Relation among power spectrum, refractory period and conduction time during ventricular fibrillation

Author(s):  
M.T. Arredondo ◽  
G. Martin ◽  
S. Guillen ◽  
M. Such ◽  
A. Quesada
1984 ◽  
Vol 62 (12) ◽  
pp. 1479-1486 ◽  
Author(s):  
Jean-Paul Clozel ◽  
Jacques Billette ◽  
Gilles Caillé ◽  
Pierre Théroux ◽  
Richard Cartier

Atrial and atrioventricular conduction variables were studied at control and at the end of each of six consecutive 45-min diltiazem administration periods in eight closed chest-anesthetized dogs. Diltiazem was given as a bolus (50 μg/kg, i.v.) followed by an infusion (0.5 μg∙kg−1∙min−1); doses were doubled in subsequent periods. The plasma concentrations, measured by gas–liquid chromatography, ranged from 8 to 1400 ng/mL and correlated strongly with the doses (r = 0.92; p < 0.01). The Wenckebach cycle length, basic conduction time, and functional refractory period of the atrioventricular (AV) node increased proportionally with plasma concentration (respective r = 0.90, 0.89, 0.80; p < 0.01). The minimum mean plasma concentrations affecting these variables significantly were 37, 83, and 175 ng/mL, respectively. Second or third degree AV blocks developed in all dogs for plasma concentrations between 379 and 1400 ng/mL. In four dogs which were given isoproterenol (0.2 μg∙kg−1∙min−1), these blocks disappeared within 1 min. Atrial conduction time and functional refractory period were slightly but significantly shortened by diltiazem with mean plasma concentrations of 175 ng/mL and over. His–Purkinje intervals were not significantly changed by diltiazem. Systolic and diastolic arterial pressures were decreased by diltiazem (r = −0.64, r = −0.79; p < 0.01) starting with a mean plasma concentration of 83 ng/mL. We conclude that AV nodal conduction variables are progressively prolonged with increasing plasma concentrations of diltiazem; plasma concentrations affecting blood pressure and AV nodal variables overlap; and the AV blocks produced by toxic concentrations of diltiazem can be corrected by isoproterenol.


1957 ◽  
Vol 191 (3) ◽  
pp. 481-486 ◽  
Author(s):  
M. J. Oppenheimer ◽  
P. R. Lynch ◽  
G. Ascanio

Slow conduction velocities play a role in pulsus alternans and digitalis intoxication and possibly in the arrhythmia due to a rapidly discharging atrial aconitine focus. In the ventricle mephentermine increases conduction velocity, shortens refractory period and A-V conduction time. The present study investigates the usefulness of mephentermine in these conditions. Pulsus alternans was reverted to a normal series of mechanical contractions by mephentermine. The same agent provided periods of regular rhythm during the presence of an atrial aconitine focus; in two cases a permanent sinus rhythm was established. The prolonged P-R interval due to intoxication with acetyl strophanthidin was restored to normal by mephentermine. The action of mephentermine is specific since compounds with addition or subtraction of one methyl group or the hydroxy-mephentermine were ineffective against a circus flutter.


1993 ◽  
Vol 265 (4) ◽  
pp. H1257-H1264 ◽  
Author(s):  
G. O'Hara ◽  
R. Gendreau ◽  
J. Billette ◽  
F. Amellal ◽  
M. Nayebpour ◽  
...  

While rate-dependent atrioventricular (AV) nodal functional properties play a major role in determining antegrade AV nodal conduction, their existence and characteristics have not been assessed during retrograde AV nodal impulse propagation. Pacing protocols were used to study selectively AV nodal recovery, facilitation, and fatigue in 6 isolated, superfused rabbit AV nodal preparations and in 11 morphine-chloralose anesthetized dogs. All three properties were identifiable during retrograde AV nodal activation in rabbits. Retrograde recovery and fatigue were clearly demonstrated in dogs, but facilitation could not be evaluated because of echo beats during retrograde premature stimulation. Functional properties were qualitatively similar during retrograde and antegrade propagation; however, important quantitative differences were noted. The time constant for recovery from activation was significantly greater in the retrograde [rabbits, 69 +/- 8 (SE) ms; dogs, 93 +/- 11 ms] compared with the antegrade direction (rabbits, 50 +/- 5 ms; dogs, 58 +/- 4 ms; P < 0.05 vs. retrograde for each species). The magnitude of fatigue resulting from sustained increases in rate was also substantially greater in the retrograde direction in both rabbits (17 +/- 2 vs. 10 +/- 1 ms antegrade, P = 0.01) and dogs (20 +/- 4 vs. 6 +/- 1 ms antegrade, P < 0.01). Conduction time and refractory period were both greater in the retrograde compared with antegrade direction, and directional differences in conduction properties were magnified as activation rate increased.(ABSTRACT TRUNCATED AT 250 WORDS)


1974 ◽  
Vol 52 (3) ◽  
pp. 624-631 ◽  
Author(s):  
Victor Elharrar ◽  
Réginald A. Nadeau ◽  
Fernand Roberge ◽  
Gérald A. Porlier ◽  
Claude Pelletier

In the anesthetized dog, the effects of ouabain injected intravenously and directly into the atrioventricular (A-V) node artery were studied. Automaticity within the A-V junction was decreased after a dose of ouabain, 30 μg/kg given intravenously (i.v.), whereas automaticity of ventricular specialized fibers was increased after a dose of 40 μg/kg i.v. The decrease of automaticity within the A-V junction was accompanied by an increased duration of the functional refractory period of this structure and by a prolongation of conduction time through the A-V junction as determined from the His bundle electrogram.


Rhabdocalyptus can arrest its feeding current. The response is initiated by mechanical or electrical stimulation, and is coordinated through the sponge by a conduction system, having a precise excitability threshold and conducting on an all-or-none basis. All parts are excitable and conduct. Individuals in colonial assemblages are coordinated. Spontaneous as well as evoked arrests are observed. There is evidence of scattered pacemaker sites. Conduction is diffuse and unpolarized, and occurs with a velocity of 0.26 ± 0.07 cm s -1 at 11 °C. The conduction system is probably the trabecular syncytium. Isolated dermal membrane (‘pure’ trabecular tissue, without flagella or contractile elements) conducts. Mechanical and chemical signalling mechanisms are discussed. It is concluded that they cannot account for the phenomena observed, but that conduction must involve electrical impulses. The effectors responsible for current arrests are almost certainly the flagella of the flagellated chambers. It is assumed that they stop beating on receiving an arrest signal through the conduction pathway. The waveforms of arrests recorded with a thermistor flowmeter are best interpreted in terms of sudden, all-or-none cessation of pumping, with slow, gradual recovery of full pumping power. The flagella probably beat feebly at first on becoming active again following an arrest. The effector response shows a refractory period of 30 s. Responses occur with short latency. Delays are attributable to conduction time. The system is fatigueable. Numerous parallels exist with the behaviour of the stigmatal cilia in the ascidian branchial sac, both in the characteristics of the effector response and in the mechanism of coordination.


2020 ◽  
Vol 116 (13) ◽  
pp. 2081-2090 ◽  
Author(s):  
Erik S Dietrichs ◽  
Karen McGlynn ◽  
Andrew Allan ◽  
Adam Connolly ◽  
Martin Bishop ◽  
...  

Abstract Aims Treatment of arrhythmias evoked by hypothermia/rewarming remains challenging, and the underlying mechanisms are unclear. This in vitro experimental study assessed cardiac electrophysiology in isolated rabbit hearts at temperatures occurring in therapeutic and accidental hypothermia. Methods and results Detailed ECG, surface electrogram, and panoramic optical mapping were performed in isolated rabbit hearts cooled to moderate (31°C) and severe (17°C) hypothermia. Ventricular activation was unchanged at 31°C while action potential duration (APD) was significantly prolonged (176.9 ± 4.2 ms vs. 241.0 ± 2.9 ms, P &lt; 0.05), as was ventricular repolarization. At 17°C, there were proportionally similar delays in both activation and repolarization. These changes were reflected in the QRS and QT intervals of ECG recordings. Ventricular fibrillation threshold was significantly reduced at 31°C (16.3 ± 3.1 vs. 35 ± 3.5 mA, P &lt; 0.05) but increased at 17°C (64.2 ± 9.9, P &lt; 0.05). At 31°C, transverse conduction was relatively unchanged by cooling compared to longitudinal conduction, but at 17°C both transverse and longitudinal conduction were proportionately reduced to a similar extent. The gap junction uncoupler heptanol had a larger relative effect on transverse than longitudinal conduction and was able to restore the transverse/longitudinal conduction ratio, returning ventricular fibrillation threshold to baseline values (16.3 ± 3.1 vs. 36.3 ± 4.3 mA, P &lt; 0.05) at 31°C. Rewarming to 37°C restored the majority of the electrophysiological parameters. Conclusions Moderate hypothermia does not significantly change ventricular conduction time but prolongs repolarization and is pro-arrhythmic. Further cooling to severe hypothermia causes parallel changes in ventricular activation and repolarization, changes which are anti-arrhythmic. Therefore, relative changes in QRS and QT intervals (QR/QTc) emerge as an ECG-biomarker of pro-arrhythmic activity. Risk for ventricular fibrillation appears to be linked to the relatively low temperature sensitivity of ventricular transmural conduction, a conclusion supported by the anti-arrhythmic effect of heptanol at 31°C.


1985 ◽  
Vol 63 (11) ◽  
pp. 1418-1422 ◽  
Author(s):  
Peter E. Dresel ◽  
A. Ogbaghebriel ◽  
R. Abraham

His-bundle electrocardiography was used to evaluate the effects of ethmozine on cardiac conduction in isolated perfused rabbit hearts electrically driven at cycle lengths of 320 and 250 ms. There was no significant change in conduction until high concentrations of ethmozine were reached. His-Purkinje and atrioventricular (AV) nodal conduction were slowed significantly at 0.1 μg/mL and atrial conduction at 1.0 μg/mL. Conduction block occurred at 10.0 μg/mL in all the hearts treated. Effects of the drug (0.1 and 0.01 μg/mL) on conduction of extrasystoles were also studied in hearts driven at a basic cycle length of 270 ms. No significant change was observed in atrial conduction of extrasystoles throughout the coupling intervals tested at both concentrations. Ethmozine (0.01 and 0.1 μg/mL) caused slowing of His-Purkinje conduction of extrasystoles but the effect of the drug did not change as a function of the coupling interval. An interval-dependent increase in AV-nodal conduction time was observed, with the maximum slowing of conduction occurring at coupling intervals close to the effective refractory period of the AV node. AV-nodal functional refractory period was increased significantly by ethmozine (0.01 and 0.1 μg/mL). The effective refractory period was significantly increased only at the higher concentration.


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