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. Efficacy of oropharyngeal lidocaine instillation on hemodynamic responses to orotracheal intubation. Partial attenuation of the cardiovascular responses to tracheal intubation with oral nisoldipine. Hemodynamic effects, myocardial ischemia, and timing of tracheal extubation with propofol-based anesthesia for cardiac surgery. Alfentanil obtunds the cardiovascular and sympathoadrenal responses to suxamethonium-facilitated laryngoscopy and intubation. The use of esmolol, nicardipine, or their combination to blunt hemodynamic changes after laryngoscopy and tracheal intubation. Arrhythmias after coronary bypass surgery. QT interval of the ECG, heart rate and arterial pressure during anaesthetic induction: comparative effects of alfentanil and esmolol. The effect of magnesium sulphate on hemodynamics and its efficacy in attenuating the response to endotracheal intubation in patients with coronary artery disease. Reduction in infarct size, arrhythmias and chest pain by early intravenous beta blockade in suspected acute myocardial infarction. Partial attenuation of hemodynamic responses to rapid sequence induction and intubation with labetalol. Small, oral dose of clonidine reduces the incidence of intraoperative myocardial ischemia in patients having vascular surgery. Attenuation of the pressor response to tracheal intubation with oral nitrendipine. Effect of labetalol or lidocaine on the hemodynamic response to intubation: a controlled randomized double-blind study. Alkalinization of intracuff lidocaine improves endotracheal tube-induced emergence phenomena. Effects of intravenous lidocaine and/or esmolol on hemodynamic responses to laryngoscopy and intubation: a double-blind, controlled clinical trial. A beta-blocker, not magnesium, is effective prophylaxis for atrial tachyarrhythmias after coronary artery bypass graft surgery. Intravenous chloroprocaine attenuates hemodynamic changes associated with direct laryngoscopy and tracheal intubation. Attenuation of hypertensive response to tracheal intubation with nitroglycerin. Comparative effects of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation. Epidural anesthesia for coronary artery bypass surgery compared with general anesthesia alone does not reduce biochemical markers of myocardial damage. Short-term effects of early intravenous treatment with a beta-adrenergic blocking agent or a specific bradycardiac agent in patients with acute myocardial infarction receiving thrombolytic therapy. Efficacy of nadolol in preventing supraventricular tachycardia after coronary artery bypass grafting. Intratracheal aerosolized etidocaine to attenuate cardiovascular and cough responses to laryngoscopy and intubation. Haemodynamic responses to laryngoscopy and tracheal intubation in geriatric patients: effects of fentanyl, lidocaine and thiopentone. Circulatory responses to laryngoscopy and endotracheal intubation in patients with and without cardiovascular disease. Effect of prophylactic practolol. Reducing the haemodynamic responses to laryngoscopy and intubation. A comparison of alfentanil with fentanyl. Prophylaxis of supraventricular and ventricular arrhythmias after coronary artery bypass grafting with low-dose sotalol. Thoracic epidural anesthesia as an adjunct to general anesthesia for cardiac surgery: effects on ventilation-perfusion relationships. Arrhythmia prophylaxis after aorta-coronary bypass. The effect of minidose propranolol. Arrhythmia prophylaxis after coronary artery bypass grafting: regimens of magnesium sulfate administration. Effect of methylprednisolone on myocardial preservation during coronary artery surgery. Topical nitroglycerin prevents the pressor response to tracheal intubation and sternotomy in patients undergoing coronary artery bypass graft surgery. Perioperative sympatholysis. Beneficial effects of the alpha 2-adrenoceptor agonist mivazerol on hemodynamic stability and myocardial ischemia. McSPI--Europe Research Group. Investigation of the effects of intravenous magnesium sulphate on cardiac rhythm in acute myocardial infarction. Morbidity outcome in early versus conventional tracheal extubation after coronary artery bypass grafting: a prospective randomized controlled trial. Effects of N-acetylcysteine on pulmonary function in patients undergoing coronary artery bypass surgery with cardiopulmonary bypass. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. The effect of clonidine premedication on hemodynamic responses to microlaryngoscopy and rigid bronchoscopy. Prevention of adriamycin-induced cardiotoxicity by prenylamine: a pilot double blind study. A comparative study of the safety of 0.25% levobupivacaine and 0.25% racemic bupivacaine for paracervical block in the first stage of labor. Lidocaine: the optimal timing of intravenous administration in attenuation of increase of intraocular pressure during tracheal intubation. Optimal dose of nicardipine for maintenance of hemodynamic stability after tracheal intubation and skin incision. Effects of intracoronary injection of mononuclear bone marrow cells on left ventricular function, arrhythmia risk profile, and restenosis after thrombolytic therapy of acute myocardial infarction. Prevention of supraventricular tachyarrhythmia with low-dose propranolol after coronary bypass. Nifedipine prevents the pressor response to laryngoscopy and tracheal intubation in patients with coronary artery disease. [Postoperative routine use of physostigmine on vigilance, cardiovascular parameters and need of analgesics]. Rocuronium combined with i.v. lidocaine for rapid tracheal intubation. Hemodynamic effects and safety of sotalol in the prevention of supraventricular arrhythmias after coronary artery bypass surgery. Effects of different steroid treatment on reperfusion-associated production of reactive oxygen species and arrhythmias during coronary surgery. Arrhythmia prophylaxis using propranolol after coronary artery surgery. Does alfentanil preserve left ventricular pump function during rapid sequence induction of anaesthesia? Magnesium substitution and postoperative arrhythmias in patients undergoing coronary artery bypass grafting. A comparison between oral antiarrhythmic drugs in the prevention of atrial fibrillation after cardiac surgery: the pilot study of prevention of postoperative atrial fibrillation (SPPAF), a randomized, placebo-controlled trial. Effect of single dose magnesium on arrhythmias in patients undergoing coronary artery bypass surgery. Effect of antagonism of mivacurium-induced neuromuscular block on postoperative emesis in children. Effects of adenosine triphosphate on the cardiovascular response to tracheal intubation.
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. To determine whether oropharyngeal instillation of lidocaine after anesthetic induction modifies the hemodynamic response to intubation.
                Prospective, randomized, double-blind, placebo-controlled study.
                Operating room of a university hospital.
                56 ASA physical status I and II adult patients scheduled for elective surgery requiring orotracheal intubation and general anesthesia.
                Patients were randomized to receive oropharyngeal instillation with either 5 mL 2% lidocaine (n = 28, lidocaine group) or 5 mL normal saline (n = 28, control group) 45 seconds after anesthetic induction bolus. Orotracheal intubation was attempted three minutes later.
                Systolic (SBP), diastolic (DBP), mean arterial pressure (MAP), and heart rate (HR) were recorded at baseline, just before intubation, and for three minutes postintubation at one-minute intervals. Occurrence of adverse events such as arrhythmias, ischemic changes in electrocardiography, and bronchospasm after intubation were also documented.
                All postintubation values of SBP, DBP, MAP, and HR were significantly lower in the lidocaine group than the control group (P < 0.01). In both groups, postintubation HRs were significantly higher than baseline values (P < 0.05). More patients (P < 0.001) became hypertensive postintubation in the control group (14/28, 50%) than the lidocaine group (2/28, 7%).
                Oropharyngeal instillation of lidocaine for three minutes before intubation attenuates the cardiovascular responses to intubation. To evaluate the efficacy and safety of nisoldipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation.
                Randomized, double-blind, placebo-controlled study.
                Induction of anesthesia for elective surgery at a university hospital.
                Thirty normotensive patients (ASA physical status I) undergoing elective surgery were assigned to one of three groups; placebo, nisoldipine 5 mg, or nisoldipine 10 mg. Each group consisted of ten patients.
                Either 5 mg of nisoldipine, 10 mg of nisoldipine, or a placebo was administered orally 2 hours before induction of anesthesia. Anesthesia was induced with thiopental sodium 5 mg/kg intravenously, and tracheal intubation was facilitated with vecuronium 0.2 mg/kg. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Laryngoscopy lasting 30 seconds was attempted 2 minutes after administration of thiopental sodium and vecuronium.
                Patients receiving the placebo showed a significant increase in mean arterial pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving nisoldipine 10 mg compared with patients receiving the placebo (p less than 0.05).
                Oral administration of nisoldipine before induction of anesthesia is a simple, practical, and safe method for attenuating pressor response to laryngoscopy and tracheal intubation. Recent interest in earlier tracheal extubation after coronary artery bypass graft (CABG) surgery has focused attention on the potential benefits of a propofol-based technique. We randomized 124 patients (34 with poor ventricular function) undergoing CABG surgery to receive either a propofol-based (5 mg.kg-1.h-1 prior to sternotomy, 3 mg.kg-1. h-1 thereafter; n = 58) or enflurane-based (0.2%-1.0%, n = 66) anesthetic. Induction of anesthesia consisted of fentanyl 15 micrograms/kg and midazolam 0.05 mg/kg intravenously in both groups. The enflurane group received an additional bolus of fentanyl 5 micrograms/kg prior to sternotomy and fentanyl 10 micrograms/kg with midazolam 0.1 mg/kg at commencement of cardiopulmonary bypass (CPB). Patients receiving propofol were extubated earlier (median 9.1 h versus 12.3 h, P = 0.006), although there was no difference in time to intensive care unit (ICU) discharge (both 22 h, P = 0.54). Both groups had similar hemodynamic changes throughout (all P > 0.10), as well as metaraminol (P = 0.49) and inotrope requirements (P > 0.10), intraoperative myocardial ischemia (P = 0.12) and perioperative myocardial infarction (P = 0.50). The results of this trial suggest that a propofol-based anesthetic, when compared to an enflurane-based anesthetic requiring additional dosing of fentanyl and midazolam for CPB, can lead to a significant reduction in time to extubation after CABG surgery, without adverse hemodynamic effects, increased risk of myocardial ischemia or infarction. Alfentanil 75 micrograms kg-1 or saline (control group) was given 1 min before induction of anaesthesia in 20 healthy patients premedicated with diazepam 0.14 mg kg-1 and pethidine 1 mg kg-1. Anaesthesia was induced with a sleep dose of thiopentone preceded by glycopyrrolate. Suxamethonium 1 mg kg-1 was used to facilitate laryngoscopy (which lasted 10 s) and tracheal intubation. Arterial pressure, heart rate and noradrenaline concentration in mixed venous plasma increased significantly after suxamethonium, and increased further after laryngoscopy and intubation in the control group (n = 10). The QT interval of the ECG was prolonged after the administration of suxamethonium, and was prolonged further after laryngoscopy and intubation. All these changes were attenuated in patients pretreated with alfentanil (n = 10), but four patients had chest wall rigidity. Changes in the QT interval correlated directly with the changes in plasma noradrenaline concentration (r = 0.67). Plasma adrenaline concentrations decreased during induction of anaesthesia in both groups. Laryngoscopy and tracheal intubation (LTI) often provoke an undesirable increase in blood pressure (BP) and/or heart rate (HR). We tested the premise that nicardipine (NIC) and esmolol (ESM) in combination (COMB) would oppose both. Adult surgical patients received pretreatment (randomized) with IV bolus NIC 30 microg/kg (n = 31), ESM 1.0 mg/kg (n = 34), or COMB (one-half dose each, n = 32). Peak BP and HR after LTI were compared with controls (CONT; n = 35) with no pretreatment. Anesthetic induction was standardized: IV thiopental (5-7 mg/kg), fentanyl (1-2 microg/kg), and succinylcholine (1.5 mg/kg). Systolic (S), diastolic (D), and mean (M) BP and HR awake before pretreatment (baseline) were similar in all test groups. No patient was treated for hypotension, bradycardia, or tachycardia after pretreatment or anesthetic induction. Peak HR after LTI was increased versus baseline in CONT and all test groups, but did not differ from CONT among the test groups. Peak SBP and DBP increased versus baseline in CONT, and with ESM and NIC, but not COMB. Peak SBP, DBP, and MBP were increased with ESM versus COMB, and peak DBP with ESM versus NIC. Compared with no pretreatment before the IV induction of general anesthesia, the peak increase in BP after LTI is best blunted by the combination of nicardipine and ESM, compared with either drug alone. No single drug or combination in the doses tested opposed increased HR.
                Compared with no pretreatment before the IV induction of general anesthesia, the peak increase in blood pressure after laryngoscopy and tracheal intubation is best blunted by the combination of nicardipine and esmolol, compared with either drug alone. No single drug or combination in the doses tested opposed increased heart rate. Ninety patients undergoing coronary bypass surgery were studied prospectively by bedside and subsequent ambulatory electrocardiographic monitoring to investigate the incidence, possible causes, and prevention of atrial fibrillation. Patients with good left ventricular function were divided randomly into a control group or groups treated with digoxin or propranolol. In the control group the incidence of atrial fibrillation was 27% and of significant ventricular extrasystoles 3%. Propranolol reduced the incidence of atrial fibrillation (14.8%), whereas digoxin had no effect and increased the incidence of ventricular extrasystoles. Age, sex, severity of symptoms, cardiomegaly, heart failure, previous myocardial infarction, and number of grafts did not affect the result. The operative myocardial ischaemic time was related to the occurrence of atrial fibrillation. There was also a significant relation between atrial fibrillation and bundle branch block. Atrial fibrillation is common after coronary artery grafting; it may be due to diffuse myocardial ischaemia or hypothermic injury. The incidence may be reduced by beta blockade. In a double-blind study the effect of esmolol and alfentanil on the QT interval of the ECG corrected by the heart rate (QTc), heart rate and arterial pressure during anaesthetic induction was studied in 59 oxycodone- and atropine-premedicated ASA class I-(II) patients with a mean age of 26 yr (range 15-50 yr). The patients were randomly allocated to one of the four groups: saline, esmolol 2 mg.kg-1, esmolol 3 mg.kg-1 or alfentanil 0.03 mg.kg-1. Both doses of esmolol prevented the prolongation of the QTc interval after thiopental and suxamethonium, but not after laryngoscopy and intubation. Alfentanil prevented the prolongation of the QTc interval following thiopental, suxamethonium and laryngoscopy but not after intubation. Esmolol did not prevent the increase in the heart rate and arterial pressure in response to laryngoscopy and intubation. No cardiovascular responses to laryngoscopy and intubation occurred in the patients treated with alfentanil. No cardiac arrhythmias occurred in the esmolol 3 mg.kg-1 group, whereas the frequency of ventricular ectopic beats was 40% in the saline group and 13-20% in the other groups. Laryngoscopy and endotracheal intubation may produce adverse hemodynamic effects. Magnesium has direct vasodilating properties on coronary arteries and inhibits catecholamine release, thus attenuating the hemodynamic effects during endotracheal intubation. We studied 36 patients with coronary artery disease (CAD) scheduled for elective coronary artery bypass grafting to evaluate the hemodynamic effects of magnesium and its efficacy in attenuating the response to endotracheal intubation. Patients received either 0.1 mL/kg (50%) magnesium sulfate (50 mg/kg) (Group A, n = 19) or isotonic sodium chloride solution (Group B, n = 17) before the induction of anesthesia and 0.05 mL/kg of isotonic sodium chloride solution (Group A) or lidocaine 2% (1 mg/kg) (Group B) before intubation. The hemodynamic variables were recorded before induction, after the trial drug, after induction, and after endotracheal intubation. Automatic ST segment analysis was performed throughout the study period. Magnesium sulfate administration was associated with increased cardiac index (P < 0.01), a minimal increase in heart rate, and a significant decrease in mean arterial pressure (MAP) and systemic vascular resistance (SVR) (P < 0.001). None of the patients in the magnesium group had significant ST depression compared with three patients in the control group. The magnesium group patients had a significantly lesser increase in MAP (P < 0.05) and SVR (P < 0.01) compared with the control group patients who received lidocaine before endotracheal intubation. Thus, magnesium is an useful adjuvant to attenuate endotracheal intubation response in patients with CAD.
                Endotracheal intubation produces adverse hemodynamic effects, which may be more detrimental in patients with coronary artery disease than in healthy patients. The present study shows that magnesium administered before endotracheal intubation can attenuate this response better than lidocaine. Four hundred seventy-seven patients suspected of having had acute myocardial infarction within less than 12 hours were randomized to receive i.v. atenolol followed by oral treatment for 10 days or to a control group. In patients with ECG changes indicative of infarction at entry, i.v. atenolol significantly reduced enzyme release by one-third and enhanced R-wave preservation. In patients without such ECG changes, treatment significantly prevented the development of infarction in a proportion of patients. There was also a significant reduction in R-on-T ectopics, repetitive ventricular arrhythmias and supraventricular arrhythmias. Treated patients had significantly greater pain relief and required fewer opiate analgesics. Significantly fewer atenolol-treated patients died by 10 days (the treatment period), had nonfatal cardiac arrests, developed heart failure, or suffered reinfarction. The effectiveness of labetalol (a combination nonselective beta and alpha-1-adrenergic receptor antagonist) in modifying hemodynamic responses associated with rapid sequence induction and tracheal intubation was evaluated. In a double-blind study, 24 ASA physical status I or II male patients scheduled for elective surgery were given either IV labetalol, 0.25 mg/kg (n = 8) or 0.75 mg/kg (n = 8), or a saline placebo (n = 8). Five minutes later, patients were given oxygen by mask and IV vecuronium, 0.01 mg/kg. Ten minutes after giving labetalol or placebo, cricoid pressure was applied and anesthesia was induced with IV sodium thiopental (4 mg/kg) and succinylcholine (1.5 mg/kg) 1 minute prior to intubation. The mean duration of laryngoscopy was 17 +/- 3 seconds. Prior to induction, the 0.25 mg/kg and 0.75 mg/kg doses of labetalol significantly (p less than 0.05) reduced mean arterial pressure by 4.4 +/- 1.9 and by 8.6 +/- 2.0 mmHg, respectively, but did not significantly alter heart rate or cardiac output. The 0.75 mg/kg dose of labetalol also significantly (p less than 0.05) decreased total peripheral resistance by 10.1 +/- 3.0%. Within 30 seconds after intubation, patients in all three groups exhibited increases in heart rate, mean arterial pressure, total peripheral resistance, and rate pressure product and a decrease in stroke volume. However, patients in the 0.25 and 0.75 mg/kg labetalol groups, compared to those in the placebo group, had significantly lower increases in peak heart rate (33 +/- 2 and 27 +/- 3 vs. 44 +/- 7 beats/minute), peak mean arterial pressure (38 +/- 6 and 38 +/- 7 vs. 58 +/- 7 mmHg), and peak rate pressure product (7,726 +/- 260 and 7,215 +/- 300 vs. 14,023 +/- 250 units). The results show that these doses of labetalol significantly blunt, but do not completely block, autonomic responses to rapid sequence induction and intubation. Most new perioperative myocardial ischemic episodes occur in the absence of hypertension or tachycardia. The ability of alpha 2-adrenoceptor agonists to inhibit central sympathetic outflow may benefit patients with coronary artery disease by increasing the myocardial oxygen supply and -demand ratio.
                A randomized double-blind study design was used in 297 patients scheduled to have elective vascular surgical procedures to evaluate the effects of 2 micrograms/kg-1 oral clonidine (n = 145) or placebo (n = 152) on the incidence of perioperative myocardial ischemic episodes, myocardial infarction, and cardiac death. Continuous real-time S-T segment trend analysis (lead II and V5) was performed during anesthesia and surgery and correlated with arterial blood pressure and heart rate before and during ischemic events. Dose requirements for vasoactive and antiischemic drugs to control blood pressure and heart rate as well as episodes of myocardial ischemia (i.e., catecholamines, beta-adrenoceptor antagonists, nitrates, and systemic vasodilators) and fluid volume load were recorded.
                Administration of clonidine reduced the incidence of perioperative myocardial ischemic episodes from 39% (59 of 152) to 24% (35 of 145) (P < 0.01). Hemodynamic patterns, percentage of ischemic time, and the number of ischemic episodes per patient did not differ. Nonfatal myocardial infarction developed after operation in four patients receiving placebo compared with none receiving clonidine (day 2 to 21; P = 0.07). The incidence of fatal cardiac events (1 vs. 2) was not different. Dose requirements for vasoactive and antiischemic drugs did not differ between the groups, but the amount of presurgical fluid volume was slightly greater in patients receiving clonidine (951 +/- 388 vs. 867 +/- 381 ml; P < 0.03).
                A small oral dose of clonidine, given prophylactically, can reduce the incidence of perioperative myocardial ischemic episodes without affecting hemodynamic stability in patients with suspected or documented coronary artery disease. The effect of nitrendipine on the cardiovascular responses to tracheal intubation was studied in a placebo-controlled, randomised, double-blind trial. Thirty patients (ASA physical status 1) undergoing elective surgery received either 5 or 10 mg nitrendipine, or a placebo orally 3 h before induction of anaesthesia (n = 10 for each group). Anaesthesia was induced with sodium thiopentone 5 mg/kg i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. Patients receiving the placebo showed a significant increase in the mean arterial pressure and the rate-pressure product in response to tracheal intubation. These increases following intubation were reduced in nitrendipine-treated patients compared with the placebo group (P < 0.05). Oral administration of nitrendipine (5 or 10 mg, 3 h before induction of anaesthesia) was able to attenuate the hypertensive response to tracheal intubation in ASA 1 patients under light anaesthesia. We propose this pharmacological technique with supplementary doses of opioids and/or benzodiazepines for the management of patients with hypertension or coronary artery disease. Labetalol, a combined alpha 1- and nonselective beta-adrenergic blocking drug, was compared to lidocaine or saline to minimize the hypertensive and tachycardic response to intubation in a controlled randomized double-blind study in patients undergoing surgical procedures under general anesthesia. Forty adult patients were divided into four groups of 10 each: placebo (saline), lidocaine 100 mg, labetalol 5 mg, or labetalol 10 mg. The double-blind preparation was administered as an IV bolus just prior to induction and 2 min before the stimulus of laryngoscopy and intubation. Heart rate and blood pressure were measured at 1-min intervals for 2 min prior to induction of anesthesia and through 6 min following induction of anesthesia. Labetalol 10 mg prevented a rise in heart rate after intubation compared to patients who received placebo, lidocaine 100 mg, or labetalol 5 mg. The hypertensive response to intubation was similar in all four groups. Labetalol 10 mg IV just prior to induction of anesthesia is a safe and cost-effective means of preventing tachycardia but not hypertension in response to laryngoscopy and intubation. We sought to evaluate the effect of filling an endotracheal tube cuff with 40 mg lidocaine alone (Group L) or alkalinized lidocaine (Group LB) in comparison to an Air Control group (Group C) on adverse emergence phenomena in a randomized controlled study (n = 25 in each group). The incidence of sore throat was decreased for Group LB in comparison to Group L during the 24 postextubation hours. The difference between Group L and Group C remained significant in the two postextubation hours only. Plasma lidocaine levels increased when lidocaine was alkalinized (C(max) were 62.5 +/- 34.0 ng/mL and 3.2 +/- 1.0 ng/mL for Groups LB and L, respectively). Cough and restlessness before tracheal extubation were decreased in Group LB compared with Group L and in Group L compared with Group C. Nausea, postoperative vomiting, dysphonia, and hoarseness were increased after extubation in Group C compared with the liquid groups, and a better tolerance was recorded with Group LB compared with Group L. The increase of arterial blood pressure and cardiac frequencies during the extubation period was less in the liquid groups than in the control group and less in Group LB compared with Group L. We concluded that use of intracuff alkalinized lidocaine is an effective adjunct to endotracheal intubation.
                Use of 40 mg of alkalinized lidocaine, rather than lidocaine or air, to fill the endotracheal tube cuff reduces the incidence of sore throat in the postoperative period. This approach also decreases hemodynamic effects, restlessness, dysphonia, and hoarseness. To evaluate the efficacy of intravenous lidocaine and two doses of esmolol for attenuating the cardiovascular responses to laryngoscopy and intubation, and to assess whether a combination of both drugs is more effective than either drug alone.
                Randomized, prospective, double-blind, placebo-controlled study.
                University hospital.
                90 ASA status I and II normotensive women scheduled for elective gynecologic procedures with general anesthesia.
                Induction of anesthesia was standardized for all patients. The first group received lidocaine 1.5 mg/kg (Group LID); the second and third groups received esmolol 1 mg/kg and 2 mg/kg, respectively (Groups E1 and E2, respectively); the fourth group received lidocaine 1.5 mg/kg and esmolol 1 mg/kg (Group LID-E1); the fifth group received lidocaine 1.5 mg/kg and esmolol 2 mg/kg (Group LID-E2); the sixth group received saline as a placebo (Group PLAC).
                Systolic blood pressure and heart rate (HR) were recorded before induction, before injection of the first test drug, immediately before laryngoscopy, and 1, 2, and 5 minutes following intubation. Duration of laryngoscopy was recorded. Only patients receiving placebo had increased HR values after intubation compared with baseline values (p < 0.05). The proportion of patients with a maximum HR exceeding 90 beats/min was significantly higher in the placebo group (8 of 15 patients) than in both esmolol groups (E1 2 of 15; E2 2 of 15) (p < 0.05). Systolic blood pressure values after tracheal intubation did not differ among groups except for those receiving the combinations of lidocaine and esmolol, and they had significantly lower blood pressure (BP) values compared with placebo (p < 0.05).
                Esmolol 1 to 2 mg/kg is reliably effective in attenuating HR response to tracheal intubation. Neither of the two doses of esmolol tested nor that of lidocaine affected the BP response. Only the combination of lidocaine and esmolol attenuated both HR and BP responses to tracheal intubation. To evaluate magnesium as a sole or adjuvant agent with currently used prophylactic drugs in suppressing postoperative atrial tachyarrhythmias (POAT) after coronary artery bypass graft (CABG) surgery.
                Single-center prospective, randomized clinical trial.
                University hospital.
                Patients (n = 400) undergoing CABG surgery.
                Patients were randomized among 6 prophylaxis regimens: (1) control (no antiarrhythmics), (2) magnesium only, (3) digoxin only, (4) magnesium and digoxin, (5) propranolol only, and (6) magnesium and propranolol. Patients randomized to a regimen including magnesium received 12 g given during 96 hours postoperatively. Patients in a digoxin regimen received 1 mg after cardiopulmonary bypass and 0.25 mg daily. Patients in a propranolol regimen received 1 mg intravenously every 6 hours until able to take 10 mg orally 4 times a day. Prophylaxis regimens were discontinued after 4 days postoperatively.
                The primary outcome was a sustained POAT or discharge from the hospital. Control patients had an incidence of POAT (38%) not significantly different from patients in magnesium-only (38%), digoxin-only (31%), and magnesium with digoxin (37%) regimens. Patients treated with propranolol had a significant reduction in POAT. Nearly identical POAT rates in the propranolol-only (18%) and propranolol with magnesium (19%) groups support the lack of efficacy of magnesium in this trial. Study design allowed analysis of and showed a beta-blocker withdrawal effect in addition to suppressive benefit of postoperative beta-blockers.
                beta-Blocker prophylaxis is indicated to reduce the incidence of POAT in CABG surgery patients and to prevent a beta-blocker withdrawal effect in patients receiving these medications preoperatively. Digoxin and magnesium as sole or adjuvant agents do not offer suppressive or ventricular rate reduction benefits in POAT.
                Copyright 2001 by W.B. Saunders Company We compared the effects of an IV administration of chloroprocaine and lidocaine on circulatory responses associated with endotracheal intubation. Thirty patients were randomly allocated to receive normal saline (placebo), lidocaine (1.5 mg/kg), or preservative-free chloroprocaine (4.5 mg/kg) 45 s before endotracheal intubation. Blood pressures and heart rate and rhythm were recorded before laryngoscopy and at 0.5, 1, 1.5, 2, 3, and 5 min after intubation. Blood samples were analyzed for catecholamine and chloroprocaine concentrations. Chloroprocaine reduced increases in blood pressure in response to intubation when compared with patients receiving normal saline and lidocaine. Systolic blood pressures at 0.5 and 1 min after intubation were significantly lower in the chloroprocaine group when compared with both the control and lidocaine groups (P < 0.05). Diastolic and mean blood pressures were significantly lower in the chloroprocaine group at all time points until 5 min after intubation (P < 0.05). Chloroprocaine and, to a lesser degree, lidocaine, produced marked attenuation of intubation-induced increases in plasma concentration of epinephrine and norepinephrine. Plasma concentrations of norepinephrine were significantly smaller in the chloroprocaine group at 0.5, 1, and 1.5 min, and plasma concentrations of epinephrine were significantly smaller at 0.5 after intubation when compared with control and lidocaine groups (P < 0.05). Measurable concentrations of chloroprocaine were recorded in plasma samples for 2 min after its administration. No adverse chloroprocaine effects (i.e., circulatory disturbances, venous irritation) were detected. The IV administration of chloroprocaine effectively blunted cardiovascular response produced by laryngoscopy and endotracheal intubation, and this effect was more pronounced when compared with IV lidocaine. To evaluate the efficacy and safety of intravenous (IV) nitroglycerin in attenuating the hypertensive response to laryngoscopy and intubation as a new application of the drug.
                Controlled, randomized, double-blind study.
                University hospital.
                Thirty normotensive patients (ASA physical status I) undergoing elective surgery were divided into three groups of ten patients each.
                Anesthesia was induced with thiopental sodium 5 mg/kg i.v., and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. During anesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Either 1.5 micrograms/kg of nitroglycerin, 2.5 micrograms/kg of nitroglycerin, or saline (control) was administered IV simultaneously with the start of laryngoscopy (lasting 30 seconds), which was attempted 2 minutes after administration of thiopental sodium and vecuronium.
                Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in nitroglycerin-treated patients compared with those in the control group (p < 0.05).
                A single, rapid IV dose of nitroglycerin is a simple, practical, effective, and safe method to attenuate the hypertensive response to laryngoscopy and tracheal intubation. To compare the safety and efficacy of lidocaine, esmolol, and nitroglycerin in modifying the hemodynamic response to laryngoscopy and intubation.
                Randomized, placebo-controlled, double-blind study.
                University-affiliated VA medical center.
                40 ASA physical status I and II patients undergoing electric surgery with general endotracheal anesthesia.
                Anesthesia was induced with thiopental sodium 5 mg/kg, and intubation was facilitated with vecuronium 0.15 mg/kg. Isoflurane (0.5% to 1%) and 50% nitrous oxide in oxygen were used for maintenance of anesthesia. In addition, patients received one of the following four study drugs intravenously (i.v.) prior to laryngoscopy: Group 1 (control) = saline 5 ml; Group 2 = lidocaine 1.5 mg/kg; Group 3 = esmolol 1.4 mg/kg; Group 4 = nitroglycerin 2 micrograms/kg.
                Mean arterial pressure (MAP) and heart rate (HR) were recorded every minute for 20 minutes following induction of anesthesia. Following laryngoscopy and intubation, MAP increased significantly in all four treatment groups (control 49% +/- 19%, lidocaine 55% +/- 26%, esmolol 25% +/- 11%, nitroglycerin 45% +/- 21%) compared with preinduction baseline values. In the esmolol-pretreated patients, the increase in HR was significantly lower (20% +/- 3%) compared with the nitroglycerin (37% +/- 8%), lidocaine (52% +/- 8%), and control (29% +/- 4%) groups.
                Lidocaine 1.5 mg/kg i.v. and nitroglycerin 2 micrograms/kg i.v. were ineffective in controlling the acute hemodynamic response following laryngoscopy and intubation. Esmolol 1.4 mg/kg i.v. was significantly more effective than either lidocaine or nitroglycerin in controlling the HR response to laryngoscopy and intubation (p < 0.05). Esmolol also was significantly more effective than lidocaine in minimizing the increase in MAP (25% vs. 55%). High thoracic epidural anesthesia/analgesia (HTEA) for coronary artery bypass grafting (CABG) surgery may have myocardial protective effects. In this prospective randomized controlled study, we investigated the effect of HTEA for elective CABG surgery on the release of troponin I, time to tracheal extubation, and analgesia. One-hundred-twenty patients were randomized to a general anesthesia (GA) group or a GA plus HTEA group. The GA group received fentanyl (7-15 microg/kg) and a morphine infusion. The HTEA group received fentanyl (5-7 microg/kg) and an epidural infusion of ropivacaine 0.2% and fentanyl 2 microg/mL until postoperative Day 3. There were no differences in troponin I levels between study groups. The time to tracheal extubation [median (interquartile range)] in the HTEA group was 15 min (10-320 min), compared with 430 min (284-590 min) in the GA group (P < 0.0001). Analgesia was improved in the HTEA group compared with the GA group. Mean arterial blood pressure poststernotomy and systemic vascular resistance in the intensive care unit were lower in the HTEA group. We conclude that HTEA for CABG surgery had no effect on troponin release but improved postoperative analgesia and was associated with a reduced time to extubation. This study was conducted to explore mechanisms that could explain the possible clinical benefit of early administration of a beta 1-selective adrenoreceptor blocking agent or a bradycardiac drug as adjunct to thrombolysis in acute myocardial infarction.
                The effects of beta-blockers given concomitantly with thrombolytic therapy in patients with acute myocardial infarction have not been fully examined. The potential role of specific bradycardiac agents lacking negative inotropism as an alternative to beta-blockers in this setting has never been studied in humans.
                In a double-blind study, we examined the effects of early intravenous and continued oral administration of a beta-blocker (atenolol), a specific bradycardiac agent (alinidine) or placebo on left ventricular function, late coronary artery patency, infarct size, exercise capacity and incidence of arrhythmias.
                A total of 292 patients with acute myocardial infarction of < or = 5 h duration and without contraindications to thrombolytic or beta-blocker therapy were studied. Of these, 100 were allocated to treatment with atenolol (5 to 10 mg intravenously followed by 25 to 50 mg orally every 12 h), 98 to alinidine (20 to 40 mg intravenously followed by 20 to 40 mg orally every 8 h) and 94 to placebo. All patients received 100 mg of alteplase over 3 h and full intravenous heparinization. No significant differences in coronary artery patency, global ejection fraction or regional wall motion were observed at 10 to 14 days among the three groups. Likewise, enzymatic and scintigraphic infarct size were also very similar. Neither atenolol nor alinidine was associated with a significant reduction in the incidence of arrhythmias during the 1st 24 h. No significant differences in clinical events were observed, with the exception of a greater incidence of nonfatal pulmonary edema in the atenolol group (6% vs. 1% in the alinidine group and 0% in the placebo group, p = 0.021).
                In the absence of contraindications, the administration of a beta-blocker or a specific bradycardiac agent together with thrombolytic therapy was safe. In this limited number of patients, these agents did not appear to enhance myocardial salvage or preservation of left ventricular function or to reduce the incidence of major arrhythmias in the early phase of infarction. To investigate the efficacy of nadolol in the prevention of supraventricular arrhythmias after coronary artery bypass graft (CABG) surgery, 148 patients undergoing elective CABG were randomized in double-blind, placebo-controlled fashion to receive either nadolol or placebo. The test medication was started on the first postoperative morning and maintained as a single daily dose for 6 weeks. Aside from routine daily clinical evaluation and postoperative electrocardiographic monitoring, patients underwent 24-hour Holter recording once preoperatively and 3 times postoperatively. Seven patients were excluded from the evaluation of efficacy analysis because of insufficient postoperative data. There were no significant differences between the patients receiving nadolol (n = 67) and those receiving placebo (n = 74) with respect to age, preoperative heart rate, previous medications (including beta blockers), incidence of previous myocardial infarction, frequency of preoperative ventricular and supraventricular arrhythmias, concomitant valvular heart disease, mean cardiopulmonary bypass time, mean aortic cross-clamp time, use of blood and crystalloid cardioplegia, mean number of bypass grafts placed, postoperative use of inotropic agents and catecholamines and incidence of perioperative myocardial infarction. Analysis of postoperative Holter recordings showed that the heart rate was consistently and significantly higher in the placebo group throughout the period of the study (p less than 0.001). The average number of premature atrial contractions was significantly smaller in the nadolol group (p less than 0.05), and nadolol patients had fewer ventricular premature complexes, couplets and non-sustained ventricular tachycardias during the first week postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS) Forty-five ASA I or II patients scheduled for elective surgery were randomized into one of three groups. Patients in Group 1 (n = 15) received no intratracheal aerosol at laryngoscopy. Patients in Group 2 (n = 15) and Group 3(n = 15) received 50 mg and 75 mg, respectively, of intratracheal aerosolized etidocaine at laryngoscopy. Cardiovascular and respiratory responses were observed at laryngoscopy and intubation and for the first ten minutes following laryngoscopy and intubation (with anesthesia provided by IV thiopental and nitrous oxide [70%] in oxygen). The magnitude and duration of blood pressure and heart rate increases caused by laryngoscopy and intubation were significantly less in the etidocaine-treated patients than in the controls (P less than .05). The incidence of coughing after intubation also was decreased significantly in the etidocaine-treated patients (P less than .05). Etidocaine did not, however, decrease the incidence of arrhythmias after intubation. The haemodynamic responses to laryngoscopy and intubation after induction of anaesthesia with thiopentone alone or in combination with 1.5 mg.kg-1 lidocaine and/or 1.5 or 3.0 microgram.kg-1 fentanyl were measured in 150 patients over 64 years of age to determine whether lidocaine, fentanyl or both lidocaine and fentanyl attenuated the pressor response. Fentanyl reduced the rises in systolic, diastolic and mean arterial pressures, heart rate, and rate pressure product and lidocaine decreased the rises in arterial blood pressure and rate pressure product (P less than 0.05). Fentanyl decreased the incidence of marked fluctuations in haemodynamic variables, often seen in geriatric patients (P less than 0.05). The haemodynamic effects of lidocaine and fentanyl were independent of each other. Complications occurred in all groups. Lidocaine-treated patients had fewer cardiac dysrhythmias (P less than 0.05) and 34 per cent of them had tinnitus. Fentanyl-treated patients had a higher incidence of hypotension (P less than 0.05). Respiratory depression developed in only one per cent of the fentanyl-treated patients. Both lidocaine and fentanyl are recommended adjuncts to induction of anaesthesia with thiopentone in geriatric patients. The effect of small intravenous doses of practolol (0.2 mg/kg body weight) on the circulatory response to laryngoscopy and endotracheal intubation, when administered with atropine (0.01 mg/kg b.w.) prior to anaesthesia was studied in 39 patients with and without cardiovascular disease. Practolol diminished significantly the rise of mean arterial pressure and pulse rate affected by laryngoscopy and endotracheal intubation when performed under thiopentone-succinylcholine anaesthesia. Arrhythmias were also less frequent through the statistical significance could not be ascertained in this small series. The small practolol dose used had no adverse circulatory effects. It is suggested that the administration of a small prophylactic dose of practolol is useful in preventing the excessive cardiovascular response due to laryngoscopy and endotracheal intubation. The effects of alfentanil and fentanyl on controlling the haemodynamic responses to laryngoscopy and intubation have been compared. Five groups of ten patients were studied. Induction was with thiopentone 4 mg/kg. Thirty seconds later group 1 received 1 ml/20 kg saline, group 2 received 15 micrograms/kg alfentanil, group 3 received 30 micrograms/kg alfentanil and group 4 received 5 micrograms/kg fentanyl one minute before induction. Suxamethonium was given 60 seconds after induction and intubation of the trachea was performed 150 seconds after the start of induction. Heart rate and mean arterial pressure were recorded every minute throughout and compared with pre-induction control values. Control patients (group 1) showed significant increases associated with tracheal intubation in all haemodynamic variables. No increases were noted in groups receiving 30 micrograms/kg alfentanil or 5 micrograms/kg fentanyl. The heart rate, but not blood pressure, increased with intubation after 15 micrograms/kg alfentanil. The mean time to movement in 50% of the control patients was 7 minutes. In those given 15 and 30 micrograms/kg alfentanil it was 11 and 12 minutes respectively. In those given 5 micrograms/kg fentanyl it was greater than 15 minutes. Alfentanil is shown to reduce the cardiovascular responses to laryngoscopy and intubation and the effect appears to have a shorter duration than that of fentanyl. Supraventricular tachyarrhythmia (SVT) commonly occurs shortly after coronary artery bypass grafting (CABG), but ventricular arrhythmias are less documented.
                On the 1st postoperative day, 206 consecutive eligible patients were prospectively randomized to a sotalol group (80 mg b.i.d.; n = 103) or a control group without beta-blockade or antiarrhythmic drugs (n = 103).
                The SVT incidence (predominantly atrial fibrillation) accounted for 16% in the sotalol group versus 48% (p < 0.00001). Multivariate analysis showed that sotalol reduced the SVT incidence (p < 0.00001, odds ratio, 0.20; 95% confidence interval, 0.09 to 0.42), whereas a lower preoperative left ventricular ejection fraction (p = 0.019) and older age (p = 0.031) were independent risk factors of SVT occurrence. The Holter electrocardiographic analysis (24 hours) demonstrated that sotalol (32 versus 92; p = 0.031) decreased the median number of ventricular events, mostly isolated premature ventricular beats. Neither ventricular proarrhythmia effect nor "torsades de pointes" were detected. Despite strict hemodynamic-based selection, sotalol had to be discontinued in 8 patients (7.8%), for reasons related to asthma in 3 or cardiac reasons in 5.
                Oral low-dose sotalol provided considerable and reliable protection in selected nondepressed cardiac function patients, reducing the occurrence of both supraventricular and ventricular arrhythmias after CABG. To determine the effects of thoracic epidural anesthesia (TEA) on ventilation-perfusion (VA/Q) relationships, atelectasis, and oxygenation before and after coronary artery bypass graft surgery (CABG).
                Prospective, controlled, unblinded, randomized trial.
                Cardiothoracic clinic at a major university referral center.
                Twenty-eight patients undergoing elective CABG.
                Perioperative and postoperative TEA was added to general anesthesia (GA) in 14 patients, and 14 patients receiving GA alone served as controls.
                VA/Q relationships were measured by the multiple inert gas elimination technique, and, 20 hours postoperatively, atelectasis was assessed by computerized tomographic scans. Arterial and mixed venous blood gases and hemodynamic variables were measured by standard techniques. TEA per se caused no change in shunt, VA/Q matching, or oxygenation. Induction of GA in the control group and induction of TEA caused similar reductions in mean arterial pressure. The TEA patients needed less morphine analgesia postoperatively and were extubated earlier. Extubation caused significant improvement in VA/Q matching. On the first postoperative day, a slight reduction in PaCO2 was seen in the TEA group, but no differences in shunt, VA/Q matching, or oxygenation compared with the GA group. Both groups showed extensive bilateral atelectasis.
                TEA can reduce respirator time and the need for morphine analgesics after CABG without negative effects on VA/Q matching, oxygenation, or atelectasis formation. After aorta-coronary bypass grafting, 164 consecutive patients were randomized to receive propranolol 5 mg every 6 hours orally (n = 82) or to serve as control subjects (n = 82). All patients were receiving beta blockers preoperatively. There were no significant differences between the two groups. The incidence of sustained supraventricular (nonsinus) tachyarrhythmias was 23% in the control group and 9.8% in the treated group (p = 0.02). The incidence of ventricular arrhythmias was 15% in the control group and 2.4% in the treated group (p = 0.005). The overall difference in clinically important arrhythmias was 38% in the control group and 12.2% in the treated group (p = 0.0002). We conclude that low-dose oral propranolol in patients who were receiving beta blockers preoperatively is effective in reducing the incidence of clinically important arrhythmias occurring after aorta-coronary bypass grafting. Arrhythmias are common after open heart surgery and may be related to hypomagnesaemia due to cardiopulmonary bypass. Although perioperative prophylactic Mg2+ administration may prevent arrhythmias after coronary artery bypass grafting (CABG), clear indications as well as the timing of Mg2+ substitution and dose regimen need to be clarified. Aim of this study was to evaluate the antiarrhythmic effects of Mg2+ infusion in patients who underwent elective CABG.
                Ninety-seven patients who underwent elective CABG were divided in four Groups. In Group A 1 g of magnesium sulfate was added to the pump prime, Group B received 1 g in the pump prime plus 5 mmol/L in the cardioplegic solution, Group C received 5 mmol/L in the cardioplegic solution, and Group D was a placebo control Group. Groups A, B, and C also received 24 h continuous infusion of magnesium sulfate at 10 mmol/L. Three-channel electrocardiogram (II-V5-V6) continuous monitoring was performed 12 hours preoperatively and 48 hours postoperatively. Blood samples were taken for subsequent Serum magnesium measurements, at five different time points before, during and after CBP.
                In all Groups serum Mg2+ levels were reduced during CPB (Time 2) and statistically significant differences from pre-anaesthesia levels (Time 1) were noted (p <0.05). In Groups A, B, and C Serum Mg2+ levels increased progressively from Time 3 to Time 5; in Group D serum Mg2+ levels were still much lower at Time 5. Significant differences (p<0.05) were noted for Groups B and C vs Groups A and D in atrial ectopics, atrial fibrillation, and ventricular arrhythmic events.
                Our results demonstrate that Mg2+ sulfate administration regimens used in Group B and C reduce postoperative arrhythmic events in patients undergoing CABG. It has been proposed that a single preoperative dose of a corticosteroid may protect the myocardium from ischemic injury during open heart surgery. To test this hypothesis, a prospective, randomized, double blind study was carried out in ninety-five patients undergoing coronary bypass surgery using intermittent ischemic arrest with systemic and local hypothermia. Half the patients received 2 gm (approximately 30 mg/kg) of methylprednisolone 2 hours prior to the initiation of cardiopulmonary bypass and the other half received a placebo. Postoperative electrocardiograms and blood levels of serum creatine phosphokinase (CPK), lactic dehydrogenase (LDH), and serum glutamic oxalacetic transaminase (SGOT) were compared in the two groups. No apparent difference was noted in the number of patients with significantly elevated levels of CPK, LDH, or SGOT or in the number with positive isoenzyme patterns of CPK and LDH. Moreover, there was no significant difference in the mean values of CPK, LDH, or SGOT between the two groups. The number of patients with electrocardiographic evidence of myocardial injury (10 per cent) was the same in both groups and no difference was noted in (1) the ease with which patients could be weaned from cardiopulmonary bypass, (2) postoperative arrhythmias, (3) postoperative bleeding, (4) postoperative respiratory insufficiency, and (5) length of hospital stay. It is concluded that a single preoperative dose of 2 gm of methylprednisolone offers no demonstrable protection to the myocardium from the effects of ischemia during coronary artery bypass surgery. Thirty adult patients who underwent coronary artery bypass graft surgery were allocated randomly to one of two equal groups to receive either 2% nitroglycerin, or a placebo ointment, applied topically over an area of 5 cm by 10 cm, in a double-blind manner, 1 h before induction of anaesthesia. Premedication consisted of oral diazepam 5-10 mg, intramuscular morphine 0.2 mg.kg-1 and promethazine 0.4 mg.kg-1. Anaesthesia was induced with morphine 0.15-0.2 mg.kg-1 and thiopentone 3-5 mg.kg-1. Laryngoscopy and tracheal intubation were facilitated by suxamethonium 1.5 mg.kg-1, and pancuronium 0.1 mg.kg-1 was used for subsequent muscle relaxation. Anaesthesia was maintained with 0.5% halothane and 40% oxygen in nitrous oxide. A significant increase in blood pressure occurred during and after laryngoscopy and tracheal intubation, and following midline sternotomy in the control group. These changes were absent in patients pretreated with topical nitroglycerin. The nitroglycerin group also maintained a lower rate-pressure product than the control group. We conclude that topical nitroglycerin is a simple and useful pretreatment to prevent the pressor response to tracheal intubation and midline sternotomy in patients undergoing coronary artery bypass graft surgery. Mivazerol hydrochloride is a new alpha 2-adrenoceptor agonist. In vitro and animal studies have demonstrated both sympatholytic and antiischemic properties. To evaluate the safety and efficacy of mivazerol in patients during perioperative stress, this multicenter phase II clinical trial studied hemodynamic stability and myocardial ischemia in patients with coronary artery disease undergoing noncardiac surgery.
                Three hundred patients, from twenty-three European medical institutions, participated in this placebo-controlled, double-blind, randomized, parallel-group trial. Ninety-eight were given high-dose mivazerol (1.5 micrograms.kg-1.h-1); 99, low-dose mivazerol (0.75 microgram.kg-1.h-1); and 103, placebo, continuously intraoperatively and for 72 h postoperatively. Blood pressure and heart rate were monitored for 96 h. Myocardial ischemia was assessed by Holter electrocardiography for at least 8 h before induction of anesthesia until 96 h after surgery. Twelve-lead electrocardiograms and creatine kinase myocardial band isoenzyme levels were obtained before and serially after surgery. Adverse cardiac events were assessed for the intraoperative, early postoperative (0-24 h), and late postoperative (24-72 h) periods.
                The incidence of tachycardia was significantly lower with high-dose mivazerol (vs. placebo) during the intraoperative (30% vs. 51%; P = 0.002), early postoperative (29% vs. 50%; P = 0.002), and late postoperative periods (46% vs. 70%; P = 0.001). Also, the percentage of patients treated for tachycardia was significantly lower with the high dose (vs. placebo) during the early (10% vs. 20%; P = 0.043) and late (6% vs. 15%; P = 0.024) postoperative periods. The incidence of hypertension was significantly lower with both high and low doses (vs. placebo) during the intraoperative period (46% and 43%, respectively, vs. 63%; P = 0.010); treatment was similar at both high and low doses (33% and 34%, respectively, vs. 46%; P = 0.066). The incidence of bradycardia was significantly higher at both dose levels than with placebo during and after drug administration (intraoperatively-3%, 7%, and 9%; early postoperative-0%, 5%, and 6%; late postoperative-0%, 4%, and 6%; after drug-0%, 6%, and 6%; placebo, low-dose, high-dose, respectively), but the need for treatment did not differ for the groups. The incidence of, and treatment for, hypotension were similar for the three groups. Intraoperative myocardial ischemia was significantly lower with high-dose mivazerol than with placebo (20% vs. 34%, respectively, P = 0.026). When intraoperative data were subdivided into emergence vs. nonemergence periods (post boc analysis), the incidence of myocardial ischemia was significantly lower with high-dose mivazerol than with placebo during emergence (11% vs. 30%; P = 0.001). Regarding blood pressure, heart rate, and ischemia, no rebound response occurred in the 12 h after discontinuation of mivazerol. The high-dose, low-dose, and placebo groups did not differ in the incidence of adverse cardiac outcomes (3%, 2%, and 8%, respectively) or the diagnosis of myocardial infarction (2%, 1%, and 6%, respectively).
                Continuous, 72-h perioperative administration of mivazerol to high-risk patients appears to be relatively safe, producing no significant hypotension or adverse events but some evidence of bradycardia not associated with adverse clinical events. Mivazerol decreased the incidence of, and treatment for, tachycardia, hypertension, and myocardial ischemia, particularly during high stress periods. Therefore, these salutary effects of mivazerol indicate further study in large-scale trials that assess mivazerol's effects on adverse cardiac outcomes, including death and myocardial infarction. To examine the effect of doubling serum magnesium concentration on the incidence of arrhythmias in patients with suspected acute myocardial infarction.
                Randomised double blind clinical trial.
                Coronary care unit of a teaching hospital.
                Clinical data were collected on 2316 randomised patients with suspected acute myocardial infarction. Holter monitoring was performed in a subgroup of 70 patients and analysed in 48 patients in whom acute myocardial infarction was confirmed.
                By random allocation, patients received either an intravenous loading dose of 8 mmol magnesium sulphate over five minutes plus 65 mmol over the next 24 hours, or equal volumes of saline.
                (a) Clinically documented arrhythmias; (b) use of antiarrhythmic treatments, cardioversion, and insertion of a pacemaker; (c) incidence of all abnormal rhythms during Holter monitoring.
                In the main trial the incidence of rhythm disturbance while in the coronary care unit (expressed as the odds ratio (OR) for magnesium: placebo and its 95% confidence interval) was not significantly different between treatment groups for ventricular fibrillation (OR 0.74; 0.46 to 1.20), ventricular tachycardia (OR 0.87; 0.63 to 1.20), supraventricular tachycardia (OR 0.69; 0.38 to 1.26), atrial fibrillation (OR 0.92; 0.69 to 1.23), or heart block of any degree (OR 1.17; 0.83 to 1.65). Sinus bradycardia was significantly more common in the magnesium group (OR 1.38; 1.03 to 1.85; p = 0.02). These findings were corroborated by the use of treatments for rhythm disturbance and the data from Holter monitoring.
                The regimen of intravenous magnesium sulphate used here had no significant effect on arrhythmia in acute myocardial infarction. The reduction in mortality that has been shown with this form of treatment is not attributable to suppression of life threatening rhythm disturbances. We undertook a prospective, randomized, controlled clinical trial to evaluate morbidity outcomes and safety of a modified anesthetic technique to provide shorter sedation and early extubation (1 to 6 hours) than those of the conventional anesthetic protocol used for prolonged sedation and extubation (12 to 22 hours) in patients after coronary artery bypass grafting.
                One hundred twenty patients undergoing elective coronary artery bypass grafting were prospectively assigned randomly to either an early extubation group (n = 60; 15 micrograms.kg-1 fentanyl and 2 to 6 mg.kg-1.hour-1 propofol and isoflurane) or to a conventional extubation group (n = 60; 50 micrograms.kg-1 fentanyl and 0.1 mg.kg-1 midazolam and isoflurane). Cardiac morbidity (postoperative myocardial ischemia, postoperative myocardial infarction, and perioperative sympathoadrenal stress response), respiratory morbidity (postextubation apnea, alveolar-arterial oxygen gradient, pulmonary shunting, oxygen consumption, atelectasis, and reintubation), hemodynamic values and vasoactive medication requirements, intraoperative awareness, postoperative cognitive function, 30 day mortality, and intensive care unit and hospital lengths of stay were compared between the two groups.
                Fifty-one of the 60 patients in each group (85%) were extubated within the defined time period. Postoperative extubation time and intensive care unit and hospital lengths of stay were significantly shorter in the early group. At 48 hours after operation, there were no significant differences between the two groups in myocardial ischemia incidences, ischemia burdens, or creatine kinase isoenzyme MB levels. Four patients in the conventional group, but not in the early group, had postoperative myocardial infaction. The extubation anesthetics used were effective in suppressing the perioperative plasma catecholamine stress response in both groups. Postextubation apnea characteristics were similar between the groups. Intrapulmonary shunt fraction improved significantly in the early group at 4 hours after extubation. The incidences and degree of atelectasis did not differ significantly between the two groups. The incidences of treated postoperative complications were comparable between the two groups, but three patients in the conventional group died as a result of stroke or postoperative myocardial infarction.
                Early extubation after coronary artery bypass grafting is safe and does not increase perioperative morbidity. There is an improvement in postextubation intrapulmonary shunt fraction and a reduction in intensive care unit and hospital lengths of stay. Cardiopulmonary bypass (CPB) has been implicated in causing poor pulmonary gas exchange postoperatively in patients undergoing coronary artery bypass grafting (CABG) procedures. In this prospective, randomized, double-blind, placebo-controlled study, we examined the pulmonary effects of N-acetylcysteine (NAC) in patients undergoing CABG. Twenty patients undergoing elective CABG and early tracheal extubation were randomized into two groups. Group I (ten patients) received a physiologic salt solution as a placebo in a continuous intravenous infusion for one hour before CPB and 24 hours after CPB; Group II (ten patients) received 100 mg/ kg NAC intravenously for one hour before CPB and 40 mg/kg/day at 24 hours after CPB. Perioperative hemodynamic and pulmonary data were recorded. Postoperative tracheal extubation was accomplished at the earliest appropriate time. The postoperative clinical course was similar in the two groups. Both groups exhibited significant postoperative increases in A-a oxygen gradient (p < 0.01), but patients in Group II exhibited significantly lower increases in postoperative A-a oxygen gradient (p < 0.006). Other hemodynamic and pulmonary data (pulmonary capillary wedge pressure, pulmonary vascular resistance (PVR), cardiac index (CI), shunt flow, dynamic lung compliance and static lung compliance) exhibited no differences between the groups. There was no significant difference in terms of intubation time. The malondialdehyde (MDA) increase in Group II following CPB was found to be significantly lower than in Group I (p = 0.043). This clinical study reveals that administration of NAC to patients undergoing elective CABG with CPB improves systemic oxygenation. There was no effect in other pulmonary parameters and in terms of intubation time. The aim of this study was to test whether the left ventricular assist device (LVAD) Impella LP2.5 (Abiomed Europe GmbH, Aachen, Germany) provides superior hemodynamic support compared with the intra-aortic balloon pump (IABP).
                Cardiogenic shock caused by left ventricular failure is associated with high mortality in patients with acute myocardial infarction (AMI). An LVAD may help to bridge patients to recovery from left ventricular failure.
                In a prospective, randomized study, 26 patients with cardiogenic shock were studied. The primary end point was the change of the cardiac index (CI) from baseline to 30 min after implantation. Secondary end points included lactic acidosis, hemolysis, and mortality after 30 days.
                In 25 patients the allocated device (n = 13 IABP, n = 12 Impella LP2.5) could be safely placed. One patient died before implantation. The CI after 30 min of support was significantly increased in patients with the Impella LP2.5 compared with patients with IABP (Impella: DeltaCI = 0.49 +/- 0.46 l/min/m(2); IABP: DeltaCI = 0.11 +/- 0.31 l/min/m(2); p = 0.02). Overall 30-day mortality was 46% in both groups.
                In patients presenting with cardiogenic shock caused by AMI, the use of a percutaneously placed LVAD (Impella LP 2.5) is feasible and safe, and provides superior hemodynamic support compared with standard treatment using an intra-aortic balloon pump. (Efficacy Study of LV Assist Device to Treat Patients With Cardiogenic Shock [ISAR-SHOCK]; NCT00417378). The usual hemodynamic response to laryngoscopy and bronchoscopy is an increase in heart rate and arterial blood pressure. Previous work has reported that 10%-18% of the patients develop ischemic ST segment changes during the procedure. Therefore, we performed a prospective, randomized, double-blinded study in 36 patients scheduled for elective microlaryngeal and bronchoscopic surgical procedures to evaluate the effects of 300-microg oral clonidine premedication (n = 18) or placebo (n = 18) on the hemodynamic alterations and the incidence of perioperative myocardial ischemic episodes. Myocardial ischemia was assessed by using continuous electrocardiographic monitoring, beginning 30 min before, and lasting until 24 h after the operation. During the procedure, patients receiving placebo exhibited a significant increase (mean +/- SD) in arterial blood pressure (the systolic increasing from 137+/-11 to 166+/-17 mm Hg, the diastolic increasing from 80+/-11 to 97+/-14 mm Hg) and heart rate (increasing from 79+/-15 to 97+/-12 bpm) compared with the baseline and with the clonidine group. A dose of 300-microg clonidine blunted the hemodynamic response to endoscopy. Ventricular arrhythmias were more frequent in patients who were not premedicated with clonidine. Two patients in the control group, but none in the clonidine group, had evidence of myocardial ischemia. These data should encourage routine premedication with clonidine in patients undergoing microlaryngoscopic and bronchoscopic procedures. Adriamycin (ADM) is an effective antineoplastic drug. However, the amount of ADM that can be administered must be limited because of the risk of developing a severe dose-dependent myocardiopathy. Prenylamine (PNL), a calcium antagonistic drug, provided partial protection against ADM-induced cardiotoxicity in mice and in the rabbit. Thus, it was considered important to evaluate the cardioprotective potential of PNL in patients given ordinary doses of ADM. Twenty-six patients were selected and randomized in two groups, and a double-blind trial was begun. Group A (n = 13): patients received ADM, i.v. at standard oncological doses up to 550 mg/m2, plus placebo, orally. Group B (n = 13): ADM was administered as in Group A, but PNL 200 mg/day was given instead of placebo. Standard ECG and chest radiographs were performed at the beginning of treatment and every two months. Mode-M echocardiograms and 24-hour ambulatory ECGs were obtained previously to the beginning of the ADM treatment and two months after the administration of the last dose of the drug. In Group A, three patients died from oncological causes, total ADM dose was 359 +/- 100 mg/m2, and the mean age was 59.7 years. One patient in this group developed a congestive myocardiopathy while another patient developed a severe supraventricular arrhythmia. In Group B, four patients died from oncological causes, total ADM dose was 367 +/- 132 mg/m2, and the mean age was 63.8 years. No myocardiopathy was found in this group. These findings suggest that simultaneous administration of PNL may mitigate ADM cardiotoxicity, but larger trials are needed to draw definite conclusions. The objective of the study was to evaluate and compare the safety of levobupivacaine and racemic bupivacaine for paracervical block (PCB) in the first stage of labor after uncomplicated pregnancy.
                Forty women in an open pilot study and 397 women in a double-blind randomized study received PCB for pain relief in the first stage of labor, either with 25 mg of levobupivacaine or with 25 mg of racemic bupivacaine. The incidence of cardiotocographic pathology was compared between the groups using Fisher's exact test. The 95% confidence intervals for the between-group difference were calculated by Newcombe's method.
                In the randomized double-blind study, the incidence of any pathological result in cardiotocography (CTG) was 10.4% in the levobupivacaine group and 12.8% in the racemic bupivacaine group. The incidence of fetal bradycardia in the groups was 2.6 and 3.8%, respectively. All the cardiotocographic changes were transient, and no operative intervention was indicated because of CTG. No difference in the analgesic effect between the drugs was found. Most of the parturients in the levobupivacaine group (97%) and in the racemic bupivacaine group (96%) had spontaneous vaginal delivery. Neonatal outcome was good in both groups.
                No difference in cardiotocographic pathology was found between PCB with levobupivacaine compared with PCB with racemic bupivacaine. The incidence of bradycardia was low. PCB was found to be a safe pain-relief method for low-risk parturients. This study was designed to examine the optimal timing of intravenous lidocaine in attenuation of increase of intraocular pressure in response to laryngoscopy and tracheal intubation during induction of anesthesia.
                One hundred and thirty five adult patients of ASA class I, aged between 20-35 years, undergoing surgical procedures irrelevant to ophthalmology were enrolled for study. Patients were randomly assigned to one of five groups. In group II, III, IV and V the patients received intravenous injection of lidocaine (2 mg/kg), 1, 3, 5, 10 min before tracheal intubation, respectively. Group I in which patients did not receive lidocaine served as the control group.
                In patients of groups I, IV and V, the intraocular pressure increased significantly after intubation, whereas in those of groups II and III, the intraocular pressure did not. All patients in the five groups showed concomitantly a surge of blood pressure, but the magnitude of increase was smallest in group III in comparison with the other groups. The values of systolic and diastolic pressures 1 min after intubation were significantly less in groups III and IV than in the control group.
                In healthy patients aged between 20 and 35 the most optimal time of administration of intravenous lidocaine to attenuate the increase of intraocular pressure seemed to be the space between 1 to 3 min before laryngoscopy and tracheal intubation. To determine the optimal dose of nicardipine (N) for maintenance of hemodynamic stability during the postinduction period, we designed a randomized, double-blind, placebo-controlled, dose-ranging study using four different doses of N administered after a standardized anesthetic induction sequence. A total of 106 patients were assigned to one of the following treatment groups: saline (control), N 0.5 mg (N0.5), N 1 mg (N1), N 2 mg (N2), and N 4 mg (N4). The study medication was administered intravenously (I.V.) in 2.5 mL of saline over 30 s 2 min before laryngoscopy. Mean arterial pressure (MAP) and heart rate (HR) were recorded at 1-min intervals for 15 min after tracheal intubation and for 5 min after skin incision. After intubation, the peak MAP values differed from the preinduction baseline MAP values by 21% +/- 20%, 9% +/- 12%, 1% +/- 13%, -10% +/- 12%, and -15% +/- 13% (mean +/- SD) in the control, N0.5, N1, N2, and N4 groups, respectively. However, the percent change in the pre- to postintubation MAP values (37% to 47%) was similar in all five groups. The highest postintubation HR values were recorded in the N4 group (P < 0.05 versus the other groups). However, the increases in MAP values after skin incision were the least in the N4 group. In conclusion, N1 I.V., administered 2 min before laryngoscopy provides optimal control of arterial blood pressure during the postinduction period. Implications: Acute increases in blood pressure during anesthesia are undesirable in patients with preexisting cardiovascular diseases. This double-blind study found that the calcium-channel blocker, nicardipine, 1 mg intravenously 2 min before tracheal intubation maintained hemodynamic stability during the intraoperative period. To assess the efficacy and safety of bone marrow cell (BMC) therapy after thrombolytic therapy of an acute ST-elevation myocardial infarction (STEMI).
                Patients with STEMI treated with thrombolysis followed by percutaneous coronary intervention (PCI) 2-6 days after STEMI were randomly assigned to receive intracoronary BMCs (n = 40) or placebo medium (n = 40), collected and prepared 3-6 h prior PCI and injected into the infarct artery immediately after stenting. Efficacy was assessed by the measurement of global left ventricular ejection fraction (LVEF) by left ventricular angiography and 2-D echocardiography, and safety by measuring arrhythmia risk variables and restenosis of the stented vessel by intravascular ultrasound. At 6 months, BMC group had a greater absolute increase of global LVEF than placebo group, measured either by angiography (mean +/- SD increase 7.1 +/- 12.3 vs. 1.2 +/- 11.5%, P = 0.05) or by 2-D echocardiography (mean +/- SD increase 4.0 +/- 11.2 vs. -1.4 +/- 10.2%, P = 0.03). No differences were observed between the groups in the adverse clinical events, arrhythmia risk variables, or the minimal lumen diameter of the stented coronary lesion.
                Intracoronary BMC therapy is associated with an improvement of global LVEF and neutral effects on arrhythmia risk profile and restenosis of the stented coronary lesions in patients after thrombolytic therapy of STEMI. Eighty-five patients receiving long-term propranolol therapy were randomized after aorta-coronary bypass grafting either to receive minidose propranolol (Group I) or to serve as controls (Group II). They were compared with 18 patients (Group III) who did not receive beta blocking agents prior to operation but were given propranolol postoperatively. Poor-risk patients (those having left ventricular aneurysms, low ejection fraction, or congestive heart failure) as well as patients who required catecholamines postoperatively were included in the study. All three groups were comparable with respect to all risk factors. Propranolol (5 to 10 mg/6 hr) was started through a nasogastric tube 6 hours after operation and continued orally in all patients in Groups I and III. Supraventricular tachyarrhythmia appeared in two of 37 patients in Group I (5%), 19 of 48 patients in Group II (40%), and five of 18 patients in Group III (27%). The incidence of supraventricular tachyarrhythmia was significantly lower in Group I than in Groups II and III (p less than 0.001, Group I versus Group II; p less than 0.01, Group I versus Group III). In conclusion, low-dose propranolol is very effective in preventing supraventricular tachyarrhythmia following aorta-coronary bypass in patients receiving beta blockers preoperatively. The increased tendency for postoperative supraventricular tachyarrhythmia to develop in these patients is attributed to hypersensitivity to adrenergic stimulation after propranolol withdrawal. The tachyarrhythmia can be prevented by early reinstitution of propranolol in low doses after the operation. The efficacy of sublingual nifedipine, administered one minute before anaesthetic induction, in order to minimise the pressor response to laryngoscopy and tracheal intubation was studied in a group of 15 patients who underwent coronary artery bypass surgery. Another group of 15 similar patients served as control. Premedication consisted of oral diazepam 5-10 mg, intramuscular morphine 0.2 mg/kg and promethazine 0.4 mg/kg. Anaesthesia was induced with morphine 0.1-0.15 mg/kg and thiopentone 3-5 mg/kg. Laryngoscopy and tracheal intubation were facilitated with suxamethonium 1.5 mg/kg. A significant increase in blood pressure occurred during and after laryngoscopy and tracheal intubation in the control group. This increase was absent in the patients pretreated with nifedipine. The nifedipine group also maintained a lower rate-pressure-product than the control group during the period of study. It is concluded that nifedipine 10 mg is a useful pretreatment to prevent the pressor response to laryngoscopy and tracheal intubation in patients with coronary artery disease. A central anticholinergic syndrome (CAS) can be related to the majority of anesthetic agents, but is often not recognized as such. Thus, most anesthesiologists seem to miss the occurrence of an anticholinergic syndrome especially when agitation and/or restlessness are the major symptoms. Therefore, the following study was undertaken to test the hypothesis that routine administration of the anticholinergic agent physostigmin is of benefit for patients in regard to vigilance, the cardiovascular system and the need of analgesics easing the time in the post anesthesia care unit (PACU).
                After approval by the local ethics committee and written informed consent, 100 patients undergoing a cholecystectomy or a struma resection, were given either physostigmin (n = 51) or saline 0.9 % (n = 49) in a randomized fashion. The study was conceived to block a possible isoflurane-N2O/O2 (opioid-based plus relaxant) induced central anticholinergic syndrome and to evaluate the effects on the cardiovascular system on vigilance and on postoperative analgesic demand. Following parameters were measured: systolic and diastolic blood pressure, heart rate, respiratory rate, and arterial blood gases. In addition, vigilance was determined and typical anticholinergic symptoms (disorientation, slurred speech, agitation, nausea, emesis, cardiac arrhythmia and muscle shivering) were determined 10, 20, 40 and 60 minutes following the intravenous injection of physostigmin. Also, the need for the postoperative analgesic pethidine was evaluated among the two groups.
                Except for a significant reduction in the need of analgesics, a reduced diastolic pressure and heart rate and a lower incidence of muscle shivering there was no difference among the two groups. One major side effect following the use of physostigmin was the higher incidence of nausea in the im mediate minutes following injection. This effect may be due to the rapid injection of the anticholinergic compound. Otherwise there were no detrimental effects of physostigmin in patients.
                From the results it can be concluded that routine administration of an anticholinergic agent results in a short term beneficial effect in regard to vigilance, a lesser incidence of muscle shivering and a lesser demand for analgesics. However, because of the low incidence of a classical central anticholinergic syndrome, routine physostigmine is only indicated when agitation is diagnosed. Rocuronium (ORG 9426) has been shown to have an onset of action more rapid than other nondepolarizing neuromuscular blocking agents and to provide intubating conditions similar to those of succinylcholine 60-90 s after administration. We compared the intubating conditions and hemodynamic changes after the administration of rocuronium 0.6 mg kg(-1) and lidocaine 1.5 mg kg(-1) with rocuronium alone and succinylcholine 60 and 90 s after administration.
                One hundred and twenty-five adult patients of ASA physical status I or II scheduled for elective surgery were randomly divided into five groups. After propofol administration in all patients, patients in group Su (succinylcholine), group R60 (rocuronium) and group RL60 (rocuronium-lidocaine) were intubated within 60 s, while groups RL90 and R90 were intubated 90 s after the administration of rocuronium and succinylcholine. Laryngoscopy was performed and intubating conditions were graded by an experienced anesthetist blind to the muscle relaxant allocation.
                In this study, groups Su, RL60, R90 and RL90 had similar intubation scores, which were significantly better than that for group R60. Heart rate did not increase after intubation in groups Su, RL60 and RL90.
                The combination of lidocaine (1.5 mg kg(-1)) and low-dose rocuronium (0.6 mg kg(-1)) along with propofol is clinically equivalent to succinylcholine, improves intubating conditions in 60 s and effectively blocks increases in heart rate after intubation. Sotalol is a beta-adrenergic blocking drug with the additional property of lengthening the cardiac action potential. These electrophysiologic properties render the drug attractive for use in the prevention of postoperative supraventricular arrhythmias (SVA), and previous studies have suggested that it was indeed effective. The hemodynamic response to sotalol and its safety early after coronary artery bypass graft (CABG) surgery were therefore studied. Forty-two patients undergoing CABG were randomly assigned either to receive sotalol to prevent postoperative SVA (25 patients) or to serve as controls (17 patients). Sotalol was started 6 hours after surgery if patients had a cardiac index > 2.8 L/min/m2 with a pulmonary capillary wedge pressure < 15 mmHg, and if they had no contraindications to the use of beta-blockers. The drug was given as a loading infusion of 1 mg/kg over 2 hours, followed by a maintenance infusion of 0.15 mg/kg/h for 24 hours. Three hours later, patients received the first oral dose of 80 mg to be repeated every 8 or 12 hours. Adverse effects necessitating discontinuation of the drug (bradycardia < 50 beats/min, systolic blood pressure < 90 mmHg, or cardiac index < 2.2 L/min/m2) occurred in six patients (24%) and were mainly related to the loading infusion. The hemodynamic data for patients who completed the study were characterized by a significant fall of the cardiac index caused by a lower heart rate without significant change of the stroke volume index. The incidence of supraventricular arrhythmias was not significantly different in the two groups (3/19 in the sotalol group, 5/17 in the control group).(ABSTRACT TRUNCATED AT 250 WORDS) During conventional cardiac surgery ischemia and reperfusion may cause excessive production of reactive oxygen species leading to tissue damage including early arrhythmias. We therefore assessed the kinetics of markers of radical stress including oxidized and reduced glutathione (GSSG/GSH), oxidized proteins (PCG) and malondialdehyde (MDA), and tested the hypothesis that different steroid treatments inhibit these markers and early reperfusion-associated supraventricular and ventricular extrasystolic beats.
                In a randomized, controlled, blinded, prospective trial 36 patients received a preoperative infusion of methylprednisolone (MP, 15 mg kg-1, n = 12), tirilazad mesylate (TM, 10 mg kg-1, n = 12) or placebo (PL, NaCl, n = 12). Coronary sinus and arterial blood was drawn at baseline and 2, 5, 15, 30, 60 and 240 min after aortic declamping. Holter-ECG analysis was used to identify arrhythmias.
                Cardiac GSSG release occurred very early (< 15 min) and was not significantly attenuated by either drug treatment. Cardiac PCG production showed biphasic increases, lasted > 4 h and was significantly reduced only by TM. Cardiac MDA release was short (< 30 min) and significantly reduced by MP and TM. Neither treatment had a significant influence on the early occurrence of ventricular or supraventricular arrhythmias. The number of patients needing cardioversions or defibrillations also were not different.
                The results indicate that cardiac production of reactive oxygen species occurs after reperfusion in humans and is not inhibited by steroid treatment. Steroid treatment effectively reduces lipid peroxidation during cardiac surgery but has no influence on arrhythmias. Sixty patients undergoing coronary artery bypass grafting operations with cold potassium cardioplegia as the method of myocardial preservation either received low-dose oral propranolol (10 mg every 6 hours; 28 patients) or served as controls (32 patients). The study period began after extubation and ended at the time of hospital discharge. On the fourth postoperative day, 24-hour Holter monitoring was performed to assess additional subtle differences in arrhythmias. The overall incidence of symptomatic postoperative arrhythmias was 31% in the control group: 6 patients (19%) had atrial fibrillation or flutter and 4 patients (12%), ventricular arrhythmias. By contrast, 1 patient (4%) in the propranolol group had atrial fibrillation, and no patient had ventricular arrhythmias. The difference in overall arrhythmia rates between the two groups is significant (p less than 0.025). Twenty-four-hour Holter monitoring demonstrated no additional differences in the frequency of simple or complex atrial or ventricular ectopy between the two groups. We conclude that the incidence of postoperative arrhythmias following coronary artery bypass operation is diminished by the oral administration of prophylactic low-dose propranolol. When compared with our previous study [1], in which the method of myocardial preservation was intermittent aortic cross-clamping and moderate hypothermia, there is no difference in the overall incidence of postoperative arrhythmias. A double-blind, randomised trial was conducted in 24 patients without cardiopulmonary disorders (20-43 years), to assess the effect of an intravenous bolus of alfentanil on the circulatory and catecholamine responses to rapid sequence induction of general anaesthesia. Induction included injection of thiopentone 5 mg/kg and suxamethonium 1.5 mg/kg in rapid succession, followed by laryngoscopy and intubation. Half of the patients received alfentanil 100 micrograms/kg immediately before thiopentone. The other half received saline. Blood pressure, heart rate, and plasma catecholamine concentrations were measured repeatedly, together with left ventricular ejection fraction assessed by radionuclide angiocardiography. The responses following laryngoscopy and intubation were completely different in the saline vs. the alfentanil group: rate pressure product +76% vs. -32%, mean arterial blood pressure +46% vs. -25%, heart +46% vs. no change, noradrenaline +117% vs. -25%, adrenaline +50% vs. -53%, and left ventricular ejection fraction -32% vs. no change. In conclusion, during rapid sequence induction of anaesthesia with thiopentone and suxamethonium, an intravenous bolus of alfentanil 100 micrograms/kg 1 min before laryngoscopy and intubation completely prevents hypertension, tachycardia, decrease in left ventricular ejection fraction, and activation of plasma catecholamines, though at the expense of moderate hypotension. Sixty coronary artery bypass grafting patients were randomized to receive either magnesium sulphate or placebo for 4 days postoperatively. The magnesium substitution reduced the duration of atrial fibrillation or flutter (p < 0.05), but not the number of patients developing these arrhythmias. The number of ventricular ectopic beats was also reduced among patients receiving magnesium sulphate compared to placebo (p < 0.05). To evaluate whether the anti-arrhythmic effect of magnesium sulphate was explained by a faster resumption of cellular potassium postoperatively, skeletal muscle electrolyte concentrations were measured pre-operatively and on the third day postoperatively. No significant difference was found in skeletal muscle potassium or magnesium contents on the third day postoperatively when comparing the two groups. The serum magnesium level declined postoperatively in the placebo group, whereas an increase was found in patients receiving magnesium sulphate. We suggest magnesium substitution as a routine postoperatively, because this treatment seems to reduce the severity of postoperative arrhythmias. Atrial fibrillation (AF) frequently occurs after cardiac surgical procedures, and beta-blockers, sotalol, and amiodarone may reduce the frequency of AF after open heart surgery. This pilot trial was designed to test whether each of the active oral drug regimens is superior to placebo for prevention of postoperative AF and whether there are differences in favor of 1 of the preventive strategies.
                We conducted a randomized, double-blinded, placebo-controlled trial in which patients undergoing cardiac surgery in the absence of heart failure and without significant left ventricular dysfunction (n = 253; average age, 65 +/- 11 years) received oral amiodarone plus metoprolol (n = 63), metoprolol alone (n = 62), sotalol (n = 63), or placebo (n = 65). Patients receiving combination therapy (amiodarone plus metoprolol) and those receiving sotalol had a significantly lower frequency of AF (30.2% and 31.7%; absolute difference, 23.6% and 22.1%; odds ratios [OR], 0.37 [95% CI, 0.18 to 0.77, P <.01 vs placebo] and 0.40 [0.19 to 0.82, P =.01 vs placebo]) compared with patients receiving placebo (53.8%). Treatment with metoprolol was associated with a 13.5% absolute reduction of AF (P =.16; OR, 0.58 [0.29 to 1.17]. Treatment effects did not differ significantly between active drug groups. Adverse events including cerebrovascular accident, postoperative ventricular tachycardia, nausea, and dyspepsia, in hospital death, postoperative infections, and hypotension, were similar among the groups. Bradycardia necessitating dose reduction or drug withdrawal occurred in 3.1% (placebo), 3.2% (combined amiodarone and metoprolol; P =.65 vs placebo), 12.7% (sotalol; P <.05 vs placebo), and 16.1% (metoprolol; P <.05 vs placebo). Patients in the placebo group had a nonsignificantly longer length of hospital stay as compared with the active treatment groups (13.1 +/- 8.9 days vs 11.3 +/- 7; P =.10), with no significant difference between the active treatment groups.
                Oral active prophylaxis with either sotalol or amiodarone plus metoprolol may reduce the rate of AF after cardiac surgery in a population at high risk for postoperative AF. Treatment with metoprolol alone resulted in a trend to a lower risk for postoperative AF. To evaluate the safety and role of prophylactic administration of magnesium in preventing arrhythmias.
                This double blind randomized placebo controlled clinical trial was conducted at Aga Khan University Hospital on coronary artery bypass surgery patients. All patients were connected to holter monitor before induction of anaesthesia and this monitoring continued for 24 hours. Study drug containing either 2-grams of magnesium or normal saline was given after intubation. Levels of serum magnesium was checked preoperatively and then in ICU at 0, 6, 12, and 24 hours. Independent t-test and chi square test were used for analysis. Statistical significance was defined as p-value < 0.05.
                A total of 104 patients consented to participate in the study, 53 patients were randomly allocated in magnesium (Mg) group and 51 in placebo group. Two (3.77%) patients in magnesium group and five patients (9.8%) in placebo group developed atrial fibrillation. Incidence of ventricular and supraventricular tachycardia was also slightly higher in placebo. Mg level after arrival in CICU (Cardiac Intensive Care Unit) showed mean of 2.1 in magnesium group and 1.6 in placebo group (p = 0.6).
                Low magnesium levels were noticed in the placebo group after cardiopulmonary bypass and although prophylactic administration of magnesium sulphate was relatively safe but significant benefit on prevention of arrhythmias could not be attained. The routine use of cholinesterase inhibitors to antagonize residual neuromuscular block may be associated with increased postoperative emesis. Rapid spontaneous recovery from mivacurium may obviate the need for these drugs. In this randomized, double-blind, placebo-controlled study of 113 healthy children who had received mivacurium as part of a standardized anesthetic regimen, we compared the incidence of postoperative complications after spontaneous recovery and after the use of neostigmine-glycopyrrolate or edrophonium-atropine. The anesthetic regimen consisted of halothane, nitrous oxide, fentanyl, 2 micrograms/kg intravenous (i.v.), mivacurium in an initial dose of 0.2 mg/kg, followed by an infusion, adjusted to maintain > or = 1 evoked contraction response to a supramaximum train-of-four stimulus. At the end of the procedure, patients received by random assignment one of three drug combinations: 1) neostigmine 70 micrograms/kg + glycopyrrolate 10 micrograms/kg, i.v., 2) edrophonium 1 mg/kg + atropine 10 micrograms/kg, i.v., and 3) saline. The trachea was extubated when evoked responses to peripheral nerve stimulation and clinical signs of adequate neuromuscular recovery were present. Postoperative pain was treated with morphine and emesis with metoclopramide. There were no significant differences between the three groups with respect to age, surgery, intraoperative fentanyl, and mivacurium use, time from the end of surgery to tracheal extubation, postanesthesia care unit (PACU) arrival and discharge, or in postoperative oxygen saturation values and analgesic requirements. Compared to the placebo group, emesis occurred more often in the PACU in patients receiving the neostigmine-glycopyrrolate combination, but not after edrophonium-atropine.(ABSTRACT TRUNCATED AT 250 WORDS) Laryngoscopy and tracheal intubation often cause hypertension and tachycardia, which may be exaggerated during rapid-sequence induction of anaesthesia. The efficacy of adenosine triphosphate (ATP) in attenuating this response was studied in patients receiving ATP 0.05 mg kg-1 or 0.1 mg kg-1 simultaneously with the start of laryngoscopy. These data were compared with those for a control group receiving saline. Each group consisted of 10 patients undergoing elective surgery. Anaesthesia was induced with thiopentone 5 mg kg-1 i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg kg-1 i.v. During anaesthesia, ventilation was assisted or controlled with 1% enflurane and 50% nitrous oxide in oxygen. Patients receiving saline showed a significant increase in mean arterial pressure and rate-pressure product associated with tracheal intubation. These increase after tracheal intubation were reduced in ATP-treated patients compared with those of the control group (P less than 0.05). The data suggest that a bolus injection of ATP is a simple, practical and effective method for attenuating the hypertensive response to laryngoscopy and tracheal intubation.
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.