Abstract
Background: Respiratory modulation of autonomic input to the sinus node results in cyclical modulation of heart rate, known as respiratory sinus arrhythmia (RSA). We hypothesized that the respiratory cycle may also exert cyclical modulation on ventricular repolarization, which may be separately measurable using local endocardial recordings. Methods and Results: The study included 16 subjects with normal ventricles undergoing routine clinical electrophysiological procedures for supraventricular arrhythmias. Unipolar electrograms were recorded from 10 right and 10 left ventricular endocardial sites. Breathing was voluntarily regulated at 5 fixed frequencies (6, 9, 12, 15, and 30 breaths per min) and heart rate was clamped by RV pacing. Activation-recovery intervals (ARI: a surrogate for APD) exhibited significant (p < 0.025) cyclical variation at the respiratory frequency in all subjects; ARI shortened with inspiration and lengthened with expiration. Peak-to-peak ARI variation ranged from 0–26 ms; the spatial pattern varied with subject. Arterial blood pressure also oscillated at the respiratory frequency (p < 0.025) and lagged behind respiration by between 1.5 s and 0.65 s from slowest to fastest breathing rates respectively. Systolic oscillation amplitude was significantly greater than diastolic (14 ± 5 vs. 8 ± 4 mm Hg ± SD, p < 0.001). Conclusions: Observations in humans with healthy ventricles using multiple left and right ventricular endocardial recordings showed that ARI action potential duration (APD) varied cyclically with respiration.
Highlights
The timing of ventricular activation exhibits rhythmic cyclical variation with the respiratory cycle, whereby the interval between heartbeats increases and decreases with expiration and inspiration respectively: respiratory sinus arrhythmia (RSA) (Anrep et al, 1936)
We hypothesized that if action potential duration (APD) exhibited localized oscillatory modulation with respiration, it might be observed in local electrical recordings from the in-situ human heart; our preliminary observations indicated the presence of a direct relationship (Gill et al, 2010)
Results of blood gas analysis showed no significant variation with the exception of a slight reduction in carbon dioxide partial pressure (PCO2) over the course of the protocol from median 4.7 to 4.1 kPa (p = 0.05, n = 5)
Summary
The timing of ventricular activation exhibits rhythmic cyclical variation with the respiratory cycle, whereby the interval between heartbeats increases and decreases with expiration and inspiration respectively: respiratory sinus arrhythmia (RSA) (Anrep et al, 1936). The mechanisms are complex (Anrep et al, 1936; Cohen and Taylor, 2002; Eckberg, 2009), RSA is generally agreed to result from waxing and waning of autonomic nerve input to the sinus node We hypothesized that these mechanisms may influence ventricular action potential repolarization. Respiratory-induced fluctuations in Abbreviations: APD, action potential duration; ARI, activation-recovery interval; LV, left ventricle; PCO2, carbon dioxide partial pressure; RSA, respiratory sinus arrhythmia; RV, right ventricle. Conclusions: Observations in humans with healthy ventricles using multiple left and right ventricular endocardial recordings showed that ARI action potential duration (APD) varied cyclically with respiration
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