Critical Care

Assessment of sedation after cardiac surgery

Stephan Jakob, MD, PhD
Department of Intensive Care Medicine
University Hospital Bern
Freiburgstrasse
CH-3010, Bern, Switzerland
Phone +41 31 632 3916
Fax +41 31 632 9644

Email: stephan.jakob@insel.ch

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Introduction

Sedation is used in most cardiac surgical patients during the postoperative period to reduce stress during rewarming and reduce cardiovascular instability. The amount of sedatives a certain patient receives usually depends on how the nurse or treating physician perceives the patient’s discomfort. Recent studies have demonstrated that using protocols to guide sedation in various groups of critically ill patients decreases both the length of mechanical ventilation as well as stay in the intensive care unit (ICU), and reduces nursing and other resource use [ 1,2]. Such protocols include quantitative assessment of sedation by using one of the several sedation scores [ 3]. However, after cardiac surgery, the adequacy of a certain sedation regimen in patients can be difficult to assess. There are several reasons for this. First, subjective discomfort and the clinically measurable level of sedation may not correlate. Second, the different hypnotic, sedative, and analgesic drugs used in the peri-operative period may have unpredictable effects on brain function. Third, the patient may have a pre-existing brain dysfunction due to a co-existing cerebral vascular disease. Finally, hypothermia, hypoperfusion, and cardiopulmonary bypass may generate some degree of brain dysfunction [ 4].

Electroencephalography is a widely available, non-invasive tool for monitoring the neuronal activity of the brain and its reaction to external input. EEG analysis is a very time consuming task, and the visual interpretation of the raw EEG signal is difficult. Signal processing of EEG is done to enhance and aid the recognition of some aspect of the EEG that correlates with the physiology and pharmacology of interest [ 5]. The bispectral (BIS) index, composed of parameters from time, frequency, and the bispectral domain of the EEG, is used to assess the depth of anesthesia and to prevent awareness. The usefulness of BIS to monitor sedation has been conversely interpreted [ 6-8]. Auditory evoked potentials are good predictors for the level of sedation and unconsciousness during propofol infusion [ 6].

This review presents a short overview on aspects of sedation in cardiac surgical patient with special focus on event related potentials.

Changing strategies in the peri-operative management of cardiac surgical patients

New surgical techniques, shorter acting drugs, and a better understanding of the peri-operative pathophysiological changes have influenced the postoperative management of cardiac surgical patients during the last several years. One recent meta-analysis on trials in cardiac surgical patients confirmed that anesthetic, sedation, and early-extubation strategies in selected cardiac surgery patients are associated with a shorter duration of mechanical ventilation, and shorter lengths of ICU and hospital stays [ 9]. However, if different drug regimes are used to achieve the same sedation end point, the time from admission to the ICU until extubation is similar [ 10]. The costs for sedation after cardiac surgery is higher when short acting drugs are used [ 11].

Sedative drugs may modulate postoperative hemodynamic responses differently [ 12]. Wahr et. Al. found a reduction of the incidence and severity of tachycardia and hypertension and an increase in the incidence of hypotension in propofol as compared to midazolam sedated patients.

Assessing sedation by using sedation scores and BIS index

Different sedation scores have been used along with the BIS index [ 7], and it has been found that BIS index is a valid measure of wakefulness after cardiac surgery. In contrast, others do not recommend the use of processed EEG monitoring (spectral edge frequency and BIS) in the assessment of postoperative sedation [ 8]. In this study, inter-individual variability was high, and neither method could consistently discriminate between conscious and unconscious sedation. One problem associated with BIS monitoring is EMG interference in patients not receiving neuromuscular blockade. It is possible that a later versions of BIS monitors with integrated EMG recognition and filtering can solve this problem, a least in part.

Active neuromonitoring in the assessment of postoperative sedation

When the brain is exposed to a stimulus, it may or may not perceive it, depending not only on wakefulness, but also on attention. Once a stimulus has gained attention by the brain ("arousal"), repeated similar stimuli will evoke a weaker responses due to a phenomenon called adaptation or habituation. Novel stimuli, on the other hand, will repeatedly gain attention. In critical illness, the processes of attention and adaptation are altered. When the level of sedation is assessed by using a sedation scores such as Ramsay Score [ 13], a huge stimulus is applied which requires a huge response, i.e. waking up. Weaker signals can be applied visually, audibly, or by invoking pain. The signals create an electrical response (evoked potential, event related potential) which can be measured. The main effects of sedative drugs such as benzodiazepines and propofol are to decrease arousal and to impair habituation such that familiar stimuli become novel again.

We have recently conducted two trials in cardiac surgical patients where postoperative sedation was assessed by using a clinical sedation score (Ramsay Score [ 13] together with auditory evoked potentials with the habituation paradigm [ 14,15] ). In one study, 30 patients scheduled for elective CABG were studied [ 14]. Anesthesia regimen (propofol-alfentanil) and postoperative sedation (propofol) were standardized. Continuous electroencephalogram (CS/3, Datex-Ohmeda, Helsinki, Finland) was recorded from frontal, temporal, and central sites , simultaneous measurement of four EEG signals. Midlatency auditory evoked potentials (MLAEP) were recorded from mastoid electrodes A1 and A2, and reffered to Cz. The stimuli used was 70 dB above normal hearing level with a stimulation rate of 7.1 Hz. Two thousand responses were recorded and averaged. One set of measurements (EEG, MLAEP) were obtained on the day before surgery (baseline), in the sedated patient preoperatively,ostoperatively in the ICU during two different clinical levels of sedation (Ramsay score 6 and 4), and on the day after surgery. We found that Pa latencies of the evoked potentials were dependent on the clinical level of sedation (p < 0,01; Figure 1). In the few patients where the Nb component of the potential was visible during clinically deep sedation (Ramsay score 6), latencies were significantly increased as compared to preoperative values (p < 0,01; Figure 1). Also, peak-to-peak amplitude (Na-Pa) was related to the level of sedation (p= 0,01).

In the other study[ 15], 40 patients were assigned to receive anaesthesia with either midazolam/fentanyl (n=20) or propofol/alfentanyl (n=20). Postoperative sedation was used with either midazolam or propofol in the respective groups in order to maintain a Ramsay score of four (prompt response to loud verbal stimuli) until the patients were warm and hemodynamically stable. Auditory evoked potentials were recorded in two-hourly intervals from ICU admission until extubation. For this purpose, brief tones were delivered to the right ear in 1 Hz-trains of four with an inter-train interval of 12 seconds. To avoid effects of shifting baselines, the evoked response was quantified as the absolute difference between the first positive and the first negative peak of the potential (Figure 2). The "arousal" response, i.e., the response to the first tone was decreased at ICU admission (Ramsay score 6; i.e. non-responsive to stimuli), and it was significantly lower in the midazolam as compared to the propofol group (p < 0.01). The arousal response remained low, even when the patients were awake (before extubation). "Habituation", i.e. a decrease in the magnitude of the evoked potentials to subsequent stimuli, was not present. This means that the subsequent stimuli were perceived as "novel". Moreover, patients on propofol even exhibited a significant (paradoxical) increase in the response to the second stimulus.

Conclusions

Cardiopulmonary bypass, anesthesia and sedation may have long lasting effects on both the central and autonomous nervous system. Active neuromonitoring can easily be added to the routine monitoring in postoperative cardiac surgical patients. Both amplitude and latencies of auditory evoked potentials are dependent on sedation, and are potentially useful for the objective assessment of sedation. Since postoperative neurophysiological changes are different in patients on different drugs, it is likely that the same clinical level of sedation is associated with a different perception of pain and other stimuli, depending on the drug. Hence, monitoring of sedation must not solely rely on clinical assessment.

Figure 1. Auditory evoked potentials in a patient with visible Nb component. 1. Baseline: on the day before operation; 3. Ramsay = 6: postoperatively, after arrival in the ICU; 4. Ramsay = 4: postoperatively, during recovery from anesthesia.

Figure 2. Auditory evoked potentials (train of four stimulus). Arousal: P50 - N100 (normal values: 15 ± 4 m V; mean ± SD; own results). Habituation: P50 - N100 / P50-N100 (normal values: 0.6 ± 0.2).

References

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Last updated: 1 April 2002Created
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