Accommodation of A-V Nodal Conduction and Fatigue Phenomenon in the His-Purkinje System

Narula, Onkar S.; Runge, M

doi:10.1007/978-94-009-9726-4_29

Cited by 24 publications

(13 citation statements)

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“…In some patients in whom TD AV block in the His-Purkinje system could be demonstrated by incremental atrial pacing, rapid ventricular pacing may also induce a high-degree AV block 12,18,19. Similar observations have been reported in an experimental model of acute ischemia of the proximal His-Purkinje system, in which PAVB could be induced by rapid atria or ventricular pacing 20.…”

Section: Td-pavbsupporting

confidence: 61%

Paroxysmal atrioventricular block: Are phase 3 and phase 4 block mechanisms or misnomers?

El‐Sherif

Jalife

2009

Heart Rhythm

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PrologueThe era of deductive analysis of the electrocardiogram was prolific in its ability to yield accurate inferences regarding the pathophysiology of a vast number of heart rhythm disorders. However, occasionally there was a tendency to infer hypothetical electrophysiological mechanisms without the benefit of direct cellular information. This turned out to be misleading in some cases in which suggested mechanisms were subsequently found to be incorrect, and it also unintentionally hampered the search for more basic mechanisms. Two cases in point are the use of the terms "phase 3" and "phase 4" block in reference to tachycardia-dependent (TD) and pause-dependent (PD) paroxysmal atrioventricular block (PAVB), 1 respectively. Not only did basic studies definitely show that TD-PAVB is not related to phase 3 block, but also significant basic studies demonstrated that PD-PAVB need not depend on a phase 4 depolarization mechanism. Here we revisit the problems of TD-and PD-PAVB and illustrate by clinical and basic science examples possible pathophysiological mechanisms.

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Section: Td-pavbsupporting

confidence: 61%

Paroxysmal atrioventricular block: Are phase 3 and phase 4 block mechanisms or misnomers?

El‐Sherif

Jalife

2009

Heart Rhythm

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“…When the duration of overdrive ventricular pacing was increased the escape rhythm recovery time was prolonged, as a result of increased suppression of the intrinsic rhythm; occasionally, it was associated with a doubling or trebling of escape rhythm recovery time probably mediated by initial exit block of the escape focus. It has been observed by Langendorff and Pick (1971) and by Narula and Runge (1976) that the AV conduction in the His-Purkinje system can be influenced by overdrive suppression during artificial pacing, and exit block induced in this way may well explain the unpredictable variations in escape rhythm recovery time seen in many patients.…”

Section: Discussionmentioning

confidence: 97%

Overdrive suppression of implanted pacemakers in patients with AV block.

Grendahl¹,

M²,

Kjekshus³

1978

Heart

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Patients being permanently paced for symptomatic AV block were studied by overdrive suppression of the QRS-inhibited pacemaker, in order to observe the underlying heart rhythm. The chest wall stimulation method was used. In complete AV block the escape rhythm recovery time proved highly reproducible on repeated testing on the same day, and in many patients remained so over months or years. Occasionally, a doubling of the escape rhythm recovery time was seen, suggesting initial exit block of the escape focus. Resetting of the escape rhythm usually followed an exponential curve until stabilisation after about 3 minutes. An early escape rhythm with a recovery time of less than 4 seconds was found on every occasion in 21 of 58 patients with complete AV block, and inconstantly in 23 more; in 14 it was never observed. Accidental pacing failure was seen in 15 patients. The overdrive suppression test was helpful in selecting pacemaker dependent patients.

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“…Perfusate Po 2 In this series of experiments, the Pc>2 of the perfusate (PaO;) of both the normoxic (95% O2) and mild hypoxic (38% or 54% O2) solution was measured prior to instrumentation of the hearts. In these hearts, the pulmonary artery was cannulated and the venous outflow diverted to the inflow port of the oxygen electrode flow chamber for measurement of venous oxygen tension (PVO2).…”

Section: Venous Oxygen Tension (Pvo 2 ) and Adenosine Release During mentioning

confidence: 99%

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine.

Jenkins

Belardinelli

1988

Circulation Research

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The progressive prolongation of atrioventricular node (AVN) conduction time to a new steady-state value caused by sadden and maintained increases in atrial rate is the most common form of AV nodal accommodation. This study was undertaken to 1) characterize AV nodal accommodation in isolated perfused guinea pig hearts, 2) investigate the influence of potential modulators of this phenomenon such as acetylcholine and adenosine, and 3) determine the physiological significance of AV nodal accommodation on cardiac function. Beat-by-beat changes in AVN conduction time caused by single-or multiple-step increases in atrial pacing rate were measured during control conditions and in the presence of atropine (1 fiM), propranolol (1 /uM), and the adenosine antagonist BW-A1433 (1 fiM). BW-A1433 was the only intervention that significantly reduced the cumulative and frequency-dependent prolongation of AVN conduction time but this was only observed at atrial cycle lengths £ 170 msec. In addition, BW-A1433 shortened the Wenckebach cycle length from 163 ±2 to 153 ±2 during normoxia and from 172 ±3 to 164 ±4 during mild hypoxia. In contrast, dipyridamole (1 fiM), an adenosine uptake blocker, markedly accentuated the AVN conduction time prolongation, accentuated the AV block associated with fast atrial rates, and significantly increased the Wenckebach cycle length. These effects of dipyridamole were prevented and antagonized by BW-A1433 and adenosine deaminase. When O 2 supply was limited and at the same time demand increased secondary to fast atrial pacing, the rate of adenosine release increased from a control of 125 ±27 to 580 ±54 pmol/min/g. This was accompanied by a significant prolongation in AVN conduction time that invariably progressed to AV block. Once AV block occurred, O 2 consumption decreased, O 2 supply-to-demand ratio improved and the rate of adenosine release dropped to 310 ±61 pmol/min/g. Reversal of the AV block with adenosine antagonists resulted in a decrease in O 2 supply-to-demand ratio and a severalfold increase in the rate of adenosine release. In this feedback system, adenosine signals the imbalance between O 2 supply and demand, causes AV block and, thus, reduces demand to compensate for the limited O 3 supply. On the other hand, adenosine deaminase and antagonists act as "error signals" by attenuating the effect of adenosine, whereas dipyridamole enhances the "gain" of the system by potentiating the effects of adenosine. We concluded that 1) AV nodal accommodation is an intrinsic property of the AVN that can be influenced by adenosine, and 2) under conditions of low O 2 supply-to-demand ratio, adenosine is produced as a negative feedback signal that protects the ventricles from excessive work by causing AV block. The wellrecognized dependence of AV conduction time on rate is consistent with this delay in recovery of excitability of the nodal cells. Furthermore, as also reported by Merideth et al, 1 the rate-dependency of AV transmission is cumulative, which indicates that the delayed recovery of excitab...

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Accommodation of A-V Nodal Conduction and Fatigue Phenomenon in the His-Purkinje System

Cited by 24 publications

References 0 publications

Paroxysmal atrioventricular block: Are phase 3 and phase 4 block mechanisms or misnomers?

Paroxysmal atrioventricular block: Are phase 3 and phase 4 block mechanisms or misnomers?

Overdrive suppression of implanted pacemakers in patients with AV block.

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine.

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