Changes in rate pressure product during induction of anaesthesia in cardiac patients. Role of topical anaesthesia of larynx.
An optimum balance of myocardial oxygen demand and supply is of great importance in patients with compromized coronary circulation. Because of this it is important to monitor such parameters as rate-pressure product (R.P.P.) which generally is an indicator of myocardial oxygen demand,  in spite of some reservation, lead V5 of E.C.G. for an early discovery of myocardial ischaemia, in addition to conventional monitoring of cardiac rate and rhythm and direct arterial and venous pressures.
By intensive monitoring and by early pharmacological intervention to keep vital signs within normal and desirable values, Moore et al showed a decrease in mortality in patients with left main coronary artery disease from 20% to 3.5%.
During induction of anesthesia and intubation there are considerable changes in the vital signs. Intubation tends to raise the blood pressure and heart rate, ,  and thereby increases the myocardial oxygen demand. Various techniques such as spraying the larynx with local anesthetics, intravenous injection of lidocaine prior to intubation and topical use of viscous lidocaine have been employed to minimize a pressure response to intubation and/or laryngoscopy., ,  Also drugs like atropine, phentolamine, propranolol and nitroprusside have been used to attenuate this response., ,  Changes in the pulse rate and blood pressure during intubation with or without the topical anesthesia of larynx have been studied. However, changes in continuously monitored R.P.P. during intubation with or without topical laryngeal anesthesia have not been studied. In the present study we looked at the changes in rate pressure product (R.P.P.) during various phases of induction, during intubation when the latter was done with or without prior administration of intralaryngeal lidocaine.
For this study, patients were divided in 2 groups. Group I consisted of 34 patients whose larynx was sprayed with 0.05 ml/kg of 4% lidocaine prior to intubation.
Group II consisted of 15 patients who did not receive topical anesthesia of the larynx.
Patients in each group were selected consecutively. Group I was studied first and group II last. Patients were discarded from the study if they manifested severe changes in pulse or blood pressure during the study period, that necessitated the use of any medication either to raise or lower the blood pressure, or to increase or decrease the heart rate. All patients received standard premedication of 0.14 mg/kg morphine and 0.4 mg atropine.
All patients had an intra-arterial line for continuous pressure monitoring, E.C.G. (lead II and V5) and catheters to monitor central venous and/or pulmonary artery pressures. All these parameters were continuously monitored. An on line computer was used to give continuous rate-pressure product. All these parameters including R.P.P. were continuously recorded on a "Grass recorder".
While breathing 100% oxygen, all patients were anesthetized with morphine 1 mg/kg up to a maximum of 75 mg (as an IN. infusion in 250 ml of 5% dextrose). At the end of morphine infusion, each patient received 0.5 mg/kg of IN. diazepam and 0.1 mg/kg pancuronium. After waiting for 5 minutes, patients in group I received 0.05 ml/kg of 4% lidocaine as a laryngeal spray. Approximately five minutes after lidocaine treatment, intubation was attempted.
R.P.P. values at different stages of induction in patients belonging to group I are shown in [Fig. 1].
Results were analyzed by analysis of variance and Student's t-test for paired data. p values of less than 0.05 were considered statistically significant.
Compared to control, R.P.P. significantly dropped after morphine (p < 0.00-1), diazepam (p < 0.001) and pancuronium (p < 0.001). Mean R.P.P. after intubation was lower than in the control, the difference between the two being statistically insignificant (p > 0.1).
R.P.P. values in 15 patients belonging to group II are shown in [Fig. 2.] R.P.P. after intubation in patients in this group was significantly higher (p < 0.001) than the control R.P.P. (12,600 ± 818.37 after intubation compared to control value of 9433.33 ± 735-08).
Ever since it was reported that cardiovascular stability was remarkably well maintained in the presence of large doses of morphine,,  use of narcotics in the anesthetic management of cardiac surgical patients is widely popular. The drop in R.P.P. after morphine is understandable. The drop in blood pressure after morphine may in part be related to its histamine releasing property. However, release of histamine might not be the cause of peripheral vasodilation., 
A drop in R.P.P. after diazepam can be explained in part due to the patient being asleep and thereby absence of anxiety of impending surgery. Liu et al observed that diazepam in small doses (0.5 mg/kg) after fentanyl had very little effect hemodynamically while larger doses (1 mg/ kg) were associated with decreased stroke volume and arterial pressure. Since the dose of diazepam in our study was 0.5 mg/kg we did not observe a significant change in R.P.P. after diazepam compared to R.P.P. after morphine.
Pancuronium leads to a slight increase in the heart rate and to some extent in the cardiac output.,  Though tachycardia is generally attributed to vagolytic action, Docherty et al observed sympathomimetic properties of pancuronium in rats. These actions explain slight increase though statistically insignificant in the mean R.P.P. after pancuronium compared to that after diazepam. R.P.P. after pancuronium bromide was significantly lower when compared to control value.
Intubation under light anesthesia is known to increase heart rate and blood pressure., , , ,  Intubation performed only under topical anesthesia leads to increase in the heart rate and blood pressure. That explains why R.P.P. after intubation in patients in group II exceeded the control R.P.P. Denlinger et al and Stoelting have found that laryngotracheal administration of lidocaine is useful in attenuating the pressure response to intubation. However, in their study laryngotracheal lidocaine did not suppress fully the pressor response to intubation as was noticed in our study. The difference can be explained on the basis of difference in anesthetic technique and secondly due to the fact that after laryngeal spray we waited 5 minutes prior to intubation. Stoelting,,, used barbiturate induction rather than morphine as in our study. Delinger et al used morphine induction but did not use diazepam. It is possible that in the latter study, patients may not be as deeply anesthetized as in our study. Suppression of pressor response to intubation is related to depth of anesthesia. However, anesthetic depth alone was not adequate in our study as can be seen in group II patients who had the same degree of anesthesia but did not receive laryngeal lidocaine spray. In this group, R.P.P. after intubation was significantly higher than the control value.