We appreciate the interest taken by Drs Bein and Tonner in the subject of our study. Patients in both groups were undergoing coronary artery bypass grafting (CABG) as well as valve replacement. No patient was in NYHA class IV. The episodes of haemodynamic disturbances were equally distributed among the various subgroups of CABG as well as the valve replacement patients although the latter showed more episodes of hypotension and tachycardia. Hypertension and bradycardia were more common in the coronary artery disease (CAD) patients and is understandable as all these patients were receiving β-adrenoceptor blocking drugs, which prevented tachycardia even in the presence of higher bispectral index (BIS) values. Detailed analysis of haemodynamic disturbances in relation to preoperative cardiac drugs and the cardiac lesion should throw more light on the cause and mechanism of these arterial pressure and heart rate changes - a small number of patients prevented us from making this subgroup analysis.
Although there was no difference in the number of patients with haemodynamic disturbances, the number of episodes of both tachycardia and hypertension was significantly higher in the control group. Sixty percent of the episodes of tachycardia were associated with BIS > 55 against a targeted BIS of 50 ± 5. BIS was >55 (the upper limit of our target, i.e. 50 ± 5) in approximately 50% of hypertensive episodes and <55 (i.e. within the set target, or below) in another 50% of such episodes; simultaneous hypertension and tachycardia was always associated with BIS > 55.
As pointed out by Drs Bein and Tonner there may be a number of factors responsible for the haemodynamic instability in cardiac patients undergoing CABG or valve replacement under cardiopulmonary bypass (CPB). In addition to the effect of anaesthetic agents, depth of anaesthesia and effects of vasoactive drugs, haemodynamic instability can also be due to poor ventricular function secondary to inadequate myocardial protection or suboptimal cardiac surgery.
Though BIS reflects the cortical state of the patient and/or cortical activity, the inhalational anaesthetics at high concentrations decrease cortical activity as well as decrease haemodynamic responses to surgical stimuli. Although narcotics may decrease these responses, even in the presence of higher BIS , movement as well as the haemodynamic responses to endotracheal intubation and surgical stimuli can also be decreased by deeper planes of anaesthesia with associated low BIS values compared to lightly anaesthetized patients with a higher BIS. Hence in the presence of high BIS values one can anticipate more hypertension and tachycardia in response to painful stimuli compared to a situation with lower BIS, though the latter is not immune to haemodynamic disturbances.
Three patients in the study group were given vasodilators (nitroglycerin) to treat hypertension before CPB with BIS ≤ 50, whereas in the control group such episodes were primarily controlled by isoflurane. This reflects the usual tendency of anaesthetists to treat haemodynamic changes by adjusting anaesthetic concentrations in the absence of a specific anaesthetic depth monitor.
Brain temperature may not only affect EEG derived variables such as BIS but also the pharmacodynamics of anaesthetic agents and hence anaesthetic requirements. Core temperature at the time of coming off CPB was 36.0-36.8°C in all patients of both groups. Hence the difference in temperature between the two groups may not be responsible for the difference in BIS while coming off CPB. Instead, the rise in BIS at this stage may be due to increased requirements, which was taken care of in the study group using BIS as an indicator while in control group the anesthesiologist was adjusting primarily haemodynamics using inotropes, vasodilators or vasoconstrictors. The temperature at the start of CPB was more variable (35.0-36.0°C in the control group and 34.5-36.0°C in the study group) but there was no difference between the two groups.
A single anesthesiologist was responsible for all the anaesthetics though he was blinded to BIS values in the control group. Hence technology learning might have affected the improvement in anaesthetic drug titration through experience and adjustment of anaesthetic concentrations. We did not analyse this aspect in the present study for reasons already explained . Previously we used to be hesitant to increase anaesthetic concentrations (especially at the time of coming off CPB) in case hypotension developed - now we use inotropes to stabilize haemodynamics while adjusting the anaesthetic concentrations using BIS.
Anaesthetic depth is quite volatile when CPB is being terminated as the patient is being warmed which changes anaesthetic requirements as well as affecting the EEG and BIS. Furthermore, during this period the anaesthetist is concentrating on the haemodynamics of the patient to ensure successful weaning from CPB - at this time mainly reacting to haemodynamic changes and trying to normalize these using inotropes or vasodilators while unknowingly accepting a lightly anaesthetized patient in the absence of objective anaesthetic depth monitoring. Though all patients had a core temperature of at least 36°C before attempting to come off CPB, minute-to-minute data over this period are lacking as it was not directly logged on to the computer - hence we are unable to make further comment. But, the core temperature in the two groups was comparable at the time of switching off CPB. We are now logging all the data directly on to the computer and we have noted that though there is gradual rise in BIS, and increased anaesthetic requirement, during the rewarming phase the BIS (as well as anaesthetic requirement for keeping BIS down) shows a sudden increase in some patients when the heart starts ejecting. Whether it is because of increased pulmonary clearance of intravenous drugs or improved tissue perfusion because of pulsatile blood flow is unknown. All these factors are responsible for the volatililty of BIS at this time and hence we also excluded this period from haemodynamic analysis.
Understandably the study group did receive more morphine though not significantly different (28 ± 3 mg in the study group compared to 25 ± 2 mg in the control group P > 0.05), as this was our first line of treatment of tachycardia and hypertension in the presence of normal or low BIS.
We cannot comment upon the economics of the anaesthetic agents in two groups, as we did not study that aspect and the data was not collected. There were some patients who were given isoflurane for treatment of hypertensive or tachycardia episodes in the control group while nitroglycerin or β-adrenoceptor blocking drugs were used in the study group. Similarly isoflurane was given infrequently and at low concentrations while coming off bypass in the control group. BIS is a useful tool to help anaesthesiologists in the rational use of drugs both anaesthetic as well as vasoactive during the surgery.
G. D. Puri
Department of Anaesthesiology and Intensive Care; Post Graduate Institute of Medical Education and Research; Chandigarh, India
S. S. Murthy
Cleveland Clinic Foundation; Cleveland; Ohio, USA
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