metric Friedman test) and 45.6 (6.3) ms after physiotherapy) ;NB amplitude showed no consistent change (-0.81 (1.4) nV, -0.81 (1.5) nV and. â 0.71 (1.3) fiV ...
British Journal of Anaesthesia 1992; 68: 349-351
EFFECT OF PHYSIOTHERAPY ON THE AUDITORY EVOKED RESPONSE OF PARALYSED, SEDATED PATIENTS IN THE INTENSIVE CARE UNIT J. R. SNEYD, D. Y. WANG, D. EDWARDS, C. J. D. POMFRETT, B. R. H. DORAN, T. E. J. HEALY AND B. J. POLLARD
SUMMARY Auditory evoked response (AER) was recorded before, during and after physiotherapy in 11 paralysed (atracurium 0.56 (SD) 0.13 mg kg'1 h~1), sedated (propofol 2.2 (1.0) mg kg~' h~'; fentanyl 4.4 (2.3) fig kg~' h~1) and critically ill patients undergoing ventilation in the intensive care unit (ICU). The latency of the negative wave, NB, was reduced by physiotherapy (mean 44.8 (SD) 7.9 ms before, 41.0 (6.8) ms during (P < 0.01, non-parametric Friedman test) and 45.6 (6.3) ms after physiotherapy) ;NB amplitude showed no consistent change (-0.81 (1.4) nV, -0.81 (1.5) nV and — 0.71 (1.3) fiV, respectively). NB latency responded to patient arousal at constant levels of sedation and this requires further evaluation as a means of monitoring sedation in paralysed patients in the ICU. KEY WORDS Brain: auditory evoked response. Intensive care: sedation. Lung: physiotherapy. Monitoring: evoked response.
Inhalation and i.v. anaesthetic agents have been shown to produce dose related changes in the early cortical components of the auditory evoked response (AER) [1,2]. Anaesthesia-induced changes in the AER are greatest in the easily recognized N B wave [3]. Surgical incision was associated with an increase in N B amplitude when end-tidal halothane concentration was kept constant and this has been cited as evidence that the early cortical AER is an index of anaesthetic depth [4]. Thornton and colleagues have proposed that an N B latency of less than 44.5 ms may be indicative of conscious awareness, even though there may be no subsequent recall [3]. Most patients undergoing controlled ventilation in the Intensive Care Unit (ICU) are sedated and many are also paralysed. Evaluation of depth of sedation is important in order to prevent excessive drug treatment whilst at the same time minimizing patient distress. Sedation scoring is useful, but cannot be applied to paralysed patients who may also show diminished or absent responses to potent stimuli such as tracheal suction. The aim of this study was to evaluate the practicality of AER monitoring in the Intensive Care Unit and to determine if a relatively standardized
form of stimulation (physiotherapy) would cause measurable changes in AER. SUBJECTS AND METHODS
The study and its consent procedures were approved by the District Ethics Committee. Critically ill patients cannot give informed consent, so we sought the agreement of relatives and proceeded after obtaining this. We studied critically ill patients who required controlled ventilation in the ICU and who were paralysed with an infusion of atracurium and sedated with infusions of fentanyl and propofol. None of the patients was known to have any preexisting hearing defect. Sedation was stable (constant infusion rates and no clinical change) for at least 2 h before the start of the study and no additional bolus doses were given before physiotherapy. Physiotherapy followed a standardized format and comprised "bag squeezing" (manual hyperinflation of the chest), percussion and shaking of the chest and passive movements of upper and lower limbs. Using a "Navigator" system (Bio-Logic System Corp., U.S.A.) binaural rarefaction click stimuli of 75 dB were given through Telephonies headphones at 6 Hz. AER was recorded using forehead and mastoid silver disc electrodes with electrode impedances of 5 kQ or less. For each AER, 1500 sweeps were averaged using the following data: high pass filter, 30 Hz; low pass filter, 500 Hz; window, 5-160 ms; 512 points per sweep; amplifier gain 150000. After collection the AER were smoothed using a 13-point running average and the major negative deflection (NB) of the early cortical AER was analysed in terms of amplitude (|iV) and latency (ms). A pilot study demonstrated that it was possible to obtain satisfactory AER from normal subjects in the ICU environment using this equipment. Consecutive pairs of AER were collected before, during and after physiotherapy. J. R. SNEYD, M.A., M.D., F.C.ANAES.; D . EDWARDS, A.S.C.T.; B. R. H. DORAN, F.C.ANAES.; B. J. POLLARD, M.D., B.PHARM.,
F.C.ANAES.; Department of Anaesthesia, Manchester Royal Infirmary, Oxford Road, Manchester. D. Y. WANG, D.MED.SC.; C. J. D . POMFRETT, B.SC, PH.D.; T . E. J. HEALY, M.SO, M.D.,
F.C.ANAES. ; Department of Anaesthesia, University Hospital of South Manchester, Withington Hospital, West Didsbury, Manchester M20 8LR. Accepted for Publication: October 30, 1991. Correspondence to B.J.P.
BRITISH JOURNAL OF ANAESTHESIA
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TABLE I. Patient data, drug treatment and outcomes for the 11 patients according to outcome (mean (range or SD))
All patients
Returned to ward
n
11
Age (yr) Sex (M/F) Weight (kg) Propofol (mg kg"1 h"1) Fentanyl (jig kg"1 h"1) Atracurium (mg kg"1 h"1) Primary diagnosis
45.2 (24-75)
5
6
41.3 (31-69)
6/5
49.8 (24-75) 3/2
3/3
75.7 (7.6) 2.2 (1) 4.4 (2.3)
0.56(0.13)
Died on ICU
72.7 (8.9) 2.1 (1) 3.3 (1.4) 0.50(0.13) Renal transplant failure Respiratory failure Septicaemia Respiratory failure Acute asthma Multiple injuries
79.4 (5.3) 2.3 (1.1) 5.7 (2.8) 0.63 (0.089) Perforated duodenal ulcer Respiratory failure Leukaemia + cytomegalovirus Pancreatic fistula After cardiac arrest
TABLE II. Haemodynamic and AER data for the 11 patients according to outcome (mean (SD)). Significant changes: *P < 0.05; **P < 0.01 (non-parametric Friedman test) Before physiotherapy All patients (n = 11) Systolic arterial pressure (mm Hg) Mean arterial pressure (mm Hg) Diastolic arterial pressure (mm Hg) Heart rate (beat min"1) N B latency (ms) N B amplitude (raV) Returned to ward (n = 6) Systolic arterial pressure (mm Hg) Mean arterial pressure (mm Hg) Diastolic arterial pressure (mm Hg) Heart rate (beat min"1) N B latency (ms) N B amplitude (mV) Died in the ICU (n = 5) Systolic arterial pressure (mm Hg) Mean arterial pressure (mm Hg) Diastolic arterial pressure (mm Hg) Heart rate (beat min"1) N B latency (ms) N B amplitude (mV)
Before
1 uV
During After
During physiotherapy
After physiotherapy
(17.2) (14.5) (14.8) (26.1) (7.9) (1.4)
124
(22.4)* 82.9 (17.1) 62 (16.1) 92 (26.7) 41.0 (6.8)** -0.81 (1.5)
114
114 (19.9) 82 (16.9) 67 (17.4) 97 (28.3) 45. .7 (8.7) - 1 . .16(0.2)
127 89 69 98
(27.8) (21.1) (18.8) (28.0) 40.1 (6.3) -1.31 (0.59)
118 83 66 93
(14.6) (10.3) (8.9) (23.6) (7.8) -0.39(2.0)
120 76 54 86
(16.1) (8.5) (7.0) (26.0) 42.2 (7.9) -0.21 (2.1)
110 72 54 81
111 78 61 90 44 .8 - 0 . .81
107 72 55 82 43. .7
(14.7) 78.4 (12.9) 61 (13.0) 88 (24.3) 45.6 (6.3) -0.71 (1.3) (16.4) (14.9) (14.2) (27.8) 45.8 (6.1) -0.92(0.3) (12.5) (7.2) (7.5) (20.4) 45.2 (7.2) -0.45(2.0)
Values for the left and right sides were averaged together, as were the pairs of AER obtained in each of the three conditions; before, during and after physiotherapy. Arterial pressure was recorded from an arterial line (radial or brachial) using a calibrated manometer system (Spacelabs, U.S.A.). Data were analysed using the non-parametric Friedman test. The package Starview II (version 1.03) was run on an Apple Macintosh computer. RESULTS
i
20
60 40 Latency (ms)
80
FIG. 1. Six consecutive recordings (redrawn) of the early and middle cortical components of the auditory evoked response from a single patient before, during and after physiotherapy. The window (5-160 ms) and filtering (high pass 30 Hz, low pass 500 Hz) result in the brain stem response not being shown. During physiotherapy the latency of the N B wave (arrow) decreased.
Data were obtained from 11 patients, of whom five died in the ICU and six returned to the general ward. Patient data, diagnoses, drug treatments and outcomes are listed in table I. We obtained satisfactory AER recordings in the ICU, although careful positioning of equipment was necessary to minimize mains interference. With careful attention to electrode placement and removal of avoidable sources of mains interference, we were able to make satisfactory recordings in all patients selected for the study. Unlike previous studies of
DOES PHYSIOTHERAPY AFFECT THE AER OF ICU PATIENTS? AER in anaesthetized patients, it was not possible to make control recordings in the awake state. The AER of sedated ICU patients is relatively flattened and the only early cortical wave which could be identified confidently in all patients was the negative wave NB. N B latency was reduced significantly by physiotherapy (P < 0.01, non-parametric Friedman test), whereas N B amplitude was not affected consistently, increasing in some patients and decreasing in others (fig. 1, table II). When the data were reanalysed according to patient outcome (table II), differences between survivors and non-survivors became apparent. The N B latency decreased markedly during physiotherapy in survivors, whilst those patients who died showed a smaller response.
DISCUSSION
We set out to recreate the definitive experiment of Thornton and colleagues [3] with appropriate modification for the ICU setting. We have demonstrated that the AER of patients in a " steady state" of paralysis and sedation on the ICU does show a reversible response to physiotherapy. Although we believe that the shortening of the N B latency which we observed was caused by cortical arousal provoked by physiotherapy, it is important to consider other possible explanations. Physiotherapy may cause profound, short lived changes in arterial blood-gas tensions and in haemodynamic state, and the possibility exists that we have witnessed an epiphenomenon of such changes. Bag squeezing with 100 % oxygen increases Pa^ and may have some effect upon P a ^ (depending upon the fresh gas flow and the amount of rebreathing which occurs). Notwithstanding this, the changes we have observed are consistent with other observations that arousal can reduce N B latency [3]. The N B latencies we have measured were less than the 44.5 ms threshold of awareness [3] or became so
351
during physiotherapy. If we extrapolate principles derived from patients studied during anaesthesia into the ICU setting, the implication is that many of our paralysed and sedated patients are in a state of conscious awareness, even if they have no recall in the event that they recover. This study did not set out to evaluate AER as an outcome predictor, and the number of patients studied is too small to draw conclusions on this subject; nevertheless, it is interesting that the group of patients who survived showed a greater reduction of N B latency in response to physiotherapy than did those who died. The patients who died received more sedation than those who did not and this could have contributed to the difference, although the additional amounts of propofol and fentanyl were relatively small. We studied each patient for a single period on one day only; repeated measurements are certainly possible, but the inconvenience of the additional equipment and the difficulty of maintaining good electrode placement may make this impractical. We conclude that AER measurement is feasible on critically ill patients in the intensive care unit and that its use should be evaluated further. Further work could usefully investigate the sensitivity and specificity of this response, or some variant of it, as an outcome predictor.
REFERENCES 1. Thornton C, Heneghan CPH, Navaratnarajah M, Jones JG. Selective effect of Althesin on the auditory evoked response in man. British Journal of Anaesthesia 1986; 58: 422^127. 2. Heneghan CPH, Thornton C, Navaratnarajah M, Jones JG. Effect of isoflurane on the auditory evoked response in man. British Journal of Anaesthesia 1987; 59: 277-282. 3. Thornton C, Barrowcliffe MP, Konieczko KM, Ventham P, Dore CJ, Newton DEF, Jones JG. The auditory evoked response as an indicator of awareness. British Journal of Anaesthesia 1989; 63: 113-115. 4. Thornton C, Konieczko K, Jones JG, Jordan C, Dore CJ, Heneghan CPH. Effect of surgical stimulation on the auditory evoked response. British Journal of Anaesthesia 1988; 60: 372-378.
