Sinus arrhythmia in man: influence of tidal volume and oesophageal pressure.
The effect of tidal volume (VT) and of the intrathoracic pressure (Poes) on the respiratory sinus arrhythmia (RSA) was studied in healthy subjects. They breathed into a spirometer with a VT of 1, 1.5, and 2 1, at a standardized, slow respiratory rate, 6-min-1 (A). Poes was varied by (B) adding a negative inspiratory pressure (NIP) of 5 cm of water and by (C) intermittent positive pressure ventilation (IPPV) at identical VT and respiratory frequency. In a separate study (D), intermittent negative pressure ventilation (INPV) was induced by applying negative pressure on the thorax. In A, increasing VT provoked an augmented RSA by a more marked tachycardia as well as bradycardia. On increasing the amplitude of Poes in B, RSA was somewhat more marked due to a lower minimum heart rate. When comparing respiratory cycles that had similar Poes but a different VT, the larger VT caused a slight increase in the RSA amplitude due to a more marked deceleration of the heart rate. IPPV almost abolished RSA, whereas INPV did not reduce the arrhythmia. It is concluded that pulmonary stretch reflexes to a minor extent contribute to RSA, whereas the hypothesis of a central nervous origin does not gain support. Cardiovascular reflexes remain the main possible cause of RSA.
D000328:Adult; D001146:Arrhythmia, Sinus / Q000503:physiopathology*; D004947:Esophagus / Q000502:physiology*; D006339:Heart Rate; D006801:Humans; D007384:Intermittent Positive-Pressure Breathing; D008176:Lung Volume Measurements; D008297:Male; D008465:Mechanoreceptors / Q000502:physiology; D011312:Pressure; D012119:Respiration; D013147:Spirometry; D013990:Tidal Volume; D014797:Vital Capacity