Cardiorespiratory interactions in patients with atrial flutter

Abstract

tory 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, whereas little is known about interactions during reentrant arrhythmias. In this study, cardiorespiratory interactions at the atrial and ventricular level were investigated during atrial flutter (AFL), a supraventricular arrhythmia based on a reentry, by using cross-spectral analysis and computer modeling. The coherence and phase between respiration and atrial (␥ AA 2 , AA) and ventricular (␥ RR 2 , RR) interval series were estimated in 20 patients with typical AFL (68.0 Ϯ 8.8 yr) and some degree of atrioventricular (AV) conduction block. In all patients, atrial intervals displayed oscillations strongly coupled and in phase with respiration (␥ AA 2 ϭ 0.97 Ϯ 0.05, AA ϭ 0.71 Ϯ 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 Ϯ 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 (␥ RR 2 ϭ 0.97 Ϯ 0.03) and in phase with respiration ( RR ϭ 1.08 Ϯ 0.80 rad). Differently, in patients with variable AV conduction, respiratory oscillations were secondary to Wencheback rhythmicity, resulting in a decreased level of coupling (␥ RR 2 ϭ 0.50 Ϯ 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 by assuming a direct mechanical action of respiration on AFL reentrant circuit. respiratory arrhythmia; heart rate variability; reentry; cross-spectral analysis; mechanoelectrical feedback THE FIRST REPORT ON AN INTERACTION between respiration and heart rate is ascribed to Ludwig and dates back as early as 1847 (34). The phenomenon, named respiratory sinus arrhythmia (RSA), was described as an acceleration of the heart rate during inspiration followed by a slowing during expiration. Since then, several studies have been performed that have revealed the complex nature of the interaction, characterized by frequency-dependent behaviors (1,4,13,21,55), and shed light on its origin. Several mechanisms have been proposed for the generation of RSA, including the direct interaction between central cardiorespiratory centers within the brain stem, pulmonary reflex pathways, respiratory gating of central arterial baroreceptor afferent input, an atrial reflex, and oscillations in arterial PCO 2...

Dynamics of AV coupling during human atrial fibrillation: role of atrial rate

“…AV response curves in our patients extend these results, since they pointed out not only the decrease of AV CRs at higher atrial rates, but also the existence of a subtle structure of n:m coupling patterns between dominant n:1 coupling regions. As concerns pattern stability, the lower stability of AV coupling and the increased variability of ventricular response at higher atrial rate observed in our patients is consistent with previous studies in patients with atrial flutter (29,30) and AF (1,14). A decreased stability of AV coupling patterns was indeed observed during the transitions from slow to rapid atrial flutter forms (30), and an increased irregularity of ventricular interval series occurred at higher atrial rates in patients with AF and congestive heart failure (14).…”

Characterization of rate and regularity of ventricular response during atrial tachyarrhythmias. Insight on atrial and nodal determinants

“…In addition, our results showed ventricular irregularity to increase as a function of the atrial rate, with complex ventricular response occurring even with regular, but high-rate atrial activation. The increase of ventricular irregularity at higher atrial rate is consistent with previous studies in patients with atrial flutter (Masè et al 2009), paroxysmal AF (Masè et al 2015), and AF with congestive heart failure (Corino 2013), and can be explained in light of nodal factors. Indeed, an increase in atrial rate may induce a shift towards advanced levels of AV block, which are intrinsically instable and associated with increased contribution of concealed conduction (Langendorf 1965, Chorro 1991, Masè et al 2012.…”

“…Nonetheless other extrinsic factors, such as respiration and autonomic tone, may influence the observed interactions. Respiration has been shown to modulate AFL rate and to combine with AV node filtering to produce complex patterns of ventricular intervals (Masè et al 2009). As well the direct influence of autonomic tone on AV conduction has been demonstrated in patients during normal sinus rhythm, atrial pacing and AF (Nollo 1994, Corino 2014).…”

Mechano-electrical feedback in the clinical setting: Current perspectives

“…Furthermore, these oscillations are not abolished by complete autonomic blockade and have been reported in the transplanted heart (Bernardi et al, 1990(Bernardi et al, , 1989. Similarly, a MEF mechanism has been suggested to cause respiratory oscillations in the cycle length of human atrial flutter (Masè et al, 2009) that persist after autonomic blockade (Ravelli et al, 2008). In the intact human heart, atrial flutter rate also fluctuates in synchrony with cyclic variations in atrial volume secondary to ventricular contractions (Lammers et al, 1991;Ravelli et al, 1994), further supporting an interplay between cardiovascular mechanisms and electrophysiological changes mediated by MEF.…”