In vivo myocardial excitability studied by simultaneous electrocardiogram and electrogram

Rogel, S.; Hasin, Y.

doi:10.1016/s0022-0736(74)80063-4

Cited by 8 publications

(4 citation statements)

References 17 publications

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“…Our observations lead us to believe that it is usually not more than 40 ms. Similar values were seen experimentally by Brooks and associates (1955), and Rogel and Hasin (1974). Increased SQ duration indicates an increase in one or more of the aforementioned time factors, and occurs as a result of severe myocardial depression.…”

Section: Significance Of the Sq Duration (Latency)supporting

confidence: 88%

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The Wenckebach phenomenon between electric pacemaker and ventricle.

Klein¹,

Segni²,

Kaplinsky³

et al. 1976

Heart

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Two cases which exhibited a Wenckebach form of exit conduction between an electrical pacemaker and the ventricular myocardium are presented. This manifests with increasing latency (stimulus to QRS intervals) and ultimate stimulus failure (block). The cycle then repeats itself. The QRS duration also increases progressively within each cycle. The phenomenon connotes an adverse prognosis. Severalpostulates regarding the mechanism are discussed.The Wenckebach phenomenon has been observed in many locations of cardiac tissue (Decherd and

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Section: Significance Of the Sq Duration (Latency)supporting

confidence: 88%

“…As early as the second hospital day, at the time of pacemaker insertion, first degree block was noted between the pacemaker and the ventricle, as reflected by a stimulus-QRS interval of 100 ms. The normal value probably does not exceed 40 ms (Brooks et al, 1955;Rogel and Hasin, 1974). The tracings shown in Fig.…”

Section: Casementioning

confidence: 90%

The Wenckebach phenomenon between electric pacemaker and ventricle.

Klein¹,

Segni²,

Kaplinsky³

et al. 1976

Heart

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“…We have previously shown that the TL current level is associated with the production of a local, non-propagated response (Rogel & Hasin, 1974). This was demonstrated by means of simultaneous recording of the surface electrocardiogram and the local tissue potential at the site of the stimulating electrode.…”

Section: Discussionmentioning

confidence: 94%

“…The lower limit of threshold (TL) is therefore that current level which is just insufficient to depolarize the heart regardless of how long it is applied or whether it follows multiple extrasystoles. With simultaneous recording and stimulating from the same electrode it has been shown that the TL current level always induces a local, nonpropagated response, which increases in magnitude with the rise in current level until general spread is manifested (Rogel & Hasin, 1974). It has also been found that within the range of stimuli between TU and TL capture is inconsistent, suggesting spontaneous variations in threshold (Rogel et al, 1970).…”

Section: Introductionmentioning

confidence: 99%

ANTIARRHYTHMIC DRUGS AND IN VIVO MYOCARDIAL EXCITABILITY IN THE DOG

Hasin

Rogel

1977

Clin Exp Pharma Physio

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S U M M A R Y1. It has been demonstrated in an earlier study that the threshold for capturing the canine ventricle in situ varies at each time interval during the relative refractory period with a wide range of current levels. Thus, there is no single threshold curve, as is commonly accepted, but rather a range defined by upper limit of threshold (T,) and a lower limit (TL). TU is the minimal current level which always produced a generalized ventricular response. A wide range of lesser current levels produced a local response but with inconsistent propagation throughout the ventricle. TL is the maximal current level which was never able t o elicit a generalized response.2. Applying the method used for the determination of these limits, the present study was undertaken to characterize the effect of quinidine, lignocaine, procainamide and verapamil in therapeutic doses on TU and TL.3. It was found that quinidine, lignocaine and procainamide elevated TU and TL during the relative refractory period, but only quinidine did so during diastole as well. Verapamil, however, did not have any significant influence on excitability. Procainamide had the least effect on the absolute refractoriness of the ventricular muscle as judged by the rightward displacement of the TU and TL curves, while quinidine and lignocaine exhibited a significant displacement regarding TU but much less so for TL.4. The proposition is entertained that TL represents true local excitability of the ventricular muscle and TU represents the stimulus needed for propagation throughout the heart during the most unfavourable conditions for such spread.5. Relative changes of TU/TL as a function of TU are considered to express the capability of the locally induced potential to evoke a generalized response: quinidine diminished, procainamide increased, and lignocaine had no effect on this parameter.

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