![]() ![]() Breathing frequency, V T, minute heart rate, cardiac output, and arterial blood pressure were not different between the conditions nonetheless artificial RSA (i.e., RSA in phase with respiration) significantly increased pulmonary gas exchange efficiency, as measured by the ratio of physiological dead space to the V T and the fraction of intrapulmonary shunt compared with no-RSA and inverse-RSA conditions. ( 13) artificially induced RSA and inverse RSA (i.e., bradycardia during inhalation and tachycardia during exhalation) via electric stimulation of the vagus in dogs after surgical elimination of endogenous autonomic efferents. That is, during inspiration, increasing heart rate in combination with increased right ventricular output (due to decreased intrathoracic pressure) increase pulmonary perfusion in time with increasing lung air volume. ( 13) have proposed that RSA serves an active physiological role in improving pulmonary gas exchange efficiency by matching blood perfusion to air flow in the lung during each respiratory cycle. That is, does RSA itself serve a physiological role or is it merely an epiphenomenon of respiratory influences on neurocardiovascular control? ![]() Other influences on the genesis and magnitude of RSA include feedback from arterial baroreceptors, a central rhythm generator in the brain stem, and intracardiac reflexes ( 3).Īlthough a great deal of research has been published concerning the physiological mechanisms mediating RSA, the question of what function, if any, RSA serves is rarely addressed. This slowing of respiration rate and increase in V T are believed to allow more time for the action of acetylcholine on muscarinic receptors at the sinoatrial node during exhalation (7, 25a). For example, changes in respiration rate and, to a lesser extent, tidal volume (V T) can affect the magnitude of RSA in the absence of any change in tonic vagal activity ( 8, 11, 15, 23). Thus measures of RSA are frequently used as an index of vagal tone (e.g., 2, 12, 19, 20).Ĭertain features of respiratory mechanics also affect the amplitude of RSA independent of changes in vagal tone. The degree to which this modulation occurs is a function of the level of tonic vagal discharge and blood pressure ( 9, 21). The tonic vagal discharge that keeps the heart rate slow decreases, and the heart rate rises. During inspiration, impulses originating in stretch receptors in the lungs travel via the vagi to inhibit the cardioinhibitory area in the medulla. Respiratory sinus arrhythmia (RSA), the increase and decrease in heart rate within each respiratory cycle, occurs mainly as a result of fluctuations of parasympathetic output to the heart, although sympathetic outflow also may influence variability ( 26). These results are consistent with previous studies and further support the theory that RSA may improve the efficiency of pulmonary gas exchange. Phase between heart rate and respiration was significantly associated with CO 2 exchange efficiency (partial r = 0.40, P = 0.03). Across subjects and paced breathing periods, RSA was significantly associated with CO 2 (partial r = −0.53, P = 0.002) and O 2 (partial r = −0.49, P = 0.005) exchange efficiency after controlling for the effects of age, respiration rate, tidal volume, and average heart rate. Pulmonary gas exchange efficiency was measured as the average ventilatory equivalent of CO 2(V˙ e/V˙ co 2) and O 2(V˙ e/V˙ o 2). ![]() Cross-spectral analysis of heart rate and respiration was computed to calculate RSA and the coherence and phase between these variables. ![]() Respiration rate, tidal volume, minute ventilation (V˙ e), exhaled carbon dioxide (V˙ co 2), oxygen consumption (V˙ o 2), and heart rate were measured in 10 healthy human volunteers during paced breathing to test the hypothesis that RSA contributes to pulmonary gas exchange efficiency. Respiratory sinus arrhythmia (RSA) may be associated with improved efficiency of pulmonary gas exchange by matching ventilation to perfusion within each respiratory cycle. ![]()
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