The wavelength of the cardiac impulse and reentrant arrhythmias in isolated rabbit atrium. The role of heart rate, autonomic transmitters, temperature, and potassium.

Abstract

We measured the wavelength of the cardiac impulse, defined as the distance traveled by the depolarization wave during the functional refractory period, in isolated narrow strips of rabbit atrium. During control, wavelength was 42 mm during pacing with 2 Hz, and was 28 mm at the maximum pacing rate; early premature beats had a wavelength as short as 23 mm. Administration of carbamylcholine (4 X 10(-7) g/ml) shortened the wavelength to 21 mm during 2 Hz, 18 mm at the maximum pacing rate Fmax, and 16 mm during an early premature impulse, respectively. The effects of epinephrine (6 X 10(-7) M) were strongly rate dependent. At slow heart rates, epinephrine clearly prolonged the wavelength (58 mm), whereas, during maximum pacing, wavelength remained unchanged (28 mm). Hypokalemia (2 mM) decreased the length of the impulse at all stimulation frequencies. Moderate hyperkalemia (5.6 and 7.0 mM) did not modify wavelength because refractoriness and conduction velocity were affected proportionally. Above 7.0 mM potassium, the wavelength became progressively prolonged because of the development of post-repolarization refractoriness. Cooling to 27 degrees C resulted in a slight lengthening of the impulse. At lower temperatures, however, wavelength prolonged significantly because of a relatively strong prolongation of the refractory period. In separate experiments in 15 X 20 mm segments of atrium, reentrant tachyarrhythmias were induced and the circuit size compared with the wavelength. The size of intraatrial circuits was similar to the magnitude of the measured wavelength during maximum pacing. Carbamylcholine and hypokalemia, both of which shorten the impulse length, also clearly decreased the size of reentrant circuits. Cooling to 27 degrees C, which affects both refractoriness and conduction velocity, only slightly prolonged the wavelength; accordingly, the size of reentrant circuits at 27 degrees C was only slightly longer than at 37 degrees C. These experiments emphasize the importance of the wavelength of the cardiac impulse in relation to the occurrence of intramyocardial reentry.

Differences in atrial fibrillation properties under vagal nerve stimulation versus atrial tachycardia remodeling

“…6). Whereas a VS increase in CV is in accordance with previous studies 70,71 , there is still controversy concerning the ATR effect on CV 75 . The varying results regarding CV changes in ATR substrate may point to the existence of multiple factors and changes that can affect CV.…”

Role of Fibrillation Cycle Length in Spontaneous and Drug-Induced Termination of Human Atrial Fibrillation-Spectral Analysis of Fibrillation Waves From Surface Electrocardiogram-

“…Sih et al 17 observed that the AF cycle length decreased just prior to spontaneous termination in 3 of 15 episodes of AF and they suggested that an increase in AF cycle length is not a universal precursor to AF termination. Spontaneous termination of AF occurring without any appreciable increase in the mean FCL indicates that maintenance of this type of AF is not dependent on multiple wavelets and may instead depend on focal mechanisms related to automatic activities from the pulmonary veins.…”

Atrial Fibrillation Produced by Prolonged Rapid Atrial Pacing Is Associated With Heterogeneous Changes in Atrial Sympathetic Innervation

“…20 Although increased vagal tone has been demonstrated to cause AF in animals 21 and humans, 20 the role of the sympathetic nervous system in AF is less understood. [21][22][23] Moreover, previous investigations of the effect of sympathetic stimulation on atrial refractoriness have found varied results. [21][22][23] In humans, an increased incidence of AF has been observed in states of increased sympathetic activity.…”