Vagal tone
Respiratory sinus arrhythmia (RSA) is a naturally occurring variation in heart rate that occurs during a breathing cycle. Heart rate increases during inhalation and decreases during exhalation. Heart rate is normally controlled by centers in the medulla oblongata. One of these centers, the nucleus ambiguus, increases parasympathetic nervous system input to the heart via the vagus nerve. The vagus nerve decreases heart rate by decreasing the rate of SA node firing. Upon expiration the cells in the nucleus ambiguus are activated and heart rate is slowed down. In contrast, inspiration triggers inhibitory signals to the nucleus ambiguus and consequently the vagus nerve remains unstimulated.
On an electrocardiogram ECG this phenomenon is seen as subtle changes in the R-R interval synchronized with respiration. The R-R interval on an ECG is shortened during inspiration and prolonged during expiration. RSA is very pronounced in children, but without sufficient cardiovascular exercise it gradually disappears in the teens. Adults in excellent cardiovascular health, such as endurance runners, swimmers, and bicyclists, are also likely to have a pronounced RSA. Meditation and relaxed breathing techniques can temporarily induce RSA. RSA becomes less prominent with age, diabetes and cardiovascular disease. [1]
Previous studies have shown that the efficiency of pulmonary gas exchange is improved by RSA, suggesting that RSA may play an active physiologic role. The matched timing of alveolar ventilation and its perfusion with RSA within each respiratory cycle could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion. Furthermore, evidence has accumulated of a possible dissociation between RSA and vagal control of that heart rate, suggesting differential controls between the respiratory modulation of cardiac vagal outflow and cardiac vagal tone. RSA or heart rate variability in synchrony with respiration is a biological phenomenon, which may have a positive influence on gas exchange at the level of the lung via efficient ventilation/perfusion matching.[2]
References
- ^ "Respiratory Sinus Arrhythmia". Retrieved 2008-05-31.
- ^ Chest. 2004 Feb;125(2):683-90 Yasuma F et al.
- Neff RA, Wang J, Baxi S, Evans C, Mendelowitz D (2003). "Respiratory sinus arrhythmia: endogenous activation of nicotinic receptors mediates respiratory modulation of brainstem cardioinhibitory parasympathetic neurons". Circ. Res. 93 (6): 565–72. doi:10.1161/01.RES.0000090361.45027.5B. PMID 12907666.
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