Atrioventricular conduction during adenosine-induced hypotension in dogs anaesthetized with sevoflurane

We have studied the effects of adenosine-induced hypotension on A-H interval (atrioventricular (AV) nodal conduction time during sinus rhythm), St-H interval (intra-atrial plus AV nodal conduction time during atrial pacing), H-V interval (His-Purkinje conduction time) and H-S interval (total ventricular conduction time) by His-bundle electrocardiography in addition to surface electrocardiogram during both sinus rhythm and atrial pacing in nine dogs anaesthetized with 1 MAC of sevoflurane. Stepwise increases in infusion rates of adenosine to 0.1, 0.3, 0.5 and 1.0 mg kg-1 min-1 produced a dose-related decrease in mean arterial pressure from 91 (6) to 38 (2) mm Hg. Adenosine significantly increased the A-H interval at infusion rates of 0.5 mg kg- 1 min-1 and above, and the St-H interval at 1.0 mg kg-1 min-1. The H-V and H-S intervals remained unchanged. Heart rate decreased significantly only at 1.0 mg kg-1 min-1 with a significant increase in the PR interval. Adenosine-induced hypotension did not have deleterious effects on AV conduction times and the surface electrocardiogram in dogs anaesthetized with 1 MAC of sevoflurane. This may indicate that the effects of adenosine on AV conduction were small and therefore are unlikely to be a contraindication to the use of adenosine for inducing hypotension in patients with initially normal conduction during sevoflurane anaesthesia.      

Atrioventricular conduction in dogs during anesthesia with isoflurane.

The effects of 1.25, 2.0, and 2.5 MAC isoflurane on atrioventricular conduction were studied by His-bindle electrocardiography during atrial pacing in ten dogs. No effect upon atrioventricular conduction as evidenced by changes in A--H interval (the time of conduction from low right atrium to His-bundle, representing primary AV nodal conduction) was found at these concentrations. Atrial pacing to 200 beats/min did not influence the A--H interval at the three anesthetic concentrations. The stability of cardiac rhythm observed clinically with isoflurane may be related to this lack of effect upon the AV node.     

Electrophysiologic effects of volatile anesthetics,sevoflurane and halothane,in a canine myocardial infarction model

The effects of sevoflurane and halothane on the effective refractory period (ERP) and ventricular activation were examined in a canine myocardial infarction model. Sevoflurane (1 MAC) reduced the heart rate and prolonged ERP in both normal and infarcted zones. A prolongation of ERP with sevoflurane was observed also during atrial pacing at a fixed rate, but the effect was less than during sinus rhythm. Sevoflurane either further delayed or blocked the delayed activation entirely in the infarcted zones with only slight effects on the activation of the normal zones. Halothane (1 MAC) prolonged ERP during sinus rhythm and atrial pacing, but to a lesser extent during the latter. Halothane also depressed ventricular activation in the infarcted zone during atrial pacing. In conclusion, sevoflurane as well as halothane selectively depresed the delayed activation and the prolongation of ERP in myocardial infarction, which may inhibit ventricular arrhythmias in myocardial infarction.     

Electrophysiological effects of intravenous dantrolene on canine heart

The electrophysiological effects of an intravenous dantrolene infusion (10 mg kg-1) were evaluated in healthy, anaesthetized dogs by intracardiac electrophysiological study. Dantrolene administration resulted in a significant prolongation of the refractory periods of the right atrium and ventricle, while the functional refractory period of the AV node was not altered. A slight increase of AV nodal conduction, measured as atrial-His bundle interval, without any change in infranodal conduction, measured as His bundle-ventricular interval, was observed during sinus rhythm. Dantrolene had no significant effects on surface ECG parameters. We conclude that intravenously administered dantrolene, at the maximal recommended doses, has primary effects on electrophysiological parameters. These findings support the hypothesis that the beneficial effects of dantrolene on cardiac arrhythmias associated with malignant hyperthermia may be related to its intrinsic activity on the electrophysiological properties of the heart, but confirmation requires further investigations on induced arrhythmias in experimental models.     

Sevoflurane Has No Effect on Sinoatrial Node Function or on Normal Atrioventricular and Accessory Pathway Conduction in Wolff-Parkinson-White Syndrome during Alfentanil/Midazolam Anesthesia

Background: The effects of sevoflurane on the electrophysiologic properties of the human heart are unknown. This study evaluated the effects of sevoflurane on the electrophysiologic properties of the normal atrioventricular conduction system, and on the accessory pathways in patients with Wolff-Parkinson-White syndrome, to determine its suitability as an anesthetic agent for patients undergoing ablative procedures.

Methods: Fifteen patients with Wolff-Parkinson-White syndrome undergoing elective radiofrequency catheter ablation were studied. Anesthesia was induced with alfentanil (20-50 [micro sign]g/kg) and midazolam (0.15 mg/kg), and vecuronium (20 mg) and maintained with alfentanil (0.5 to 2 [micro sign]g [middle dot] kg-1 [middle dot] min-1) and midazolam (1 or 2 mg every 10-15 min, as required). An electrophysiologic study measured the effective refractory period of the right atrium, atrioventricular node, and accessory pathway; the shortest conducted cycle length of the atrioventricular node and accessory pathway during atrial pacing; the effective refractory period of the right ventricle and accessory pathway; and the shortest retrograde conducted cycle length of the accessory pathway during ventricular pacing. Parameters of sinoatrial node function included sinus node recovery time, corrected sinus node recovery time, and sinoatrial conduction time. Intraatrial conduction time and the atrial-His interval were also measured. Characteristics of induced reciprocating tachycardia, including cycle length, atrial-His, His-ventricular, and ventriculoatrial intervals, also were measured. Sevoflurane was administered to achieve an end-tidal concentration of 2% (1 minimum alveolar concentration), and the study measurements were repeated.

Results: Sevoflurane had no effect on the electrophysiologic parameters of conduction in the normal atrioventricular conduction system or accessory pathway, or during reciprocating tachycardia. However, sevoflurane caused a statistically significant reduction in the sinoatrial conduction time and atrial-His interval, but these changes were not clinically important. All accessory pathways were successfully identified and ablated.     

Halothane effects on conductivity of the AV node and His-Purkinje system in the dog

His-bundle electrocardiography was used to evaluate the effect of halothane on AV nodal and His-Purkinje system conduction times in the spontaneously beating dog heart. During artrial pacing at basic heart rates of 120 or 200 beats per minute (bpm), an extrastimulus (cycle length longer or shorter than that of the basic rate) was delivered to test the effect of halothane on several parameters of AV nodal conductivity. Included were the functional refractory period, basal conduction time, and fatigue effect (prolongation of basal conduction time as heart rate was increased from 120 to 200 bpm). Increasing MAC level of halothane (1.25 to 2.75 MAC) prolonged both AV node and His-Purkinje conduction times, yet had little effect on the parameters of nodal conductivity tested for. These effects of halothane could be potentially dangerous in the clinical setting for patients with defective AV conduction. In addition, changes in conduction may be in part responsible for arrhythmias seen during halothane anesthesia.     

Sinus nodal function and risk for atrial fibrillation after coronary artery bypass graft surgery

BACKGROUND: Nonsurgical patients with sinus node dysfunction are at high risk for atrial tachyarrhythmias, but whether a similar relation exists for atrial fibrillation after coronary artery bypass graft surgery is not clear. The purpose of this study was to evaluate sinus nodal function before and after coronary artery bypass graft surgery and to evaluate its relation with the risk for postoperative atrial arrhythmias. METHODS: Sixty patients without complications having elective coronary artery bypass graft surgery underwent sinus nodal function testing by measurement of sinoatrial conduction time (SACT) and corrected sinus nodal recovery time (CSNRT). Patients were categorized based on whether postoperative atrial fibrillation developed. RESULTS: Twenty patients developed atrial fibrillation between postoperative days 1 through 3. For patients remaining in sinus rhythm (n = 40), sinoatrial conduction times were no different and corrected sinus nodal recovery times were shorter after surgery when compared with measurements obtained after anesthesia induction. Sinus node function test results before surgery were similar between the sinus rhythm and the atrial fibrillation groups. After surgery, patients who later developed atrial fibrillation had longer sinoatrial conduction times compared with the sinus rhythm group (P = 0.006), but corrected sinus nodal recover time was not different between these groups. A sinoatrial conduction time > 96 ms measured at this time point was associated with a 7.3-fold increased risk of postoperative atrial fibrillation (sensitivity, 62%; specificity, 81%; positive and negative predictive values, 56% and 85%, respectively; area under the receiver operator characteristic curve, 0.72). CONCLUSIONS: These data show that sinus nodal function is not adversely affected by uncomplicated coronary artery bypass surgery. Patients who later developed atrial fibrillation, however, had prolonged sinoatrial conduction immediately after surgery compared with patients remaining in sinus rhythm. These results suggest that injury to atrial conduction tissue at the time of surgery predisposes to postoperative atrial fibrillation and that assessment of sinoatrial conduction times could provide a means of identifying patients at high risk for postoperative atrial fibrillation.     

Effects of Volatile Anesthetics on Atrial and AV Nodal Electrophysiological Properties in Guinea Pig Isolated Perfused Heart

Background: Knowledge of the anesthetic effects on atrial and atrioventricular (AV) nodal electrophysiologic properties is fundamental to understand the modulatory role of anesthetics on the pathogenesis of supraventricular tachycardias, and to individualize the perioperative management of patients with supraventricular tachycardias or AV nodal conduction disturbances. Therefore the authors studied the effects of three commonly used volatile anesthetics on the electrophysiologic properties of the atrium and AV node.

Methods: The concentration-dependent electrophysiologic effects of halothane, isoflurane, and desflurane (0 - 2 minimum alveolar concentration [MAC]) were studied in guinea pig Langendorff-perfused hearts fit with instruments to simultaneously measure atrial and AV nodal conduction times and atrial monophasic action potential duration. Atrial and AV nodal effective refractory periods were measured simultaneously using a computer-assisted premature stimulation protocol. The concentrations of anesthetics in the gas phase were monitor by an infrared gas analyzer.

Results: Volatile anesthetics caused markedly different concentration-dependent effects on atrial conduction, repolarization, and refractoriness, and on AV nodal function. At equianesthetic concentrations, halothane depressed atrial conduction the most, whereas desflurane caused the greatest shortening of atrial monophasic action potential duration. Halothane had no significant effect on atrial refractoriness, whereas at 2 MAC desflurane significantly shortened and isoflurane significantly prolonged atrial effective refractory periods by 18.1 +/- 13.5% and 13.2 +/- 14.7%, respectively. On an equi-MAC basis, the rank order of potency for the anesthetics to prolong AV nodal conduction time and AV nodal ERP was halothane > desflurane > isoflurane.     

Electrophysiologic assessment of the effects of enflurane, halothane, and isoflurane on properties affecting supraventricular re-entry in chronically instrumented dogs

Most paroxysmal forms of clinical supraventricular tachycardia (SVT) are likely due to re-entrant excitation. Electrophysiologically demonstrated mechanisms for re-entrant SVT include, in descending order of importance, atrioventricular (AV) node, AV node and accessory (AV bypass) pathway, sinus node, or atrial re-entry. Except for sinus node re-entry, none of these mechanisms for re-entrant SVT can be reliably reproduced in animal models. The authors suspected, however, that anesthetic effects on atrial and AV nodal electrophysiologic properties might be used to predict their actions against suspected re-entrant SVT. Awake-to-anesthetized (1.2 and 1.6 MAC) comparisons for the effects of enflurane (ENF), halothane (HAL), and isoflurane (ISO) on atrial and AV nodal electrophysiologic properties were made in ten chronically instrumented dogs. Studies were carried out with and without pharmacologic autonomic blockade with atropine, propranolol, and hexamethonium. By ANOVA, significant (P less than 0.05) effects of the anesthetics included: prolongation of AV nodal conduction time and the Wenckebach point in dogs with autonomic blockade (ENF, HAL, ISO); increased atrial effective and functional refractory periods in dogs without autonomic blockade (ENF, ISO); increased atrial functional refractory period in dogs without autonomic blockade (HAL); increased AV nodal functional refractory period in dogs with and without autonomic blockade (ENF, ISO), or with autonomic blockade (HAL). Sinus node re-entry, manifest by atrial echo beats during high right atrial stimulation, could be demonstrated in several dogs of each anesthetic test group during awake electrophysiologic testing. All anesthetics, with or without autonomic blockade and autonomic blockade in awake dogs, invariably abolished such re-entry. It is concluded that any anesthetic that increases atrial and AV nodal refractoriness should not be conducive to SVT caused by AV node or atrial re-entry. All of the anesthetics tested also appear effective against sinus node re-entry in dogs in which this mechanism can be demonstrated. Finally, no conclusions can be reached concerning anesthetic effects on re-entry requiring participation of both AV node and AV bypass pathways, since anesthetic effects on AV bypass pathways were not tested.     

Sinus Nodal Function and Risk for Atrial Fibrillation after Coronary Artery Bypass Graft Surgery

Background: Nonsurgical patients with sinus node dysfunction are at high risk for atrial tachyarrhythmias, but whether a similar relation exists for atrial fibrillation after coronary artery bypass graft surgery is not clear. The purpose of this study was to evaluate sinus nodal function before and after coronary artery bypass graft surgery and to evaluate its relation with the risk for postoperative atrial arrhythmias.

Methods: Sixty patients without complications having elective coronary artery bypass graft surgery underwent sinus nodal function testing by measurement of sinoatrial conduction time (SACT) and corrected sinus nodal recovery time (CSNRT). Patients were categorized based on whether postoperative atrial fibrillation developed.

Results: Twenty patients developed atrial fibrillation between postoperative days 1 through 3. For patients remaining in sinus rhythm (n = 40), sinoatrial conduction times were no different and corrected sinus nodal recovery times were shorter after surgery when compared with measurements obtained after anesthesia induction. Sinus node function test results before surgery were similar between the sinus rhythm and the atrial fibrillation groups. After surgery, patients who later developed atrial fibrillation had longer sinoatrial conduction times compared with the sinus rhythm group (P = 0.006), but corrected sinus nodal recover time was not different between these groups. A sinoatrial conduction time > 96 ms measured at this time point was associated with a 7.3-fold increased risk of postoperative atrial fibrillation (sensitivity, 62%; specificity, 81%; positive and negative predictive values, 56% and 85%, respectively; area under the receiver operator characteristic curve, 0.72).     

Vecuronium-induced neuromuscular block during xenon or sevoflurane anaesthesia in humans

Twitch response using accelerometry and plasma concentrations, of vecuronium and its metabolite were studied in 27 surgical patients during xenon or sevoflurance anaesthesia after administration of vecuronium 0.05 mg kg-1. Anaesthesia was maintained using oxygen-xenon (MAC = 71%) or oxygen-sevoflurane (MAC = 2%) at an end-tidal concentration equal to 0.8 MAC (i.e. 57% xenon and 1.6% sevoflurane). Mean time from administration of vecuronium to 25% recovery of the first twitch of the train-of-four response was significantly shorter in the xenon group than in the sevoflurane group (12.9 (SD 2.5) min vs 19.4 (6.0) min, respectively). Plasma concentrations of vecuronium at 25% recovery were significantly higher during xenon than during sevoflurane anaesthesia (187 (49) ng ml-1 vs 136 (40) ng ml-1, respectively), while those of 3-desacetylvecuronium were similar in both groups.      

Pentobarbital Plasma Concentrations and Cardiac Electrophysiology During Prolonged Pentobarbital Infusion Anaesthesia in the Dog

There is need for a prolonged stable level of anaesthesia, and we therefore investigated the cardiac electrophysiological effects of continuous pentobarbital infusion after initial pentobarbital injection to induce anaesthesia in dogs. Plasma concentrations of pentobarbital were measured by gas-liquid chromatography. Heart rate, atrial, atrioventricular (AV) nodal and His-Purkinje conduction times were measured by His bundle electrography, and atrial, AV nodal and ventricular refractoriness by programmed electrical stimulation. Over a 5-h observation period, continuous infusion of pentobarbital 3.5 mg · kg^-1 h^-1 after an initial pentobarbital injection of 25 mg · kg^-1 intravenously gave stable mean plasma concentrations of 140-135 μmol · l^-1. The cardiac electrophysiological variables studied did not change significantly during this period. We conclude that a stable experimental model for cardiac electrophysiological studies can be obtained for several hours by-continuous pentobarbital infusion.     

Effect of incremental doses of sevoflurane on cerebral pressure autoregulation in humans

We have examined cerebral pressure autoregulation while awake, and during 0.5 and 1.5 MAC of sevoflurane anaesthesia in 10 patients undergoing non-intracranial neurosurgical procedures. All patients received a standardized anaesthetic comprising premedication with temazepam 20 mg orally, a sleep dose of propofol, fentanyl 1 microgram kg-1 and vecuronium 0.1 mg kg-1. After tracheal intubation, the lungs were ventilated with a mixture of air and oxygen to mild hypocapnia. Routine monitors included ECG, continuous and intermittent non-invasive arterial pressure, pulse oximetry and end-tidal capnography. In addition, blood flow velocity (vmca) was measured by insonating the middle cerebral artery transtemporally using a 2-MHz transcranial Doppler probe. Cerebral pressure autoregulation was tested by increasing mean arterial pressure (MAP) by approximately 20 mm Hg using an infusion of phenylephrine and simultaneously recording vmca. The index of autoregulation (IOR) during each period of the study, calculated as the ratio of percentage change in estimated cerebral vascular resistance (CVRe = MAP/vmca) to percentage change in MAP, was compared using ANOVA. vmca during 0.5 and 1.5 MAC of sevoflurane anaesthesia was significantly lower than that while awake (mean 79 (SD 24), 54 (15) and 51 (12) cm s-1, respectively; P < 0.05). There was no significant change in vmca with the increase in MAP while awake, or during 0.5 or 1.5 MAC of sevoflurane anaesthesia and IOR was similar under the three conditions (0.82 (0.11), 0.83 (0.04) and 1.0 (0.03), respectively). We conclude that cerebral pressure autoregulation remained intact during sevoflurane anaesthesia in humans.      

Propofol does not affect the canine cardiac conduction system under autonomic blockade

PURPOSE: To determine the effects of propofol on the cardiac conduction system in dogs with pharmacological autonomic blockade. METHODS: In eight mongrel dogs receiving 6 mg.kg-1.hr-1 propofol and vecuronium under pharmacological autonomic blockade with atropine and propranolol the infusion rates of propofol were increased from 6, (baseline), to 12, 18 and 24 mg.kg-1.hr-1 at 60-min intervals. An electrophysiological study assessed sinus rate, sinus node recovery time, corrected sinus node recovery time, intraatrial conduction time, AV nodal effective refractory period, Wenckebach cycle length and AV conduction times. Electrocardiographical variables and arterial pressures were also measured. All measurements were repeated at 30 min after the beginning of each infusion of propofol. RESULTS: Propofol did not produce direct effects on the electrophysiological or electrocardiographical variables at any infusion rates. Heart rates did not change at higher infusion rates in the presence of decreases in arterial pressures. CONCLUSION: Propofol did not affect the cardiac conduction system in the presence of autonomic blockade. Thus, the direct cardiac effects of propofol do not play a causative role in the genesis of propofol-associated bradyarrhythmias.     

Augmentation of the neuromuscular blocking effects of cisatracurium during desflurane, sevoflurane, isoflurane or total i.v. anaesthesia

We have evaluated the enhancement of cisatracurium-induced neuromuscular block by potent inhalation anaesthetic agents, by constructing dose-effect curves for cisatracurium in 84 patients during anaesthesia with 1.5 MAC (70% nitrous oxide) desflurane, sevoflurane, isoflurane or total i.v. anaesthesia (TIVA). Acceleromyography (TOF- Guard) and train-of-four (TOF) stimulation of the ulnar nerve were used (2 Hz every 12 s). Cisatracurium was administered in increments of 15 micrograms kg-1 until depression of T1/T0 > 95% was reached. ANOVA was used for statistical analysis (alpha = 0.05, beta = 0.2). Depression of T1/T0 during potent inhalation anaesthesia was enhanced compared with TIVA. ED50 and ED95 values of cisatracurium were 15 (SD 5) and 34 (10) micrograms kg-1 for desflurane; 15 (4) and 32 (7) micrograms kg-1 for sevoflurane; and 15 (5) and 33 (9) micrograms kg-1 for isoflurane. These were significantly lower than the values for TIVA (21 (4) and 51 (13) micrograms kg-1) (P < 0.01 in each case). After equi-effective dosing, times to T1/T0 = 25% were similar in all groups (19 (7), 19 (5), 20 (5) vs 16 (4) min). Recovery index25-75% and time to a TOF ration of 0.70 were prolonged significantly by desflurane and sevoflurane compared with TIVA (18 (5), 19 (8) vs 12 (4) min and 43 (11), 44 (10) vs 35 (5) min, respectively), whereas the difference was not significant for isoflurane (14 (6) and 41 (7) min).      

Multiple electrocardiographic anomalies during anaesthesia in an athlete

A 22-year-old athlete was scheduled for a minor surgical procedure under general anaesthesia. During anaesthesia, his electrocardiogram demonstrated multiple episodes of dysrhythmias including complete bundle branch block, atrioventricular (AV) block, isorhythmic atrioventricular dissociation with junctional rhythm. Administration of atropine 1.0 mg IV terminated the last episode of dysrhythmias. Postoperatively, a resting 12-lead electrocardiogram showed first degree AV block, ST-segment elevation and prominent U waves. A 24 hour Holter recording demonstrated first degree atrioventricular block, episodes of marked sinus arrhythmias and one episode of sinus tachycardia at a rate of 152 beats ·min^-1. Treadmill stress testing revealed peak achieved heart rate of 200 beats·min^-1 without ischaemia. These findings collectively indicated athletic heart syndrome. Implications of athletic heart syndrome for the anaesthetist are reviewed and discussed.     

Effects of magnesium sulphate on the cardiovascular system, coronary circulation and myocardial metabolism in anaesthetized dogs

We have studied the effects of i.v. bolus doses of magnesium sulphate (MgSO4) 60, 90 and 120 mg kg-1 on haemodynamic state, the coronary circulation and myocardial metabolism in nine dogs anaesthetized with pentobarbitone and fentanyl. MgSO4 produced dose-dependent decreases in arterial pressure, heart rate, left ventricular dP/dtmax and left ventricular minute work index (LVMWI) and an increase in the time constant of left ventricular isovolumic relaxation. Stroke volume increased, systemic vascular resistance decreased and cardiac output did not change significantly. MgSO4 produced decreases in coronary perfusion pressure, coronary vascular resistance and myocardial oxygen consumption (MVO2). Coronary sinus blood flow, lactate extraction ratio and the ratio of LVMWI to myocardial MVO2, that is an index of cardiac efficiency, did not change significantly. This study indicated that the depressant effect of MgSO4 on cardiac function was offset by lowering of peripheral vascular resistance, so that cardiac pump function remained effective, and the almost constant coronary sinus blood flow resulted from the decrease in coronary vascular resistance even at higher doses.      

Effects of intravenous lidocaine on cardiac sympathetic nerve activity and A–V conduction in halothane–anesthetized cats

To study neural contributions to the alterations in intracardiac conduction induced by IV lidocaine, we measured cardiac sympathetic nerve activity (CSNA) simultaneously with sinus cycle length (SCL) and AV conduction time using His–bundle electrocardiography following IV lidocaine in cats. Sixteen cats were anesthetized with halothane in oxygen and mid–sternotomized. The His–bundle electrogram and CSNA were recorded from an electrode placed in the interatrial septum and from the left ventrolateral or ventromedial nerve, respectively. Atrium–His (A–H), His–Purkinje (H–V), and total intraventricular (H–S) conduction times were measured during atrial pacing conducted at a cycle length of 300 ms. In eight cats, 1 MAC, 2 MAC, and 3 MAC halothane were given during IV lidocaine (Groups H–l, H–2 and H–3). In the other eight cats, anesthesia was switched from halothane to IV alpha–chloralose (30–50 mg–kgBW^-1; Group C). A significant decrease in CSNA with IV lidocaine, 2 mg–kgBW^-1' was recognized in Groups C and H–l, but not in Groups H–2 and H–3. Prolongations of SCL during the spontaneous cycle, A–H and H–V in the paced mode following IV lidocaine were significant in Groups C, H–l and H–2, but not significant in Group H–3. We conclude that IV lidocaine induces a significant decrease in CSNA during alpha–chloralose or 1 MAC halothane anesthesia which partly contributes to the control of intracardiac conduction.     

Esmolol prevents and suppresses arrhythmias during halothane anaesthesia in dogs

The antiarrhythmic effect of esmolol, a selective beta 1 adrenoreceptor blocker, was evaluated in the presence of epinephrine induced arrhythmias in dogs (n = 6). The arrhythmogenic dose of epinephrine (ADE) during 1.2 MAC halothane in dogs was increased from 3.23 +/- 0.25 (mean +/- SD) to 30.90 +/- 3.56 micrograms.kg-1.min-1 (P less than 0.001) by the prior administration of esmolol 0.5 microgram.kg-1 bolus followed by an infusion at the rate of 150 micrograms.kg-1.min-1. Higher esmolol infusion doses of 200 micrograms.kg-1.min-1 further increased ADE to 99.0 +/- 2.92 micrograms.kg-1.min-1 (P less than 0.001). After discontinuation of esmolol and during continued halothane anaesthesia, ventricular tachycardia was induced by increasing the infusion rate of the 100 micrograms.ml-1 solution of epinephrine. In all dogs ventricular tachycardia was restored to sinus rhythm by a bolus dose of esmolol (1 microgram.kg-1). We conclude that esmolol pretreatment increases the ADE during halothane anaesthesia in dogs. Our data suggest that esmolol may be useful as an antiarrhythmic agent in the management of epinephrine-related ventricular arrhythmias during anaesthesia in man.     

Magnesium inhibits the hypertensive but not the cardiotonic actions of low-dose epinephrine

Intravenous magnesium supplementation is often used to control cardiac arrhythmias and coronary artery vasospasm resulting from disturbances of magnesium homeostasis after coronary artery bypass surgery. Many such patients also require inotropic drug support of depressed myocardial function. However, increased serum magnesium concentrations directly depress cardiac contractility in animals and may interfere with catecholamine actions. To determine whether small intravenous doses of magnesium sulfate (MgSO4) interfere with the cardiotonic actions of epinephrine, we examined the hemodynamic effects of MgSO4 and epinephrine infusion in 17 cardiac surgical patients on their 1st postoperative day in a prospective, controlled study. In 11 patients, infusion of MgSO4 (7-mg.kg-1 bolus followed by 10 mg.kg-1.h-1 as a continuous infusion) increased serum magnesium concentrations by 44% (mean +/- standard error of the mean [SEM] of 0.8 +/- 0.1 to 1.2 +/- 0.1 mM; P less than 0.01) but had no significant effect on heart rate; mean arterial, central venous, or pulmonary arterial occlusion pressures; or cardiac output. Epinephrine infusion (30 ng.kg-1.min-1) significantly increased cardiac index (2.7 +/- 0.1 to 3.1 +/- 0.21.min-1.m-2; P less than 0.05); this effect was not altered by MgSO4 administration (n = 11). However, MgSO4 significantly blunted epinephrine's hypertensive action and prevented a significant increase in mean arterial pressure during concurrent MgSO4-epinephrine administration. Six placebo control patients were given two sequential infusions of epinephrine separated by a placebo infusion to rule out an effect of time on the hemodynamic response to epinephrine. Mean arterial pressure and cardiac index responses to epinephrine were identical before and after placebo infusion.(ABSTRACT TRUNCATED AT 250 WORDS)