sevoflurane exerts protective effects against myocardial ischaemia and reperfusion injury during coronary bypass surgery which improves the post-CPB contractility of myocardium ,,, . The reduction of myocardial stunning by sevoflurane might also contribute to the cardio protective effects of sevoflurane on ischemic myocardium  . Sevoflurane was shown to reduce the ischaemia induced metabolic changes in myocardium associated with decreased systemic haemodynamic parameters. Sevoflurane preconditioning significantly decreases the postoperative release of brain natriuretric peptide, a sensitive marker of myocardial contractile dysfunction in patients undergoing CABG surgery  . De Hert et al  demonstrated that sevoflurane but not propofol preserve cardiac function after CPB. They observed a higher cardiac output after coronary bypass surgery in patients who were anaesthetized with sevoflurane as compared to propofol treated patients. Nader et al  found that sevoflurane decreases the inflammatory response and improves myocardial function after CPB, as assessed by RWMA and LVSWI. Sevoflurane-mediated reduction in cardiac troponin was associated with improved long-term outcomes in one study  .
In a large clinical trial, Parker et al  demonstrated significantly shorter time to tracheal extubation with sevoflurane anaesthesia as compared to target control propofol anaesthesia in patients undergoing CABG surgery. However, there was no difference in duration of ICU stay between the groups  . The duration of post operative ventilation and ICU stay was not statistically different among groups in present study.
Despite the differences in early postoperative cardiac function, the postoperative complications and outcome variables did not differ between the groups. The incidence of myocardial ischaemia was 13% in sevoflurane group which is comparable to other studies ,. As the incidence of postoperative cardiac events was low in both groups, we would have required more patients to show a difference in the outcome.
In conclusion, vital capacity rapid inhalational induction with sevoflurane offers a smooth and safe technique, and may be an alternative for induction of anaesthesia in patients with known CAD. Sevoflurane supplemented with low-dose fentanyl has no deleterious haemodynamic effects when used as main induction and maintenance agent in patients undergoing CABG surgery. Compared with total intravenous technique, the sevoflurane based volatile anaesthetic technique offers better control of blood pressure during perioperative period and preserve cardiac function after CPB. However, our results cannot be extended to the patients with severe left ventricular dysfunction or with valvular disease. Further studies are required to prove the efficacy of sevoflurane induction and maintenance of anaesthesia in patients with severely impaired left ventricular function (EF<30%).
| References|| |
|1.||Kirklin JW, Naftel DC, Blackstone EH, Pohost GM. Summary of a consensus concerning death and ischemic events after coronary artery bypass grafting. Circulation 1989; 79: 181-91. |
|2.||Yu CH, Beattie WS. The effects of volatile anesthetics on cardiac ischemic complications and mortality in CABG: a meta-analysis. Can J Anesth 2006; 53: 906-18. [PUBMED] |
|3.||De Hert SG, Cromheecke S, ten Broecke PW, Els Mertens, De Blier IG, et al. Effects of propofol, desflurane and sevoflurane on recovery of myocardial function after coronary surgery in elderly high-risk patients. Anesthesiology 2003; 99: 314-23. |
|4.||Hall JE, Stewart IM, Harmer M. Single breath induction of sevoflurane anaesthesia with and without nitrous oxide: a feasibility study in adults and comparison with an intravenous bolus of propofol. Anaesthesia 1997; 52: 410-5. |
|5.||Yurino M, Kimura H. A comparison of vital capacity breath and tidal breathing techniques for induction of anaesthesia with high sevoflurane concentrations in nitrous oxide and oxygen. Anaesthesia 1995; 50: 308-11. [PUBMED] |
|6.||Nader ND, Li CM, Khadra WZ, Reedy R, Panos AL. Anesthetic myocardial protection with sevoflurane. J Cardiothorac Vasc Anesth 2004; 18: 269-74. [PUBMED] [FULLTEXT] |
|7.||Toller WG, Kersten JR, Pagel PS, Hettrick DA, Warltier DC. Sevoflurane reduces myocardial infarct size and decreases the time threshold for ischemic preconditioning in dogs. Anesthesiology 1999; 91: 1437-46. [PUBMED] [FULLTEXT] |
|8.||Samarkandi AH, Mansour AK. Induced preconditioning of cardiac performance in coronary bypass surgery - sevoflurane vs propofol. Middle East J Anesthesiol 2004; 17: 833-44. [PUBMED] |
|9.||Gracia C, Julier K, Bestmann L, Zollinger A, Von Segesser LK et al. Preconditioning with sevoflurane decreases PECAM-1 expression and improves one-year cardiovascular outcome in coronary artery bypass graft surgery. Br J Anaesth 2005; 94: 159-65. |
|10.||Julier K, Da Silva R, Gracia C, Bestmann L, Frascarolo P et al. Preconditioning by sevoflurane decreases biochemical markers and renal dysfunction in coronary artery bypass graft surgery: a double-blinded, placebocontrolled, multicenter study. Anesthesiology 2003; 98:1315-27. |
|11.||De Heart S, ten Broecke PW, Els Mertens, Van Sommeren EW, De Blier IG. Sevoflurane but not propofol preserves myocardial function in coronary surgery patients. Anesthesiology 2002; 97: 42-9. |
|12.||El Azab SR, Scheffer GJ, Rosseel PMJ, de Lange JJ. Induction and maintenance of anaesthesia with sevoflurane in comparison to high dose opioid during coronary artery bypass surgery. Eur J Anaesthesiol 2000; 17: 336-8. |
|13.||Gravel NR, Searle NR, Taillefer J, Carrier M, Roy M and Gagnon L. Comparison of the haemodynamic effects of sevoflurane anesthesia induction and maintenance vs TIVA in CABG surgery. Can J Anesth 1999; 46: 240-6. |
|14.||Wang JYY, Winship SM, Thomas SD, Gin T, Russell GN. Induction of anaesthesia in patients with coronary artery disease: a comparison between sevofluraneremifentanil and fentanyl-etomidate. Anaesthesia Intensive Care 1999; 27: 363-8. |
|15.||Djaiani GN, Hall J, Pugh S, Peaston RT. Vital capacity inhalation induction with sevoflurane: an alternative to standard intravenous induction for patients undergoing cardiac surgery. J Cardiothorac Vas Anesth 2001; 15: 169-74. |
|16.||Yurino M, Kimura H. Efficient inspired concentration of sevoflurane for vital capacity rapid inhalational induction (VCRII) technique. J Clin Anesth 1995; 7: 228-31. [PUBMED] [FULLTEXT] |
|17.||Vidal MA, Calderon E, Martinez E, Pernia A, Torres LM. Comparison of 2 techniques of inhaled anesthetic induction with sevoflurane in coronary artery revascularization. Rev Esp Anesthesiol Reanim 2006; 53: 639-42. |
|18.||Schultz JE, Hsu AK, and Gross GJ.Morphine mimics the cardioprotective effect of ischemic preconditioning via a glibenclamide-sensitive mechanism in the rat heart. Cir Res 1996: 78: 1100-4. |
|19.||Parker FC, Story DA, Poustie S, Liu G, McNicol L. Time to tracheal extubation after coronary artery surgery with isoflurane, sevoflurane, or target-controlled propofol anesthesia: a prospective, randomized, controlled trial. J Cardiothorac Vasc Anesth 2004; 18: 613-9. [PUBMED] [FULLTEXT] |
|20.||Searle NR, Martineau RJ, Conzen P, Al-Hasani A, Mark L, et al. Comparison of sevoflurane/fentanyl and isoflurane fentanyl during elective coronary artery bypass surgery. Can J Anesth 1996; 43: 890-9. [PUBMED] |
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]