Respiratory Sinus Arrhythmia : A Phenomenon Improving Pulmonary Gas Exchange and Circulatory Efficiency

The correlations of 11 indexes of heart rate variability were examined with pharmacologically determined cardiac vagal tone in 15 normal subjects at supine rest. After sympathetic influences by intravenous propranolol were eliminated, RR interval variability was measured for 10 minutes under controlled respiration (0.25 Hz), and cardiac vagal tone was determined as the decrease in mean RR interval following complete vagal blockade with atropine. Time domain indexes (standard deviation, coefficient of variance and mean successive difference) correlated strongly with vagal tone (r = 0.87, 0.81 and 0.92, respectively; p less than 0.001 for all). The same was true for frequency domain indexes for the high-frequency (0.25 Hz) component calculated both by autoregressive spectrum analysis (square root of power and coefficient of component variance) and by fast Fourier transform (mean amplitude) (r = 0.91, 0.85 and 0.86, respectively; p less than 0.0001 for all). However, frequency domain indexes for the low-frequency spectral component (0.03 to 0.15 Hz) correlated less strongly (r = 0.69, 0.55 and 0.70, respectively), and the fraction of power [power/(total power greater than 0.03 Hz)] of both components showed no correlation. Principal component analysis showed that the first 6 indexes with strong correlations contained solely the first principal component closely related to vagal tone, whereas the remaining 5 indexes also contained the second component unrelated to vagal tone. These results indicate that most of the time and frequency domain analyses in use provides an accurate and common measure of cardiac vagal tone at rest. Show more

Cardiovascular variables such as heart rate, arterial blood pressure, stroke volume and the shape of electrocardiographic complexes all fluctuate on a beat to beat basis. These fluctuations have traditionally been ignored or, at best, treated as noise to be averaged out. The variability in cardiovascular signals reflects the homeodynamic interplay between perturbations to cardiovascular function and the dynamic response of the cardiovascular regulatory systems. Modern signal processing techniques provide a means of analyzing beat to beat fluctuations in cardiovascular signals, so as to permit a quantitative, noninvasive or minimally invasive method of assessing closed loop hemodynamic regulation and cardiac electrical stability. This method promises to provide a new approach to the clinical diagnosis and management of alterations in cardiovascular regulation and stability. Show more

Since changes of heart period follow changes of cardiac vagal efferent activity quantitatively with nearly fixed latencies, measurements of respiratory sinus arrhythmia may provide insights into human central vagal mechanisms. Accordingly, I measured intervals between heartbeats during controlled breathing (at breathing intervals of 2.5-10 s and nominal tidal volumes of 1,000 and 1,500 ml) in six healthy young men and women. As breathing interval increased, the longest heart periods became longer, the shortest heart periods became shorter, and the peak-valley P-P intervals increased asymptotically. Peak-valley P-P intervals also increased in proportion to tidal volume. However, this influence was small: a 50% increase of tidal volume increased the average peak-valley P-P interval by only about 15%. The phase angles between heart period changes and respiration varied as linear functions of breathing interval. Heart period shortening (cardioacceleration) began in inspiration at short breathing intervals and in expiration at long breathing intervals. Heart period lengthening, however, began in early expiration at all breathing intervals studied. These results point toward a close relationship between variations of respiratory depth and interval and the quantity, periodicity, and timing of vagal cardiac outflow in conscious humans. They suggest that, at usual breathing rates, phasic respiration-related changes of vagal motoneuron activity began in expiration, progress slowly, and are incompletely expressed at fast breathing rates. Show more