Abstract
The pathophysiology of paroxysmal A V block (PAVB) was studied in 20 anesthetized dogs after ligation of the anterior septal artery. Simultaneous recording of leads II and aV(R), as well as intracardiac recordings from the His bundle (Hb) and both bundle branches, were monitored. In 18 of 20 experiments, PAVB was localized in the Hb. In all experiments, PAVB occurred subsequent to Mobitz type II A V block. In 8 experiments, PAVB occurred spontaneously during sinus rhythm and was preceded by a period of Wenckebach periodicity superimposed upon a 2:1 A V block. Vagal induced slowing of the sinus rate resulted in immediate resumption of 1:1 A V conduction. In 18 experiments, PAVB was induced by atrial pacing at a critical heart rate in each case (180-300 beats/min). Evidence is presented that A V conduction was consistently blocked below a critical H H interval. Slowing the pacing rate, termination of pacing or increasing the pacing rate until physiological A V nodal block occurred, all could result in a longer H H interval and immediate resumption of A V conduction. When the critical heart rate for PAVB was maintained, a slow idioventricular escape rhythm occurred. Five patients who developed PAVB after acute myocardial ischemia are also reported providing the clinical counterpart for the experimental observations. In all 5 cases, PAVB occurred on acceleration of the sinoatrial rate (105-140 beats/min) which was spontaneous in 2 and induced by drugs given for varied therapeutic indications in 3 (isoprenaline in 2 and atropine sulfate in 1). In all 5, PAVB was associated with Mobitz type II and/or 2:1 A V block. These experimental and clinical observations suggest that PAVB after acute myocardial ischemia appears to be due to a tachycardia dependent repetitive concealed conduction in the ischemic His Purkinje system, probably mainly in the Hb. The clinical observations point out potential consequences of a rapid atrial rate in patients with acute myocardial ischemia and type II A V block.
| Original language | English |
|---|---|
| Pages (from-to) | 515-528 |
| Number of pages | 14 |
| Journal | Circulation |
| Volume | 50 |
| Issue number | 3 |
| State | Published - Dec 1 1974 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
Cite this
The pathophysiology of tachycardia dependent paroxysmal atrioventricular block after acute myocardial ischemia. Experimental and clinical observations. / el-Sherif, N.; Scherlag, B. J.; Lazzara, R.; Hope, R.; Williams, D. O.; Samet, P.
In: Circulation, Vol. 50, No. 3, 01.12.1974, p. 515-528.Research output: Contribution to journal › Article
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TY - JOUR
T1 - The pathophysiology of tachycardia dependent paroxysmal atrioventricular block after acute myocardial ischemia. Experimental and clinical observations
AU - el-Sherif, N.
AU - Scherlag, B. J.
AU - Lazzara, R.
AU - Hope, R.
AU - Williams, D. O.
AU - Samet, P.
PY - 1974/12/1
Y1 - 1974/12/1
N2 - The pathophysiology of paroxysmal A V block (PAVB) was studied in 20 anesthetized dogs after ligation of the anterior septal artery. Simultaneous recording of leads II and aV(R), as well as intracardiac recordings from the His bundle (Hb) and both bundle branches, were monitored. In 18 of 20 experiments, PAVB was localized in the Hb. In all experiments, PAVB occurred subsequent to Mobitz type II A V block. In 8 experiments, PAVB occurred spontaneously during sinus rhythm and was preceded by a period of Wenckebach periodicity superimposed upon a 2:1 A V block. Vagal induced slowing of the sinus rate resulted in immediate resumption of 1:1 A V conduction. In 18 experiments, PAVB was induced by atrial pacing at a critical heart rate in each case (180-300 beats/min). Evidence is presented that A V conduction was consistently blocked below a critical H H interval. Slowing the pacing rate, termination of pacing or increasing the pacing rate until physiological A V nodal block occurred, all could result in a longer H H interval and immediate resumption of A V conduction. When the critical heart rate for PAVB was maintained, a slow idioventricular escape rhythm occurred. Five patients who developed PAVB after acute myocardial ischemia are also reported providing the clinical counterpart for the experimental observations. In all 5 cases, PAVB occurred on acceleration of the sinoatrial rate (105-140 beats/min) which was spontaneous in 2 and induced by drugs given for varied therapeutic indications in 3 (isoprenaline in 2 and atropine sulfate in 1). In all 5, PAVB was associated with Mobitz type II and/or 2:1 A V block. These experimental and clinical observations suggest that PAVB after acute myocardial ischemia appears to be due to a tachycardia dependent repetitive concealed conduction in the ischemic His Purkinje system, probably mainly in the Hb. The clinical observations point out potential consequences of a rapid atrial rate in patients with acute myocardial ischemia and type II A V block.
AB - The pathophysiology of paroxysmal A V block (PAVB) was studied in 20 anesthetized dogs after ligation of the anterior septal artery. Simultaneous recording of leads II and aV(R), as well as intracardiac recordings from the His bundle (Hb) and both bundle branches, were monitored. In 18 of 20 experiments, PAVB was localized in the Hb. In all experiments, PAVB occurred subsequent to Mobitz type II A V block. In 8 experiments, PAVB occurred spontaneously during sinus rhythm and was preceded by a period of Wenckebach periodicity superimposed upon a 2:1 A V block. Vagal induced slowing of the sinus rate resulted in immediate resumption of 1:1 A V conduction. In 18 experiments, PAVB was induced by atrial pacing at a critical heart rate in each case (180-300 beats/min). Evidence is presented that A V conduction was consistently blocked below a critical H H interval. Slowing the pacing rate, termination of pacing or increasing the pacing rate until physiological A V nodal block occurred, all could result in a longer H H interval and immediate resumption of A V conduction. When the critical heart rate for PAVB was maintained, a slow idioventricular escape rhythm occurred. Five patients who developed PAVB after acute myocardial ischemia are also reported providing the clinical counterpart for the experimental observations. In all 5 cases, PAVB occurred on acceleration of the sinoatrial rate (105-140 beats/min) which was spontaneous in 2 and induced by drugs given for varied therapeutic indications in 3 (isoprenaline in 2 and atropine sulfate in 1). In all 5, PAVB was associated with Mobitz type II and/or 2:1 A V block. These experimental and clinical observations suggest that PAVB after acute myocardial ischemia appears to be due to a tachycardia dependent repetitive concealed conduction in the ischemic His Purkinje system, probably mainly in the Hb. The clinical observations point out potential consequences of a rapid atrial rate in patients with acute myocardial ischemia and type II A V block.
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M3 - Article
C2 - 4416401
AN - SCOPUS:0016275435
VL - 50
SP - 515
EP - 528
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 3
ER -