Orthotopic Heart Transplantation

Introduction

• Orthotopic heart transplantation (OHT) is the definitive therapy for end-stage heart failure due to ischemic or nonischemic cardiomyopathy, refractory arrhythmias, infiltrative disease, or complex congenital heart defects.

Allocation Criteria

• In 2018, the heart transplant allocation system was revised from a 3-tier system to a 6-tier system.² This was due to the increasing number of patients and advancements in mechanical circulatory support systems (Table 3).

Transplant Techniques

• There are 3 different techniques for cardiac transplantation, the most common being bicaval OHT.³ Total OHT is largely outdated and rarely used.

Anesthetic Considerations⁴

• During OHT important considerations include the induction of anesthesia with slow titration of anesthetic medications.
• In addition to standard American Society of Anesthesiologists monitors, an arterial line, a large-bore central venous catheter, a pulmonary artery catheter, a TEE probe, and cerebral oximetry are utilized.
• Sometimes these patients have a mechanical circulatory device in place, which requires constant monitoring.
• The surgery takes place under cardiopulmonary bypass (CPB) and is performed at institutions with appropriate resources and trained staff.
• Weaning from CPB and the early postoperative period for heart transplantation have their own unique challenges.
  • Management of the denervated heart
    • The transplanted heart lacks autonomic innervation, so direct-acting inotropic and chronotropic agents are often required to maintain adequate cardiac output.
    • Epicardial atrial and ventricular pacing wires are commonly used to treat postoperative bradycardia, with a target heart rate of 100–130 bpm to optimize cardiac output.
  • Causes of difficulty weaning from CPB
    • Primary graft dysfunction (PGD): Typically results from ischemia–reperfusion injury or unrecognized donor heart pathology.
    • Secondary graft dysfunction: May be caused by hyperacute rejection, surgical complications, or right ventricular failure due to pressure or volume overload.
    • Right heart failure: Frequently related to elevated pulmonary vascular resistance or preexisting pulmonary hypertension.
    • Refractory vasoplegia: Another common challenge that can impair adequate perfusion despite normal graft function.
  • Role of TEE
    • Posttransplant TEE assessment focuses on evaluating biventricular function, tricuspid regurgitation, and evidence of obstruction at anastomotic sites.

Postoperative Complications⁵

• Common postoperative complications include arrhythmias, tricuspid regurgitation, acute kidney injury, and graft failure.
• Arrhythmias
  • Arrhythmias are frequent after heart transplantation, especially early bradyarrhythmias due to denervation and disruption of the conduction system.
  • Supraventricular tachyarrhythmias can arise from atrial suture lines or signal rejection or graft vasculopathy.
  • Management includes pacing for bradycardia and antiarrhythmics or ablation for atrial arrhythmias; new arrhythmias later in recovery require evaluation for rejection.
• Tricuspid Regurgitation (TR)
  • TR is the most common valvular complication and is often related to endomyocardial biopsy–associated injury.
  • Other contributors include right ventricular dilation, size mismatch, and surgical technique.
  • While mild TR is well tolerated, significant TR may worsen renal function, cause congestion, and reduce long-term survival; severe symptomatic cases may require valve intervention.
• Acute kidney injury
  • Acute kidney injury occurs frequently after transplant due to perioperative hemodynamic instability, ischemia-reperfusion injury, vasopressor use, preexisting kidney dysfunction, and calcineurin inhibitor toxicity and is associated with increased mortality and prolonged hospitalization.
  • Management centers on hemodynamic optimization, nephrotoxin avoidance, adjustment of immunosuppressants, and renal replacement therapy as needed.
• PGD
  • PGD is the leading cause of early mortality and presents within 24 hours as severe left ventricular, right ventricular, or biventricular failure unrelated to rejection or surgical complications.
  • Risk factors include ischemia-reperfusion injury, prolonged cold ischemic time, marginal donors, and inflammatory responses.
  • Treatment requires aggressive hemodynamic support and often mechanical circulatory support such as extracorporeal membrane oxygenation.

Anesthetic Considerations After Heart Transplantation⁶

• Postheart transplant patients have denervation of the donor heart and thus have altered autonomic physiology and response to medications. During the early posttransplantation period (6-12 months), elective procedures are deferred due to a greater risk of complications.
• Special anesthetic considerations in posttransplant patients include the following
  • Cardiac autonomic denervation results in varying hemodynamic effects
    • Loss of sympathetic innervation
    • Loss of reflex sympathetic tachycardia in response to decreases in blood volume or pressure
    • Loss of parasympathetic innervation
    • Higher resting heart rate of 90-130 bpm
    • Loss of baroreceptor reflexes (ineffective Valsalva maneuvers and carotid massage)
    • Loss of visceral innervation
    • Classic chest pain from myocardial ischemia is absent
  • The Starling effect is retained. The denervated heart is significantly dependent on intravascular volume and adequate preload to maintain stroke volume and cardiac output. Therefore, it is critically important to avoid perioperative hypovolemia.
  • Pharmacologic changes
    • Only direct-acting vasopressors (e.g., phenylephrine, norepinephrine, vasopressin) and chronotropic agents (e.g., isoproterenol) are effective
    • Indirect agents (e.g., ephedrine) and anticholinergics (e.g., atropine, glycopyrrolate) are not effective.
    • Vasodilator agents (e.g., nitroglycerin, hydralazine) may lead to profound hypotension due to loss of reflex tachycardia.
    • Adenosine will have a prolonged and profound bradycardic effect.
    • Neuromuscular blocking agents will not exert their usual effects on heart rate.
    • Reversal agents that are acetylcholinesterase inhibitors do not cause bradycardia.
    • Due to chronic steroid administration causing adrenal suppression, stress dose steroids may be necessary.
  • Patients are at a higher risk for myocardial infarction due to cardiac allograft vasculopathy, or transplant-related coronary artery disease.
  • Common EKG abnormalities include dual p-waves (due to the presence of native atrial cuff tissue and the transplanted atrium), right bundle branch block (due to frequent endomyocardial biopsies), and atrial dysrhythmias (due to the lack of vagal tone and increased endogenous catecholamines).