Description
- Heart transplantation has become an established therapeutic modality for patients with end-stage heart disease.
- Refined transplantation techniques, improved patient selection, cyclosporine immunosuppression, improved monitoring and anesthetic management techniques as well as appropriate postoperative care have enhanced the survival rate of recipients.
- Consequently, many more of these patients present for elective or emergency operations.
Epidemiology
Etiology/Risk Factors
The two most common indications for transplantation are ischemic cardiomyopathy and idiopathic dilated cardiomyopathy. Together, they comprise 90% of all transplant recipients.
Physiology/Pathophysiology
- Denervated heart: The post-transplant heart retains normal Frank–Starling mechanisms, impulse formation and conductivity, as well as intact
and 
receptors that respond to circulating catecholamines. However, it lacks normal responses and variations to respiration, carotid massage, and Valsalva maneuvers. The denervated heart has a faster basal resting heart rate, increased incidence of cardiac dysrhythmias, and a preload-dependent cardiac output. - Allograft rejection: Most episodes occur within the first 3 months with a peak at about 4–6 weeks. The pathogenesis involves cellular (lymphocyte infiltration) and/or humoral (antibody) mechanisms. The clinical spectrum of rejection includes fatigue, ventricular dysrhythmias, congestive heart failure, silent myocardial infarction, and sudden death. Early diagnosis is by endocardial biopsy. The time course involves a hyperacute stage (first 24 hours after transplant), an acute stage (within 6–8 weeks), and a chronic stage (months to years after transplant). Treatment involves augmented steroid therapy.
- Infection: Immunosuppressive agents should be continued indefinitely, making infection an ever-present risk. The leading cause is direct contact with contaminated material. Infections are most prevalent in the first few weeks after transplantation, and include mediastinitis and opportunistic infections (CMV, Pneumocystis carinii, toxoplasma, and Legionella).
- Effects of immunosuppressive agents on anesthetic management: Cyclosporine enhances the effects of muscle relaxants. Thus, a prolonged blockade may be seen after vecuronium or pancuronium.
- Effects of anesthetic management on immunosuppressive agents: Cyclosporine or tacrolimus levels must be kept within indicated therapeutic range.
- Dilution with massive fluid infusion and cardiopulmonary bypass can result in significant reductions in levels.
- Drugs that decrease blood levels: Phenobarbital, phenytoin, carbamazepine, and ticlopidine
- Drugs that increase blood levels: Many antibiotics, antifungal agents, metoclopramide, verapamil, and diltiazem
- Propofol does not appear to affect cyclosporine blood levels
- Data on the effects of general anesthesia and cyclosporine pharmacokinetics are limited.
- Allograft coronary artery disease (CAD): Present in ~21% of patients 5 years post-transplant; it is the leading cause of death 3–5 years post-transplant. The coronary arteries undergo an accelerated process of coronary atherosclerosis (CAV). The etiology appears to be multifactorial; risk factors include pre-existing CAD, female donors, female recipients, and congenital cardiac disease.
- Post-transplant hypertension: Present in ~67% of patients at 5 years post-transplant. Cyclosporine therapy appears to be an important etiologic factor. Treatment with nifedipine is poorly tolerated because of vasodilation, and beta-blockers are best avoided. Diltiazem and ACE inhibitors are the drugs of choice (note that diltiazem can increase cyclosporine levels and dose needs to be adjusted accordingly).
- Renal dysfunction: Present in ~13% of patients at 5 years post-transplant. Cyclosporine therapy appears to be an important etiologic factor. In addition, it may be worsened by the simultaneous administration of NSAIDs or trimethoprim/sulfamethoxazole. Erythromycin and diltiazem elevate cyclosporine blood concentrations and can further deteriorate renal function.
- The physiology of the denervated heart needs to be understood and appropriate medications should be chosen to treat bradycardia and hypotension.
- Heart transplant patients may be undergoing rejection and manifesting myocardial dysfunction; additionally, they have increased CAV and cardiac dysrhythmias. A thorough evaluation of the cardiovascular system is mandated.
- Strict aseptic precautions need to be followed and maintained; all intravascular and airway equipment should be handled with sterile gloves.