The Experts below are selected from a list of 177 Experts worldwide ranked by ideXlab platform
Philip R. Reid - One of the best experts on this subject based on the ideXlab platform.
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effects of flecainide encainide and clofilium on ventricular Refractory Period extension by transcardiac shocks
Pacing and Clinical Electrophysiology, 1996Co-Authors: Robert J. Sweeney, Robert M. Gill, Mitchell I. Steinberg, Philip R. ReidAbstract:OBJECTIVE: The mechanisms by which pharmacological agents alter electrical defibrillation are not fully understood. It has been proposed that, in addition to directly stimulating tissue, defibrillation may involve Refractory Period extension (RPE) produced by the shock. Accordingly, pharmacological agents might modulate defibrillation by altering RPE. This study examined the effect of Class I and Class III antiarrhythmic agents on RPE by transcardiac shocks. METHODS: In four groups of pentobarbital anesthetized dogs, RPE was measured during rapid ventricular pacing before and after administration of either the Class I agents flecainide (n = 7) or encainide (n = 7), the Class III agent clofilium (n = 7), or vehicle (n = 5). Measurements included QRS duration during sinus rhythm and a conduction time, QTC interval and Refractory Period, and RPE for 4- to 10-V/cm shocks delivered 20-80 ms before the end of the tissue absolute Refractory Period. For the 6-V/cm shocks, the interval after the shock during which tissue remained Refractory (RIAS) was also computed. RESULTS: Drugs affected QRS duration, conduction time, QTC, and Refractory Period ( without shocks) in accordance with their anticipated Class I and Class III actions. Without drugs, significant RPE was observed in all animals for all shocks delivered 40 ms or less before the end of the Refractory Period. Clofilium, encainide, and flecainide had a tendency to increase RPE but only clofilium produced a significant increase. For 6-V/cm shocks with different timings, the minimum RIAS was found to be approximately 43 ms, and occurred for shocks given 20-30 ms before the end of the Refractory Period. CONCLUSIONS: At drug dosages that produced moderate Class III ( approximately equal to 15%) or strong Class I (approximately equal to 35%) effects, only the Class III agent significantly increased RPE and RIAS. Thus, in addition to altering tissue excitability, the effect of antiarrhythmic agents to increase RPE and the minimum RIAS may help explain their influence on defibrillation threshold.
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Countershock strength-duration relationship for myocardial Refractory Period extension.
Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 1995Co-Authors: Robert J. Sweeney, Robert M. Gill, Philip R. ReidAbstract:Objectives: To determine the strength-duration relationship for Refractory Period extension (RPE) in order to understand better the influence of shock waveform on RPE. Methods: In six open-chest pentobarbital-anesthetized dogs, the RPE was measured by rectangular transcardiac shocks that produced 2– to 32-V/cm local voltage gradients at the measurement site. At each intensity, measurements were made for shocks with 2– to 32-msec durations delivered 30 msec before the end of the tissue Refractory Period. Results: These shocks produced up to 40% RPE. The RPE varied strongly with shock intensity and duration, with more RPE for stronger or longer shocks. At 32 V/cm, early portions of the shock waveform contributed most to RPE. At 8 and 16 V/cm, later portions made relatively larger contributions that were still smaller than those of the early portions. At 4 V/cm, the contributions to total RPE were spread over the entire waveform. At 2 V/cm, shocks failed to produce significant RPE. Conclusions: For rectangular shock waveforms, the relationship between RPE and duration is approximately linear at low intensity, but at higher intensity greater RPE is produced by earlier, rather than later, portions of the waveform. This may be because RPE by early portions of the waveform changes the effective timing in the Refractory Period for later portions of the same waveform. These results' provide new insight into the possible role of waveform on defibrillation efficacy.
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Characterization of Refractory Period extension by transcardiac shock.
Circulation, 1991Co-Authors: Robert J. Sweeney, Robert M. Gill, Philip R. ReidAbstract:BACKGROUND To better understand the Refractory Period extension (RPE) produced by transcardiac shocks and its possible role in defibrillation, we measured RPE under various experimental conditions. METHODS AND RESULTS Using ventricular pacing in pentobarbital-anesthetized dogs, we characterized RPE in relation to the anatomic site of pacing, the local voltage gradient (LVG) produced by the shocks at the pacing site, and the pacing rate and pacing current used to make the measurements. We also determined if RPE persisted into the next Refractory Period after the shock and measured RPE at the end of 30-second episodes of acute ischemia to the pacing site, which were caused by occluding the left anterior descending artery. Each anatomic site tested showed RPE, which increased sharply with increasing LVG at lower levels but less sharply at higher LVG. The RPE versus LVG was approximated with an exponential curve that had an exponential constant of about 5-6 V/cm. At faster pacing rates, RPE occurred earlier in the Refractory Period but was unchanged when expressed as a percent increase of Refractory Period. RPE did not vary with the pacing current and was present only in the Refractory Period during which the shock was delivered. The RPE was not significantly altered by acute ischemia. These results show that transcardiac shocks selectively extend the Refractory Period of tissue proportional to the LVG and the timing of the shock in the Refractory Period. They are consistent with the concept that RPE prevents depolarization from tissue directly excited by a shock from propagating to tissue that was Refractory to that same shock. CONCLUSIONS The insensitivity of RPE to short ischemic episodes and the presence of RPE at increased activation rates suggest that RPE might exist under conditions of fibrillation and be a major determinant of the success or failure of defibrillation.
Robert J. Sweeney - One of the best experts on this subject based on the ideXlab platform.
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effects of flecainide encainide and clofilium on ventricular Refractory Period extension by transcardiac shocks
Pacing and Clinical Electrophysiology, 1996Co-Authors: Robert J. Sweeney, Robert M. Gill, Mitchell I. Steinberg, Philip R. ReidAbstract:OBJECTIVE: The mechanisms by which pharmacological agents alter electrical defibrillation are not fully understood. It has been proposed that, in addition to directly stimulating tissue, defibrillation may involve Refractory Period extension (RPE) produced by the shock. Accordingly, pharmacological agents might modulate defibrillation by altering RPE. This study examined the effect of Class I and Class III antiarrhythmic agents on RPE by transcardiac shocks. METHODS: In four groups of pentobarbital anesthetized dogs, RPE was measured during rapid ventricular pacing before and after administration of either the Class I agents flecainide (n = 7) or encainide (n = 7), the Class III agent clofilium (n = 7), or vehicle (n = 5). Measurements included QRS duration during sinus rhythm and a conduction time, QTC interval and Refractory Period, and RPE for 4- to 10-V/cm shocks delivered 20-80 ms before the end of the tissue absolute Refractory Period. For the 6-V/cm shocks, the interval after the shock during which tissue remained Refractory (RIAS) was also computed. RESULTS: Drugs affected QRS duration, conduction time, QTC, and Refractory Period ( without shocks) in accordance with their anticipated Class I and Class III actions. Without drugs, significant RPE was observed in all animals for all shocks delivered 40 ms or less before the end of the Refractory Period. Clofilium, encainide, and flecainide had a tendency to increase RPE but only clofilium produced a significant increase. For 6-V/cm shocks with different timings, the minimum RIAS was found to be approximately 43 ms, and occurred for shocks given 20-30 ms before the end of the Refractory Period. CONCLUSIONS: At drug dosages that produced moderate Class III ( approximately equal to 15%) or strong Class I (approximately equal to 35%) effects, only the Class III agent significantly increased RPE and RIAS. Thus, in addition to altering tissue excitability, the effect of antiarrhythmic agents to increase RPE and the minimum RIAS may help explain their influence on defibrillation threshold.
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Countershock strength-duration relationship for myocardial Refractory Period extension.
Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 1995Co-Authors: Robert J. Sweeney, Robert M. Gill, Philip R. ReidAbstract:Objectives: To determine the strength-duration relationship for Refractory Period extension (RPE) in order to understand better the influence of shock waveform on RPE. Methods: In six open-chest pentobarbital-anesthetized dogs, the RPE was measured by rectangular transcardiac shocks that produced 2– to 32-V/cm local voltage gradients at the measurement site. At each intensity, measurements were made for shocks with 2– to 32-msec durations delivered 30 msec before the end of the tissue Refractory Period. Results: These shocks produced up to 40% RPE. The RPE varied strongly with shock intensity and duration, with more RPE for stronger or longer shocks. At 32 V/cm, early portions of the shock waveform contributed most to RPE. At 8 and 16 V/cm, later portions made relatively larger contributions that were still smaller than those of the early portions. At 4 V/cm, the contributions to total RPE were spread over the entire waveform. At 2 V/cm, shocks failed to produce significant RPE. Conclusions: For rectangular shock waveforms, the relationship between RPE and duration is approximately linear at low intensity, but at higher intensity greater RPE is produced by earlier, rather than later, portions of the waveform. This may be because RPE by early portions of the waveform changes the effective timing in the Refractory Period for later portions of the same waveform. These results' provide new insight into the possible role of waveform on defibrillation efficacy.
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Characterization of Refractory Period extension by transcardiac shock.
Circulation, 1991Co-Authors: Robert J. Sweeney, Robert M. Gill, Philip R. ReidAbstract:BACKGROUND To better understand the Refractory Period extension (RPE) produced by transcardiac shocks and its possible role in defibrillation, we measured RPE under various experimental conditions. METHODS AND RESULTS Using ventricular pacing in pentobarbital-anesthetized dogs, we characterized RPE in relation to the anatomic site of pacing, the local voltage gradient (LVG) produced by the shocks at the pacing site, and the pacing rate and pacing current used to make the measurements. We also determined if RPE persisted into the next Refractory Period after the shock and measured RPE at the end of 30-second episodes of acute ischemia to the pacing site, which were caused by occluding the left anterior descending artery. Each anatomic site tested showed RPE, which increased sharply with increasing LVG at lower levels but less sharply at higher LVG. The RPE versus LVG was approximated with an exponential curve that had an exponential constant of about 5-6 V/cm. At faster pacing rates, RPE occurred earlier in the Refractory Period but was unchanged when expressed as a percent increase of Refractory Period. RPE did not vary with the pacing current and was present only in the Refractory Period during which the shock was delivered. The RPE was not significantly altered by acute ischemia. These results show that transcardiac shocks selectively extend the Refractory Period of tissue proportional to the LVG and the timing of the shock in the Refractory Period. They are consistent with the concept that RPE prevents depolarization from tissue directly excited by a shock from propagating to tissue that was Refractory to that same shock. CONCLUSIONS The insensitivity of RPE to short ischemic episodes and the presence of RPE at increased activation rates suggest that RPE might exist under conditions of fibrillation and be a major determinant of the success or failure of defibrillation.
Robert M. Gill - One of the best experts on this subject based on the ideXlab platform.
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effects of flecainide encainide and clofilium on ventricular Refractory Period extension by transcardiac shocks
Pacing and Clinical Electrophysiology, 1996Co-Authors: Robert J. Sweeney, Robert M. Gill, Mitchell I. Steinberg, Philip R. ReidAbstract:OBJECTIVE: The mechanisms by which pharmacological agents alter electrical defibrillation are not fully understood. It has been proposed that, in addition to directly stimulating tissue, defibrillation may involve Refractory Period extension (RPE) produced by the shock. Accordingly, pharmacological agents might modulate defibrillation by altering RPE. This study examined the effect of Class I and Class III antiarrhythmic agents on RPE by transcardiac shocks. METHODS: In four groups of pentobarbital anesthetized dogs, RPE was measured during rapid ventricular pacing before and after administration of either the Class I agents flecainide (n = 7) or encainide (n = 7), the Class III agent clofilium (n = 7), or vehicle (n = 5). Measurements included QRS duration during sinus rhythm and a conduction time, QTC interval and Refractory Period, and RPE for 4- to 10-V/cm shocks delivered 20-80 ms before the end of the tissue absolute Refractory Period. For the 6-V/cm shocks, the interval after the shock during which tissue remained Refractory (RIAS) was also computed. RESULTS: Drugs affected QRS duration, conduction time, QTC, and Refractory Period ( without shocks) in accordance with their anticipated Class I and Class III actions. Without drugs, significant RPE was observed in all animals for all shocks delivered 40 ms or less before the end of the Refractory Period. Clofilium, encainide, and flecainide had a tendency to increase RPE but only clofilium produced a significant increase. For 6-V/cm shocks with different timings, the minimum RIAS was found to be approximately 43 ms, and occurred for shocks given 20-30 ms before the end of the Refractory Period. CONCLUSIONS: At drug dosages that produced moderate Class III ( approximately equal to 15%) or strong Class I (approximately equal to 35%) effects, only the Class III agent significantly increased RPE and RIAS. Thus, in addition to altering tissue excitability, the effect of antiarrhythmic agents to increase RPE and the minimum RIAS may help explain their influence on defibrillation threshold.
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Countershock strength-duration relationship for myocardial Refractory Period extension.
Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 1995Co-Authors: Robert J. Sweeney, Robert M. Gill, Philip R. ReidAbstract:Objectives: To determine the strength-duration relationship for Refractory Period extension (RPE) in order to understand better the influence of shock waveform on RPE. Methods: In six open-chest pentobarbital-anesthetized dogs, the RPE was measured by rectangular transcardiac shocks that produced 2– to 32-V/cm local voltage gradients at the measurement site. At each intensity, measurements were made for shocks with 2– to 32-msec durations delivered 30 msec before the end of the tissue Refractory Period. Results: These shocks produced up to 40% RPE. The RPE varied strongly with shock intensity and duration, with more RPE for stronger or longer shocks. At 32 V/cm, early portions of the shock waveform contributed most to RPE. At 8 and 16 V/cm, later portions made relatively larger contributions that were still smaller than those of the early portions. At 4 V/cm, the contributions to total RPE were spread over the entire waveform. At 2 V/cm, shocks failed to produce significant RPE. Conclusions: For rectangular shock waveforms, the relationship between RPE and duration is approximately linear at low intensity, but at higher intensity greater RPE is produced by earlier, rather than later, portions of the waveform. This may be because RPE by early portions of the waveform changes the effective timing in the Refractory Period for later portions of the same waveform. These results' provide new insight into the possible role of waveform on defibrillation efficacy.
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Characterization of Refractory Period extension by transcardiac shock.
Circulation, 1991Co-Authors: Robert J. Sweeney, Robert M. Gill, Philip R. ReidAbstract:BACKGROUND To better understand the Refractory Period extension (RPE) produced by transcardiac shocks and its possible role in defibrillation, we measured RPE under various experimental conditions. METHODS AND RESULTS Using ventricular pacing in pentobarbital-anesthetized dogs, we characterized RPE in relation to the anatomic site of pacing, the local voltage gradient (LVG) produced by the shocks at the pacing site, and the pacing rate and pacing current used to make the measurements. We also determined if RPE persisted into the next Refractory Period after the shock and measured RPE at the end of 30-second episodes of acute ischemia to the pacing site, which were caused by occluding the left anterior descending artery. Each anatomic site tested showed RPE, which increased sharply with increasing LVG at lower levels but less sharply at higher LVG. The RPE versus LVG was approximated with an exponential curve that had an exponential constant of about 5-6 V/cm. At faster pacing rates, RPE occurred earlier in the Refractory Period but was unchanged when expressed as a percent increase of Refractory Period. RPE did not vary with the pacing current and was present only in the Refractory Period during which the shock was delivered. The RPE was not significantly altered by acute ischemia. These results show that transcardiac shocks selectively extend the Refractory Period of tissue proportional to the LVG and the timing of the shock in the Refractory Period. They are consistent with the concept that RPE prevents depolarization from tissue directly excited by a shock from propagating to tissue that was Refractory to that same shock. CONCLUSIONS The insensitivity of RPE to short ischemic episodes and the presence of RPE at increased activation rates suggest that RPE might exist under conditions of fibrillation and be a major determinant of the success or failure of defibrillation.
Ding Zhi-jian - One of the best experts on this subject based on the ideXlab platform.
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Atrial Refractory Period Dispersion and Atrial Fibrillation
Advances in Cardiovascular Diseases, 2010Co-Authors: Ding Zhi-jianAbstract:Atrial fibrillation is one of the most common clinical arrhythmias,and has a high rate of morbidity and mortality.There are many hypotheses regarding the mechanisms of atrial fibrillation.Atrial electrical remodeling,which involves the shortening of the atrial effective Refractory Period,an increase of the atrial effective Refractory Period dispersion,and a slowing of the electrical conduction,has been proven to promote the initiation and maintenance of atrial fibrillation.This article reviews the relationship between the atrial effective Refractory Period dispersion and atrial fibrillation and factors influencing the former.
Qiu Han - One of the best experts on this subject based on the ideXlab platform.
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Effects of rhomotoxin on ventricular Refractory Period in the rabbit heart
Chinese Pharmacological Bulletin, 1997Co-Authors: Qiu HanAbstract:AIM:Effect of rhomotoxin (Rh) 12 5 μg·kg -1 or 25 μg·kg -1 iv on ventricular Refractory Period was observed. METHOD:Using ventricular plunge electrode. RESULTS:At 20, 40, 60 and 80 min (after Rh 12 5 μg·kg -1 iv); VDT, ERP and RRP had no significant changes; but at 20, 40, 60 and 80 min, Rh 25 μg·kg -1 iv caused significant prolongation of ERP and (or) RRP ( P 0 05). CONCLUSIONS :That Rh wight have effect of prolongating ventricular Refractory Period.
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Effects of propafenone on changes of ventricular Refractory Period caused by subthreshold conditioning stimulation in the rabbit ventricle
Chinese Pharmacological Bulletin, 1993Co-Authors: Qiu HanAbstract:Effect of propafenone (Pro) 3 mg·kg-1iv on changes of ventricular Refractory Period caused by subthreshold conditioning stimulation in the rabbit ventricle was observed by using plunge electrode. The results indicate that Pro may cause significant prolongation of Refractory Period by S1St method. When stimulation strength of St was 2V, Refractory Period by S1-Stmethod was longer than that by S1-S2method; 4 V or beyond 4 V, prolongation value(Refractory Period of S1S2 method) of Refractory Period caused by S1-St method was decreased (vs pre-medication) and even Refractory Period by S1-S2(330 Hz, 50 ms,6V) method was shorter than that by S1S2 method. Pro may cause increase of minimal inhibitory voltages (Ss) that can inhibit ventricualr depolarization by S2,but this change had no significant difference (vs pre-medication ).
