Cardiac Transplant Patient: Non-Cardiac Surgery Considerations
ASA ACE Program, 2009
Patients after cardiac transplantation have the following characteristics:
• lack of cardiac innervation
• risk for allograft rejection
• accelerated coronary artery disease
• increased risk for malignancy
• chronic use of corticosteroids and other immunosuppressive agents
After heart transplantation, the donor heart is denervated. Lack of this innervation restricts the ability of the new heart to increase heart rate in response to sympathetic stimulation, as occurs with hypotension or hypovolemia. A patient with a transplanted heart is considered to be preload dependent. A perioperative goal would be to maintain normovolemia and not restrict intravenous fluids.
A patient with a transplanted heart may regenerate cardiac innervation after approximately one year. These patients will then experience tachycardia in response to conditions such as hypovolemia, hypotension, myocardial ischemia, and hypoglycemia.
Premedication with atropine is not routinely required. In the absence of regenerated cardiac innervation, the administration of an indirect-acting anticholinergic such as atropine or glycopyrrolate will not be effective (ie, produce tachycardia). If a medication is required for increasing heart rate, administration of a direct-acting agent (e.g., epinephrine, isoproterenol) is recommended.
Corticosteroids are commonly administered chronically to patients after cardiac transplantation. Strong consideration should be given to providing a stress dose of corticosteroids for patients who continue to receive steroids for immunosuppression. Many patients will have the side effects associated with long-term administration including hypertension and diabetes mellitus.
Patients with a transplanted heart are at increased risk for accelerated coronary artery disease (CAD), thereby warranting use of ST segment monitoring even in children or adolescents. The detection of myocardial ischemia can be challenging if the patient is unable to sense the chest pain from myocardial ischemia. The detection of CAD in patients after cardiac transplantation is typically determined by cardiac angiography. The presence of CAD in patients with transplanted hearts generally increases proportionally from the time of cardiac transplantation. A recent study reports that approximately half of patients are free of angiographic evidence of CAD nine years after cardiac transplantation.
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