The effect of nitroglycerin on response to tracheal intubation. Assessment by radionuclide angiography. Myocardial ischemia in untreated hypertensive patients: effect of a single small oral dose of a beta-adrenergic blocking agent. Failure of intravenous nitroglycerin to prevent intraoperative myocardial ischemia during fentanyl-pancuronium anesthesia. Modification of the haemodynamic responses to induction of anaesthesia and tracheal intubation with alfentanil, esmolol and their combination. The effect of various administration routes of lidocaine on hemodynamics and ECG rhythm during endotracheal intubation. Attenuation of the cardiovascular and catecholamine responses to tracheal intubation with oral guanabenz. Partial attenuation of the cardiovascular responses to tracheal intubation with oral manidipine. Comparison of nicardipine, diltiazem and verapamil for controlling the cardiovascular responses to tracheal intubation. Sedation, topical pharyngeal anesthesia and cardiorespiratory safety during gastroscopy.
The effect of intravenous (IV) nitroglycerin (NTG) on perioperative myocardial ischemia as detected by single pass radionuclide angiocardiography was studied in 20 patients scheduled for elective coronary artery bypass grafting (CABG). Ten patients, selected at random, received IV NTG 1 microgram.kg-1.min-1 (NTG group) and 10 others, IV saline (control group). Anesthetic induction consisted of midazolam 0.2 mg.kg-1, vecuronium 0.1 mg.kg-1, and 50% N2O in O2. ECG leads I, II, and V5 were monitored for ST segment changes. Single pass radionuclide angiocardiography (RNA) was performed at 5 times: prior to induction, prior to tracheal intubation, and at 1, 3.5, and 6 min following intubation. The presence of new regional wall motion abnormalities (RWMA) was determined from each RNA study as compared with the preinduction measurement. Apart from one patient in the control group who developed a new "v" wave after intubation, there was no evidence of ischemia by pulmonary capillary wedge pressure. No ECG evidence of ischemia was detected in any patient. Despite this, new regional wall motion abnormalities were observed in 3 patients in the control group and 1 patient in the NTG group. Blood pressure and heart rate responses of patients with new RWMA were not significantly different from other patients. The low incidence of ischemia in this population precludes a definitive statement regarding the efficacy of IV NTG, but the lower incidence of RWMA in the NTG group suggests a protective effect. In a non-double-blind, prospective, randomized study, the intra-operative electrocardiograms of 128 mildly hypertensive surgical patients were examined in order to determine the incidence of myocardial ischemia during anesthesia. No patient had been receiving chronic antihypertensive therapy prior to the study, but a single small oral dose of a beta-adrenergic blocking agent (labetalol, atenolol, or oxprenolol) was given to 89 of them along with premedication. Forty-four per cent of the untreated control patients and 61% of the patients pretreated with a beta-adrenergic blocking agent had normal preoperative electrocardiograms and no risk factors for coronary artery disease other than hypertension (this difference between groups was not statistically significant). During tracheal intubation and/or emergence from anesthesia, a brief, self-limited episode of myocardial ischemia was detected in 11 of 39 untreated control patients, and in two of 89 patients pretreated with a beta-adrenergic blocking agent (P less than 0.001). Tachycardia always accompanied the ischemic events, but a conspicuous increase in blood pressure did not. The authors conclude that mild hypertension, when untreated prior to the induction of anesthesia, is associated with a high incidence of myocardial ischemia; and that a single small oral dose of a beta-adrenergic blocking agent, given with pre-medication, can significantly reduce that risk. Twenty patients undergoing coronary artery bypass grafting under fentanyl-pancuronium anesthesia were studied. Continuous electrocardiographic (ECG) recording by a Holter Monitor was utilized to determine the incidence of ECG changes of myocardial ischemia during the precardiopulmonary bypass period and to determine the efficacy of an intravenous nitroglycerin (iv NTG) infusion for preventing ischemic ECG changes. Patients in Group 1 (n = 9) received a 0.5 microgram . kg-1 . min-1 iv NTG infusion 20 min prior to induction of anesthesia and throughout the study. Patients in Group 2 (n = 11) received placebo. A randomized double-blind protocol was employed. Anesthesia was induced with fentanyl 3 micrograms . kg-1 . min-1. After fentanyl 25 micrograms/kg and pancuronium 0.1 microgram/kg, the trachea was intubated. After fentanyl 50 micrograms/kg surgery commenced. Prior to induction of anesthesia, iv NTG caused significant decreases in mean arterial pressure and pulmonary capillary wedge pressure, whereas placebo had no effect. However, subsequent to induction of anesthesia, hemodynamics in the two groups were identical. Fifty per cent of patients developed ECG changes of myocardial ischemia during the period from induction of anesthesia to commencement of cardiopulmonary bypass. The incidence of ischemic ECG changes was virtually identical in Group 1 (5/9) and Group 2 (5/11). Ischemic ECG changes were associated with increases in heart rate, mean arterial pressure, and rate pressure product, and decreases in the endocardial viability ratio (DPTI/SPTI). Increases in pulmonary capillary wedge pressure were not associated with myocardial ischemia. Fentanyl-pancuronium anesthesia, as administered in this study, was associated with a high incidence of myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS) The purpose of this double-blind randomized work was to study the effect of alfentanil and esmolol and their half-dose combination on the increases of heart rate and arterial pressure and on the prolongation of the QTc interval of the ECG occurring during anaesthetic induction. Sixty ASA class I-II patient with mean age ranging from 26 to 32 yr among the groups. Patients were allocated to one of four equal groups to receive saline, esmolol 2 mg.kg-1, alfentanil 0.03 mg.kg-1 and alfentanil 0.015 mg.kg-1+esmolol 1 mg.kg-1. Anaesthesia was induced with thiopentone. Succinylcholine was used to facilitate tracheal intubation. Haemodynamic variables were measured non-invasively and the QTc interval with the aid of a microcomputer. Comparisons between the groups were performed using two-way analysis of variance with repeated measures. Both alfentanil and alfentanil-esmolol prevented the increase of heart rate and arterial pressure caused by intubation whereas esmolol prevented only the increase of the heart rate. None of the treatments prevented prolongation of the QTc interval after intubation and only alfentanil prevented that after succinylcholine. The present results suggest that in the prevention of the haemodynamic responses to tracheal intubation, the half-dose combination of alfentanil and esmolol is as effective as alfentanil and superior to esmolol. The combination is preferable to relatively large doses of either drug in circumstances where side effects, such as respiratory depression due to alfentanil or bradycardia due to both drugs should be minimized. Observations of arterial blood pressure, heart rate and cardiac rhythm during endotracheal intubation and within a five minute period thereafter were made in 80 patients randomly assigned into four groups. The aim was to study the cardiovascular changes following endotracheal intubation using a standard anesthesia technique and to compare the efficacy of lidocaine in controlling cardiovascular changes using different administration techniques. Anesthesia was induced with thiopentone and succinylcholine followed by endotracheal intubation. In group A, the control group, no lidocaine was given. In groups B, C, and D, lidocaine as laryngotracheal spray, transtracheal injection or intravenous injection in a dosage of 1 mg/kg BW was administered prior to endotracheal intubation. In the control group, laryngoscopy and endotracheal intubation caused a significant rise in blood pressure and heart rate with a high percentage (60%) of cardiac dysrhythmias including serious types. In the lidocaine groups, we observed significantly lower values of blood pressure and cardiac dysrhythmias as compared to the control group. Only 20-25% of the cases showed sinus tachycardia. No significant differences were noticed between the lidocaine groups. We conclude from our study that those patients who had received lidocaine prior to endotracheal intubation showed minimal cardiovascular changes. Lidocaine should therefore routinely be used prior to endotracheal intubation. We conducted a randomized, placebo-controlled, and double-blind study to evaluate the efficacy of oral guanabenz, an alpha 2-adrenergic agonist, in attenuating the cardiovascular and catecholamine responses to laryngoscopy and tracheal intubation in 30 normotensive (ASA physical status 1) patients undergoing elective surgery. They were allocated to one of three groups (n = 10 for each): placebo, 4 mg, or 6 mg of guanabenz groups. These tablets were administered 2 h before the induction of anesthesia. Anesthesia was induced with thiopental 5.0 mg/kg intravenously (IV), and tracheal intubation was facilitated by the administration of vecuronium, 0.2 mg/kg IV. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after the administration of thiopental and vecuronium. Patients receiving placebo showed a significant increase in mean arterial blood pressure, heart rate, and plasma catecholamine concentrations in response to tracheal intubation. These changes were significantly smaller in patients receiving either dose of guanabenz (P < 0.05). Oral administration of guanabenz before induction of anesthesia is a simple and effective method for attenuating the pressor and tachycardic responses to laryngoscopy and tracheal intubation with the drug acting at least partly via inhibition of the increases in plasma catecholamines concentrations. We conducted a placebo-controlled, randomized, and double-blinded study to evaluate the efficacy of manidipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation. Thirty normotensive patients (ASA physical status 1) undergoing elective surgery were allocated to one of three groups (n = 10 for each); placebo, 5 mg manidipine, and 10 mg manidipine groups. These tablets were orally administered 3 h before induction of anaesthesia. Anaesthesia was induced with thiopentone 5 mg.kg-1 iv, and tracheal intubation was facilitated with vecuronium 0.2 mg.kg-1. Laryngoscopy lasting 30 sec was attempted 2 min after induction of anaesthesia. Patients receiving placebo showed a significant increase in systolic and diastolic blood pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving manidipine 10 mg compared with patients receiving placebo or manidipine 5 mg (P < 0.05). Oral administration of manidipine 10 mg before induction of anaesthesia is a simple and effective method for attenuating pressor response to laryngoscopy and tracheal intubation. We stressed that the potential beneficial effect of a reduced haemodynamic reaction to intubation might be obtained at the expense of hypotension later on. We have compared the efficacy of three calcium channel blockers, nicardipine, diltiazem and verapamil, in attenuating the cardiovascular responses to laryngoscopy and intubation in 60 normotensive patients (ASA I) undergoing rapid sequence induction of anaesthesia with thiopentone and fentanyl. We also examined whether or not these blockers inhibited catecholamine release induced by intubation. The patients were allocated to one of four groups (n = 15 for each): saline (control), nicardipine 30 micrograms kg-1, diltiazem 0.2 mg kg-1 or verapamil 0.1 mg kg-1. Verapamil and the three other drugs were administered 45 s and 60 s before the start of direct laryngoscopy, respectively, in a double-dummy design. Anaesthesia was induced with thiopentone 4 mg kg-1 i.v. and fentanyl 2 micrograms kg-1 i.v. Tracheal intubation was facilitated with vecuronium 0.2 mg kg-1. During anaesthesia, ventilation was assisted or controlled with 1% isoflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 s was attempted 2 min after administration of thiopentone and vecuronium. Patients receiving saline exhibited significant increases in systolic and diastolic arterial pressures (AP), heart rate (HR) and plasma concentrations of catecholamines associated with tracheal intubation. The increase in AP was attenuated in patients treated with any calcium channel blocker. The greatest effect was elicited by verapamil, which attenuated the increase in HR, although nicardipine seemed to enhance tachycardia. All three drugs failed to suppress the increase in plasma catecholamine concentrations in response to tracheal intubation. These findings suggest that bolus injection of verapamil 0.1 mg kg-1 was a more effective method of controlling hypertension and tachycardia associated with intubation than diltiazem 0.2 mg kg-1 or nicardipine 30 micrograms kg-1, and that these prophylactic effects were not caused by inhibition of the catecholamine response. In a prospective, double-blind study, we examined the effects of routine sedation and pharyngeal anesthesia on cardiorespiratory parameters during gastroscopy.
                Intravenous sedation and topical pharyngeal anesthesia are used to alleviate the discomfort during upper gastrointestinal endoscopy. Cardiorespiratory changes during gastroscopy are common.
                Two hundred fifty two consecutive outpatients undergoing gastroscopy were assigned into 4 groups: (1) sedation with intravenous midazolam and placebo throat spray (midazolam group), (2) placebo sedation and pharyngeal anesthesia with lidocaine throat spray (lidocaine group), (3) placebo sedation and placebo throat spray (placebo group), and (4) no intravenous cannula nor throat spray (control group). Arterial oxygen saturation (SaO2), systolic and diastolic blood pressure and continuous electrocardiogram were recorded before, during, and after the endoscopic procedure.
                Gastroscopy increased heart rate in all study groups. Premedication with intravenous midazolam or lidocaine spray alleviated this rise (P<0.001, repeated measures analysis of variance) and decreased the incidence of tachycardia. Similarly, sedation with midazolam or topical pharyngeal anesthesia decreased the rise in systolic blood pressure (P<0.001). Midazolam produced lower SaO2 values during gastroscopy compared with lidocaine, placebo or control groups (P<0.001). However, episodes of desaturation (SaO2 </=92) were no more common in the midazolam group than in other groups.
                Premedication with midazolam alleviated the rise in heart rate and systolic blood pressure but induced a statistically significant decrease in arterial oxygen saturation. However, gastroscopy proved to be a safe procedure both with and without sedation.
The risk of arrhythmias associated with tracheal intubation was significantly reduced with pre-induction administration of local anaesthetics, calcium channel blockers, beta blockers and narcotics compared to placebo. Pharmacological intervention also reduced the risk of ECG evidence of myocardial ischaemia in the pooled data. Lignocaine pretreatment showed a significant effect but evidence came from one study only. The data suggested that there may be a reduction in ECG evidence of myocardial ischaemia with beta blocker pretreatment but this difference was not statistically significant. There is a need to focus on outcomes rather than haemodynamic measurements alone when studying this response in future trials.