Purpose of review: To evaluate arterial pulselessness and the no-touch time of 5 min in defining irreversible cessation of cardiorespiratory functions in nonheart-beating donation (NHBD).
Recent findings: Experimental NHBD studies identified compensatory neurohumoral mechanisms elicited in controlled terminal shock after withdrawal of life support. The neurohumoral mechanisms can preserve the viability of the cardiovascular and central nervous systems by: 1) diverting systemic blood flow from nonvital to vital organs; and 2) maintaining the perfusion pressure (arterial to venous pressure gradient minus interstitial tissue pressure) and microcirculation in vital organs. These compensatory mechanisms cause an early onset of splanchnic hypoperfusion and antemortem ischaemia of transplantable organs and preclude irreversible cessation of cardiorespiratory functions after brief periods of circulatory arrest. Allograft ischaemia is associated with primary nonfunction or delayed function in transplant recipients similar in aetiology to organ dysfunction in the postresuscitation phase of shock.
Summary: In-situ perfusion can reverse ceased cardiac and neurological functions after arterial pulselessness and a no-touch time of 5 min in experimental models. Perfusion pressures are superior to arterial pulselessness in determining reversibility of ceased cardiac and neurological functions in circulatory arrest. Utilizing physiologically relevant circulatory and neurological parameters in NHBD protocols is essential for ascertaining irreversible cessation of vital functions in donors.