Purpose: The American Heart Association published a study focused on cardiac failure post-transplant, and how it may be associated with myocardial changes that occur in the organ donor after brain death, prior to procurement and transplantation.  This study specifically analyzed changes that occurred in the myocardium during the catecholamine storm. In this controlled study, brain death was induced in animal subjects and intercranial pressures were increased through inflation of a subdurally placed balloon which mirrored the herniation process. Researchers monitored hemodynamic stability, ventricular pressures, and output volumes.  These measurements were done prior to herniation induction, and in intervals over seven hours once brain death had been confirmed. Biopsies were also collected from the left ventricle cardiac tissue before brain death induction and 6-7 hours afterwards. The change relevant to this abstract was specific to the myocardium Beta-adrenergic receptor density. Post brain death, the Beta-adrenergic receptor density increased significantly, from 291±64 to 353±56 units/mg, or roughly 21%.  The control subjects in the study underwent the same biopsies as the test subjects and there was no significant change noted in the control group.

Methods: To review the process of brain death and how its associated physiologic changes could potentially alter the mechanisms of beta-agonist bronchodilators as it relates to BD donor management. We propose that transitioning from Albuterol to Levalbuterol in donor management could lead to improved donor stability and reduce the need for additional medications to control Albuterol induced tachycardia. We have revised our Pediatric and Adult BD Donor Management Order Sets to transition to Levalbuterol from Albuterol and are currently gathering data to review for any reduction in cardiac arrhythmia occurrence with our donors over the next year.

Results: As our data populates with the results of our post-case analysis over the next year, we anticipate that we will realize a reduction in tachycardia in our donors with a subsequent reduction in additional medications that would otherwise be indicated to control Albuterol-induced tachycardia.

Conclusions: Albuterol being a dual-isomer medication that initiates response in both the Beta-2 adrenergic receptors in the lungs (intended) as well as the Beta-1 adrenergic receptors in the heart (unintended). These Beta-1 receptors are the receptors that increased 21% post brain death induction in the study. With the increased concentration of Beta-1 adrenergic receptors in the heart because of the brain death herniation process, it follows that the potential for cardiac arrhythmias and other side effects also increases. Levalbuterol is another Beta-agonist bronchodilator used to open the airways in the lungs. It differs from Albuterol because it is a single-isomer medication and is specific to the Beta-2 adrenergic receptors in the lungs.