"Non-Heart-Beating," or "Cardiac Death," Organ Donation: Why We Should Care

Mohamed Y. Rady, MD, PhD, FRCS (Eng.), FRCP (UK), FCCM; Joseph L. Verheijde, PhD, MBA; Joan McGregor, PhD

Disclosures

Journal of Hospital Medicine. 2007;2(5):324-334. 

In This Article

Organ Procurement and the Dead Donor Rule

Organ procurement is only permitted when the donor is already dead (ie, the dead donor rule), and the act of organ recovery cannot have been the immediate act to cause that death.[10,11] There are 2 criteria for death as defined in the Uniform Determination of Death Act (UDDA; Table 1 ): an individual who has sustained irreversible cessation of either (1) circulatory and respiratory functions or (2) all functions of the entire brain, including the brain stem, is considered dead and this determination of death must have been made in accordance with accepted medical standards.[12] When organs are procured from an individual in whom all brain function has ceased but normal cardiac pump activity is continuing, it is referred to as heart-beating organ donation. Organ procurement after cessation of cardiac pump activity and cardiorespiratory functions is referred to as non-heart-beating organ donation (NHBOD). Organ procurement from an individual in imminent or cardiac death is considered NHBOD.

Non-heart-beating organ donors can be neurologically intact and do not fulfill the brain death criterion prior to cessation of cardiac pump activity. In response to this dilemma, the University of Pittsburgh Medical Centre developed a protocol for donation of organs that permitted their procurement from patients who were pulseless and apneic for 2 minutes and did not fulfill brain criteria and who had previously given consent for organ donation.[13] Because it is uncertain if cessation of cardiorespiratory function is irreversible after only a short time, the Institute of Medicine (IOM) extended the time required for pulselessness and apnea from 2 to 5 minutes before permitting organ procurement.[14] Waiting longer than 5 minutes for the determination of death would compromise the quality of procured organs because of warm ischemia time and would influence the functioning of grafts in transplant recipients.

One of the pivotal assumptions for NHBOD acceptance is that 5 minutes of pulselessness and apnea eliminates the possibility that the procurement process itself could be the cause of death and fulfills the "dead donor rule."[14,15] The cardiorespiratory death criteria were derived from observations that did not evaluate delayed autoresuscitation (spontaneous return of circulation) or simultaneous cessation of brain electrical activity (as recorded in brain death).[16–18] The death criteria applied for organ procurement must also comply with the irreversibility requirement of the UDDA.[11,12]

The true incidence, temporal characteristics, and predictors of autoresuscitation in humans remain unknown because of underreporting in the literature. However, there have been case reports of autoresuscitation with return of neurologic function (also called the Lazarus phenomenon) after 10 minutes of cardiac asystole.[19,20] Maleck et al. and Adhiyaman et al. described autoresuscitation 5 minutes or longer after cardiorespiratory arrest in 44% and 50% of the published case reports, respectively.[19,20] Although cardiac asystole leads to the loss of arterial pulse pressure, circulatory arterial mean pressure is maintained in diastole by arteriolar vasomotor tone. The relaxation (diastole) phase systemic arterial to venous pressure gradient provides the perfusion pressure for vital organs and the spontaneous return of circulation after circulatory arrest.[21] It is likely that autoresuscitation occurs because of the persistence of circulatory vasomotor tone after cessation of cardiac function. The time course of systemic vascular tone after circulatory arrest has not been well characterized in humans. However, the IOM criteria did not account for the incidence of delayed autoresuscitation in humans even though the Maastricht protocol (developed by the University of Zurich, Zurich, Switzerland) acknowledged this phenomenon and required at least 10 minutes to elapse after cardiorespiratory arrest before starting organ procurement.[22] The 10 minute waiting time did not compromise the quality of the organs procured.

The cardiorespiratory death criteria for organ procurement also ignore cardiac electrical activity (such as pulseless electrical activity or ventricular fibrillation) on an electrocardiogram. Research with cardiac ultrasonography and indwelling arterial catheters confirms that pulseless cardiac electrical activity can be associated with cardiac mechanical contractions, although these contractions are too weak to be detected by blood pressure monitoring.[23] The presence of cardiac electrical activity on an electrocardiogram can also increase the likelihood that delayed autoresuscitation will occur.[19,20] Furthermore, whether there is brain electrical activity or neurologic function when cardiac electrical activity is still observed on an electrocardiogram remains unknown.[24] It can be argued that donors who have already suffered severe neurologic injury cannot have meaningful neurologic function at the time of cardiorespiratory death. However, the presence of brain activity becomes relevant for organ donors with intact neurologic and brain function prior to cardiorespiratory arrest when only cardiorespiratory criteria for organ procurement are being used.[4,8,9]

In situ circulatory support with extracorporeal perfusion in organ donors has also refuted that cardiorespiratory arrest for 5 minutes fulfills the UDDA requirement because reversibility can occur during the procurement process. In situ extracorporeal perfusion is initiated 5 minutes after cardiorespiratory arrest of donors in order to preserve organs for procurement.[25] Coronary and cerebral reperfusion can lead to the return of cardiac and neurologic functions (also called reanimation) of donors during the procurement process. Mechanical occlusion of the aortic arch and pharmacological agents are required to suppress donor reanimation during organ procurement.[26] Martin et al. documented that in situ extracorporeal perfusion returned full neurologic and cardiac function 25 minute after cardiorespiratory arrest that occurred outside the hospital.[27] Similar observations of full neurologic recovery and survival to hospital discharge were reported after in situ extracorporeal perfusion for in-hospital cardiorespiratory arrest.[28] These observations confirm that the time required for irreversible loss of neurologic function after cessation of circulation is much longer than the 2-5 minutes of cardiorespiratory arrest required to begin the process of organ procurement in NHBOD.

The incidence of donor reanimation during procurement is unknown because its reporting violates the dead donor rule and can create legal concerns.[11] It can be argued that reanimation of organ donors is irrelevant because it does not mean survival. However, the occurrence of reanimation invalidates the premise that the cardiorespiratory criteria for organ procurement comply with the uniform determination of death. Others have accepted the inaccuracy of these criteria for determining death for procurement of organs from deceased donors and proposed abandoning the dead donor rule in order to permit recovery of transplantable organs before death.[29]

In the face of the uncertainty in determining death and in response to a media and marketing campaign by organ procurement organizations (OPOs) to promote public enrollment in deceased organ donation, the transplant community renamed NHBOD "cardiac death" organ donation.[30,31] The use of the term cardiac death is scientifically inaccurate and perhaps misleading. This term is used to denote the cessation of circulation and cardiac pump activity. The term cardiac death can be misinterpreted as meaning the heart has irreversibly ceased at the time of procurement, thus contradicting the scientific evidence for spontaneous resumption of cardiac function and autoresuscitation.[19,20] Alternatively, the use of this term can falsely imply that neurologic activity or brain stem function has ceased irreversibly after loss of cardiac activity, when scientific evidence suggests that brain stem function can remain after cardiac arrest.[32]

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