Theoretical analysis predicts that respiratory sinus arrhythmia does not accurately measure efferent vagal activity during anesthesia.

The respiratory sinus arrhythmia (RSA) is an oscillation of cardiac cycle length (CCL) at the frequency of breathing. RSA is a non-invasive measure of efferent vagal activity, during controlled experimental conditions. Our goal is to assess whether existing theory predicts that RSA amplitude reliably measures efferent vagal activity during and after anesthesia. To do so we combine several existing mathematical models to predict the respiratory sinus arrhythmia. Computer simulation shows that for positive-pressure ventilation without spontaneous breathing efforts, increasing mean arterial pressure causes increase in efferent vagal activity, but not RSA amplitude. Therefore, for positive-pressure ventilation, RSA amplitude does not predict efferent vagal effects on CCL. In contrast, for spontaneous breathing, increasing mean arterial pressure causes increase in both efferent vagal activity and RSA amplitude. Therefore, during spontaneous breathing, RSA amplitude does predict efferent vagal activity. Nevertheless, RSA amplitude also depends on factors that have little effect on efferent vagal activity. For example, RSA amplitude is decreased by increasing respiratory rate or administering acetylcholinesterase and muscarinic antagonists. We conclude that current theory provides little or no justification for using RSA amplitude as a surrogate for efferent vagal activity during anesthesia.