title: Respiratory sinus arrhythmia. A phenomenon improving pulmonary gas exchange and circulatory efficiency.
abstract: BACKGROUND
  The primary mechanisms of respiratory sinus arrhythmia (RSA) are understood to be the modulation of cardiac vagal efferent activity by the central respiratory drive and the lung inflation reflex, and the degree of RSA increases with cardiac vagal activity. However, it is unclear whether RSA serves an active physiological role or merely reflects a passive cardiovascular response to respiratory input. We hypothesized that RSA benefits pulmonary gas exchange by matching perfusion to ventilation within each respiratory cycle.
  
  
  RESULTS
  In seven anesthetized dogs, a model stimulating RSA was made. After elimination of endogenous autonomic activities, respiration-linked heartbeat fluctuations were generated by electrical stimulation of the right cervical vagus during negative pressure ventilation produced by phrenic nerve stimulation (diaphragm pacing). The vagal stimulation was performed in three conditions; phasic stimulation during expiration (artificial RSA) and during inspiration (inverse RSA) and constant stimulation (control) causing the same number of heartbeats per minute as the phasic stimulations. Although tidal volume, cardiac output, and arterial blood pressure were unchanged, artificial RSA decreased the ratio of physiological dead space to tidal volume (VD/VT) and the fraction of intrapulmonary shunt (Qap/Qt) by 10% and 51%, respectively, and increased O2 consumption by 4% compared with control. Conversely, reverse RSA increased VD/VT and Qap/Qt by 14% and 64%, respectively, and decreased O2 consumption by 14%.
  
  
  CONCLUSIONS
  These results support our hypothesis that RSA benefits the pulmonary gas exchange and may improve the energy efficiency of pulmonary circulation by "saving heartbeats."
authors.affiliation: Third Department of Internal Medicine, Nagoya City University Medical School, Japan. hayano@med.nagoya-cu.ac.jp
authors.forename: J
authors.initials: J
authors.lastname: Hayano
authors.forename: F
authors.initials: F
authors.lastname: Yasuma
authors.forename: A
authors.initials: A
authors.lastname: Okada
authors.forename: S
authors.initials: S
authors.lastname: Mukai
authors.forename: T
authors.initials: T
authors.lastname: Fujinami
mesh_terms: D000818:Animals; D001146:Arrhythmia, Sinus / Q000503:physiopathology*; D001794:Blood Pressure; D004285:Dogs; D004562:Electrocardiography; D005263:Femoral Artery; D001239:Inhalation; D008168:Lung / Q000502:physiology / Q000503:physiopathology*; D010100:Oxygen / Q000032:analysis / Q000097:blood; D010313:Partial Pressure; D011652:Pulmonary Circulation; D012016:Reference Values; D012119:Respiration; D013990:Tidal Volume; D014630:Vagus Nerve / Q000503:physiopathology
chemical_list: D010100:Oxygen