Determination of effects of internal countershock by direct cardiac recordings during normal rhythm

Colavita, Paul G.; Wolf, Patrick D.; Smith, William M.; Bartram, Frederick R.; Hardage, Mike; Re, Ideker

doi:10.1152/ajpheart.1986.250.5.h736

Cited by 7 publications

(5 citation statements)

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“…The time required to activate both the septum and the epicardium (the cardiac activation time) was determined by subtracting the time of earliest recorded activation of either the septum or epicardium from the latest recorded activation time for each map. The areas directly depolarized by the 20-V and 100-V shocks delivered during sinus rhythm were also calculated to indicate regions of high-and low-field strength generated by the shock (9).…”

Section: Surgical Preparationmentioning

confidence: 99%

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Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

Chen¹,

Shibata²,

Dixon³

et al. 1986

J. Clin. Invest.

239

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To test the hypothesis that a defibrillation shock is unsuccessful because it fails to annihilate activation fronts within a critical mass of myocardium, we recorded epicardial and transmural activation in 11 open-chest dogs during electrically induced ventricular fibrillation (VF). Shocks of 1-30 J were delivered through defibrillation electrodes on the left ventricular apex and right atrium. Simultaneous recordings were made from septal, intramural, and epicardial electrodes in various combinations. Immediately after all 104 unsuccessful and 116 successful defibrillation shocks, an isoelectric interval much longer than that observed during preshock VF occurred. During this time no epicardial, septal, or intramural activations were observed. This isoelectric window averaged 64±22 ms after unsuccessful defibrillation and 339±292 ms after successful defibrillation (P < 0.02). After the isoelectric window of unsuccessful shocks, earliest activation was recorded from the base of the ventricles, which was the area farthest from the apical defibrillation electrode. Activation was synchronized for one or two cycles following unsuccessful shocks, after which VF regenerated.Thus, (a) after both successful and unsuccessful defibrillation with epicardial shocks of 21 J, an isoelectric window occurs during which no activation fronts are present; (b) the postshock isoelectric window is shorter for unsuccessful than for successful defibrillation; (c) unsuccessful shocks transiently synchronize activation before fibrillation regenerates; (d) activation leading to the regeneration of VF after the isoelectric window for unsuccessful shocks originates in areas away from the defibrillation electrodes. The isoelectric window does not support the hypothesis that defibrillation fails solely because activation fronts are not halted within a critical mass of myocardium. Rather, unsuccessful epicardial shocks of 21 J halt all activation fronts after which VF regenerates.

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Section: Surgical Preparationmentioning

confidence: 99%

“…We have modified our mapping system to record soon after a countershock without amplifier saturation (9). The purpose of this study was to use this modified mapping system during ventricular fibrillation (VF)' to test the critical mass hypothesis of electrical defibrillation.…”

Section: Introductionmentioning

confidence: 99%

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

Chen¹,

Shibata²,

Dixon³

et al. 1986

J. Clin. Invest.

239

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“…Tissue under electrodes that did not record an activation after S 2 stimulation was considered to be directly excited by the stimulus as described previously. 14,15 To quantify the effect of the incision on the activation sequence, the time interval was determined from the begin- Figure 1. Effect of an intracellular discontinuity on current flow.…”

Section: Discussionmentioning

confidence: 99%

Myocardial Discontinuities

et al. 1998

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Background-Theoretical models suggest that an electrical stimulus causes regions of depolarization and hyperpolarization on either side of a myocardial discontinuity. This study determined experimentally whether an artificial discontinuity gives rise to an activation front in response to an electrical stimulus, consistent with the creation of such polarized regions. Methods and Results-After a thoracotomy in six dogs, a 504-unipolar-electrode plaque was sutured to the right ventricular epicardium to map activations. From a line electrode parallel to one side of the plaque, 10 S 1 stimuli were delivered, followed by S 2 and S 3 stimuli (S 1 S 1 , S 1 S 2 , S 2 S 3 intervalϭ300 ms). S 1 and S 3 stimuli were 25 mA; 5-ms S 2 stimuli of both polarities were initially 25 mA and increased in 25 mA increments. The plaque was removed, and a transmural incision was made through the ventricular wall in the middle of the mapped region and sutured closed. The plaque was replaced and the stimulation protocol repeated. Before the incision, S 2 stimuli directly activated tissue only near the stimulation site. An activation front arose at the border of the directly activated region and propagated across the plaque. As the S 2 stimulus strength was increased, the size of the directly activated region increased. After the incision, sufficiently large S 2 stimuli caused direct activation of tissue adjacent to the transmural incision as well as at the stimulation site. Activation fronts that arose adjacent to the transmural incision either propagated proximally toward the stimulation site and collided with the activation front originating from the stimulation wire or propagated distally away from the incision. Minimum S 2 stimulus strengths activating areas adjacent to the incision were only 45Ϯ14% (cathode) and 39Ϯ18% (anode) of the strengths required to directly activate the same area before the incision was formed (PϽ.05). Conclusions-Myocardial discontinuities can give rise to activation fronts after a stimulus, suggesting the presence of polarized regions adjacent to the discontinuity. (Circulation. 1998;97:1738-1745.)

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“…Continuity of I i at the intercellular junction, i.e., I i | x5 0 2 5 I i | x5 0 1 3. Applicability of Kirchhoff's voltage law at the junction, i.e., V m | x5 0 2 2 V m | x5 0 1…”

Section: Theoreticalmentioning

confidence: 99%

Theoretical and Experimental Study of Sawtooth Effect in Isolated Cardiac Cell‐Pairs

Sharma

Tung

2001

Cardiovasc electrophysiol

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Determination of effects of internal countershock by direct cardiac recordings during normal rhythm

Cited by 7 publications

References 0 publications

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

Activation during ventricular defibrillation in open-chest dogs. Evidence of complete cessation and regeneration of ventricular fibrillation after unsuccessful shocks.

Myocardial Discontinuities

Theoretical and Experimental Study of Sawtooth Effect in Isolated Cardiac Cell‐Pairs

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