SLOWING OF THE ATRIAL-FLUTTER RATE DURING 1-1 ATRIOVENTRICULAR-CONDUCTION IN HUMANS AND DOGS - AN EFFECT MEDIATED THROUGH ATRIAL PRESSURE AND VOLUME

Introduction: During atrial flutter the effects of 1:1 atrioventricular (AV) conduction on the rate of atrial flutter was studied in 12 patients and 14 dogs. Methods and Results: (A) In all patients, the development of 1:1 AV conduction was associated with a significant increase in flutter cycle length (261.7 +/- 9.9 to 281.8 +/- 12.1 msec, mean increase 20.3 +/- 3.2 msec, P < 0.001). The flutter cycle length returned to control values when 1:1 AV conduction ceased. In four patients in whom atrial pressure was monitored, the prolongation of the atrial flutter cycle interval during 1:1 AV conduction was associated with an immediate rise in atrial pressure (4.0 +/- 0.4 to 6.5 +/- 0.7 mmHg, P < 0.003). (B) In order to examine the mechanism of this phenomenon, similar studies were carried out in dogs with experimentally induced atrial flutter. 1:1 AV conduction consistently lengthened the flutter cycle length during control conditions or following vagotomy and during the administration of isoproterenol. This was always associated with a rise in atrial filling pressure. Inferior vena cava occlusion consistently shortened the flutter cycle length and this was also independent of vagotomy and isoproterenol administration. The atrial filling pressure fell during inferior vena cava occlusion. During 1:1 AV conduction, the prolonged flutter cycle length was shortened by inferior vena cava occlusion to values prior to 1:1 AV conduction. Conclusion: The rate of atrial flutter is accelerated by reductions in atrial pressure, and slowed by increased atrial pressure. These effects are independent of the vagus nerve or an adrenergic agonist. Changes in atrial pressure and volume affect characteristics of the atrial flutter circuit, and thus can modulate the rate of atrial flutter.