Response of tertiary centres to pressure changes. Is there a mechano-electrical association?
OBJECTIVE
To investigate the mechanism of pressure related ventricular arrhythmias by examining them during atrioventricular (AV) block.


METHODS
Complete AV block, where all ventricular beats are ectopic, was induced by AV node ablation and/or by toxic digitalisation, and rhythm changes were studied while arterial blood pressure was repeatedly raised and lowered.


METHODS
15 anaesthetised mongrel dogs, weight 15-28 kg, were used. AV block was induced in eight by chemical or mechanical ablation of the AV node. In five of these and in seven other dogs, 5.0-7.5 mg digoxin was also given.


RESULTS
Following AV block due to ablation, a heart rate increase (or no change) was found in 87.5% of 56 arterial pressure increases produced by elevation of an open arterial blood reservoir or by metaraminol infusion, but in only 21.8% of 55 pressure decreases caused by arterial bleeding (p much less than 0.001). Following AV block due to digitalisation, the equivalent figures were 96% of 50 pressure increases and 27.3% of 55 pressure decreases (p much less than 0.001). While arterial pressure was increased there was moderate acceleration of the escape rhythm, then appearance of premature ventricular beats, then non-sustained and finally sustained ventricular tachycardia. The reverse occurred, with some hysteresis, on decreasing the arterial pressure. In five of the digitalised animals, arterial pressure reduction to nearly zero caused reproducible sudden arrest, with resumption of the ordinary escape rhythm on increasing the pressure again.


CONCLUSIONS
The findings suggest the possibility of two kinds of ectopic rhythm in AV block: the "normal" escape rhythm which is only moderately affected by arterial pressure changes; and an "abnormal" faster pressure dependent rhythm which is generated by high arterial pressure and abolished by pressure near zero, as if there were a mechano-electrical association. This abnormal rhythm may prevail completely in digitalis toxicity so that if cardiac arrest occurs, no automaticity can be expected to appear unless arterial pressure is raised.
Sideris
D A
DA
Department of Clinical Therapeutics, Medical School, Athens University, Alexandra General Hospital, Greece.
Toumanidis
S T
ST
Kostis
E B
EB
Stagiannis
K
K
Spyropoulos
G
G
Moulopoulos
S D
SD
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001283:Atrioventricular Node / Q000187:drug effects / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology*; D004077:Digoxin / Q000494:pharmacology; D004285:Dogs; D004562:Electrocardiography; D005557:Formaldehyde / Q000494:pharmacology; D006327:Heart Block / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000503:physiopathology; D008465:Mechanoreceptors / Q000503:physiopathology*; D013610:Tachycardia / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000503:physiopathology
D005557:Formaldehyde; D004077:Digoxin