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1 University of Trento
2 S. Chiara Hospital
* To whom correspondence should be addressed. E-mail: mase{at}science.unitn.it.
Respiratory sinus arrhythmia (RSA) is generally known as the autonomically-mediated modulation of the sinus node pacemaker frequency in synchrony with respiration. Cardiorespiratory interactions have been largely investigated during sinus rhythm, while little is known during reentrant arrhythmias. In this study cardiorespiratory interactions at the atrial and ventricular level were investigated during atrial flutter, a supraventricular arrhythmia based on a reentry, by cross-spectral analysis and computer modeling. The coherence and phase between respiration and atrial (
2AA,
AA) and ventricular (
2RR,
RR) interval series were estimated in 20 patients with typical atrial flutter (68.0 ± 8.8 years) and some degree of atrioventricular (AV) conduction block. In all patients atrial intervals displayed oscillations strongly coupled and in phase with respiration (
2AA = 0.97 ± 0.05,
AA = 0.71 ± 0.31 rad), corresponding to a paradoxical lengthening of intervals during inspiration. The modulation pattern was frequency-independent, with in phase oscillations and short time delays (0.40 ± 0.15 s) for respiratory frequencies in the range 0.1-0.4 Hz. Ventricular patterns were affected by AV conduction type. In patients with fixed AV conduction, ventricular intervals displayed oscillations strongly coupled (
2RR = 0.97 ± 0.03) and in phase with respiration (
RR = 1.08 ± 0.80 rad). Differently, in patients with variable AV conduction, respiratory oscillations were secondary to Wencheback rhythmicity, resulting in a decreased level of coupling (
2RR = 0.50 ± 0.21). Simulations with a simplified model of AV conduction showed ventricular patterns to originate from the combination of a respiratory modulated atrial input with the functional properties of the AV node. The paradoxical frequency-independent modulation pattern of atrial interval, the short time delays and the complexity of ventricular rhythm characterize respiratory arrhythmia during AFL and distinguish it from normal RSA. These peculiar features can be explained assuming a direct mechanical action of respiration on AFL reentrant circuit.
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