Extreme respiratory sinus arrhythmia in response to superimposed head-down tilt and deep breathing

Respiratory sinus arrhythmia (RSA) is characterized by normal fluctuations in heart rate in phase with the respiratory cycle. There are many proposed mechanisms underlying the RSA phenomenon, including respiratory-induced cardiac loading (i.e., Bainbridge reflex), arterial baroreflex activation, vagal feedback from pulmonary stretch receptors, and central neural mechanisms. It is currently unclear to what extent these mechanisms are responsible for eliciting RSA in humans, particularly in response to stressors.

Here we present a case report of a healthy 26-yr-old woman (BMI 22.95 kg · m(-2)) who developed extreme RSA when exposed to the simultaneous cardiac loading stressors of 45° head-down tilt (HDT) and increased tidal volume during CO2 rebreathing. During baseline breathing in both supine and 45° HDT position, RSA magnitude was similar (mean ∼10-14 bpm). RSA was tidal volume-dependent, whereby in the supine position the RSA magnitude doubled with an approximate doubling in tidal volume during rebreathing (mean ∼20 bpm). However, when HDT and rebreathing were superimposed, extreme RSA was elicited (mean ∼45 bpm; range ∼38-110 bpm), approximately 450% over baseline breathing in the supine position. ECG analysis and follow up medical assessment revealed no underlying cardiac pathology.

The existence of extreme RSA when HDT and increased inspired volumes were superimposed suggests that the dual cardiac loading stimuli acted synergistically, increasing RSA magnitude over either stimulus alone. This case report may be relevant to situations where orthostatic stress and augmented tidal volumes are superimposed, or more generally when conflicting sympathetic and parasympathetic activation is simultaneous.