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HYPERTENSIVE AND CATECHOLAMINE RESPONSE TO TRACHEAL INTUBATION IN PATIENTS WITH PREGNANCY-INDUCED HYPERTENSION
Br. J. Anaesth. (1989), 63, 429-434
HYPERTENSIVE AND CATECHOLAMINE RESPONSE TO TRACHEAL INTUBATION IN PATIENTS WITH PREGNANCY-INDUCED HYPERTENSION N. G. LAVIES, B. H. MEIKLEJOHN, A. E. MAY, K. J. ACHOLA AND D. FELL
PATIENTS AND METHODS
We studied 10 patients with PIH, undergoing elective or emergency Caesarean section (group I) and 10 normotensive mothers undergoing elective N . G. LAVIES, B.SC, M.B., CH.B., F.F.A.R.C.S.; B. H . MEIKLEJOHN, B.SC, M.B., CH.B., F.F.A.R.C.S.; A . E. MAY, M.B., B.S., Caesarean section under general anaesthesia F.F.A.R.C.S.; Department of Anaesthesia, Leicester Royal (group II). PIH was denned as an arterial pressure Infirmary, Leicester LEI 5WW. K. J. ACHOLA, M.SC, PH.D.; greater than 140/90 mm Hg on two or more D. FELL, M.B., CH.B., F.F.A.R.C.S.; University Department of separate occasions appearing initially in the Anaesthesia, Leicester Royal Infirmary. Accepted for Pubsecond or third trimesters. Informed consent was lication: March 16, 1989. obtained from each patient for their inclusion in Correspondence to N. G. L.
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
An increase in arterial pressure is known to accompany laryngoscopy with or without tracheal SUMMARY intubation, and this response is accompanied by an increase in plasma noradrenaline concentration The pressor and catecholamine responses to [1-3]. An exaggerated pressor response to tracheal laryngoscopy and intubation were studied in intubation has been reported in hypertensive nine patients with pregnancy-induced hyperpatients [4], but those treated with beta-adreno- tension (PIH) and in eight normotensive conceptor blocking drugs appear to respond in this trols. Five of the PIH patients had received oral respect similarly to normotensive subjects, whilst labetalol as antihypertensive therapy. Mean exhibiting greater increases in noradrenaline con- arterial pressure (MAP) increased significantly from the pre-induction value in all groups 1 min centration [5]. Patients with severe pre-eclampsia or preg- after intubation, and also at 3 min in those with nancy-induced hypertension (PIH) also exhibit PIH who had not received labetalol. Arterial marked hypertensive responses to tracheal in- pressure was significantly greater in both PIH tubation, despite the use of vasodilator drugs [6, groups than in the control group at all times. 7]. However, previous studies have not examined However, the percentage increase in MAP on the response in normotensive parturients for intubation was significantly less in the labetalol comparison. Furthermore, the role of catechol- treated group than in either the untreated or the amines in pre-eclampsia is uncertain, as plasma control groups. There were no significant differconcentrations of noradrenaline have been repor- ences between the groups in plasma concented to be lower than [8], higher than [9], or no trations of either noradrenaline or adrenaline; different from [10] normotensive controls. Adrena- noradrenaline concentration increased signifiline concentrations are also inconsistent [10, 11]. cantly after intubation only in the control group. In order to investigate further the hypertensive Labetalol appears to confer some protection and catecholamine responses to tracheal intu- against the pressor response to intubation in parturients with PIH. bation in PIH, we have measured these responses in an unselected group of parturients with PIH and compared them with those of normotensive controls.
430
BRITISH JOURNAL OF ANAESTHESIA 50 % nitrous oxide and 0.5 % halothane in oxygen. The lungs were ventilated using a Manley ventilator delivering a minute volume of 120 ml kg"1; in a pilot study this had been found to maintain PaCo, in the range 3.5-4.5 kPa. Neuromuscular block was maintained with atracurium which was given before the effects of the suxamethonium had terminated in order to prevent coughing. At 1, 3 and 5 min after intubation, 10-ml samples of blood were withdrawn from the i.v. cannula without the use of a tourniquet and placed in evacuated lithium-heparin tubes. Heart rate and arterial pressure were recorded at these times. In group II, surgery was delayed until completion of blood sampling, but in some patients in group I the urgency of the situation dictated that surgery commenced before the 5-min sample had been taken. Blood was centrifuged within 1 h at 4 °C and the separated plasma was stored at — 70 °C until analysis for catecholamine concentration was carried out by High Pressure Liquid Chromatography as detailed elsewhere [2]. The data were analysed statistically using Student's paired t test and one-way ANOVA for
TABLE I. Description of patient groups
Group I Group II
n
Mean (SEM) age (yr)
Mean (SEM) weight (kg)
Primip.
Multip.
Infant wt (mean) (g)
9 8
28 (2.5) 32(1.0)
74 (6.5) 72 (6.2)
7 0
2 8
1963 3356
TABLE 11. Details of patients with PIH (group I). * Severe PIH. CS = Caesarean section
(yr)
Parity
(kg)
Max. SAP/DAP before CS (mm Hg)
1*
23
0
77
200/120
3+
2 3* 4
38 24 29
2 0 0
102 48 73
150/100 160/110 150/110
— 3+ —
6 10* 11*
26 36 22
0 0 0
77 95 57
150/100 160/110 200/130
1+ 1+ 3+
17*
20
0
74
170/120
2+
18*
35
1
63
180/105
3+
Wt
Age No.
Proteinuria (g)
Medication Phenobarbitone, labetalol + hydrallazine None Phenobarbitone Phenobarbitone, labetalol + methyl dopa Phenobarbitone None Phenobarbitone, labetalol + hydrallazine Phenobarbitone labetalol + hydrallazine Phenobarbitone, labetalol
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
the study, which was approved by the District Ethics Committee. Each patient received premedication with 0.3molar sodium citrate 30 ml, but no sedative agents were given, with the exception of antihypertensive or anticonvulsant therapy which had been prescribed. During pre-oxygenation in the operating theatre, an additional 18-gauge i.v. cannula was inserted under local anaesthesia into an antecubital vein on the arm contralateral to that with the existing i.v. infusion. An automatic arterial pressure cuff (Dinamap 845) was placed on the arm receiving the i.v. infusion, and the ECG was monitored. Heart rate and arterial pressure were recorded before induction and a 10-ml blood sample was withdrawn from the i.v. cannula. Each group received the same anaesthetic technique: after full pre-oxygenation, standard rapid sequence induction of anaesthesia was commenced using thiopentone 4-5 mg kg"1 i.v., suxamethonium l.Smgkg""1 i.v. and application of cricoid pressure. Intubation of the trachea was accomplished as soon as neuromuscular block was achieved and anaesthesia was continued using
RESPONSES TO TRACHEAL INTUBATION IN PARTURIENTS
431
200
140i
180
130-
160
120-
1
I
140 120
_ 100
•i no-
J
100
S 9080-
80 70-
60 60-
40 Before nduction
3
1
50
5
Before induction
After intubation (rrm )
FIG. 1. Mean (SEM) systolic and diastolic arterial pressures in groups la ( 0 ) , Ib ( • ) and II ( • ) . *P < 0.02; **P < 0.01 within group comparison with baseline; -fP<0.05 groups la v. Ib.
1
3 After intubation (min)
FIG. 2. Mean (SEM) heart rates in groups I (-•- ) and II
*P < 0.05 within group comparison with baseline; **P < 0.01 between groups.
(-)•
TABLE III. Effect of labetalol on mean (SEM) MAP (mm Hg). A = Before induction; B = 1 min; C = 3 min; D = 5 min after intubation; "Significant difference in % increase in MAP between groups la and Ib, and between la and II (P < 0.01)
D
B
Group la (treated) Group Ib (untreated) Group II
119 (5.6) 124(3.5) 95 (3.8)
135(8.4) 154(4.6)** 118(3.8)
118(9.5) 139(5.4) 96 (3.8)
117(6.1) 126 (6.9) 92 (5.5)
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
Patients in group I have been allocated to two within group comparisons and unpaired t test for between group comparisons. P < 0.05 was con- subgroups on the basis of receiving labetalol (la) or not (Ib). In groups Ib and II SAP and DAP sidered to be significant. increased significantly from pre-induction values at 1 min; in group Ib they were increased also at RESULTS 3 min. In group la, only DAP increased signifiTwo patients in group II and one patient in group cantly at 1 min (fig. 1). Other values were not I were excluded because of incomplete data, significantly different from baseline. However, leaving nine in group I and eight in group II. The arterial pressure was significantly higher at all demographic details of the patients are given in times in both PIH groups than in the control table I and details of individual patients in group group. I are given in table II. Five patients were classified There was a 25 % increase in MAP 1 min after as severely pre-eclamptic, that is, with an arterial intubation in groups Ib and II. However, patients pressure of 160/110 mm Hg or more on two receiving labetalol (group la) showed an increase separate occasions, proteinuria of > 5 g/24 h, or of only 13%, which was significantly less than both [12]. Three patients were receiving anti- that of both the other groups (table III). hypertensive treatment comprising labetalol There were no significant differences in heart 400 mg three times a day orally and hydrallazine rate between labetalol-treated (la) and untreated i.m.; one received labetalol only, and one labetalol (Ib) patients, therefore their results have been and methyl dopa. combined. The pre-induction value was signifi-
432
BRITISH JOURNAL OF ANAESTHESIA 3.0-
PIH untreated with labetalol, although the absolute values were obviously higher in the latter patients. The actual (as opposed to percentage) 2.6increase in MAP in group II closely resembled 2.4that reported by Millar-Forbes and Dally [13] for a similar induction technique in gynaecological patients. 2.0The increase in MAP on intubation in group Ib (30 mm Hg) was less than that reported by Hodgkinson, Husain and Hayashi (45 mm Hg) 1.6 [6], and by Connell, Dalgleish and Downing 1.4 (43 mm Hg) [7]. However, these workers used 1.2 direct intra-arterial monitoring and reported 1.0 increases from post-induction values and not preinduction as in this study, and this may explain the 0.8 discrepancy. We did not feel it justified to wait for 0.6 an indirect reading of arterial pressure between 0.4 induction and intubation and it is also possible that transient pressure peaks were missed using an 0.2 oscillotonometric method. Before induction Two other differences between this and Con3 5 nelPs study make comparison difficult: the After intubation (min) previous study included only severely affected FIG. 3. Mean (SEM) noradrenaline concentrations in groups ) and II (•)• *P < 0.05 within group comparison with patients, whereas only six of the nine patients in group I of our study were in this category, and our baseline. patients with PIH were mostly primiparous and of average age 28 yr, compared with more multicantly higher in group II, but thereafter there parae and a younger mean age (23.6 yr) in were no differences. Within both groups I and II, ConnelPs study. values at 1 and 3 but not 5 min after tracheal Patients in group la who had received oral intubation were significantly higher than before labetalol as antihypertensive treatment showed a induction (fig. 2). significantly reduced pressor response compared At 1 min after intubation there was a 28 % with both untreated hypertensives and normotenincrease in plasma concentration of noradrenaline sive controls. The fact that most of this group in group II, which was significant compared with were also in a severe category of PIH/prebaseline (fig. 3). There was a 33% increase in eclampsia makes this observation striking. noradrenaline concentration after 1 min in group Labetalol, a mixed alpha and beta-adrenergic I patients, but this was not significant. There were blocking agent, has become popular with obsteno significant differences between the groups in tricians for the treatment of PIH and is now the noradrenaline concentration at any study point, first-line treatment in our unit. Pure beta-blocking no significant changes in plasma concentration of drugs, for example metoprolol, given orally have adrenaline in each group and no differences been shown to attenuate hypertensive responses between groups. in non-pregnant patients undergoing general anaesthesia [14]. More recently, one oral dose of labetalol has been shown also to be effective [15]. DISCUSSION In contrast, i.v. practolol given immediately Although previous studies have described the before intubation seems to be ineffective, at least cardiovascular changes during general anaesthesia in normotensive subjects [16]. It is interesting to in patients with pre-eclampsia [6, 7] they have note that 60% of patients in ConnelFs series had not included a group of normotensive parturients received i.v. practolol, with obviously ineffective for comparison. We have demonstrated that the results [7]. percentage increase in MAP after intubation was Labetalol did not always prevent peaks of similar in healthy parturients and in patients with arterial pressure; one patient in group la had an 2.8-
I
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
Jl
I
I
RESPONSES TO TRACHEAL INTUBATION IN PARTURIENTS
intubation. British Journal of Anaesthesia 1983; 55: 855-859. 3. Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. British Journal of Anaesthesia 1987; 59: 295-299. 4. Prys-Roberts C, Greene LT, Meloche R, Foex P. Studies of anaesthesia in relation to hypertension II: Haemodynamic consequences of induction and endotracheal intubation. British Journal of Anaesthesia 1971; 43: 531-547. 5. Low JM, Harvey JT, Prys-Roberts C, Dagnino J. Studies of anaesthesia in relation to hypertension. VII: Adrenergic responses to laryngoscopy. British Journal of Anaesthesia 1986; 58: 471-477. 6. Hodgkinson R, Husain FJ, Hayashi RH. Systemic and pulmonary blood pressures during Caesarean section in parturients with gestational hypertension. Canadian Anaesthetists Society Journal 1980; 27: 389-393. 7. Connell H, Dalgleish J, Downing JW. General anaesthesia in mothers with severe pre-eclampsia/eclampsia. British Journal of Anaesthesia 1987; 59: 1375-1380. 8. Tunbridge RDG, Donnai P. Plasma noradrenaline in normal pregnancy and in hypertension of late pregnancy. British Journal of Obstetrics and Gynaecology 1981; 88: 105-108. In conclusion, our results indicate that there 9. Davey DA, Macnab MF. Plasma adrenaline, noradrenawas no quantitative difference in the pressor or line and dopamine in pregnancy hypertension. British Journal of Obstetrics and Gynaecology 1981; 81: 611. catecholamine response to intubation experienced by normotensive and untreated hypertensive 10. Pederson EB, Rasmussen AB, Christensen NJ, Johannesen P, Lauritsen JG, Kristensen S, Wohlert M. Plasma parturients, although the number of patients noradrenaline and adrenaline in pre-eclampsia, essential studied was relatively small. Our findings do not hypertension in pregnancy and normotensive control subjects. Ada Endocrinologica 1982; 99: 594-600. support the concept of vascular hyperactivity to pressor agents in pre-eclampsia which has been 11. Abboud T, Anal R, Sarkis F, Henriksen EH, Kammula RK. Sympathoadrenal activity, maternal, fetal, and neopropounded [19]. However, the potential clinical natal responses after epidural anesthesia in the preeffect of a surge in arterial pressure is much eclamptic patient. American Journal of Obstetrics and greater if the basal value is higher, as it is more Gynecology 1982; 144: 915-918. likely to exceed the upper limit of cerebral 12. Wright JP. Anesthetic considerations in pre-eclampsiaeclampsia. Anesthesia and Analgesia 1983; 63: 590-601. autoregulation. 13. Millar Forbes A, Dally FG. Acute hypertension during In view of the high proportion of deaths caused induction of anaesthesia and endotracheal intubation of by cerebral haemorrhage and oedema in hypernormotensive man. British Journal of Anaesthesia 1970; 42: 618-624. tensive diseases of pregnancy [20] and the known morbidity from intubation [21], it seems 14. Magnusson J, Thulin T, Werner O, Jarhult J, Thompson D. Haemodynamic effects of pre-treatment with metoprudent to attempt to limit the maximum MAP prolol in hypertensive patients undergoing surgery. after intubation to 130 mm Hg, the upper limit of British Journal of Anaesthesia 1986; 58: 251-260. autoregulation in man [22]. Labetalol given orally 15. Stone JG, Foex P, Sear JW, Johnson LL, Khambatta HJ, Triner L. Myocardial ischaemia in untreated hypertensive may be a useful agent to help attenuate hyperpatients: Effect of a single oral dose of a beta-adrenergic tensive responses to airway manipulation, but blocking agent. Anesthesiology 1988; 68: 495-500. its use requires more careful evaluation in a larger 16. Achola KJ, Jones MJ, Mitchell RWD, Smith G. Effects of number of patients. beta-adrenoceptor antagonism on the cardiovascular and catecholamine responses to tracheal intubation. Anaesthesia 1988; 43: 433-^136. REFERENCES 17. Lawes EG, Downing JW, Duncan PW, Bland B, Lavies NG, Gane GAC. Fentanyl-droperidol supplementation 1. Russell WJ, Morris RG, Frewin DB, Drew SE. Changes of rapid sequence induction in the presence of severe in plasma catecholamine concentrations during endopregnancy-induced and pregnancy-aggravated hypertentracheal intubation. British Journal of Anaesthesia 1981; sion. British Journal of Anaesthesia 1987; 59: 1381-1391. 53: 837-839. 2. Derbyshire DR, Chmielewski A, Fell D, Vater M, Achola 18. Shnider SM, Abboud T, Levinson G, Wright RG, Kim S, Henriksen E, Hughes SC, Roizen MF, Johnson J. K, Smith G. Plasma catecholamine responses to tracheal
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
SAP greater than 200 mm Hg. An alternative or additional approach might be to use a rapidly acting potent opioid as part of the induction sequence; fentanyl has been found effective in this respect in severe pre-eclampsia [17]. Plasma concentrations of noradrenaline increased significantly 1 min after tracheal intubation in group II, and this has been found to occur in most studies of non-pregnant subjects. Shnider and colleagues [18] reported a 21 % increase in plasma concentration of noradrenaline following intubation in normotensive parturients having Caesarean section. This is comparable to our finding (28%), but, to our knowledge, catecholamine concentrations have not been reported previously in relation to tracheal intubation in pre-eclampsia. Although the increase in the PIH group was not significant because of large variability, it is likely that more patients would have yielded a significant result.
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BRITISH JOURNAL OF ANAESTHESIA
General anesthesia for Cesarean section: maternal and fetal norepinephrine levels and neonatal neurobehavioural status. Anesthesiology 1980; 53: S302. 21. 19. Talledo OE, Chesley LC, Zuspan FP. Renin-angiotensin system in normal and toxemic pregnancies. American Journal of Obstetrics & Gynecology 1968; 100: 218-221. 22. 20. Department of Health and Social Security. Report on Confidential Enquiry into Maternal Deaths in England and
Wales, 1979-1981. London: Her Majesty's Stationary Office. Fox EJ, Sklar GS, Hill CH, Villanueva R, King BD. Complications related to the pressor response to endotracheal intubation. Anesthesiology 1977; 47: 524-525. Lassen NA, Christensen MS. Physiology of cerebral blood flow. British Journal of Anaesthesia 1976; 48: 719-734.
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HYPERTENSIVE AND CATECHOLAMINE RESPONSE TO TRACHEAL INTUBATION IN PATIENTS WITH PREGNANCY-INDUCED HYPERTENSION N. G. LAVIES, B. H. MEIKLEJOHN, A. E. MAY, K. J. ACHOLA AND D. FELL
PATIENTS AND METHODS
We studied 10 patients with PIH, undergoing elective or emergency Caesarean section (group I) and 10 normotensive mothers undergoing elective N . G. LAVIES, B.SC, M.B., CH.B., F.F.A.R.C.S.; B. H . MEIKLEJOHN, B.SC, M.B., CH.B., F.F.A.R.C.S.; A . E. MAY, M.B., B.S., Caesarean section under general anaesthesia F.F.A.R.C.S.; Department of Anaesthesia, Leicester Royal (group II). PIH was denned as an arterial pressure Infirmary, Leicester LEI 5WW. K. J. ACHOLA, M.SC, PH.D.; greater than 140/90 mm Hg on two or more D. FELL, M.B., CH.B., F.F.A.R.C.S.; University Department of separate occasions appearing initially in the Anaesthesia, Leicester Royal Infirmary. Accepted for Pubsecond or third trimesters. Informed consent was lication: March 16, 1989. obtained from each patient for their inclusion in Correspondence to N. G. L.
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
An increase in arterial pressure is known to accompany laryngoscopy with or without tracheal SUMMARY intubation, and this response is accompanied by an increase in plasma noradrenaline concentration The pressor and catecholamine responses to [1-3]. An exaggerated pressor response to tracheal laryngoscopy and intubation were studied in intubation has been reported in hypertensive nine patients with pregnancy-induced hyperpatients [4], but those treated with beta-adreno- tension (PIH) and in eight normotensive conceptor blocking drugs appear to respond in this trols. Five of the PIH patients had received oral respect similarly to normotensive subjects, whilst labetalol as antihypertensive therapy. Mean exhibiting greater increases in noradrenaline con- arterial pressure (MAP) increased significantly from the pre-induction value in all groups 1 min centration [5]. Patients with severe pre-eclampsia or preg- after intubation, and also at 3 min in those with nancy-induced hypertension (PIH) also exhibit PIH who had not received labetalol. Arterial marked hypertensive responses to tracheal in- pressure was significantly greater in both PIH tubation, despite the use of vasodilator drugs [6, groups than in the control group at all times. 7]. However, previous studies have not examined However, the percentage increase in MAP on the response in normotensive parturients for intubation was significantly less in the labetalol comparison. Furthermore, the role of catechol- treated group than in either the untreated or the amines in pre-eclampsia is uncertain, as plasma control groups. There were no significant differconcentrations of noradrenaline have been repor- ences between the groups in plasma concented to be lower than [8], higher than [9], or no trations of either noradrenaline or adrenaline; different from [10] normotensive controls. Adrena- noradrenaline concentration increased signifiline concentrations are also inconsistent [10, 11]. cantly after intubation only in the control group. In order to investigate further the hypertensive Labetalol appears to confer some protection and catecholamine responses to tracheal intu- against the pressor response to intubation in parturients with PIH. bation in PIH, we have measured these responses in an unselected group of parturients with PIH and compared them with those of normotensive controls.
430
BRITISH JOURNAL OF ANAESTHESIA 50 % nitrous oxide and 0.5 % halothane in oxygen. The lungs were ventilated using a Manley ventilator delivering a minute volume of 120 ml kg"1; in a pilot study this had been found to maintain PaCo, in the range 3.5-4.5 kPa. Neuromuscular block was maintained with atracurium which was given before the effects of the suxamethonium had terminated in order to prevent coughing. At 1, 3 and 5 min after intubation, 10-ml samples of blood were withdrawn from the i.v. cannula without the use of a tourniquet and placed in evacuated lithium-heparin tubes. Heart rate and arterial pressure were recorded at these times. In group II, surgery was delayed until completion of blood sampling, but in some patients in group I the urgency of the situation dictated that surgery commenced before the 5-min sample had been taken. Blood was centrifuged within 1 h at 4 °C and the separated plasma was stored at — 70 °C until analysis for catecholamine concentration was carried out by High Pressure Liquid Chromatography as detailed elsewhere [2]. The data were analysed statistically using Student's paired t test and one-way ANOVA for
TABLE I. Description of patient groups
Group I Group II
n
Mean (SEM) age (yr)
Mean (SEM) weight (kg)
Primip.
Multip.
Infant wt (mean) (g)
9 8
28 (2.5) 32(1.0)
74 (6.5) 72 (6.2)
7 0
2 8
1963 3356
TABLE 11. Details of patients with PIH (group I). * Severe PIH. CS = Caesarean section
(yr)
Parity
(kg)
Max. SAP/DAP before CS (mm Hg)
1*
23
0
77
200/120
3+
2 3* 4
38 24 29
2 0 0
102 48 73
150/100 160/110 150/110
— 3+ —
6 10* 11*
26 36 22
0 0 0
77 95 57
150/100 160/110 200/130
1+ 1+ 3+
17*
20
0
74
170/120
2+
18*
35
1
63
180/105
3+
Wt
Age No.
Proteinuria (g)
Medication Phenobarbitone, labetalol + hydrallazine None Phenobarbitone Phenobarbitone, labetalol + methyl dopa Phenobarbitone None Phenobarbitone, labetalol + hydrallazine Phenobarbitone labetalol + hydrallazine Phenobarbitone, labetalol
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
the study, which was approved by the District Ethics Committee. Each patient received premedication with 0.3molar sodium citrate 30 ml, but no sedative agents were given, with the exception of antihypertensive or anticonvulsant therapy which had been prescribed. During pre-oxygenation in the operating theatre, an additional 18-gauge i.v. cannula was inserted under local anaesthesia into an antecubital vein on the arm contralateral to that with the existing i.v. infusion. An automatic arterial pressure cuff (Dinamap 845) was placed on the arm receiving the i.v. infusion, and the ECG was monitored. Heart rate and arterial pressure were recorded before induction and a 10-ml blood sample was withdrawn from the i.v. cannula. Each group received the same anaesthetic technique: after full pre-oxygenation, standard rapid sequence induction of anaesthesia was commenced using thiopentone 4-5 mg kg"1 i.v., suxamethonium l.Smgkg""1 i.v. and application of cricoid pressure. Intubation of the trachea was accomplished as soon as neuromuscular block was achieved and anaesthesia was continued using
RESPONSES TO TRACHEAL INTUBATION IN PARTURIENTS
431
200
140i
180
130-
160
120-
1
I
140 120
_ 100
•i no-
J
100
S 9080-
80 70-
60 60-
40 Before nduction
3
1
50
5
Before induction
After intubation (rrm )
FIG. 1. Mean (SEM) systolic and diastolic arterial pressures in groups la ( 0 ) , Ib ( • ) and II ( • ) . *P < 0.02; **P < 0.01 within group comparison with baseline; -fP<0.05 groups la v. Ib.
1
3 After intubation (min)
FIG. 2. Mean (SEM) heart rates in groups I (-•- ) and II
*P < 0.05 within group comparison with baseline; **P < 0.01 between groups.
(-)•
TABLE III. Effect of labetalol on mean (SEM) MAP (mm Hg). A = Before induction; B = 1 min; C = 3 min; D = 5 min after intubation; "Significant difference in % increase in MAP between groups la and Ib, and between la and II (P < 0.01)
D
B
Group la (treated) Group Ib (untreated) Group II
119 (5.6) 124(3.5) 95 (3.8)
135(8.4) 154(4.6)** 118(3.8)
118(9.5) 139(5.4) 96 (3.8)
117(6.1) 126 (6.9) 92 (5.5)
Downloaded from http://bja.oxfordjournals.org/ at University of Manitoba on June 25, 2015
Patients in group I have been allocated to two within group comparisons and unpaired t test for between group comparisons. P < 0.05 was con- subgroups on the basis of receiving labetalol (la) or not (Ib). In groups Ib and II SAP and DAP sidered to be significant. increased significantly from pre-induction values at 1 min; in group Ib they were increased also at RESULTS 3 min. In group la, only DAP increased signifiTwo patients in group II and one patient in group cantly at 1 min (fig. 1). Other values were not I were excluded because of incomplete data, significantly different from baseline. However, leaving nine in group I and eight in group II. The arterial pressure was significantly higher at all demographic details of the patients are given in times in both PIH groups than in the control table I and details of individual patients in group group. I are given in table II. Five patients were classified There was a 25 % increase in MAP 1 min after as severely pre-eclamptic, that is, with an arterial intubation in groups Ib and II. However, patients pressure of 160/110 mm Hg or more on two receiving labetalol (group la) showed an increase separate occasions, proteinuria of > 5 g/24 h, or of only 13%, which was significantly less than both [12]. Three patients were receiving anti- that of both the other groups (table III). hypertensive treatment comprising labetalol There were no significant differences in heart 400 mg three times a day orally and hydrallazine rate between labetalol-treated (la) and untreated i.m.; one received labetalol only, and one labetalol (Ib) patients, therefore their results have been and methyl dopa. combined. The pre-induction value was signifi-
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PIH untreated with labetalol, although the absolute values were obviously higher in the latter patients. The actual (as opposed to percentage) 2.6increase in MAP in group II closely resembled 2.4that reported by Millar-Forbes and Dally [13] for a similar induction technique in gynaecological patients. 2.0The increase in MAP on intubation in group Ib (30 mm Hg) was less than that reported by Hodgkinson, Husain and Hayashi (45 mm Hg) 1.6 [6], and by Connell, Dalgleish and Downing 1.4 (43 mm Hg) [7]. However, these workers used 1.2 direct intra-arterial monitoring and reported 1.0 increases from post-induction values and not preinduction as in this study, and this may explain the 0.8 discrepancy. We did not feel it justified to wait for 0.6 an indirect reading of arterial pressure between 0.4 induction and intubation and it is also possible that transient pressure peaks were missed using an 0.2 oscillotonometric method. Before induction Two other differences between this and Con3 5 nelPs study make comparison difficult: the After intubation (min) previous study included only severely affected FIG. 3. Mean (SEM) noradrenaline concentrations in groups ) and II (•)• *P < 0.05 within group comparison with patients, whereas only six of the nine patients in group I of our study were in this category, and our baseline. patients with PIH were mostly primiparous and of average age 28 yr, compared with more multicantly higher in group II, but thereafter there parae and a younger mean age (23.6 yr) in were no differences. Within both groups I and II, ConnelPs study. values at 1 and 3 but not 5 min after tracheal Patients in group la who had received oral intubation were significantly higher than before labetalol as antihypertensive treatment showed a induction (fig. 2). significantly reduced pressor response compared At 1 min after intubation there was a 28 % with both untreated hypertensives and normotenincrease in plasma concentration of noradrenaline sive controls. The fact that most of this group in group II, which was significant compared with were also in a severe category of PIH/prebaseline (fig. 3). There was a 33% increase in eclampsia makes this observation striking. noradrenaline concentration after 1 min in group Labetalol, a mixed alpha and beta-adrenergic I patients, but this was not significant. There were blocking agent, has become popular with obsteno significant differences between the groups in tricians for the treatment of PIH and is now the noradrenaline concentration at any study point, first-line treatment in our unit. Pure beta-blocking no significant changes in plasma concentration of drugs, for example metoprolol, given orally have adrenaline in each group and no differences been shown to attenuate hypertensive responses between groups. in non-pregnant patients undergoing general anaesthesia [14]. More recently, one oral dose of labetalol has been shown also to be effective [15]. DISCUSSION In contrast, i.v. practolol given immediately Although previous studies have described the before intubation seems to be ineffective, at least cardiovascular changes during general anaesthesia in normotensive subjects [16]. It is interesting to in patients with pre-eclampsia [6, 7] they have note that 60% of patients in ConnelFs series had not included a group of normotensive parturients received i.v. practolol, with obviously ineffective for comparison. We have demonstrated that the results [7]. percentage increase in MAP after intubation was Labetalol did not always prevent peaks of similar in healthy parturients and in patients with arterial pressure; one patient in group la had an 2.8-
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intubation. British Journal of Anaesthesia 1983; 55: 855-859. 3. Shribman AJ, Smith G, Achola KJ. Cardiovascular and catecholamine responses to laryngoscopy with and without tracheal intubation. British Journal of Anaesthesia 1987; 59: 295-299. 4. Prys-Roberts C, Greene LT, Meloche R, Foex P. Studies of anaesthesia in relation to hypertension II: Haemodynamic consequences of induction and endotracheal intubation. British Journal of Anaesthesia 1971; 43: 531-547. 5. Low JM, Harvey JT, Prys-Roberts C, Dagnino J. Studies of anaesthesia in relation to hypertension. VII: Adrenergic responses to laryngoscopy. British Journal of Anaesthesia 1986; 58: 471-477. 6. Hodgkinson R, Husain FJ, Hayashi RH. Systemic and pulmonary blood pressures during Caesarean section in parturients with gestational hypertension. Canadian Anaesthetists Society Journal 1980; 27: 389-393. 7. Connell H, Dalgleish J, Downing JW. General anaesthesia in mothers with severe pre-eclampsia/eclampsia. British Journal of Anaesthesia 1987; 59: 1375-1380. 8. Tunbridge RDG, Donnai P. Plasma noradrenaline in normal pregnancy and in hypertension of late pregnancy. British Journal of Obstetrics and Gynaecology 1981; 88: 105-108. In conclusion, our results indicate that there 9. Davey DA, Macnab MF. Plasma adrenaline, noradrenawas no quantitative difference in the pressor or line and dopamine in pregnancy hypertension. British Journal of Obstetrics and Gynaecology 1981; 81: 611. catecholamine response to intubation experienced by normotensive and untreated hypertensive 10. Pederson EB, Rasmussen AB, Christensen NJ, Johannesen P, Lauritsen JG, Kristensen S, Wohlert M. Plasma parturients, although the number of patients noradrenaline and adrenaline in pre-eclampsia, essential studied was relatively small. Our findings do not hypertension in pregnancy and normotensive control subjects. Ada Endocrinologica 1982; 99: 594-600. support the concept of vascular hyperactivity to pressor agents in pre-eclampsia which has been 11. Abboud T, Anal R, Sarkis F, Henriksen EH, Kammula RK. Sympathoadrenal activity, maternal, fetal, and neopropounded [19]. However, the potential clinical natal responses after epidural anesthesia in the preeffect of a surge in arterial pressure is much eclamptic patient. American Journal of Obstetrics and greater if the basal value is higher, as it is more Gynecology 1982; 144: 915-918. likely to exceed the upper limit of cerebral 12. Wright JP. Anesthetic considerations in pre-eclampsiaeclampsia. Anesthesia and Analgesia 1983; 63: 590-601. autoregulation. 13. Millar Forbes A, Dally FG. Acute hypertension during In view of the high proportion of deaths caused induction of anaesthesia and endotracheal intubation of by cerebral haemorrhage and oedema in hypernormotensive man. British Journal of Anaesthesia 1970; 42: 618-624. tensive diseases of pregnancy [20] and the known morbidity from intubation [21], it seems 14. Magnusson J, Thulin T, Werner O, Jarhult J, Thompson D. Haemodynamic effects of pre-treatment with metoprudent to attempt to limit the maximum MAP prolol in hypertensive patients undergoing surgery. after intubation to 130 mm Hg, the upper limit of British Journal of Anaesthesia 1986; 58: 251-260. autoregulation in man [22]. Labetalol given orally 15. Stone JG, Foex P, Sear JW, Johnson LL, Khambatta HJ, Triner L. Myocardial ischaemia in untreated hypertensive may be a useful agent to help attenuate hyperpatients: Effect of a single oral dose of a beta-adrenergic tensive responses to airway manipulation, but blocking agent. Anesthesiology 1988; 68: 495-500. its use requires more careful evaluation in a larger 16. Achola KJ, Jones MJ, Mitchell RWD, Smith G. Effects of number of patients. beta-adrenoceptor antagonism on the cardiovascular and catecholamine responses to tracheal intubation. Anaesthesia 1988; 43: 433-^136. REFERENCES 17. Lawes EG, Downing JW, Duncan PW, Bland B, Lavies NG, Gane GAC. Fentanyl-droperidol supplementation 1. Russell WJ, Morris RG, Frewin DB, Drew SE. Changes of rapid sequence induction in the presence of severe in plasma catecholamine concentrations during endopregnancy-induced and pregnancy-aggravated hypertentracheal intubation. British Journal of Anaesthesia 1981; sion. British Journal of Anaesthesia 1987; 59: 1381-1391. 53: 837-839. 2. Derbyshire DR, Chmielewski A, Fell D, Vater M, Achola 18. Shnider SM, Abboud T, Levinson G, Wright RG, Kim S, Henriksen E, Hughes SC, Roizen MF, Johnson J. K, Smith G. Plasma catecholamine responses to tracheal
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SAP greater than 200 mm Hg. An alternative or additional approach might be to use a rapidly acting potent opioid as part of the induction sequence; fentanyl has been found effective in this respect in severe pre-eclampsia [17]. Plasma concentrations of noradrenaline increased significantly 1 min after tracheal intubation in group II, and this has been found to occur in most studies of non-pregnant subjects. Shnider and colleagues [18] reported a 21 % increase in plasma concentration of noradrenaline following intubation in normotensive parturients having Caesarean section. This is comparable to our finding (28%), but, to our knowledge, catecholamine concentrations have not been reported previously in relation to tracheal intubation in pre-eclampsia. Although the increase in the PIH group was not significant because of large variability, it is likely that more patients would have yielded a significant result.
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General anesthesia for Cesarean section: maternal and fetal norepinephrine levels and neonatal neurobehavioural status. Anesthesiology 1980; 53: S302. 21. 19. Talledo OE, Chesley LC, Zuspan FP. Renin-angiotensin system in normal and toxemic pregnancies. American Journal of Obstetrics & Gynecology 1968; 100: 218-221. 22. 20. Department of Health and Social Security. Report on Confidential Enquiry into Maternal Deaths in England and
Wales, 1979-1981. London: Her Majesty's Stationary Office. Fox EJ, Sklar GS, Hill CH, Villanueva R, King BD. Complications related to the pressor response to endotracheal intubation. Anesthesiology 1977; 47: 524-525. Lassen NA, Christensen MS. Physiology of cerebral blood flow. British Journal of Anaesthesia 1976; 48: 719-734.
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