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Biomedical subjects

J L Atlee

Publications and source records attributed to J L Atlee.

54 records · Page 3Linked to original sources
PubMed1986

Thiopental and epinephrine-induced dysrhythmias in dogs anesthetized with enflurane or isoflurane.

Epinephrine-induced dysrhythmias were studied in 19 dogs anesthetized with 1.25 MAC enflurane or isoflurane, or the same preceded by thiopental (20 mg/kg). In 11 (group 1) dogs, thiopental reduced the dose of epinephrine required for production of ventricular ectopy, bigeminy and tachycardia with enflurane, and only ventricular tachycardia with isoflurane (P less than 0.05). Thiopental potentiation of epinephrine-induced dysrhythmias with enflurane lasted 4 hr after induction. In eight (group 2) dogs, the arrhythmic dose (ADE in microgram/ml) and plasma level of epinephrine (PLE in ng/ml) for four or more ventricular extrasystoles in 15 sec were determined in the same animal under each of the four test conditions. ADE and PLE values (X +/- SEM) were, respectively, enflurane, 9.1 +/- 1.0 and 141 +/- 24 (8/8 dogs); enflurane-thiopental, 5.0 +/- 0.6 and 63 +/- 16 (8/8 dogs); isoflurane, 28.3 and 330 (1/7 dogs); and isoflurane-thiopental, 15.2 +/- 2.8 and 265 +/- 59 (5/7 dogs). In addition, thiopental had no effect on plasma epinephrine levels reached during epinephrine infusions with 1.0 (enflurane only), 2.0 (enflurane, isoflurane) and 4.0 micrograms X kg-1 X min-1 (isoflurane only). Nor were epinephrine levels reached during enflurane or enflurane-thiopental different from those reached during isoflurane or isoflurane-thiopental. It is concluded that thiopental potentiates several types of epinephrine-induced ventricular dysrhythmias with enflurane, but only ventricular tachycardia with isoflurane. Furthermore, isoflurane or isoflurane-thiopental were less sensitizing than enflurane or enflurane-thiopental. Finally, neither thiopental nor the anesthetic agents affected plasma epinephrine levels reached during epinephrine infusions lasting 3 min.

Animals↗
PubMed1985

Anaesthesia and cardiac electrophysiology.

Cardiac dysrhythmias occur in 60% or more of anaesthetized patients. While most are not immediately life-threatening, they are serious when 1) accompanied by atrioventricular (A-V) dyssynchrony and impaired myocardial performance, 2) a favourable myocardial oxygen balance is jeopardized, or 3) there is likelihood of progression to life-threatening dysrhythmias. Partial A-V dyssynchrony occurs with non-sinus origin supraventricular and A-V junctional rhythms, and complete A-V dyssynchrony with ventricular rhythms and advanced heart-block. Any tachydysrhythmia may increase the myocardial oxygen demand, and possibly reduce oxygen supply as well. Certain supraventricular tachydysrhythmias and most sustained ventricular rhythm disturbances are likely to predispose to life-threatening dysrhythmias. Thus, any cardiac rhythm disturbance should be of concern to the anaesthetist since it is a departure from normal and a sign of an untoward drug effect or altered physiological state. The purpose of this article is to summarize our current understanding of cardiac electrophysiological mechanisms, particularly how these apply to dysrhythmias that occur during anaesthesia, and to review the actions of, and indications for, antidysrhythmic drugs. A better understanding of electrophysiological mechanisms by anaesthetists should lead to improved patient management; hence, a reduced likelihood that dysrhythmias will occur that require specific drug or electrical management.

Action Potentials↗
PubMed1985

Epinephrine-induced ventricular arrhythmias in dogs anesthetized with halothane: potentiation by thiamylal and thiopental.

Epinephrine-induced ventricular arrhythmias were studied in 8 dogs anesthetized at weekly intervals with halothane (1.09% end-tidal concentration) preceded by thiamylal or thiopental (20 mg/kg of body weight). Lead II, bundle of His and high right atrial electrograms, and femoral artery and airway pressures were recorded. Epinephrine was infused in logarithmically spaced increasing rates (initial rate = 0.25 micrograms/kg/min) for a maximum of 2.5 minutes. The maximal (greater than or equal to 4 ventricular premature depolarizations within 15 s of each other) and minimal (all other ventricular or junctional rhythms) arrhythmogenic doses were calculated (infusion rate X time to arrhythmia). The mean (+/- SD) minimal arrhythmogenic dosages for the thiamylal-halothane, thiopental-halothane, and halothane-only groups were 1.84 +/- 0.66, 1.83 +/- 0.64, and 3.69 +/- 1.32 micrograms/kg, respectively; the mean (+/- SD) maximal arrhythmogenic dosages were 2.32 +/- 0.77, 3.37 +/- 1.30, and 8.86 +/- 4.40 micrograms/kg, respectively, with no change after 4 hours of anesthesia. During infusion of the maximal arrhythmogenic dosages, the mean infusion of the maximal arrhythmogenic dosages, the mean percentage increase in serum K+ for thiamylal-halothane, thiopental-halothane, and halothane-only groups was 33 +/- 14%, 31 +/- 13%, and 38 +/- 18%, respectively.

Anesthesia, General↗
PubMed1982

Potentiation by thiopental of halothane--epinephrine-induced arrhythmias in dogs.

Epinephrine-induced arrhythmias were studied in 14 dogs (Group 1) anesthetized with halothane alone (1.09% end-tidal), and on another occasion, at the same halothane concentration following intravenous thiopental (20 mg/kg). Surface (Lead II), catheter His bundle and high right atrial electrocardiograms, and airway and femoral arterial pressures were recorded. Graded doses of epinephrine (EPI-least dose 0.25 microgram . kg-1 . min-1) were infused over five minutes, but terminated sooner if ventricular tachycardia occurred (maximal sensitization). Sensitizing EPI doses (microgram . kg-1) were calculated (dose X time to arrhythmia) for: Shift in or wandering atrial pacemaker (SAP-WAP), atrial ectopy (At Ect), A-V dissociation (AVD), and ventricular ectopy, bigeminy, or tachycardia (V Ect, V Bigem, V Tach). With halothane alone, SAP-WAP occurred at the least dose of EPI followed by At Ect, AVD, V Ect, V Bigem, and V Tach in order of increasing EPI dose. Following thiopental, EPI doses for AVD, V Ect, V Bigem, and V Tach were reduced, as well as EPI dose differences for At Ect, AVD, V Ect, and V Bigem. In an additional seven dogs (Group 2), anesthesia was induced with thiopental (20 mg/kg) followed by halothane (1.09% end-tidal). These animals were observed for arrhythmias during graded EPI infusions at 1-2 h and 3-4 h following thiopental. Sensitizing EPI doses for SAP-WAP and V Tach were similar at each time period. The authors concluded that with halothane and increasing EPI dose, sensitization constitutes a spectrum of arrhythmias, beginning with atrial and progressing to severe ventricular arrhythmias. Thiopental reduces the EPI dose needed for AVD and ventricular, but not atrial, arrhythmias. It also reduces the EPI dose discrepancies for atrial and ventricular arrhythmias.

Animals↗
PubMed1981

Halothane and hypocapnia: effects on electrically stimulated atrial arrhythmias in digitalized dogs.

To assess the effectiveness of halothane as an antiarrhythmic agent against atrial arrhythmias brought about by hyperventilation of digitalized subjects, the effects of halothane end-tidal (ET) = 1.0% and hypocapnia (PCO2ET = 25 vs 40 torr) on stimulated atrial arrhythmias (atrial echoes [echoes]; repetitive atrial firing [RAF]) and supraventricular conduction and refractoriness were assessed digitalized dogs. Ten dogs received low dose (LD, 22 microgram/kg/day X 7 days) and nine dogs received high dose (HD, 44 microgram/kg/day X 7 days) digoxin. Serum digoxin levels following LD were 0.5 to 1.8 ng/ml (mean +/- 1 SD = 1.16 +/- 0.31) and following HD were 2.0 to 4.0 ng/ml (3.06 +/- 0.71 ng/ml). High right atrial pacing and extrastimulation and catheter His bundle electrocardiography were used. Spontaneous arrhythmias or conduction disturbances were not observed. Halothane enhanced RAF but not echoes in dogs given LD and HD. It also increased supraventricular conduction time and refractoriness. Hypocapnia had no effect on echoes or RAF and minimal effects on conduction and refractoriness. By analysis of variance, digoxin had no effects on echoes, RAF, refractory periods, or conduction. It is concluded that halothane affords no protection against stimulated arrhythmias in hypocapneic or eucapneic, nontoxic digitalized dogs.

Animals↗
PubMed1980

Diagnosis and therapy of perioperative arrhythmias.

Cardiac arrhythmias are extremely common in the perioperative setting. They only require treatment when they (1) interfere significantly with normal tissue perfusion; (2) adversely affect the normal balance between myocardial oxygen supply and demand; or (3) predispose the patient to ventricular tachycardia or fibrillation. Usually, the treatment is simple: correct the underlying cause or causes. In some instances, either the cause will not be apparent or time will not permit adequate identification of the precipitating events. In these instances, drug treatment or electrical therapy is indicated. The classification of arrhythmias and the actions, indications, dosages and routes, and major side effects of the drugs commonly used in their treatment are summarized in Tables 1 through 3. The indications for electrical therapy, including pacemakers and cardioversion, were discussed in the sections dealing with bradyarrhythmias, tachyarrhythmias, and AV conduction block.

Anesthesia, General↗
PubMed1980

Mechanical hyperventilation: effect on specialized atrioventricular conduction, supraventricular refractoriness, and experimental atrial arrhythmias in dogs anesthetized with pentobarbital or pentobarbital-halothane.

The effect of hypocapnia (PCO2ET 25 vs 40 torr) on specialized atrioventricular (AV) conduction, supraventricular refractory periods, and experimental atrial arrhythmias provoked by premature atrial stimulation (atrial echoes-echoes, repetitive atrial firing (RAF)) was assessed in dogs anesthetized with pentobarbital or pentobarbital-halothane (1.0% end-tidal). Catheter His bundle electrocardiography was used. Both hypocapnia and halothane prolonged AV nodal conduction, but the effect of halothane was more pronounced. Halothane prolonged the atrial functional (AtFRP), atrial effective (AtERP), and AV nodal functional refractory (AVFRP) periods. These effects of halothane were linked to an increased incidence of RAF but not to echoes. Hypocapnia prolonged the AVFRP (less than halothane), had no effect on the AtFRP and shortened the AtERP. These effects of hypocapnia were associated with an increased incidence of echoes, but not with RAF. Echoes and RAF are thought to be caused by reentry within the sinus node, atria, and AV node. The differing effects of halothane and hypocapnia on the incidence of these arrhythmias may be due to differning effects on supraventricular refractoriness.

Anesthesia↗
PubMed1975

Diphenylhydantoin and lidocaine modification of A-V conduction in halothane-anesthetized dogs.

The effect of halothane on A-V conduction was evaluated in gods during atrial pacing using the technique of His-bundle electrocardiography. In addition, the effects of lidocaine and diphenylkydantoin (DPH) on A-V conuction were examined during halothane anesthesia. Effects of these drugs on three subintervals of A-V conduction were compared. These included the -H (stimulus atifact of His-bundle deflection-atrioventricular conduction), H-Q (His-budnle deflection onset of QRS complex-His-Purkinje conduction), and H-S intervals(His-bundle delfection to end of QRS COmplex-total intraventricular conduction). Linear regression best described the relationship between duration of interval (P-H, H-V,and H-S) and heart rate during incremental increases in the atrial paced rate. Data from these experiments were fitted to a multiple lenear regression model that predicted the effect of increasing concentrations of halothan, lidocaine, and DPH on slope and intercept coefficients. In creasing concentrations of halothan ( 30 and 45 mg/100 ml arterial). Both lidocaine and DPH further depressed conduction at all levels of halothan anesthesia. The P-H interval was particularly sensitive todrug effefts. This may represent potentiation of the normal slowing of conduction through the AVnode in response to incremental increases in heart rate (fatigue response.) We conclude thatboth lidocaine and DPH fail to reverse the depressant effect of halothane on A-V conduction. This may explain their ineffectiveness in treating certain types of arrhythmias during halothane anesthesia.

Anesthesia, Inhalation↗
PubMedDate not supplied

Chronic recording from the His bundle of the awake dog.

The conventional catheter method for measuring specialized A-V nodal and His-ventricular conduction times in the intact dog heart precludes an unanesthetized control. This control is necessary for meaningful studies of the effect of drugs or drug-drug interactions on A-V conduction times. At right thoracotomy (halothane anesthesia), mongrel dogs had bipolar electrodes sutured to the epicardial surface of both atrial appendages, junctions of the sulcus terminalis with both vena cavae, and right ventricle. A unipolar needle electrode, referenced to a unipolar electrode on the ascending aorta, was inserted into the interatrial septum from the aortic root for recording the His bundle electrogram. After one to three weeks for stabilization, weekly measurements were made of A-V nodal conduction time (AVN) and His-ventricular conduction time (H-V) for up to 52 weeks (4 to 52 weeks). Mean values (13 dogs) for spontaneous cycle length, AVN and H-V conduction times were 477 +/- 25, 82 +/- 3, and 30 +/- 1 msec, respectively. Simultaneous recordings from catheter and implanted His bundle electrodes were made during changes in atrial paced rate (five dogs, pentobarbital anesthesia). Values for AVN and H-V conduction times from catheter or implanted electrodes were the same. AVN conduction time increased, H-V conduction time remained constant during increases in atrial rate. Atropine shortened and propranolol prolonged AVN conduction time in six unanesthetized, unsedated dogs; neither affected H-V conduction time. Histologic examination of electrode sites in two dogs at 43 and 52 weeks showed no evidence of damage to underlying myocardial recording sites. This preparation provides reproducible awake values for AVN and H-V conduction times, and hence a more meaningful control for pharmacologic investigations.

Animals↗
PubMedDate not supplied

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.

Anesthesia↗