Anesthesia: Essays and Researches  Login  | Users Online: 790 Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
Home | About us | Editorial board | Ahead of print | Search | Current Issue | Archives | Submit article | Instructions | Copyright form | Subscribe | Advertise | Contacts


 
Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 11  |  Issue : 1  |  Page : 47-51  

Attenuation of cardiovascular response to direct laryngoscopy and intubation, comparative study of lignocaine, nifedipine, and placebo during general anesthesia


Department of Anaesthesia, NRI Medical College and Hospital, Guntur, Andhra Pradesh, India

Date of Web Publication16-Feb-2017

Correspondence Address:
Dr. Venkata Sesha Sai Krishna Manne
Saibaba Road, 4-21-5, Chaitanyapuri, Guntur - 522 007, Andhra Pradesh
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0259-1162.200227

Rights and Permissions
   Abstract 

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.

Keywords: Intubation, laryngoscopy, lignocaine, nifedipine


How to cite this article:
Manne VS, Paluvadi VR. Attenuation of cardiovascular response to direct laryngoscopy and intubation, comparative study of lignocaine, nifedipine, and placebo during general anesthesia. Anesth Essays Res 2017;11:47-51

How to cite this URL:
Manne VS, Paluvadi VR. Attenuation of cardiovascular response to direct laryngoscopy and intubation, comparative study of lignocaine, nifedipine, and placebo during general anesthesia. Anesth Essays Res [serial online] 2017 [cited 2022 Dec 5];11:47-51. Available from: https://www.aeronline.org/text.asp?2017/11/1/47/200227


   Introduction Top


Laryngoscopy and intubation are almost always associated with hemodynamic changes due to sympathetic discharge caused by epipharyngeal and laryngopharyngeal stimulation.[1],[2],[3]

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.[2],[4],[5] In healthy patients, these responses are generally well tolerated. Various attempts are made to block this stress response, but they are only partially successful.[6],[7],[8],[9],[10]

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.[11],[12],[13]


   Materials and Methods Top


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 Top


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

Click here to view


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

Click here to view


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

Click here to view


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

Click here to view


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 Top


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).[15],[16],[17],[18]

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.[10],[19],[20]


   Conclusion Top


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.

 
   References Top

1.
Forbes AM, Dally FG. Acute hypertension during induction of anaesthesia and endotracheal intubation in normotensive man. Br J Anaesth 1970;42:618-24.  Back to cited text no. 1
    
2.
Prys-Roberts C, Greene LT, Meloche R, Foëx P. Studies of anaesthesia in relation to hypertension. II. Haemodynamic consequences of induction and endotracheal intubation. Br J Anaesth 1971;43:531-47.  Back to cited text no. 2
    
3.
Reid LC, Brace DE. Irritation of the respiratory tract and its reflex effect upon heart. Surg Gynaecol Obstet 1940;70:157-62.  Back to cited text no. 3
    
4.
Masson AH. Pulmonary edema during or after surgery. Anesth Analg Curr Res 1964;43:440-51.  Back to cited text no. 4
    
5.
Braunwald E. Control of myocardial oxygen consumption: Physiologic and clinical considerations. Am J Cardiol 1971;27:416-32.  Back to cited text no. 5
    
6.
Stoelting RK. Attenuation of blood pressure response to laryngoscopy and tracheal intubation with sodium nitroprusside. Anesth Analg 1979;58:116-9.  Back to cited text no. 6
    
7.
Curran J, Crowley M, O'Sullivan G. Droperidol and endotracheal intubation. Attenuation of pressor response to laryngoscopy and intubation. Anaesthesia 1980;35:290-4.  Back to cited text no. 7
    
8.
Hamill JF, Bedford RF, Weaver DC, Colohan AR. Lidocaine before endotracheal intubation: Intravenous or laryngotracheal? Anesthesiology 1981;55:578-81.  Back to cited text no. 8
    
9.
Kautto UM. Attenuation of the circulatory response to laryngoscopy and intubation by fentanyl. Acta Anaesthesiol Scand 1982;26:217-21.  Back to cited text no. 9
    
10.
Fassoulaki A, Kaniaris P. Intranasal administration of nitroglycerine attenuates the pressor response to laryngoscopy and intubation of the trachea. Br J Anaesth 1983;55:49-52.  Back to cited text no. 10
    
11.
Pedersen OL, Mikkelsen E. Acute and chronic effects of nifedipine in arterial hypertension. Eur J Clin Pharmacol 1978;14:375-81.  Back to cited text no. 11
    
12.
Beer N, Gallegos I, Cohen A, Klein N, Sonnenblick E, Frishman W. Efficacy of sublingual nifedipine in the acute treatment of systemic hypertension. Chest 1981;79:571-4.  Back to cited text no. 12
    
13.
Moses JW, Wertheimer JH, Bodenheimer MM, Banka VS, Feldman M, Helfant RH. Efficacy of nifedipine in rest angina refractory to propranolol and nitrates in patients with obstructive coronary artery disease. Ann Intern Med 1981;94 (4 pt 1):425-9.  Back to cited text no. 13
    
14.
Stoelting RK. Circulatory changes during direct laryngoscopy and tracheal intubation: Influence of duration of laryngoscopy with or without prior lidocaine. Anesthesiology 1977;47:381-4.  Back to cited text no. 14
    
15.
Hodgkinson R, Husain FJ, Hayashi RH. Systemic and pulmonary blood pressure during caesarean section in parturients with gestational hypertension. Can Anaesth Soc J 1980;27:389-94.  Back to cited text no. 15
    
16.
Connell H, Dalgleish JG, Downing JW. General anaesthesia in mothers with severe pre-eclampsia/eclampsia. Br J Anaesth 1987;59:1375-80.  Back to cited text no. 16
    
17.
Lawes EG, Downing JW, Duncan PW, Bland B, Lavies N, Gane GA. Fentanyl-droperidol supplementation of rapid sequence induction in the presence of severe pregnancy-induced and pregnancy-aggravated hypertension. Br J Anaesth 1987;59:1381-91.  Back to cited text no. 17
    
18.
Miyake W, Oda Y, Ikeda Y, Tanaka K, Hagihira S, Iwaki H, et al. Effect of remifentanil on cardiovascular and bispectral index responses following the induction of anesthesia with midazolam and subsequent tracheal intubation. J Anesth 2010;24:161-7.  Back to cited text no. 18
    
19.
Guazzi M, Olivari MT, Polese A, Fiorentini C, Magrini F, Moruzzi P. Nifedipine, a new antihypertensive with rapid action. Clin Pharmacol Ther 1977;22 (5 Pt 1):528-32.  Back to cited text no. 19
    
20.
Reves JG, Kissin I, Lell WA, Tosone S. Calcium entry blockers: Uses and implications for anesthesiologists. Anesthesiology 1982;57:504-18.  Back to cited text no. 20
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]


This article has been cited by
1 Comparison of dexmedetomidine, lidocaine, magnesium sulfate, and remifentanil in cough suppression during endotracheal extubation: A double-blind, randomized clinical trial
Ehsan Jafarzadeh, Hesameddin Modir, Esmail Moshiri, Farzad Zamani Barsari, Amir Almasi-Hashiani
Bali Journal of Anesthesiology. 2022; 0(0): 0
[Pubmed] | [DOI]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
    Materials and Me...
    Observation and ...
   Discussion
   Conclusion
    References
    Article Tables

 Article Access Statistics
    Viewed2255    
    Printed44    
    Emailed0    
    PDF Downloaded136    
    Comments [Add]    
    Cited by others 1    

Recommend this journal