Attenuation of Haemodynamic Responses to Laryngoscopy & Intubation following Nitroglycerin and Esmolol infusion
P Gupta, B Panda, R Verma, P Ranjan, S Mathur, G Sinha
esmolol, hemodynamic response: intubation, nitroglycerin
P Gupta, B Panda, R Verma, P Ranjan, S Mathur, G Sinha. Attenuation of Haemodynamic Responses to Laryngoscopy & Intubation following Nitroglycerin and Esmolol infusion. The Internet Journal of Anesthesiology. 2009 Volume 22 Number 2.
In 1940, Reid and Brace1 first described hemodynamic response to laryngoscopy and intubation. Laryngoscopy and tracheal intubation are known to cause sympathoadrenal stimulation. This manifests as hypertension and tachycardia. Usually these transient changes have no deleterious consequences in healthy individual, but in some patients they can provoke left ventricular failure, myocardial ischemia and cerebral hemorrhage2,3. These complications are more likely to occur in the presence of coronary or cerebral atheroma or pre-existing hypertension4. The present study was conducted to study the efficacy of intravenous infusions of nitroglycerin and esmolol in attenuating these responses.
Materials and methods
Group C - Normal saline infusion (control group)
Group E - Esmolol hydrochloride infusion 100 g/kg/min
Group N - Nitroglycerin infusion 0.5 g/kg/min
All patients were premedicated with alprazolam 0.5 mg two hours before operation. On arrival in the operation theatre patients’ baseline heart rate, systolic, diastolic and mean blood pressures were recorded and 0.2 mg glycopyrrolate and 0.5 mg/kg of pentazocine were administered intravenously. The infusion of normal saline/ study drug was started. The induction was done with thiopentone sodium 1-2 mg/kg and neuromuscular blockade was achieved by succinylcholine 1.5 mg/kg. Direct laryngoscopy was done and tracheal intubation was completed within 30 sec in all the patients. Serial measurement of heart rate, systolic blood pressure, diastolic blood pressure and mean arterial pressure were done with a bioview monitor. The infusion (study drug/ saline) was stopped 5 minutes after intubation. Anaesthesia was maintained with 66% nitrous oxide in oxygen and vecuronium bromide. Data was analyzed by Chi square test and Students‘t’ test as applicable.
The three groups were comparable with respect to age, weight and gender (Table 1).
No significant difference in mean age, weight and sex ratio in the three groups
Haemodynamic changes before and after intubation are shown in tables 2 - 5. Heart rate increased significantly in group C, 1 min after intubation (p < 0.01) and increased further 3 and 4 min after intubation (p < 0.001). In group N the heart rate increased one minute after intubation and continued to increase at subsequent intervals. The increase was statistically significant 3, 4 and 5 minutes after intubation (p < 0.05). In group E the changes in heart rate following intubation were statistically not significant (fig 1).
Five minutes after the start of infusion and just before intubation systolic blood pressure decreased in all the three groups but the change was statistically significant in group N (p<0.05) and group E (p<0.01). Following intubation it increased significantly, 1, 3 and 5 minutes after intubation in group C (p<0.001) and 3 and 5 minutes after in group N (p<0.01 and <0.05 respectively). This rise in the group N was significantly less than group C (p<0.05). In group E systolic blood pressure did not increase following intubation (figure 2).
There was a significant rise in diastolic blood pressure, 1 and 3 minutes after intubation in group C (p<0.01). Diastolic blood pressure did not change significantly in group N and group E (Figure 3).
Mean arterial pressure increased significantly in the control group following intubation after 1 min (p<0.01) and after 3 and 5 min (<0.001). In group N the rise in mean arterial pressure was statistically significant only 3 min after intubation (p<0.001). In the esmolol group mean arterial pressure decreased significantly (p<0.05) 1 minute after intubation. It increased subsequently but was not significantly different from the initial value (Figure 4).
Hypertension and tachycardia subsequent to tracheal intubation have been well documented2. In susceptible patients even this short period (2-7 minutes) of hypertension and tachycardia can result in myocardial ischaemia or increased intracranial pressure. Complications resulting from these haemodynamic events after intubation include left ventricular dysfunction,8,9 hypertensive crises4, pulmonary oedema4, cardiac dysrhythmias10,12, myocardial ischaemia,3,13 and myocardial necrosis3.
Many agents have been used to attenuate undesirable haemodynamic responses to laryngoscopy and intubation with varying success. These include intravenous opioids4, vasodilators5, calcium channel blockers6, intravenous and topical lignocaine7 and adrenoceptor blocking drugs alone8 or in combination with other drugs9, 10. In the present study esmolol and nitroglycerin were selected because of their similar pharmacokinetic profile i.e. rapid onset of action, short duration of action, rapid elimination and termination of action on discontinuation of infusion. Many studies have been done to assess the effect of these drugs when given as a bolus injection9-11, but very few studies have been done with intravenous infusion. We preferred to use nitroglycerin and esmolol in the form of an infusion as it would be less likely to cause acute fluctuations in heart rate and blood pressure.
In the present study nitroglycerin prevented a rise in diastolic blood pressure and attenuated the increase in systolic blood pressure following intubation. It failed to attenuate ionotropic response to intubation. The reason for this could have been the tendency of nitroglycerin to cause tachycardia. This finding is similar to that of Singh et al.12 and Vanden Berg et al13
It can be concluded from the present study that esmolol (100 gm/kg/min) was superior to nitroglycerin (0.5 gm/kg/min) in attenuating the hemodynamic responses to laryngoscopy and intubation.