Attenuation of Cardiovascular Response to Direct Laryngoscopy and Intubation, Comparative Study of Lignocaine, Nifedipine, and Placebo During General Anesthesia.

BACKGROUND/
OBJECTIVE: The purpose of the study was to compare the attenuation of cardiovascular response to direct laryngoscopy and intubation using lignocaine, nifedipine, and placebo during general anesthesia.
MATERIALS AND METHODS: This prospective study was done in sixty patients undergoing noncardiac surgeries of American Society of Anesthesiologists health status Class I and II between the age groups of 18-60 years. They were randomly divided into three groups of 20 each (lignocaine group, nifedipine group, and placebo group) and cardiovascular response (heart rate [HR] and blood pressure [BP]) to direct laryngoscopy and intubation were compared.
RESULTS: The rise in HR and BP was most significant in the placebo group and insignificant in lignocaine and nifedipine groups.
CONCLUSION: Nifedipine is effective than lignocaine in attenuating hypertensive response, and lignocaine is effective in attenuating rate pressure product than nifedipine.

RCT Entities:   Population Interventions Outcomes

INTRODUCTION

Laryngoscopy and intubation are almost always associated with hemodynamic changes due to sympathetic discharge caused by epipharyngeal and laryngopharyngeal stimulation.[123]

This stimulation is associated with an increase in plasma norepinephrine concentration. The circulatory perturbations consist of elevation in heart rate (HR), systolic blood pressure (BP) (Stoelting, 1978), pulmonary arterial pressure (Sorenson et al. 1977), and cardiac arrhythmias (anesthesia by Ronald D. Miller, 5th Edition, Vol. 1) which occasionally lead to myocardial ischemia, heart failure, and cardiovascular catastrophes (Fox et al., 1977) in susceptible patients.[245] In healthy patients, these responses are generally well tolerated. Various attempts are made to block this stress response, but they are only partially successful.[678910]

This response is undesirable and dangerous in patients with heart disease (limited coronary or myocardial reserve-myocardial ischemia or failure may follow), valvular heart disease, hypertension, cerebrovascular disease, intracranial vascular anomaly, abdominal aortic aneurysm, dissecting aortic aneurysm, pheochromocytoma, preeclamptic toxemia, etc.

The various methods used to suppress the cardiovascular response to laryngoscopy and intubation are systemic and topical local anesthetics, vasodilators such as nitroglycerine, sodium nitroprusside, isosorbide dinitrate, centrally acting drugs such as clonidine, and calcium channel blockers. No single agent has been established as the most appropriate drug of choice. Many studies have been done using a combination of drugs to suppress the pressor response to laryngoscopy. In our study, we used lignocaine and nifedipine separately to observe the cardiovascular response to laryngoscopy and intubation.

The use of lignocaine hydrochloride intravenous (IV) in treating arrhythmias after myocardial infarction is well established. Use of IV bolus followed by IV infusion of lignocaine hydrochloride to control ventricular tachycardia and arrhythmias both intraoperatively and intensive therapy is well known. It is a local anesthetic with membrane stabilizing action on cardiac muscle and thereby decreasing the cardiac excitabilities.

Nifedipine is a widely used calcium channel blocker with profound smooth muscle relaxant properties thereby reducing BP. It is rapidly absorbed by sublingual route which is simple, economical, noninvasive method of controlling BP.[111213]

MATERIALS AND METHODS

The present study was done to evaluate the efficacy of IV lignocaine and sublingual nifedipine against each other and against placebo in attenuating stress response induced (rise of BP and HR) during direct laryngoscopy and intubation.

Sixty patients undergoing noncardiac surgeries of American Society of Anesthesiologists (ASA) health status Class I and II between the age groups of 18–60 years and comparable height and weight were selected for this study. Patients were randomly divided into three groups of twenty each (Groups 1, 2, and 3).

Group 1 - Placebo

Group 2 - Lignocaine

Group 3 - Nifedipine.

All patients were normotensive and had a normal HR, electrocardiogram (ECG), hemoglobin, and electrolytes preoperatively.

The procedure to be undertaken was explained and informed consent obtained from all patients and randomly assigned to receive a preinduction dose of either normal saline, lignocaine 1.5 mg/kg IV, or sublingual nifedipine 10 mg.

Exclusion criteria: HR of <60 bpm and systolic BP of <100 mm of Hg; the presence of first, second, or third degree heart block; congestive heart failure, myocardial ischemia within the previous 6 months; history of bronchospastic disease or asthma; hepatic or renal disease; ingestion of beta-blocking drugs in the past 24 h.

Demographic data included age, sex, weight, and ASA physical status were recorded.

After proper preanesthetic checkup, following premedication was given:

Injection midazolam 0.1 mg/kg (intramuscularly)

Injection glycopyrrolate 0.2 mg IV

Injection tramadol HCl 2 mg/kg IV.

Study medication was administered; normal saline 5 ml, 1 min before; IV lignocaine 1.5 mg/kg, 90 s before; sublingual nifedipine 10 mg, 15 min before induction of anesthesia.

The arterial pressure was recorded by Korotkoff method using a sphygmomanometer and basal HR by means of a pulse oximeter and it is designated as preinduction basal values (before administering study medication).

Patients were preoxygenated with 100% O2 for 3 min and were induced with thiopentone 5 mg/kg and succinylcholine 1.5 mg/kg. Direct laryngoscopy and endotracheal intubation were performed 90 s after time 0. Anesthesia was maintained with N2O 50% and oxygen 50%. Neuromuscular blockade was achieved with pancuronium 0.1 mg/kg.

HR and BP were monitored by pulse oximeter and BP every 1 min for 5 m from 0 time and designated as T0, T1, T2, T3, T4, and T5, respectively.

Surgery was not commenced on any patient until the study protocol was completed. Any deleterious cardiovascular events were noted.

Parametric data including weight, baseline HR, and arterial pressure were compared using unpaired Student's t-test. Changes in HR and arterial pressure were analyzed using unpaired Student's t-test. A significant level of P < 0.05 was chosen.

OBSERVATION AND RESULTS

Sixty normotensive, healthy adult patients of ASA health status Class I and II belonging to both sexes and undergoing elective noncardiac surgery were studied. They were randomly divided into three groups comprising twenty patients each.

Anthropometric details of three groups:

Table 1 shows the demographic data of the patients.

Table 1

Demographic data

The majority of the patients were in the range of 41–60 years in all the groups.

In the control group, the mean age of the patient was 37.9, whereas it was 37–85 years in Group 2 and 31.65 years in Group 3.

The mean weight of the patient was 51.55 kg in Group 1, 51.15 in Group 2, and 49.35 in Group 3. There was no significant difference between the three groups in age, sex, and weight.

The changes in HR are given in Table 2. The baseline HR in all the groups was comparable among the three groups.

Table 2

Heart rate values

The mean HR before induction was 87.2/min in Group 1, 93.65/min in Group 2, and 87.15/min in Group 3 (values before administering study drugs).

HRs increased after administering 10 mg of sublingual nifedipine from basal mean value of 87.12–108.7.

At time 0, there was most highly significant rise of HR observed in Group 1 and 3, and highly significant rise in Group 2.

At 1 min, HRs were a most highly significant rise in Group 1 and 3, whereas a significant rise in Group 2.

At 3 min, the rise in HRs in Group 1 and 3 was most highly significant and insignificant in Group 2, the values being 102 in Group 1, 95.1 in Group 2, and 107.25 in Group 3.

At 4 min, the HRs were a most highly significant rise in Group 1, a significant rise in Group 3, and insignificant in Group 2.

At 5 min, HRs were most highly significant in Group 1 and insignificant in Group 2 and 3.

Table 3 shows the mean arterial pressure (MAP) values.

Table 3

Mean arterial pressure values

Basal MAP values (93.3 in Group 1, 94.4 in Group 2, and 89.2 in Group 3) in three groups are statistically comparable.

At 0 min, the mean MAP values were most highly significant in all the groups.

At 1 min, the mean MAP values were most highly significant in all the groups.

At 2 min, the changes in MAP values in Group 1 and 2 were most significant and highly significant in Group 3.

At 3 min, most highly significant rise was seen in Group 1, significant rise in Group 2, and insignificant change in Group 3 were observed.

At 4 min, highly significant rise in MAP was observed in Group 1, whereas insignificant changes were seen in Group 2 and 3.

At 5 min, a significant rise in MAP was observed in Group 1 and insignificant changes in Group 2 and 3.

Changes in rate pressure products (RPPs) are shown in Table 4.

Table 4

Rate pressure product values

Basal mean RPP values are 10,627.2 in Group 1 with standard deviation (SD) of 1396.94; 11,312.9 in Group 2 with SD of 1352.75; and 10,245.4 in Group 3 with SD of 744.05.

At the time of intubation, mean RPP in Group 1 was 17,330 with SD of 2198.8, 14,765.5 in Group 2 with SD of 2014.64, and 14,872.7 in Group 3 with SD of 863.67. There is most highly significant use in all the three groups.

At 1 min after intubation, the mean RPP values were most highly significant use in the three groups.

At 2 min after intubation, mean RPP values were most highly significant use in Group 1 and 3 and significant change in Group 2.

At 3 min after intubation, mean RPP values were most highly significant change in Group 1 and 3 and significant change in Group 2.

At 4 min after intubation, the mean RPP values were most highly significant use in Group 1, highly significant rise in Group 3, and insignificant use in Group 2 were observed.

At 5 min after intubation, the mean RPP values were showing most highly significant rise in Group 1 and insignificant rise in Group 2 and 3.

DISCUSSION

Reflex cardiovascular responses to laryngoscopy and intubation are tachycardia and hypertension were first reported by King (1951). There is a positive increase in sympathoadrenal activity and definite increase in plasma adrenaline, noradrenaline, and dopamine levels in patients undergoing endotracheal intubation.[14]

The magnitude of change of clinical parameters in MAP and cardiac rhythm paralleled the significant increase in catecholamines – Russell et al. (1981).

These reflex responses are a potential cause for increased morbidity and mortality during anesthesia.

These complications include pulmonary edema, cardiac failure and cerebrovascular accidents (Fox et al. 1977), abnormal rhythms (Burnstein et al., 1950, and Kunneral, 1967), and myocardial ischemia (Prys-Roberts, 1971).[15161718]

Pressure by the laryngoscope blade on the deep tissues adjacent to the epiglottis probably contributed to the ECG changes (Tukeshima et al. 1964).

Sympathetic reflex provoked by stimulation of the epipharynx and laryngopharynx (Tomosi and Widdicombe 1969).

Hypertensive response to laryngoscopy can be significantly decreased by simple lignocaine spray (Masson and Eckon Hoff 1971). However, spraying of laryngopharynx is difficult in awake patients without laryngoscopy. Hence, in our study lignocaine was administered intravenously.

IV lignocaine also produces a central sedative effect and suppresses the cough reflex. The membrane stability action of lignocaine prevents the occurrence of dysrhythmics potentiate the action of inhalation anesthetics and neuromuscular blocking drugs and thus becomes a good adjunct to the balanced anesthesia.

An attempt was made in this study to alternate the reflex cardiovascular responses using lignocaine intravenously and nifedipine sublingually.

The effect of nitroglycerine ointment in attenuating pressor response during laryngoscopy was studied by Karma, Wig, Sapra (1986). They proved that the maximum rise in systolic BP was significantly lower than the control group. However, in our study, the rise in MAPs was significantly lower than the control group.

The effect of IV lignocaine on pressor response to laryngoscopy in normotensive patients was studied by Arrixica, Murica et al. (1981) proved that lignocaine significantly attenuated the response. Similar response was also noted in our study.

The results of the present study showed that both drugs are effective in attenuating cardiovascular response to laryngoscopy and intubation, which in other studies showed a similar type of response.[101920]

CONCLUSION

In our study, the comparative study of two drugs regarding their clinical efficacy in attenuating hemodynamic responses following laryngoscopy and intubation lignocaine is effective in attenuating RPP, whereas nifedipine is effective in attenuating MAP.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.