Table 1.
Cardiac medication management.
Fig 1.
Algorithm for management of a hemodynamically unstable primate.
An algorithm for vasoactive infusions and isotonic IV fluid boluses needed to augment the animal’s blood pressure is outlined above.
Table 2.
Interpretation of ventilation and oxygenation disturbances on ABG.
Table 3.
AAN guidelines prior to confirmation of brain death.
Fig 2.
Confirmation of brain death: Apnea challenge.
All but one animal (#2) were stable enough from a respiratory standpoint to undergo a successful apnea challenge. All animal experienced respiratory acidosis and a rise in pCO2 of greater than 20mmHg without a spontaneous breath, consistent with brain death. Other than the single animal who became extremely hypoxic, the remaining animals were able to maintain pO2>70 during the challenge with pre-oxygenation techniques.
Fig 3.
Hemodynamics of brain death: Systolic blood pressure and heart rate.
When examining the change is systolic blood pressure (SBP), there was a predicable hypertension, followed by hypotension before return to baseline. Fig 3B shows the individual SBP response to brain death and Fig 3A shows the average response for all animals. When change in HRs with BD there was a trend of slightly delayed tachycardia at 15 minutes after brain death, followed by slow return to a HR approximately 10–15 bpm above the animal’s original baseline by 1 hour post brain death. Fig 3C shows the individual HR response to brain death and Fig 3D shows the average response for all animals.
Fig 4.
Maintenance of brain death—Vital signs.
We were able to maintain hemodynamic stability throughout brain death with MAP>60 and HR within 20 bpm of the animal’s baseline.
Table 4.
Vasoactive drug use by animal.
Fig 5.
Maintenance of brain death—Ventilation and oxygenation.
Using by following serial ABGs and making appropriate ventilator adjustment, we were able to maintain adequate oxygenation and ventilation throughout brain death.
Table 5.
Management and severity of diabetes insipidus.
Fig 6.
Urine output throughout brain death.
Although there was variability among animals (Fig 6B), the average peak UO occurred 5–8 hour after BD induction (Fig 6A). All but one animal exceeded the 4ml/kg/hr of urine output at some time point in the experiment.
Table 6.
Histological analysis of brain dead vs. naïve primates.
Fig 7.
Biopsy A shows Kidney H&E of naïve rhesus, age 18 years, diagnosed as normal. Biopsy B shows Kidney H&E of naïve rhesus, age 15 years, diagnosed with mild acute tubular injury, focal mild arteriosclerosis. Biospy C shows Kidney H&E of brain dead rhesus, age 16 years, diagnosed normal. Biopsy D shows Kidney H&E of naïve rhesus, age 19 years, diagnosed with mild acute tubular injury, focal mild arteriosclerosis.
Fig 8.
Biopsy A shows Liver H&E of naïve rhesus, age 15 years, diagnosed 5–10% macrovesicular fatty infiltrates, moderate/marked vacuolization. Biopsy B shows Liver H&E of brain dead rhesus, age 18 years, diagnosed 5–10% macrovesicular fatty infiltrates, moderate vacuolization.
Fig 9.
Biopsy A shows H&E of naïve rhesus, age 21 years, diagnosed mild apoptosis, minimal lobular atrophy. Biopsy B shows H&E of brain dead rhesus, age 17 years, diagnosed mild apoptosis, minimal lobular atrophy.