Asphyxia-activated corticocardiac signaling accelerates onset of cardiac arrest

Proc Natl Acad Sci U S A. 2015 Apr 21;112(16):E2073-82. doi: 10.1073/pnas.1423936112. Epub 2015 Apr 6.


The mechanism by which the healthy heart and brain die rapidly in the absence of oxygen is not well understood. We performed continuous electrocardiography and electroencephalography in rats undergoing experimental asphyxia and analyzed cortical release of core neurotransmitters, changes in brain and heart electrical activity, and brain-heart connectivity. Asphyxia stimulates a robust and sustained increase of functional and effective cortical connectivity, an immediate increase in cortical release of a large set of neurotransmitters, and a delayed activation of corticocardiac functional and effective connectivity that persists until the onset of ventricular fibrillation. Blocking the brain's autonomic outflow significantly delayed terminal ventricular fibrillation and lengthened the duration of detectable cortical activities despite the continued absence of oxygen. These results demonstrate that asphyxia activates a brainstorm, which accelerates premature death of the heart and the brain.

Keywords: asphyxic cardiac arrest; autonomic nervous system; coherence; directed connectivity; near-death experience.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Arrhythmias, Cardiac / complications
  • Arrhythmias, Cardiac / physiopathology
  • Asphyxia / complications*
  • Asphyxia / physiopathology*
  • Cerebral Cortex / physiopathology*
  • Electrocardiography
  • Electroencephalography
  • Evoked Potentials
  • Heart / physiopathology*
  • Heart Arrest / complications*
  • Heart Arrest / physiopathology*
  • Heart Function Tests
  • Heart Rate
  • Male
  • Neurotransmitter Agents / metabolism
  • Rats, Wistar
  • Time Factors
  • Ventricular Fibrillation / complications
  • Ventricular Fibrillation / physiopathology


  • Neurotransmitter Agents