title: Sinus arrhythmia in man: influence of tidal volume and oesophageal pressure.
abstract: 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.
mesh_terms: 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