Preterminal gasping and effects on the cardiac function

Abstract

Gasping, also known as agonal respirations, is the terminal pattern that occurs after anoxia or ischemia and is a universal phenomenon in mammals. In this article we review the physiology of gasping, the prevalence and significance of gasping in cardiac arrest, and the effects of gasping on cardiac function. Review relevant human and animal literature on gasping and cardiac function during gasping. Gasping originates in the medullary area of the central nervous system. Gasping is prevalent during cardiac arrest: it occurs in all animals during ventricular fibrillation, in a majority of infants (31 of 32) with sudden infant death syndrome, and in 30-40% of witnessed episodes of cardiac arrest in adults. Animal studies demonstrated that gasping is associated with a decrease in intrathoracic pressure during the inspiratory phase, which promotes venous return and an increase in intrathoracic pressure during the expiratory phase, which favors coronary perfusion. Gasping increases cardiac output and cardiac contractility in immature animals exposed to anoxia. Gasping is auto-resuscitative in immature mammals and improves the outcome of cardiopulmonary resuscitation in mature mammals. Gasping is associated with important cardiorespiratory changes: improved pulmonary gas exchange, increased venous return to the heart, increased cardiac output, cardiac contractility, aortic pressure, and coronary perfusion pressure.