Acta Anaesthesiol Scand 1992: 36: 2 1-24
Timing of peak pressor response following endotracheal intubation S. HICKEY, A. E. CAMERON, A. J. ASBURY and G. D. MURRAY Departments of Anaesthesia and Surgery, Western Infirmary, Glasgow and Department of Anaesthesia, Vale of Leven District General Hospital, Alexandria, Scotland, UK
The study was designed to measure the timing of the peak cardiovascular response following laryngoscopy and endotracheal intubation. Thirty patients ASA 1 or 2 were studied, with arterial pressure being continuously monitored using the Ohmeda 2300 Finapres. Patients were randomised to receive either propofo12.5 mg. kg-’ (Group A) or thiopentone 4.5 mg. kg-’ (Group B). The mean time to complete laryngoscopy and intubation was 26 s in Group A and 20 s in Group B. The peak response occurred on average 31 s after the start of the stimulus in Group A and after 32 s in Group B. In 8 out of the 30 cases the peak response occurred during the period of stimulation. Systolic pressure fell on average by 2.6 kPa (20 mmHg) (range 0 to 5.9 (45 mmHg)) from its peak value to the value measured at the 1-min time mark in the propofol group, and by 2.3 kPa ( 1 7 mmHg) (range 0.4 (3 mmHg) to 3.8 (29 mmHg)) in the thiopentone group. We conclude that the use of slow arm-cuff-based arterial pressure measurement techniques may miss important hypertensive episodes during laryngoscopy and endotracheal intubation. The effectiveness of agents in obtunding the pressor response may thus be misinterpreted. Received 4 November I9N, acceptedfor publication 13 May I991
Key words: Anesthetics, intravenous: propofol, thiopentone; equipment: finapres; complications: pressor response; laryngoscopy.
The cardiovascular response to laryngoscopy and endotracheal intubation has been well documented. Much has been written about the magnitude of this pressor response (1-3), its consequences (4-6), and the manoeuvres which might obtund it (7-1 7). However, less has been written about the actual timing of this peak response, and values quoted range from 7 to 120 s (18, 19). Information on the precise timing of this response (particularly if it is a consistent response) will not only help in the recognition of the response, but might also help in the timing of administration of drugs which obtund the response. With the introduction of the finger arterial pressure monitor, it has become possible to measure arterial pressure continuously and non-invasively, and therefore to identify accurately the timing of the peak pressor response. We felt that this may provide additional useful information, since non-invasive arm cuff techniques of measuring arterial pressure can take up to 30 s to measure arterial pressure, during which time the peak response may be waning, or may be lost completely. In addition, many investigators in this field have relied on measuring arterial pressure at 1 or 2min intervals from the time of stimulus (12-15, 17), during which the arterial pressure might change significan tl y. An investigation was therefore designed to measure
the timing and duration of the pressor response to laryngoscopy and endotracheal intubation; to compare peak values with values measured at 1-min intervals; and to compare differences in the above between two groups of patients induced with either propofol or thiopentone.
PATIENTS AND METHODS Thirty patients ASA grade 1 or 2, aged between 16 and 70 years, were studied. Patients were scheduled for elective gynaecological, general surgical, or orthopaedic procedures. The protocol excluded any patient with a history of hypertension or epilepsy, or those who were regularly taking sedative drugs. The study was approved by the local Ethics Committee. All patients were premedicated with temazepam 20 mg for females, 30 mg for males, plus metoclopramide 10 mg, both given orally, approximately 90 min before induction. On arrival in the anaesthetic room, a 20-g cannula was inserted under local anaesthesia, and the patient was connected to an Ohmeda 2300 Finapres arterial pressure monitor, which allowed continuous non-invasive pressure measurement. Output from the Finapres was taken to a Hewlett-Packard “Think-Jet” printer, which printed continuously. Arterial pressure measurements were made at minute intervals for 5 min prior to the induction of anaesthesia. The mean of these was taken as the baseline value. The patients were randomly allocated using an opaque envelope system into two groups. In Group A patients, anaesthesia was induced by injecting 2.5 mg.kg-’ of propofol intravenously over 30 s. In Group B patients, anaesthesia was induced by injecting 4.5 mg . kg-’
22
S. HICKEY ET AL.
of thiopcntone over the same time period. Thereafter the management of patients in both groups was identical. From time zero, the start of the injection of the induction agent, arterial pressure measurements were printed out at 5-s intervals. (The Finapres will make measurements continuously, i.e. for every heart beat. This can lead to overload of the printer, however, which is why we chose to limit measurements to 5-s intervals, and measured the time to completion of tracheal intubation on the same scale.) Following completion of the injection of induction agent, the venous cannula was flushed with 2-3 ml of normal saline. The patients breathed 66% nitrous oxide in oxygen (total fresh gas flow 9 1. min- ’) through a face mask connected to a Bain system. Ventilation was gently assisted as necessary. At the 40-s mark 1.5 mg. kg-’ of suxamethonium was injected intravenously as a bolus, and the cannula once again flushed. At the 90-s mark laryngoscopy and tracheal intubation were performed, using a MacIntosh laryngoscope. The endotracheal tubes were lubricated with a water-based gel. The time taken to place the endotracheal tube was recorded, with inflation of the tube cuff used as the end point (timed to the nearest 5 s). Enflurane I % was added to the gas mixture when the breathing system was reconnected, and ventilation assisted as appropriate. Arterial pressure measurements continued at 5-s intervals for a further 3 min following insertion of the endotracheal tube. This allowed the time to peak arterial pressure to be identified at a later stage from the print-out, and allowed comparison of peak values with the values measured at the 1-min time marks. The serial measurements were analysed using summary measures as recommended by Matthews and his colleagues (20). Prior to analysis the data were “smoothed” using a running median technique (21). This procedure emphasises the underlying trend in serial measurements, while reducing the possible misinterpretation resulting from extreme data points. For each subject the pressor response was calculated as a function of the magnitude of the rise in systolic pressure above the baseline and the duration of this rise. Systolic pressure was plotted for each individual from the start of laryngoscopy until the end of the study period (Fig. I ) . The area under the curve (AUC) was calculated, from which a mean rise in systolic pressure over the study period was then determined (AUC divided by number of time intervals (36 5-s intervals = 180 s). Where the systolic pressure fell below baseline, the rise was taken as 0 kPa, i.e. no negative values were taken into account in calculating the AUC. This analysis provided three summary measures: peak systolic pressure, time to peak systolic pressure, and mean rise in systolic pressure above baseline. Between-group analysis of these summary
Systollc BP (kPa)
Systollc BP (mmHg) 180 AUC 1TO 180 160
10.9 18.6
10.6
0
,140
1
20
1
44
60
80
100
120
UO
180
10
Time ( 8 ) from start of laryngorcopy +Pallmi A l l
+Bamollna BP
Fig. I . Plot of systolic pressure vs time for Patient no. I I in Group A, showing how ‘‘area under the curve” was calculated.
Table I Demographic data.
Age in years mean (range) Weight in kg mean (range) Sex ratio F:M
Group A ( n = 15)
Group B ( n = 15)
39 ( 1 7 6 6 )
37 (22-63)
65 (52-78)
65 (48-90)
14: I
14: 1
measures was performed using the Mann-Whitney U test. A probability value of less than 0.05 is considered significant.
RESULTS Table 1 shows that the groups were similar in terms of age and weight. Both groups showed a heavy bias towards female patients (14 out of 15 patients in each group), which is explained in part by the inclusion of gynaecological patients. The timing of the peak pressor response, and the time to complete laryngoscopy and tracheal intubation, is given for each patient in Table 2. The mean time to peak response was 31 s in the propofol group and 32 s in the thiopentone group. The mean time to complete laryngoscopy and tracheal intubation was similar in both groups: 26 s (range 10 to 50) in the propofol group and 20 s (range 10 to 40) in the thiopentone group. In 8 out of the 30 cases, peak pressure occurred during the period of stimulus (Table 2). There was no correlation between the rise in arterial pressure (from post-induction trough level to peak pressure) and the duration of the stimulus. The groups were similar in terms of baseline (preop) systolic pressures (Table 2). Following induction of anaesthesia, the mean fall in systolic pressure was 5.1 kPa (39 mmHg) (range -0.8 ( - 6 mmHg) to 9.8 (74 mmHg)) in the propofol group, and 3.2 kPa (24 mmHg) (range - 0.4 ( - 3 mmHg) to 5.2 (39 mmHg)) in the thiopentone group (P=0.005). There was no significant difference in peak systolic pressure between the groups (Table 2). The mean rise in systolic pressure above baseline was 1.5 kPa ( 1 1 mmHg) (range 0 to 4.6 (34 mmHg)) in the propofol group and 2.6 kPa (20 mmHg) (range 0.3 (2 mmHg) to 7.1 (53 mmHg)) in the thiopentone group (P=0.06). In three cases in the propofol group it can be seen that the systolic pressure did not rise above baseline at any point during the study period (Table 2). The difference in mean systolic pressure between peak values and those measured 1 min after the start of the stimulus was 2.6 kPa (20 mmHg) (range 0 to 5.9 (45 mmHg)) in the propofol group, and 2.3 kPa
TIMING OF PRESSSOR RESPONSE Table 2 Summary of systolic pressure changes associated with laryngoscopy and tracheal intubation. Time to peak BP measured from start of laryngoscopy. BP measured in mmHg.
Patient Baseline No BP
Peak BP
Duration of Time to Peak BP stimulus (s)
(s)
BP at 1 min
Overall mean BP rise (see text)
Group A (propofol) 30 1 1 I5 96 0 20 92 30 2 132 138 0.8 20 I20 30 3 I10 186 15 141 25.2 4 I15 153 6.5 25 25 121 30 5 140 205 19.8 35 I76 198 30 6 129 30 22.7 162 7 I I3 154 25 13.3 20 126 35 8 112 125 3.5 25 109 0 60 9 151 127 25 127 10 128 155 50 50 143 5.2 I1 137 164 4.5 30 25 139 30 12 116 125 110 25 1.2 75 10 13 129 181 175 34.4 0 15 20 158 14 175 162 100 168 31.9 40 40 15 147 Mean 127 156 11.3 26 31 136 (range) (100-1 75) (96-205) ( 15-75) ( 10-50) (92-1 75) (0-34.4) Group B (thiopentone) 1 152 203 30 25 175 13.2 10 188 38.9 2 127 197 30 3 I06 150 75 15 146 27.0 4 128 180 50 20 172 18.5 5 144 198 25 20 169 25.4 6 119 154 80 25 151 19.0 7 99 117 30 40 100 4.0 8 92 124 30 10 116 10.5 10 170 21.0 9 I39 I95 35 10 147 258 40 25 235 53.4 II 112 178 25 10 157 27.8 12 125 158 30 25 138 6.5 13 161 224 40 30 216 20.8 14 I38 I70 25 20 147 7.7 15 102 121 20 20 95 2.0 Mean 126 175 32 20 158 19.7 (range) (92-161) ( I 17-258) (20-80) (10-40) (95-235) (2.0-53.4)
(17 mmHg) (range 0.4 (3 mmHg) to 3.8 (29 mmHg)) in the thiopentone group. DISCUSSION A number of contrasting results are to be found regarding the efficacy of particular agents in treating the cardiovascular response following laryngoscopy and intubation. One contributing factor to this is the confusion caused by different methods of measuring arterial pressure. Direct intra-arterial pressure measurement will always identify the peak response irrespective of its timing and duration. However, the invasive nature of arterial cannulation limits its use to situations where it is of proven benefit.
23
Indirect measurement of arterial pressure using an arm cuff may miss the peak response, and therefore lead the authors to conclude that a particular agent completely abolishes the pressor response, while in reality the response is only attenuated. This may, for example, explain conflicting results in patients pretreated with 5 pg. kg-' of fentanyl (9, 13). With the introduction of the Finapres, beat-by-beat arterial pressure can now be recorded non-invasively, in most patients. The rapid response time of the Finapres has been reported previously, with simultaneous tracings of intra-arterial pressure and pressure measured by the Finapres being virtually identical (22,23). We feel that using this device has enabled us to identify the timing of the peak pressor response accurately, and to show that there is no difference in the time to the peak response between the above two groups. Harris and his colleagues reported that 2.5 mg . kg-' of propofol did not abolish the pressor effect 1 min after intubation in comparison with arterial pressure immediately before; but they stated that the pressure did not rise above pre-induction values ( 17). The present study agrees that the arterial pressure at 1 min was not significantly different from pre-induction values, but continuous monitoring revealed a peak before this point. In this study, reporting the systolic pressure 1 min after the start of the stimulus would underestimate the true peak value by 2.6 kPa (20 mmHg) in the propofol group. Comparison of the peak systolic pressure and the mean rise in systolic pressure suggests that propofol has no effect on obtunding the pressor response to laryngoscopy and tracheal intubation compared with thiopentone. This is, again, in contrast to the results of Harris and his colleagues (17). The failure of propofol to protect against the pressor response occurred despite a significantly greater fall in systolic pressure following the induction of anaesthesia in this group. While the mean rise in systolic pressure above baseline was smaller in the propofol group, the difference did not reach statistical significance. In this study the peak pressor response occurred during the stimulus in 8 out of the 30 cases. It is important therefore when measuring the pressor response to start at the beginning of the stimulus rather than after the stimulus has ended. Whether or not this has been done in previous investigations is not always clear from the description of the method.
ACKNOWLEDGEMENTS The authors gratefully acknowledge the co-operation of the anaesthetists, surgeons, nursing staff and theatre technicians of the Vale of Leven Hospital. The Finapres was kindly loaned by Ohmeda.
24
S. HICKEY ET AL.
REFERENCES I . King B D, Harris L C Jnr, Greifenstein F E, Elder J D, Dripps R D. Reflex circulatory response to direct laryngoscopy and tracheal intubation performed during general anesthesia. Anesthesiologv I95 1 : 12: 556-566. 2. Wycoff C C. Endotracheal intubation: effects on blood pressure and pulse rate. Anesthesiology 1960: 21: 153-158. 3. Prys-Roberts C, Green L T, Meloche R, Foex P. Studies of anaesthesia in relation to hypertension 11: haemodynamic consequence of induction and endotracheal intubation. BY 3 Anaesth 1971: 4 3 531-547. 4. Forbes A M, Dally F G. Acute hypertension during induction of anaesthesia and endotracheal intubation in normotensive man. B r J Anaesth 1970: 42: 618424. 5. Fox E J, Sklar G S, Hill C F, Villanueva R, King B D. Complications related to the pressor response to endotracheal intubation. Anesthesiology 1977: 47: 524-525. 6. M o a t E A, Sethna D H, Bussel J A, Raymond M J, Matloff J, Gray R J. Effects of intubation on coronary blood flow and myocardial oxygenation. Can Anaesth Soc 3 1985: 32: 105-1 11. 7. Abou-Madi M N, Kexzler H, Yacoub J M. Cardiovascular reactions to laryngoscopy and tracheal intubation following small and large intravenous doses of lidocaine. Can Anaesth SOC3 1977: 24: 12-19. 8. Stoelting R K. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesth Anal8 1979: 58: 116-1 19. 9. Dahlgren N, Messeter K. Treatment ofstress response to laryngoscopy and intubation with fentanyl. Anaesthesia I98 I: 36: 1022-1026. 10. Kautto U M. Attenuation of the circulatory response to laryngoscopy and intubation by fentanyl. Acta Anaesthesiol Scand 1982: 26: 217-221. 11. Bedford R F, Marshall W K. Cardiovascular response to endotracheal intubation during four anaesthetic techniques. Acta Anaesthesiol Scand 1984: 28: 563-566. 12. Black T E, Kary B, Healy T E J. Reducing the haemodynamic responses to laryngoscopy and intubation - a comparison of alfentanil with fentanyl. Anaesfhesia 1984: 39: 883-887. 13. Kay B, Healy T E J, Bolder P M. Blocking the circulatory
responses to tracheal intubation - a comparison of fentanyl and nalbuphine. Anaesthesia 1985: 40:960-963. 14. Kay B, Nolan D, Mayall R, Healy T E J. The effect ofsufentanil on the cardiovascular responses to tracheal intubation. .4naesthesia 1987: 42: 382-386. 15. Achola K J, Jones M J, Mitchell W D, Smith G. Effects of betaadrenoceptor antagonism on the cardiovascular and catecholamine responses to tracheal intubation. Anaesthesia 1988: 43: 433-436. 16. Kale S C, Mahajan R P, Jayalakshami T S, Raghavan V, Das B. Nifedipine prevents the pressor response to laryngoscopy and tracheal intubation in patients with coronary artery disease. Anaesthesia 1988: 43: 495-497. 17. Harris C E, Murray A M, Anderson J M, Grounds R M, Morgan M. Effects of thiopentone, etomidate and propofol on the haemodynamic response to tracheal intubation. Anaesthesia 1988: 43: 32-36. 18. Stoelting R K. Circulatory changes during laryngoscopy and tracheal intubation: influence of duration of laryngoscopy with or without prior lidocaine. Anesthesiologv 1977: 47: 381-384. 19. Mills P. Poole T, Curran J. Cricoid pressure and the pressor response to tracheal intubation. Anaesthesia 1988: 43: 788-791, 20. Matthews J N S, Altman D G, Campbell M J, Royston P. Analysis of serial measurements in medical research. Br Med 3 1990: 300: 230-235. 21. Velleman P F. Definition and comparison of robust nonlinear data smoothing algorithms. 3 A m Stat Assoc 1980: 75: 609-615. 22. Van Egmond J, Hasenbos M, Crul J F. Invasive v. non-invasive measurement of arterial pressure -comparison of two automatic methods and simultaneously measured direct intra-arterial pressure. Br 3 Anaesth 1985: 57: 434444. 23. Imholz B P M, Van Montfrans G A, Settels J J, Van de Hoevan G M A, Karemaker J M, Wieling W. Continuous non-invasive blood pressure monitoring: reliability of Finapres device during the Valsalva manoeuvre. Cardiovasc Res 1988: 22: 39G397. Address: Stephen Hickey Division of Anaesthesia Royal Infirmary Glasgow Scotland, U K
Timing of peak pressor response following endotracheal intubation S. HICKEY, A. E. CAMERON, A. J. ASBURY and G. D. MURRAY Departments of Anaesthesia and Surgery, Western Infirmary, Glasgow and Department of Anaesthesia, Vale of Leven District General Hospital, Alexandria, Scotland, UK
The study was designed to measure the timing of the peak cardiovascular response following laryngoscopy and endotracheal intubation. Thirty patients ASA 1 or 2 were studied, with arterial pressure being continuously monitored using the Ohmeda 2300 Finapres. Patients were randomised to receive either propofo12.5 mg. kg-’ (Group A) or thiopentone 4.5 mg. kg-’ (Group B). The mean time to complete laryngoscopy and intubation was 26 s in Group A and 20 s in Group B. The peak response occurred on average 31 s after the start of the stimulus in Group A and after 32 s in Group B. In 8 out of the 30 cases the peak response occurred during the period of stimulation. Systolic pressure fell on average by 2.6 kPa (20 mmHg) (range 0 to 5.9 (45 mmHg)) from its peak value to the value measured at the 1-min time mark in the propofol group, and by 2.3 kPa ( 1 7 mmHg) (range 0.4 (3 mmHg) to 3.8 (29 mmHg)) in the thiopentone group. We conclude that the use of slow arm-cuff-based arterial pressure measurement techniques may miss important hypertensive episodes during laryngoscopy and endotracheal intubation. The effectiveness of agents in obtunding the pressor response may thus be misinterpreted. Received 4 November I9N, acceptedfor publication 13 May I991
Key words: Anesthetics, intravenous: propofol, thiopentone; equipment: finapres; complications: pressor response; laryngoscopy.
The cardiovascular response to laryngoscopy and endotracheal intubation has been well documented. Much has been written about the magnitude of this pressor response (1-3), its consequences (4-6), and the manoeuvres which might obtund it (7-1 7). However, less has been written about the actual timing of this peak response, and values quoted range from 7 to 120 s (18, 19). Information on the precise timing of this response (particularly if it is a consistent response) will not only help in the recognition of the response, but might also help in the timing of administration of drugs which obtund the response. With the introduction of the finger arterial pressure monitor, it has become possible to measure arterial pressure continuously and non-invasively, and therefore to identify accurately the timing of the peak pressor response. We felt that this may provide additional useful information, since non-invasive arm cuff techniques of measuring arterial pressure can take up to 30 s to measure arterial pressure, during which time the peak response may be waning, or may be lost completely. In addition, many investigators in this field have relied on measuring arterial pressure at 1 or 2min intervals from the time of stimulus (12-15, 17), during which the arterial pressure might change significan tl y. An investigation was therefore designed to measure
the timing and duration of the pressor response to laryngoscopy and endotracheal intubation; to compare peak values with values measured at 1-min intervals; and to compare differences in the above between two groups of patients induced with either propofol or thiopentone.
PATIENTS AND METHODS Thirty patients ASA grade 1 or 2, aged between 16 and 70 years, were studied. Patients were scheduled for elective gynaecological, general surgical, or orthopaedic procedures. The protocol excluded any patient with a history of hypertension or epilepsy, or those who were regularly taking sedative drugs. The study was approved by the local Ethics Committee. All patients were premedicated with temazepam 20 mg for females, 30 mg for males, plus metoclopramide 10 mg, both given orally, approximately 90 min before induction. On arrival in the anaesthetic room, a 20-g cannula was inserted under local anaesthesia, and the patient was connected to an Ohmeda 2300 Finapres arterial pressure monitor, which allowed continuous non-invasive pressure measurement. Output from the Finapres was taken to a Hewlett-Packard “Think-Jet” printer, which printed continuously. Arterial pressure measurements were made at minute intervals for 5 min prior to the induction of anaesthesia. The mean of these was taken as the baseline value. The patients were randomly allocated using an opaque envelope system into two groups. In Group A patients, anaesthesia was induced by injecting 2.5 mg.kg-’ of propofol intravenously over 30 s. In Group B patients, anaesthesia was induced by injecting 4.5 mg . kg-’
22
S. HICKEY ET AL.
of thiopcntone over the same time period. Thereafter the management of patients in both groups was identical. From time zero, the start of the injection of the induction agent, arterial pressure measurements were printed out at 5-s intervals. (The Finapres will make measurements continuously, i.e. for every heart beat. This can lead to overload of the printer, however, which is why we chose to limit measurements to 5-s intervals, and measured the time to completion of tracheal intubation on the same scale.) Following completion of the injection of induction agent, the venous cannula was flushed with 2-3 ml of normal saline. The patients breathed 66% nitrous oxide in oxygen (total fresh gas flow 9 1. min- ’) through a face mask connected to a Bain system. Ventilation was gently assisted as necessary. At the 40-s mark 1.5 mg. kg-’ of suxamethonium was injected intravenously as a bolus, and the cannula once again flushed. At the 90-s mark laryngoscopy and tracheal intubation were performed, using a MacIntosh laryngoscope. The endotracheal tubes were lubricated with a water-based gel. The time taken to place the endotracheal tube was recorded, with inflation of the tube cuff used as the end point (timed to the nearest 5 s). Enflurane I % was added to the gas mixture when the breathing system was reconnected, and ventilation assisted as appropriate. Arterial pressure measurements continued at 5-s intervals for a further 3 min following insertion of the endotracheal tube. This allowed the time to peak arterial pressure to be identified at a later stage from the print-out, and allowed comparison of peak values with the values measured at the 1-min time marks. The serial measurements were analysed using summary measures as recommended by Matthews and his colleagues (20). Prior to analysis the data were “smoothed” using a running median technique (21). This procedure emphasises the underlying trend in serial measurements, while reducing the possible misinterpretation resulting from extreme data points. For each subject the pressor response was calculated as a function of the magnitude of the rise in systolic pressure above the baseline and the duration of this rise. Systolic pressure was plotted for each individual from the start of laryngoscopy until the end of the study period (Fig. I ) . The area under the curve (AUC) was calculated, from which a mean rise in systolic pressure over the study period was then determined (AUC divided by number of time intervals (36 5-s intervals = 180 s). Where the systolic pressure fell below baseline, the rise was taken as 0 kPa, i.e. no negative values were taken into account in calculating the AUC. This analysis provided three summary measures: peak systolic pressure, time to peak systolic pressure, and mean rise in systolic pressure above baseline. Between-group analysis of these summary
Systollc BP (kPa)
Systollc BP (mmHg) 180 AUC 1TO 180 160
10.9 18.6
10.6
0
,140
1
20
1
44
60
80
100
120
UO
180
10
Time ( 8 ) from start of laryngorcopy +Pallmi A l l
+Bamollna BP
Fig. I . Plot of systolic pressure vs time for Patient no. I I in Group A, showing how ‘‘area under the curve” was calculated.
Table I Demographic data.
Age in years mean (range) Weight in kg mean (range) Sex ratio F:M
Group A ( n = 15)
Group B ( n = 15)
39 ( 1 7 6 6 )
37 (22-63)
65 (52-78)
65 (48-90)
14: I
14: 1
measures was performed using the Mann-Whitney U test. A probability value of less than 0.05 is considered significant.
RESULTS Table 1 shows that the groups were similar in terms of age and weight. Both groups showed a heavy bias towards female patients (14 out of 15 patients in each group), which is explained in part by the inclusion of gynaecological patients. The timing of the peak pressor response, and the time to complete laryngoscopy and tracheal intubation, is given for each patient in Table 2. The mean time to peak response was 31 s in the propofol group and 32 s in the thiopentone group. The mean time to complete laryngoscopy and tracheal intubation was similar in both groups: 26 s (range 10 to 50) in the propofol group and 20 s (range 10 to 40) in the thiopentone group. In 8 out of the 30 cases, peak pressure occurred during the period of stimulus (Table 2). There was no correlation between the rise in arterial pressure (from post-induction trough level to peak pressure) and the duration of the stimulus. The groups were similar in terms of baseline (preop) systolic pressures (Table 2). Following induction of anaesthesia, the mean fall in systolic pressure was 5.1 kPa (39 mmHg) (range -0.8 ( - 6 mmHg) to 9.8 (74 mmHg)) in the propofol group, and 3.2 kPa (24 mmHg) (range - 0.4 ( - 3 mmHg) to 5.2 (39 mmHg)) in the thiopentone group (P=0.005). There was no significant difference in peak systolic pressure between the groups (Table 2). The mean rise in systolic pressure above baseline was 1.5 kPa ( 1 1 mmHg) (range 0 to 4.6 (34 mmHg)) in the propofol group and 2.6 kPa (20 mmHg) (range 0.3 (2 mmHg) to 7.1 (53 mmHg)) in the thiopentone group (P=0.06). In three cases in the propofol group it can be seen that the systolic pressure did not rise above baseline at any point during the study period (Table 2). The difference in mean systolic pressure between peak values and those measured 1 min after the start of the stimulus was 2.6 kPa (20 mmHg) (range 0 to 5.9 (45 mmHg)) in the propofol group, and 2.3 kPa
TIMING OF PRESSSOR RESPONSE Table 2 Summary of systolic pressure changes associated with laryngoscopy and tracheal intubation. Time to peak BP measured from start of laryngoscopy. BP measured in mmHg.
Patient Baseline No BP
Peak BP
Duration of Time to Peak BP stimulus (s)
(s)
BP at 1 min
Overall mean BP rise (see text)
Group A (propofol) 30 1 1 I5 96 0 20 92 30 2 132 138 0.8 20 I20 30 3 I10 186 15 141 25.2 4 I15 153 6.5 25 25 121 30 5 140 205 19.8 35 I76 198 30 6 129 30 22.7 162 7 I I3 154 25 13.3 20 126 35 8 112 125 3.5 25 109 0 60 9 151 127 25 127 10 128 155 50 50 143 5.2 I1 137 164 4.5 30 25 139 30 12 116 125 110 25 1.2 75 10 13 129 181 175 34.4 0 15 20 158 14 175 162 100 168 31.9 40 40 15 147 Mean 127 156 11.3 26 31 136 (range) (100-1 75) (96-205) ( 15-75) ( 10-50) (92-1 75) (0-34.4) Group B (thiopentone) 1 152 203 30 25 175 13.2 10 188 38.9 2 127 197 30 3 I06 150 75 15 146 27.0 4 128 180 50 20 172 18.5 5 144 198 25 20 169 25.4 6 119 154 80 25 151 19.0 7 99 117 30 40 100 4.0 8 92 124 30 10 116 10.5 10 170 21.0 9 I39 I95 35 10 147 258 40 25 235 53.4 II 112 178 25 10 157 27.8 12 125 158 30 25 138 6.5 13 161 224 40 30 216 20.8 14 I38 I70 25 20 147 7.7 15 102 121 20 20 95 2.0 Mean 126 175 32 20 158 19.7 (range) (92-161) ( I 17-258) (20-80) (10-40) (95-235) (2.0-53.4)
(17 mmHg) (range 0.4 (3 mmHg) to 3.8 (29 mmHg)) in the thiopentone group. DISCUSSION A number of contrasting results are to be found regarding the efficacy of particular agents in treating the cardiovascular response following laryngoscopy and intubation. One contributing factor to this is the confusion caused by different methods of measuring arterial pressure. Direct intra-arterial pressure measurement will always identify the peak response irrespective of its timing and duration. However, the invasive nature of arterial cannulation limits its use to situations where it is of proven benefit.
23
Indirect measurement of arterial pressure using an arm cuff may miss the peak response, and therefore lead the authors to conclude that a particular agent completely abolishes the pressor response, while in reality the response is only attenuated. This may, for example, explain conflicting results in patients pretreated with 5 pg. kg-' of fentanyl (9, 13). With the introduction of the Finapres, beat-by-beat arterial pressure can now be recorded non-invasively, in most patients. The rapid response time of the Finapres has been reported previously, with simultaneous tracings of intra-arterial pressure and pressure measured by the Finapres being virtually identical (22,23). We feel that using this device has enabled us to identify the timing of the peak pressor response accurately, and to show that there is no difference in the time to the peak response between the above two groups. Harris and his colleagues reported that 2.5 mg . kg-' of propofol did not abolish the pressor effect 1 min after intubation in comparison with arterial pressure immediately before; but they stated that the pressure did not rise above pre-induction values ( 17). The present study agrees that the arterial pressure at 1 min was not significantly different from pre-induction values, but continuous monitoring revealed a peak before this point. In this study, reporting the systolic pressure 1 min after the start of the stimulus would underestimate the true peak value by 2.6 kPa (20 mmHg) in the propofol group. Comparison of the peak systolic pressure and the mean rise in systolic pressure suggests that propofol has no effect on obtunding the pressor response to laryngoscopy and tracheal intubation compared with thiopentone. This is, again, in contrast to the results of Harris and his colleagues (17). The failure of propofol to protect against the pressor response occurred despite a significantly greater fall in systolic pressure following the induction of anaesthesia in this group. While the mean rise in systolic pressure above baseline was smaller in the propofol group, the difference did not reach statistical significance. In this study the peak pressor response occurred during the stimulus in 8 out of the 30 cases. It is important therefore when measuring the pressor response to start at the beginning of the stimulus rather than after the stimulus has ended. Whether or not this has been done in previous investigations is not always clear from the description of the method.
ACKNOWLEDGEMENTS The authors gratefully acknowledge the co-operation of the anaesthetists, surgeons, nursing staff and theatre technicians of the Vale of Leven Hospital. The Finapres was kindly loaned by Ohmeda.
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