Attenuation of Hemodynamic Responses to Endotracheal Intubation: Comparison of Clonidine, Esmolol, Lignocaine and Placebo

2010 
INTRODUCTION: The hemodynamic responses to laryngoscopy and endotracheal intubation have been recognised since 1951. The induction of anaesthesia, laryngoscopy, tracheal intubation and surgical stimulation often evoke cardiovascular responses characterised by alteration in systemic arterial blood pressure, heart rate and cardiac rhythm1. The response following laryngoscopy and intubation peaks at 1.2 minutes and return to baseline within 5 to 10 minutes. Though the sympathoadrenal responses are probably of little consequence in healthy patients, it is hazardous to those patients with hypertension, coronary heart disease, cerebrovascular disease, intracranial pathology and hyperactive airways. In such cases, reflex circulatory responses such as an increase in heart rate, systemic arterial pressure and disturbances in cardiac rhythm need to be suppressed. Prof. King et al., (1951) documented myocardial ischemic changes due to reflex sympathoadrenal responses immediately following laryngoscopy and intubation with a mean increase in systolic pressure of 40mmHg even in normotensive individuals. Pyrs Roberts et al., (1971) showed exaggerated form of this response in hypertensive patients. Various systemic as well as topical agents have been used to reduce these untoward hemodynamic responses during laryngoscopy. When compared to systemic agents, administration of local anaesthetic solutions are likely to be of limited value. The commonest strategies adopted are narcotics, vasodilators, β-blockers, calcium channel blockers, lignocaine, clonidine and other sympatholytics. In our study, we have compared lignocaine, clonidine, esmolol and placebo in suppressing stress responses to laryngoscopy and intubation. Since clonidine, lignocaine3 and esmolol have been known to blunt sympathetic responses to intubation , their efficacy has been compared with control (placebo) in the Department of anaesthesiology, MMC (GGH), Chennai. AIM OF THE STUDY: For the safe conduct of anaesthesia, the hemodynamic responses to laryngoscopy and intubation should be abolished or at least attenuated to balance the myocardial oxygen supply and demand. This study was done to compare the efficacy of intravenous clonidine, esmolol, lignocaine and placebo in attenuating the hemodynamic stress responses to laryngoscopy and intubation. MATERIALS AND METHODS: One hundred and twenty patients of ASA physical status 1 or 2 undergoing elective surgical procedure under general anaesthesia with endotracheal intubation were included in this study. Patients belonging to age group 15 to 60 years of both the sexes were included. It is a prospective randomized controlled study. The study was approved by our institution ethical committee and after obtaining written, informed consent from the patient, this study was conducted. The study was done during the period from June 2009 to august 2009 in the Department of Anaesthesiology, Govt. General Hospital, Chennai. Inclusion Criteria: 1) ASA 1 or 2. 2) Patients with airway with modified mallampatti grade class 1 or 2 3) Age group 15 to 60 years of both sexes. Exclusion Criteria: 1. Patients with full stomach, 2. Patients posted for emergency surgery, 3. Patients with difficult airway, 4. Hypertension, diabetes, ischemic heart disease and pregnancy, 5. Patients with contraindications to study drugs, 6. Patient refusal. MATERIALS: 1. Injection thiopentone 2.5% solution, 2. Injection suxamethonium, 3. Injection glycopyrollate, 4. Injection fentanyl, 5. Injection esmolol hydrochloride( esocard) 100mg/10ml vial, 6. Injection ligocaine 2% (preservative free), 7. Injection clonidine 0.15mg/ml ampoule, 8. Normal saline, 9. Disposable 10 ml syringe, 10. Larynyngoscope with blades 3 and 4, 11. Endotracheal tubes of various sizes. SUMMARY: This prospective randomised study was designed to evaluate the efficacy of intravenous clonidine, esmolol, lidocaine and placebo in suppressing the hemodynamic changes during endotracheal intubation. A total of one hundred and twenty patients belonging to ASA 1 and 2 were randomly divided into four groups. Patients in group C received clonidine 2 mcg/kg, in group E received esmolol 1 mg/kg, in group L received lidocaine 1.5 mg/kg and in group P received normal saline two minutes prior to induction. The following observations were made: 1. Patients in group C showed the maximum attenuation of both heart rate and blood pressure following endotracheal intubation. 2. Patients in group E showed a significant attenuation of heart rate as effective as group C but attenuation of blood pressure (though effective than groups L and P) was not as effective as group C. 3. Patients in group L showed no significant difference from group P in attenuating circulatory responses and both lignocaine and placebo were ineffective. 4. All the patients were recovered well from anaesthesia and none of them developed complications like severe bradycardia( HR< 50/min) or profound hypotension (SBP < 80 mmHg). CONCLUSION: From the above study it is concluded that the hemodynamic changes associated with endotracheal intubation can be safely and effectively obtunded by using intravenous clonidine prior to induction of anaesthesia. Clonidine is found to be effective in blunting hemodynamic responses to laryngoscopy and intubation, followed by esmolol. Lignocaine and placebo were ineffective in attenuating these responses to laryngoscopy and endotracheal intubation.
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