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J L Atlee

Publications and source records attributed to J L Atlee.

At least 37 records · Page 2Linked to original sources
PubMed1991

Atrial pacing thresholds measured in anesthetized patients with the use of an esophageal stethoscope modified for pacing.

Transesophageal atrial pacing (TAP) with the use of standard, thermistor-equipped, esophageal stethoscopes, modified for pacing by incorporation of a 4-French, bipolar TAP probe (pacing esophageal stethoscope [PES]), was evaluated in 100 adult patients under general anesthesia. A commercially available TAP pulse generator supplied 10-ms pulses with current variable between 0 and 40 mA. Pacing distances (in centimeters) were measured from the infraalveolar ridge to midway between PES electrodes (1.5-cm interelectrode distance). Pacing thresholds (milliamperes) were measured at the point of a maximum-amplitude P-wave (PMAX) in the bipolar esophageal electrogram and points 1 cm proximal or 1, 2, or 3 cm distal to PMAX. TAP (70-100 beats per min) was used for sinus bradycardia less than or equal to 60 beats per min (36 patients) or atrioventricular (AV) junctional rhythm (2 patients) and blood pressure changes with TAP documented. In male patients (n = 49), PMAX was 32.7 +/- 0.3 cm (mean +/- SE) and minimum pacing threshold 5.1 +/- 0.4 mA (range, 1-13 mA) at 33.6 +/- 0.3 cm (range, 30-37 cm). In female patients (n = 51), PMAX was 30.4 +/- 0.4 cm and minimum pacing threshold 4.4 +/- 0.4 mA (range, 2-14 mA) at 31.1 +/- 0.4 cm (range, 26-40 cm). TAP produced an average 13-16 mmHg increase in systolic, diastolic, or mean arterial pressure in patients with sinus bradycardia or AV junctional rhythm. There were no subjective patient complaints (epigastric discomfort, dysphagia) that could be attributed to TAP; objective evaluation (esophagoscopy) was not performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Anesthetics and automaticity in latent pacemaker fibers. II. Effects of halothane and epinephrine or norepinephrine on automaticity of dominant and subsidiary atrial pacemakers in the canine heart.

Knowledge of anesthetic effects on the automaticity of dominant and subsidiary cardiac pacemakers is fundamental to an understanding of mechanisms of arrhythmia during anesthesia, as well as to the management of patients with sinus node dysfunction or atrioventricular (AV) conduction block. Among potential pacemakers of the heart are subsidiary atrial pacemakers (SAP), which are located outside the classic sinoatrial (SA) node region but still within the right atrium. SAP have a higher inherent rate of automaticity than AV junctional pacemakers, may contribute to a multicentric atrial pacemaker complex, and can control the rhythm of the heart when the SA node is absent or inhibited. How halothane, epinephrine (E), or norepinephrine (NE), alone or in combination, would affect the relation between the automaticity of the SA node and SAP was tested using an isolated, perfused canine right atrial preparation (n = 78). This preparation was perfused via the SA node artery with Krebs' solution (36.0 +/- 0.5 degrees C) equilibrated with 97% oxygen-3% carbon dioxide. Delivered concentrations of halothane of 1 or 2% corresponded to measured perfusate concentrations of 0.50 +/- 0.02 or 0.80 +/- 0.04 mM in experiments with E (n = 24) and 0.45 +/- 0.02 or 0.75 +/- 0.04 mM in experiments with NE (n = 54). E or NE perfusate concentrations were 1, 2, and 5 micrograms/l or 2, 5, and 10 micrograms/l, respectively. To determine the site of earliest activation (SEA), extracellular recordings were made from the SA node region and distal sites (approximately 1, 2, and 3 cm) along the sulcus terminalis, the previously reported locations of SAP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Anesthetics and automaticity in latent pacemaker fibers. III. Effects of halothane and ouabain on automaticity of the SA node and subsidiary atrial pacemakers in the canine heart.

Atrial tachyarrhythmias are a common manifestation of digitalis toxicity. Such arrhythmias could be due to enhanced automaticity of subsidiary atrial pacemakers (SAP) compared to the sinoatrial (SA) node. Halothane is known to oppose digitalis-induced ventricular arrhythmias. Its effect on digitalis-caused atrial arrhythmias is unknown. Therefore, we tested two hypotheses, as follows. First, increasing ouabain concentrations would enhance automaticity of SAP compared to the SA node and that such enhanced automaticity could explain digitalis-caused atrial tachyarrhythmias. Second, halothane would oppose such enhanced automaticity of SAP, thereby opposing digitalis-caused atrial tachyarrhythmias. A canine right atrial preparation was perfused via the SA node artery with Krebs' solution (36.0 +/- 0.5 degrees C) equilibrated with 97% oxygen-3% carbon dioxide. Four bipolar extracellular electrodes recorded the site of earliest activation (SEA), which in this preparation could be the SA node or increasingly remote sites of SAP approximately 1, 2, and 3 cm distal to the SA node along the sulcus terminalis. Pacemaker shifts to SAP during exposure to drugs were scored for magnitude of shift as 1, 2, or 3 depending on which SAP site was the SEA. Magnitude scores were summed for each test condition and normalized by dividing the total number of preparations tested. Preparations (n = 48) were exposed to 1 or 2% halothane (perfusate concentrations of 0.51 +/- 0.01 or 0.79 +/- 0.03 mM, respectively) and/or to low- or mid-therapeutic (2.5 or 5 x 10(-8) M) or borderline toxic ouabain (1 x 10(-7) M). Normalized magnitude scores were not significantly different from zero (control value) with any halothane or ouabain concentration alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Halothane, enflurane and isoflurane on abnormal automaticity and triggered rhythmic activity of Purkinje fibers from 24-hour-old infarcted canine hearts.

The effects of inhalation anesthetics halothane, enflurane, and isoflurane on spontaneous impulse initiation (automaticity) and triggered sustained rhythmic activity were examined in Purkinje fibers derived from normal (n = 38) and 24-h-old infarcted canine hearts (n = 27) to further understanding of their influence on the cellular mechanisms underlying generation of cardiac arrhythmias. Purkinje fibers from normal or infarcted hearts were superfused with modified Krebs' solution (37 degrees C) with or without epinephrine (2 or 15 microM) and equilibrated with a 97% O2-3% CO2 gas mixture (control). Transmembrane action potentials were recorded using conventional microelectrode techniques, and Purkinje fibers were exposed to anesthetic concentrations equivalent to 2.0 MAC. Normal Purkinje fibers were not spontaneously active unless exposed to epinephrine. All anesthetics (enflurane greater than halothane, isoflurane; P less than 0.05) increased automaticity of normal Purkinje fibers exposed to either epinephrine concentration. Partially depolarized Purkinje fibers from infarcted hearts were either spontaneously active or were quiescent. For ischemic fibers that beat spontaneously, abnormal automaticity was sustained (duration greater than 300 s) or periodic (duration less than 300 s). Sustained abnormal automaticity was elicited by epinephrine (15 microM) in some quiescent partially depolarized fibers. None of the anesthetics affected the rate of sustained abnormal automaticity, regardless of whether the induction of such automaticity required epinephrine, nor did anesthetics significantly affect the duration of trains of periodic abnormal automaticity. Finally, quiescent, partially depolarized Purkinje fibers were tested for triggered rhythmic activity during pacing at a cycle length of 800 ms.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1991

Comparison of logdose and bracket protocols for determination of epinephrine arrhythmia thresholds in dogs anesthetized with thiopental-halothane.

Previous studies in dogs of anesthetic-epinephrine arrhythmias have used logdose or bracketed epinephrine infusion protocols to determine the arrhythmic dose of epinephrine (ADE) or plasma level of epinephrine at arrhythmias (PCE). Reported logdose ADE values for halothane preceded by thiopental induction (thiopental-halothane) are twice those with the bracket protocol. There are no reported PCE data for the bracket protocol, and neither protocol has been directly compared in the same dogs. Therefore, direct comparisons were made of thiopental-halothane ADE and PCE in seven dogs (group 1). Dogs were induced with thiopental (20 mg/kg), followed by halothane inhalation at end-tidal concentrations equivalent to MAC 1.25. Epinephrine infusion protocols were compared on two weekly test occasions, with the sequence and order of protocol testing randomized. Logdose ADE for four or more ventricular beats within 15 s was 3.92 +/- 0.60 micrograms/kg (mean +/- standard error), higher than the bracket ADE (2.54 +/- 0.34 micrograms/ml) (P less than 0.05). PCE at ADE were similar for both protocols, but six separate infusions of epinephrine were required to establish ADE with the logdose compared to four with the bracket protocol (P less than 0.05). These findings suggested enhanced epinephrine clearance with the logdose protocol. Therefore, five additional but similarly anesthetized dogs (group 2) were tested to determine if physiologic or hemodynamic conditions prior to epinephrine infusions ("initial conditions") were equivalent for both protocols. Protocols were modified to avoid provocation of ventricular arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Prolongation of the QT interval by enflurane, isoflurane, and halothane in humans.

Previous investigations in laboratory animals have documented the ability of the volatile anesthetics to prolong the QT interval and the QT interval corrected for level of heart rate, QTc. The purpose of the present investigation was to evaluate the direct electrocardiographic and hemodynamic effects of enflurane, isoflurane, and halothane in healthy, unpremedicated patients using an inhalation induction to avoid the confounding effects of other anesthetic agents. Experiments were conducted in 22 adult male patients, (ASA physical status I or II) divided into three groups given either enflurane (n = 6), isoflurane (n = 8), or halothane (n = 8) anesthesia. Twenty-four-hour preoperative, preinduction, and postinduction hemodynamic and electrocardiographic measurements were obtained. Anesthetic blood concentrations, levels of plasma electrolytes, and arterial blood gas tensions were also quantitated. Halothane administration (0.81 +/- 0.06 mM) did not significantly alter the PR interval or QRS duration but significantly increased the QT (0.38 +/- 0.01 to 0.45 +/- 0.01 s) and QTc intervals (0.39 +/- 0.01 to 0.44 +/- 0.02 s). Isoflurane anesthesia (1.04 +/- 0.11 mM) did not significantly change QRS duration or PR and QT intervals but significantly prolonged the QTc interval (0.42 +/- 0.01 to 0.47 +/- 0.14 s). Similarly, enflurane anesthesia (2.16 +/- 0.13 mM) significantly prolonged the QTc (0.40 +/- 0.01 to 0.46 +/- 0.14 s) without change in QRS duration or PR and QT intervals. Plasma electrolyte levels and arterial gas tensions remained within normal limits in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1991

Anesthetics and automaticity in latent pacemaker fibers: I. Effects of halothane, enflurane, and isoflurane on automaticity and recovery of automaticity from overdrive suppression in Purkinje fibers derived from canine hearts.

Knowledge of arrhythmic or antiarrhythmic actions of anesthetics on automaticity of latent pacemaker fibers has relevance to the intraoperative management of patients with bradyarrhythmia due to sinus node dysfunction or heart block. The authors determined the effects of halothane, enflurane, and isoflurane on automaticity and recovery of automaticity from overdrive suppression in canine Purkinje fibers derived from normal hearts. Purkinje fibers were superfused with a modified Krebs' solution (37 degrees C) containing epinephrine (2 or 15 microM) and equilibrated with a 97% O2-3% CO2 gas mixture (control). Transmembrane action potentials (AP) were recorded using standard microelectrode techniques. Purkinje fibers were then exposed to anesthetics at vaporizer settings of 0.75 or 1.5% (halothane), 1.75 or 3.5% (enflurane), and 1 or 2% (isoflurane), which were equivalent to measured superfusate concentrations of 0.22 or 0.47 mM (halothane), 0.44 or 0.94 mM (enflurane), and 0.28 or 0.53 mM (isoflurane). Compared to control, there was no significant effect of either concentration of the anesthetics on upstroke (phase 0) depolarization, AP amplitude or duration (50% repolarization), or maximum diastolic potential. All three anesthetics increased spontaneous rate. The increase in rate with all three anesthetics was due to enhanced diastolic depolarization (rate dV/dt, phase-4 depolarization). Recovery times from overdrive suppression were determined after 30 or 60 s of pacing at drive cycle lengths of 800, 500, and 400 ms and only at higher anesthetic concentrations. Recovery of automaticity was shortened by halothane only in slowly paced fibers exposed to the lower concentration of epinephrine. Under all other conditions recovery times were not affected by halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Effects of diltiazem, verapamil, and inhalation anesthetics on electrophysiologic properties affecting reentrant supraventricular tachycardia in chronically instrumented dogs.

Paroxysmal supraventricular tachycardia (PSVT) is likely due to reentry involving the atrioventricular (AV) node, AV node with AV bypass pathway, sinus node, or atria. Intravenous diltiazem (DIL) or verapamil (VER) might be used to treat PSVT in anesthetized patients, and either drug could be more or less effective or produce adverse circulatory effects in this circumstance because the available inhalation anesthetics are known to elevate plasma concentrations of acutely administered iv DIL or VER. Because human studies were precluded and there are no reliable animal models for most reentrant PSVT, the authors determined the effects of iv DIL or VER and potent inhalation anesthetics (enflurane, halothane, isoflurane) on supraventricular electrophysiologic (EP) properties affecting the likelihood of reentrant PSVT in chronically instrumented dogs. Measurements of supraventricular EP properties in awake dogs without drugs served as control. DIL and VER were then administered iv to achieve clinically relevant plasma concentrations in awake dogs and EP properties were again measured. Finally, anesthetic effects on EP properties in dogs with DIL or VER were tested at end-tidal concentrations equivalent to 1.2 or 1.6 MAC for enflurane, halothane, or isoflurane. In awake dogs, DIL or VER increased AV node conduction time. Wenckebach point and functional refractoriness, and also reduced the range of premature atrial intervals for and likelihood of producing sinus node interpolation or reentry with atrial extrastimulation (P less than 0.05, ANOVA). AV node conduction time, Wenckebach point, and functional refractoriness were further increased in anesthetized dogs (all agents) with DIL or VER compared with control (P less than 0.05, ANOVA). All anesthetics with DIL or VER abolished sinus node interpolation and reentry. Atrial effective and functional refractory periods were not affected by DIL or VER in awake dogs and were increased by any of the anesthetics in dogs with DIL (P less than 0.05, ANOVA). Atrial refractory periods were little affected by anesthetics with VER. Adverse circulatory effects, including systolic arterial pressure less than 50 mmHg and second-degree (type 1) AV block or sinus arrest with escape rhythms, were most common with VER and any (especially enflurane) of the anesthetics. Finally, anesthetized animals with sinus arrest and escape rhythms (any test condition) could be paced from the atrium at physiologic rates (up to 120 beats/min).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

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.

Animals↗
PubMed1988

Conscious state comparisons of the effects of the inhalation anesthetics and diltiazem, nifedipine, or verapamil on specialized atrioventricular conduction times in spontaneously beating dog hearts.

The effects of enflurane (ENF), halothane (HAL), and isoflurane (ISO) on specialized atrioventricular (AV) conduction times were contrasted to awake (control) in 22 chronically instrumented dogs. Dogs were studied with and without diltiazem (DIL), nifedipine (NIF), vehicle for NIF (VEH), or verapamil (VER). These calcium channel blockers (CCB) were administered iv to achieve clinically effective steady-state plasma levels in awake dogs. CCB plasma levels in awake dogs, subsequently anesthetized with ENF (N = 10), HAL (N = 10), or ISO (N = 11), were: DIL = 94 +/- 13 to 124 +/- 9 ng/ml, NIF = 4 +/- 1 to 7 +/- 2 ng/ml, VER 108 +/- 23 to 147 +/- 9 ng/ml. Anesthetized dogs had approximate two-fold increases in plasma levels of DIL or VER. There was no anesthetic effect on plasma levels for NIF. In the absence of CCBs, HAL increased AV nodal conduction time (AVN) compared to awake. There was a 4-10% increase in His-Purkinje (HP) and ventricular (VENT) conduction time with each anesthetic. The CCBs did not alter HP or VENT in awake dogs, but AVN was increased 15-23% by DIL and 28-38% by VER. Three of ten dogs with VER developed complete heart block or AV junctional escape rhythm at each level of ENF. One dog with VER developed type I, 2 degrees (Wenckebach) AV block at each level of HAL and ISO. No dogs with DIL had heart block or escape rhythms during anesthesia. In anesthetized dogs without heart block or escape rhythms, the increase in AVN with VER ranged from 46 to 69%, and with DIL from 36 to 55%. The CCB had no added effects on HP or VENT with any anesthetic. Finally, there were no effects of NIF alone or with the anesthetics on specialized conduction that could not be attributed to VEH. The authors conclude that with the inhalation anesthetics, antiarrhythmic plasma levels of DIL or VER prolong AV nodal most compared to infranodal conduction time. Additionally, heart block or escape rhythms appear more likely with VER and any of the potent inhalation anesthetics.

Anesthesia, Inhalation↗
PubMed1986

Conscious-state comparisons of the effects of inhalation anesthetics on specialized atrioventricular conduction times in dogs.

The effects of 1.2, 1.7, and 2.3 MAC enflurane (ENF), halothane (HAL), and isoflurane (ISO) on specialized atrioventricular (AV) conduction times were compared with awake (control) in 23 dogs that were chronically instrumented for His bundle studies. Compared with awake, 1.2 MAC ENF and HAL produced 17% and 18% increases in AV nodal conduction time, respectively. There was little added prolongation related to depth of ENF or HAL. ISO did not prolong AV nodal conduction compared with awake at 1.7 (9%) and 2.3 MAC (12%). All agents produced an approximate 5% increase in His-Purkinje and ventricular conduction times compared with awake, with little additional effect related to depth of anesthesia. In separate experiments in ten of these dogs, anesthetic effects on conduction were determined following combined autonomic blockade with atropine and propranolol. During autonomic blockade, there was no effect of any anesthetic compared with awake, or to increased level of anesthesia, on specialized AV conduction times. The authors conclude that of the major inhalation anesthetics in current clinical use, ISO is least depressant of and ENF and HAL about equally depressant of AV nodal and His-Purkinje conduction times. Furthermore, depression of AV nodal conduction appears to be an indirect rather than direct effect of anesthesia. Finally, most depression of conduction occurs with light anesthesia, with little added depression related to depth of anesthesia over levels likely to be encountered clinically.

Anesthesia, Inhalation↗