Cardiorespiratory interactions and blood flow generation during cardiac arrest and other states of low blood flow.
OBJECTIVE
Recent advances in cardiopulmonary resuscitation have shed light on the importance of cardiorespiratory interactions during shock and cardiac arrest. This review focuses on recently published studies that evaluate factors that determine preload during chest compression, methods that can augment preload, and the detrimental effects of hyperventilation and interrupting chest compressions.


RESULTS
Refilling of the ventricles, so-called ventricular preload, is diminished during cardiovascular collapse and resuscitation from cardiac arrest. In light of the potential detrimental effects and challenges of large-volume fluid resuscitations, other methods have increasing importance. During cardiac arrest, active decompression of the chest and impedance of inspiratory airflow during the recoil of the chest work by increasing negative intrathoracic pressure and, hence, increase refilling of the ventricles and increase cardiac preload, with improvement in survival. Conversely, increased frequency of ventilation has detrimental effects on coronary perfusion pressure and survival rates in cardiac arrest and severe shock. Prolonged interruption of chest compressions for delivering single-rescuer ventilation or analyzing rhythm before shock delivery is associated with decreased survival rate.


CONCLUSIONS
Cardiorespiratory interactions are of profound importance in states of cardiovascular collapse in which increased negative intrathoracic pressure during decompression of the chest has a favorable effect and increased intrathoracic pressure with ventilation has a detrimental effect on survival rate.
Sigurdsson
Gardar
G
Cardiac Arrhythmia Center, University of Minnesota, Minneapolis, Minnesota 55455, USA.
Yannopoulos
Demetris
D
McKnite
Scott H
SH
Lurie
Keith G
KG
D000328:Adult; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D003326:Coronary Circulation / Q000502:physiology; D004195:Disease Models, Animal; D006323:Heart Arrest / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D012143:Respiratory Physiological Phenomena; D016276:Ventricular Function / Q000502:physiology