EFFECT OF LARYNGOSCOPY AND INTUBATION ON PLASMA CATECHOLAMINE LEVELS DURING INTRAVENOUS INDUCTION OF ANAESTHESIA

Transcription

1 Brit. J. Anaesth. (1972), 44,1323 EFFECT OF LARYNGOSCOPY AND INTUBATION ON PLASMA CATECHOLAMINE LEVELS DURING INTRAVENOUS INDUCTION OF ANAESTHESIA S. TAKKI, T. TAMMISTO, P. NIKKI AND A. JAATTELA SUMMARY The effect of laryngoscopy and the introduction of a bronchography tube on blood pressure, heart rate, rhythm and plasma catecholamines was studied in 30 patients during three different modes of anaesthesia induction (thiopentone 5 mg/kg followed by suxamethonium 1 mg/kg, propanidid 7 mg/kg followed by suxamethonium 0.2 mg/kg and propanidid 10 mg/kg). Laryngoscopy and intubation caused an increase in systolic blood pressure in all groups, although the increase was not statistically significant after propanidid alone. Levels of total plasma catecholamines, measured during and two minutes after laryngoscopy, remained unchanged in all groups. The preanaesthetic content of noradrenaline as a percentage of total catecholamines was higher in those patients who developed a more marked increase in blood pressure during laryngoscopy and intubation. In man laryngoscopy and endotracheal intubation cause tachycardia and arterial hypertension. These changes have been assumed to depend on increased cardiac output (Prys-Roberts et al., 1971). Reflex cardiovascular responses to mechanical stimulation of the upper respiratory tract have been described in cats also (Tomori and Widdicombe, 1969). These authors observed that the responses were associated with enchanced neuronal activity in the cervical sympathetic efferent fibres. It has been suggested that in man, too, these responses may depend on sympathetic overactivity, and specific beta-adrenergic blocking agents have therefore been recommended to inhibit this increased cardiac overactivity in hypertensive patients (Prys-Roberts et al., 1971). In the present study we compared the cardiovascular changes caused by three different types of anaesthesia induction to changes in plasma catecholamine levels. The three modes of induction were: propanidid followed by suxamethonium, propanidid alone, and thiopentone followed by suxamethonium. METHODS There were 30 adult patients scheduled for bronchography. Table I shows their distribution between the three treatment groups. The general condition of the patients was good, and their cardiovascular function was normal as shown by clinical and X-ray examinations and electrocardiography (12 leads). All the patients received the same preanaesthetic medication of atropine 0.01 mg/kg and pethidine 1 mg/kg by intramuscular injection. The measurements were performed in the induction room. The largest accessible vein was cannulated and a slow infusion of 10% invert sucrose started. Once cardiovascular stability had been achieved (three consecutive similar readings of blood pressure and heart rate) control blood samples were taken. At time zero the anaesthesia was induced either with thiopentone 5 mg/kg followed by suxamethonium 1 mg/kg, or with propanidid 7 mg/kg followed by suxamethonium 0.2 mg/kg, or with propanidid 10 mg/kg alone. The drugs were injected through the side arm of the drip over 60 sec. When suxamethonium was used it was injected immediately after the anaesthetic and ventilation was assisted and then controlled by manual ventilation with a facepiece at a rate of b.p.m. using oxygen 8 l./min. At about the 3rd minute, a curved blade laryngoscope was inserted, the larynx and trachea were sprayed with 2 ml of 4% lignocaine solution and then a thin bronchography tube was passed. Lignocaine gel (Xylocaine) was used to lubricate the tube. The tube was passed by the same anaesthetist (T.T.) on all occasions, and the laryngoscopy was standardized to last 30 sec. The reactions of patients during intuba- S. TAKKI, M.D.; T. TAMMISTO, M.D.; P. NIKKI, M.D.; A. JAATELLA, M.D.; Department of Anaesthesia, Helsinki University Central Hospital, and Department of Pharmacology, University of Helsinki, Helsinki, Finland,

2 1324 BRITISH JOURNAL OF ANAESTHESIA Induction agents TABLE I. Age, sex and weight distributions of the three treatment groups. Pulse Systolic Diastolic rate Age Sex Weight pressure pressure (beats (yr) M/F (kg) (mm Hg) (mmhg) min) Thiopentone 5 ing/kg+ suxamethonium 1 mg/kg / ± ±5.21 Propanidid 7 mg/kg+ suxamethonium 0.2 mg/kg 40.0±5.62 5/ Propanidid 10 mg/kg /5 64.4± Systolic and diastolic blood pressures and pulse rates before the treatment are shown. Mean values with SE. tion were recorded. After intubation, IPPV was continued at a rate of b.p.m. until consciousness returned. The patients then breathed spontaneously for as long as the recording period continued. Blood pressure and pulse rate were measured by auscultation before and at 1, 2, 3, 4, 5, 7, 9, 13 and 15 min after induction. Lead II of the electrocardiogram was recorded continuously. Micro-Astrup analysis of the capillary blood was performed before anaesthesia and immediately after awakening. Blood samples for catecholamine measurements were collected from the cannulated cubital vein as described in detail in a previous paper (Tammisto et al., 1971), before induction, at the time of laryngoscopy and about 2 minutes later. Catecholamine determinations The details of the technique used for quantitative determination of adrenaline (A) and noradrenaline (NA) in the plasma were the same as in the previous paper (Tammisto et al., 1971). The method was based on the principles described by Vendsalu (1960). Propanidid 7 mg/kg + Suxamethonium 0.2mg/kg x Propanidid 10 mg/kg Thiopentone 5 mg/kg + Suxamethonium t mg/kg «FIG. 1. The change in arterial systolic and diastolic pressure and heart rate in the three different treatment groups. Mean±SE U 15

3 EFFECT OF LARYNGOSCOPY AND INTUBATION 1325 RESULTS The data are presented in three ways. First a comparison of the circulatory responses and catecholamine changes between the three different modes of induction is made. Figure 1 shows the mean values of heart rate and blood pressure curves in the three different treatment groups. In all groups there was an initial decrease in systolic pressure, which in the propanidid groups amounted to and mm Hg (SE) during the first minute after induction. In the thiopentone group the decrease was less, amounting to mm Hg (SE). At 2 minutes an increase in arterial pressure was seen in every treatment group. This reached its maximum in all groups 3-4 min after induction, thus corresponding to the time of laryngoscopy and intubation. The mean maximum increase in systolic pressure amounted to 31 ±11 (SE) mm Hg (P<0.02) above the preanaesthetic level in the thiopentone-suxamethonium group, to mm Hg (P<0.001) in the propropanidid-suxamethonium group and to (P>0.05) in propanidid group. Thereafter the arterial pressure fell progressively in all groups. It remained slightly above the conscious control level in the propanidid groups but fell to a mean value of 7 mm Hg below the control level in the thiopentone group. Diastolic pressure changes were similar but slightly less. The increase in heart rate seemed to be more marked in the propanidid groups. The mean maximum increase was recorded at the time of laryngoscopy except after the higher dose (10 mg/kg) of propanidid, where the maximum increase ( (SE) beats/min, P<0.01) occurred before laryngoscopy. In the thiopentone-suxamethonium group the mean maximum increase amounted to 15+4/min (P<0.01) and in the propanidid-suxamethonium group to /min (P<0.01). Differences between the groups did not, however, take on statistical significance. Isolated ventricular extrasystoles were seen during laryngoscopy in two patients after propanididsuxamethonium and in one patient after propanidid. After thiopentone-suxamethonium nodal rhythm or wandering pacemaker were seen in three patients. Plasma catecholamine levels before the treatment are shown in table II. There were no statistically significant changes in the catecholamine levels of the three different groups. Thus the mean values of the catecholamines did not correlate with the changes in blood pressure or pulse rate. Secondly, the behaviour of catecholamines in relation to the extent of circulatory response was analysed in each induction group. For this purpose the patients in each treatment group were divided into two subgroups according to the increase in systolic blood pressure above or below the median increase of the group during intubation. The comparison of catecholamine changes measured in the fourth blood sample, taken about 2 min after intubation, was made between the two subgroups in each treat- TABLE II. Plasma catecholamine levels before the treatment are shown. Catecholamines 0*g/l.) Induction agents NA + A NA Thiopentone 5 mg/kg+suxamethonium 1 mg/kg 0.98± Propanidid 7 mg/kg+suxamethonium 0.2 mg/kg 0.86± ± Propanidid 10 mg/kg 1.02± ± Mean values with SE. TABLE III. Change in plasma catecholamine levels (ng/l.)±se after different modes of induction in patients with an increase in systolic blood pressure above or below the median increase during laryngoscopy and intubation. above the median increase Change in plasma catecholamines (jug/l.) below the median increase Induction agents NA + A NA NA + A NA Thiopentone 5 mg/kg + suxamethonium 1 mg/kg Propanidid 7 mg/kg + suxamethonium 0.2 mg/kg Propanidid 10 mg/kg ± ± ± ±

4 1326 BRITISH JOURNAL OF ANAESTHESIA ment group. As seen in table HI, there were no appreciable differences between the subgroups except in the propanidid group. In this group there was an increase in adrenaline and decrease in noradrenaline in those patients who responded to laryngoscopy and intubation with an increase in systolic blood pressure above the median increase, whereas adrenaline and noradrenaline appeared to fluctuate in the opposite way in the other subgroup. The difference between changes in the adrenaline level between the subgroups receiving propanidid alone is statistically significant (P<0.05). Thirdly a comparison was made between the preanaesthetic catecholamine levels in the subgroups. Table IV lists the total catecholamine levels and the percentage content of adrenaline and noradrenaline of these subgroups before treatment. Those patients who responded to laryngoscopy and intubation with an increase in systolic blood pressure above the median increase in the groups showed in the thiopentone and propanidid groups higher levels of total catecholamines with a higher percentage content of noradrenaline in all groups than those whose response was below the median increase. The results of blood-gas analysis performed before and after anaesthesia revealed no significant differences. Coughing and straining during laryngoscopy or after intubation were noted in 8 patients after propanidid followed by suxamethonium, in 7 patients after propanidid but in only 3 patients after thiopentone followed by suxamethonium. Vomiting occurred once in the propanidid group. Three patients had signs of residual neuromuscular block after propanidid-suxamethonium at the time of awakening. DISCUSSION Tachycardia and hypertension are well documented complications of laryngoscopy and tracheal intubation in normal patients (Reid and Brace, 1940; Burstein, LoPinto and Newman, 1950; King et al., 1951; Takeshima, Noda and Higaki, 1964; Forbes and Dally, 1970). This phenomenon has been studied in detail in cats by Tomori and Widdicombe (1969), who found it to be associated with an increased impulse traffic in the cervical sympathetic efferent fibres. This nervous activity was especially increased by the stimulation of the epipharyngeal and laryngopharyngeal regions, and was accompanied by the largest hypertensive response. Beside this finding the authors assume that the hypertension could be a result of the release of catecholamines by adrenals. This mechanism does not seem to have been studied in man. In the present study a statistically significant increase in systolic blood pressure occurred immediately after intubation in the thiopentone-suxamethonium and the propanidid-suxamethonium groups. In the thiopentone group the increase in systolic blood pressure on average reached mm Hg (SE) from the awake level. This agrees with data from other studies in normal patients (Takeshima, Noda and Hegaki, 1964; Forbes and Dally, 1970) and in hypertensive patients (Prys-Roberts, Meloche and TABLE IV. Preanaesthetic plasma catecholamines (i'g/l.)±se after different modes of induction in patients with an increase in systolic blood pressure above or below the median increase during the procedure. above the median increase Preanaesthetic plasma catecholamines O'g/1.) below the median increase Induction agent NA + A NA NA + A NA Thiopentone 5 mg/kg + suxamethonium 1 mg/kg Propanidid 7 mg/kg + suxamethonium 0.2 mg/kg Propanidid 10 mg/kg ± ± ± ±0.20 (76.4±7.65%) (23.6±7.65%) 0.57±0.10 (76.5 ±8.35%) 0.22± ( %) 1.05 ± ±0.15 (69.8±15.5%) (3O.2±15.5%) 0.39± (60.2±16.14%) (39.8±16.14%) 0.39 ±0.14 (38.6 ±8.60%) The percentages ± SE refer to proportion of the total catecholamines (61.4 ±8.60%) 0.27 ± (45.2±12.03%) (54.8±12.03%)

5 EFFECT OF LARYNGOSCOPY AND INTUBATION 1327 Foex, 1971) but is less than that reported for patients with mitral stenosis (Dottori, Lof and Ygge, 1970). After propanidid and suxamethonium, laryngoscopy caused a circulatory response similar to that after thiopentone and suxamethonium. The finding that the increase in systolic blood pressure after propanidid alone was not statistically significant is probably accounted for by the deeper level of anaesthesia, since the dose of propanidid in this group was 10 mg/kg as against 7 mg/kg in the propanididsuxamethonium group. This finding supports the suggestion that a deeper level of anaesthesia before endotracheal intubation in patients with cardiovascular disease is beneficial (King et al., 1951). Since the laryngoscopy and intubation procedures were standardized and performed by the same anaesthetist in all cases, the stimulation was probably similar in all groups. The role played by suxamethonium is difficult to assess. Takeshima, Noda and Higaki (1964) did not observe an increase in blood pressure when injection of suxamethonium was not followed by intubation, but opposing suggestions have been put forward (Koelle, 1970). Since propanidid prolongs the action of suxamethonium (Clarke, Dundee and Daw, 1964), suxamethonium was here used in a smaller dosage after propanidid than after thiopentone. Despite similar circulatory responses observed in these groups coughing and straining were more marked after propanidid. However, residual neuromuscular block was seen in 3 patients after propanidid-suxamethonium. This supports the suggestion of Clarke (1969) that propanidid should be avoided when suxamethonium is also given without nitrous oxide supplementation. No other factors that may possibly modify the hypertensive reaction such as hypoxia or hypercarbia seem to be involved, since the patients' lungs were ventilated with oxygen and there were no changes in blood-gas values. We did not find an increase in total catecholamine levels, although the samples were collected both during and 2 minutes after the maximum increase in blood pressure. On the grounds of the animal experiments (Tomori and Widdicombe, 1969) this might be explained by assuming that the increased sympathetic activity of cervical efferents is regionally too limited to be reflected by increase in catecholamine levels in the general circulation. On the other hand, general sympathetic stimulation has also been assumed (Tomori and Widdicombe, 1969). Here the lack of increase in catecholamines may be due to inaccuracies in the determination method. This explanation is not supported by the results of previous studies (Tammisto et al., 1971), in which parenterally administered adrenaline and noradrenaline (0.25 /ig/kg) each caused a pressure response similar to that found here and a demonstrable increase in plasma catecholamine levels. Pentazocine 1.2 mg/kg i.v. also caused a similar pressure response, associated with an increase in catecholamine levels. The significance of the varying percentage content of adrenaline and noradrenaline found in the subgroups remains unclear. It might suggest that the behaviour of the blood pressure during induction depends on the initial ratio of adrenaline to noradrenaline, but more detailed studies are required to support this view. REFERENCES Burstein, C. L., Lo Pinto, F. J., and Newman, W. (1950). Electrocardiographic studies during endotracheal intubation. I: Effects during usual routine techniques. Anesthesiology, 11, 224. Clarke, R. S. J. (1969). The eugenols propanidid. Int. Anesth. Clin., 7, 43. Dundee, J. W., and Daw, R. H. (1964). Clinical studies of induction agents. XI: The influence of some intravenous anaesthetics on the respiratory effects and sequelae of suxamethonium. Brit. J. Anaesth., 36, 307. Dottori, O., L6f, B. A., and Ygge, H. (1970). Heart rate and arterial blood pressure during different forms of induction of anaesthesia in patients with mitral stenosis and constrictive pericarditis. Brit. J. Anaesth., 42, 849. Forbes, A. M., and Dally, F. G. (1970). Acute hypertension during induction of anaesthesia and endotracheal intubation in normotensive man. Brit. J. Anaesth., 42, 618. King, B. D. ; Harris, L. C. jr, Greifenstein, F. E., Elder, J. D., and Dripps, R. D. (1951). Reflex circulatory responses to direct laryngoscopy and tracheal intubation performed during general anesthesia. Anesthesiology, 12, 556. Koelle, G. B. (1970). Neuromuscular blocking agents; in The Pharmacological Basis of Therapeutics (eds. Goodman. L. S., and Gilman, A.), 4th edn., p New York: Macmillan. Prys-Roberts, C, Greene, L. T., Meloche, R., and Foex, P. (1971). Studies on anaesthesia in relation to hypertension. II: Haemodynamic consequences of induction and endotracheal intubation. Brit. J. Anaesth., 43, 531. Meloche, R., and Foex, P. (1971). Studies of anaesthesia in relation to hypertension. I: Cardiovascular responses of treated and untreated patients. Brit. J. Anaesth., 43, 122. Reid, L. C, and Brace, D. E. (1940). Irritation of the respiratory tract and its reflex effect upon the heart. Surg. Gynec. Obstet., 70, 157. Takeshima, K., Noda, K., and Higaki, M. (1964). Cardiovascular response to rapid anesthesia induction and endotracheal intubation. Anesth. Analg. Curr. Res., 43, 201.

6 1328 BRITISH JOURNAL OF ANAESTHESIA Tammisto, T., Jaattela, A., Nikki, P., and Takki, S. (1971). Effect of pentazocine and pethidine on plasma catecholamine levels. Ann. Clin. Res. 3, 22. Tomori, Z., and Widdicombe, J. G. (1969). Muscular, bronchomotor and cardiovascular reflexes elicited by mechanical stimulation of the respiratory tract. J. Physiol. (Lond.), 200, 25. Vendsalu, A. (1960). Studies on adrenaline and noradrenaline in human plasma. Acta physiol. scand., 49, Suppl EFFETS ENGENDRES PAR LA LARYNGOSCOPIE ET L'INTUBATION TRACHEALE SUR LE TAUX DES CATECHOLAMINES PLASMATIQUES AU COURS D*UNE INDUCTION ANESTHESIQUE PAR VOIE INTRAVEINEUSE SOMMARE Les effets engendre's par la laryngoscopie et l'introduction d'un tube en vue d'une bronchographie, sur la pression sanguine, la frequence et le rythme cardiaque, ainsi que sur le taux des catecholamines plasmatiques, ont it etudies chez trente malades, au cours de trois types diff6rents d'induction anesthe'sique: administration de thiopentone (5 mg/kg) suivie de celle de suxamethonium (1 m g/kg)> administration de propanidide (7 mg/kg) suivie de celle de suxamethonium (0,2 mg/kg), et administration de propanidide seule (10 mg/kg). La laryngoscopie et l'intubation tracheale ont entraine dans toutes les series une augmentation de la pression art^rielle systolique, bien que cet accroissement tensionnel n'ait pas h.6 statistiquement significatif apres administration de propanidid seule. Dans tous les groupes, le taux des catecholamines plasmatiques totales, mesure au cours de la laryngoscopie et deux minutes apres celle-ci, n'a present^ aucune modification. Le taux preanesthe'sique de noradrenaline, exprim en pourcentage par rapport au taux des catecholamines totales, a 6t6 plus elevd chez les malades ayant accus6 une elevation tensionnelle plus marquee au cours de la laryngoscopie et de 1'intubation tracheale. WIRKUNG VON LARYNGOSKOPIE UND INTUBATION AUF DIE PLASMAKATECHOLAMINSPIEGEL WAHREND INTRAVEN6SER NARKOSEEINLEITUNG ZUSAMMENFA SSUNG Die Wirkung der Laryngoskopie und der Einfiihrung eines Bronchographie-Katheters auf Blutdruck, Herzfrequenz, Herzrhythmus und Plasmakatecholamine wurde an 30 Patienten wahrend drei verschiedener Arten der Narkoseeinleitung (Thiopental mg/kg, anschlieffcnd Suxamethonium 1 mg/kg; Propanidid 7 mg/kg, anschliefiend Suxamethonium 0,2 mg/kg; Propanidid 10 mg/kg) untersucht. Die Larnygoskopie und Intubation verursachten einen Anstieg des systolischen Blutdrucks in alien Gruppen, obgleich der Anstieg nach Propanidid allein nicht statistisch signifikant war. Die wahrend und 2 Minuten nach der Laryngoskopie gemessenen Spiegel der Gesamtkatecholamine im Plasma blieben in alien Gruppen unverandert. Der Noradrenalingehalt vor Narkose als prozentualer Ausdruck der Gesamtkatecholamine war bei denjenigen Patienten hoher, die wahrend der Laryngoskopie und Intubation einen ausgepragteren Blutdruckanstieg entwickelten. EFECTO DE LA LARINGOSCOPIA E INTUBACION SOBRE LOS NIVELES DE CATECOLAMINAS EN EL PLASMA DURANTE LA INDUCCION INTRA- VENOSA DE LA ANESTESIA RESUMEN Fue estudiado en treinta pacientes el efecto de la laringoscopia e introduction de un tubo de broncografia sobre la presion arterial, frecuencia cardiaca, ritmo y catecolaminas del plasma durante tres modos diferentes de inducci6n anestesica (5 mg de tiopentona/kg seguidos por 1 mg de suxametonio/kg, 7 mg de propanidid/kg seguidos por 0,2 mg/de suxametonio/kg y 10 mg de propanidid/kg). La laringoscopia e intubacidn causaron un incremento de la presi6n arterial sistolica en todos estos grupos, aunque el incremento no era estadisticamente significativo despues de propanidid solo. Los niveles de las catecolaminas totales del plasma, medidos durante y dos minutos despues de la laringoscopia, permanecieron sin cambio en todos los grupos. El contenido preanestesico de noradrenalina como porcentaje de catecolaminas totales fue ma's elevado en los pacientes que desarrollaron un incremento mas acusado de la presion arterial durante la laringoscopia e intubation.