Hyperthermia-induced cardiac arrest in monkeys: limited efficacy of standard CPR

Successful resuscitation from heatstroke cardiopulmonary arrest has been only partially explored and the data covering the post resuscitation pathophysiology leading to secondary arrest is, in most cases, insufficient.

Following heatstroke-cardiopulmonary arrest, successful resuscitation may be achieved by standard CPR with surface cooling and administration of glucose. We ponder the sequence of early circulatory responses and the pathophysiological changes following successful resuscitation.

We exposed 12 pigtail monkeys to total-body hyperthermia (cerebral T 42 degrees C) until cardiac arrest ensued. Standard external CPR with surface cooling and glucose 5% IV were administered for up to 30 min. Control group A (n = 6) was compared with experimental group B (n = 6), which received additional steroid, glucagon and hypertonic glucose during CPR attempts.

No significant differences were found between the outcome of the two groups. The 30-min CPR attempt succeeded in restoration of spontaneous circulation (ROSC) in 8/12 monkeys-5 animals from group A and 3 in group B. The animals in whom resuscitation was unsuccessful had significantly prolonged periods of rectal temperature exceeding 42.5 degrees C (p < 0.05), and significantly higher rectal temperatures at the end of 30 min of CPR and cooling (p < 0.05). All the resuscitated animals later rearrested at 158 +/- 68 (95-228) min after ROSC; pulmonary edema occurred in 6/8 animals.

We conclude that experimentally-induced heatstroke can be transiently reversed by standard resuscitative procedures, but is followed by a delayed, irreversible, secondary shock state, which could not be prevented by the treatment we employed. We were, however, able to document in detail the pathophysiologic processes involved in the resuscitation, and the irreversible shock one sees after "successful" CPR.