Pathophysiology of oscillatory breathing during sleep and exercise in heart failure patients (1132.12)

Abstract

Background: There is OB during sleep and exercise in HF. However, mechanism is unclear. Since 2011, we reported new theory system of integrated control/regulation of respiration-circulation. For breath, the next breath is dominantly initiated by this breath, by magnitude of oscillatory PaO2, PaCO2 and [H+] via fast peripheral chemical receptors (PCR); and its gain/sensitivity is adjusted by slow central chemical receptors (CCR) with long time delay (~30s). It appears to be clear to explain mechanism of OB. Pathophysiology: 1.Ventricle Mixed Effect: It decreased oscillatory signals in blood which dominantly effected by LVEF. The poor ventricle function (lower LVEF) , the lower oscillatory magnitude from pulmonary vein o artery. The normal breath signals, via HF ventricle, only generate smaller next breath; and so on襃 the final breath should be very small or disappeared (apnea). 2. Time Phase difference: Then delayed averaged/mean signal arrived at central chemical receptors will change gain to adjust the sensitivity to make larger breath襃 There is a time phase difference between PCR (close to lung) and CCR, i.e. PCR-lung hyperventilation with CCR hypoventilation and PCR-lung hypoventilation with CCR hyperventilation. Combined two of Ventricle Mixed Effect and Time Phase Difference, HF patients should have oscillatory breathing pattern. Grant Funding Source: Chinese National High Technology Research and Development Program (863 Program) Project 2012AA021009