The transplanted heart rarely provides the recipient with completely normal cardiac function. The organ’s intrinsic muscle function may be preserved, but its altered physiology results from denervation and the anatomical consequences of surgical implantation [1, 4, 17].

Electrophysiology. Both sympathetic and parasympathetic efferent nerve fibres are severed during surgical implantation as well as sensory afferents. Reinnervation may occur, in some cases detectable as early as 5 months post-implantation, though more usually is not physiologically significant [18–20]. Denervation will result in symptomless ischaemia (no angina pectoris), increase in body water and left atrial pressures and elevated resting heart rate (approx. 90–110 bpm). The denervated heart will not mount a tachycardia as part of any reflex sympathetic response. Thus, any increase in cardiac output will be dependent on increasing heart rate and increasing circulating volume. The cardiovascular responses to surgical stimulation are lost. Carotid sinus massage and the Valsalva manoeuvre do not affect heart rate.

A significant fraction of patients exhibit conduction defects, especially right bundle branch block and implantation of a permanent pacemaker. Dysrhythmias are common and likely contributing factors include absent vagal tone, rejection (previous or active episodes) and raised endogenous catecholamines.

Cardiac performance. Exercise function may be reduced to 60–70% of that of normal subjects due to the absence of reflex tachycardia to exercise, increasing preload-related filling pressures and coexistent diastolic dysfunction [3, 4, 17].

The neuroendocrine response to heart transplantation may include elevation of plasma renin, natriuretic peptides, vasopressin and noradrenaline. This may contribute to diastolic dysfunction and the exaggerated hypertensive disease seen in patients and limit the heart’s response to the demands of exercise.

Skeletal muscle mass and function may be diminished by poor preoperative condition, as end-stage cardiac failure progresses, and the need for corticosteroids postoperatively as part of the immunosuppressive regime.

Cardiac allograft vasculopathy. CAV is a diffuse, nonfocal concentric thickening of the donor coronary arteries [21, 22]. The predominant pathological feature is concentric intimal hyperplasia as opposed to the discrete endothelial lipid core seen in atherosclerotic coronary arterial disease. The final common pathway is one of the immune activation leading to intimal hyperplasia most likely due to the cumulative injury from ischaemia-reperfusion injury, mechanical damage, cytomegalovirus infection and inherent endothelial damage (hypertension, diabetes, immunosuppression, hyperlipidaemia). The diffuse and extensive nature of the disease reduces the chances of successful revascularisation treatments significantly. Within 5 years of transplantation, only 70% of patients are CAV-free and this drops to 40% by 10 years.

Conversely, direct chronotropes and pressors are required to increase heart rate and systemic vascular resistance. Isoprenaline, dobutamine, metaraminol, adrenaline and noradrenaline all exert a direct adrenoceptor action. Ephedrine may be less effective as at least some of its activity is presynaptic, and myocardial catecholamine storage is chronically depleted.

Most antiarrhythmic drugs remain effective, but their potent negative inotropy may be revealed, as the heart is unable to initiate any reflexes to counter this. Amiodarone is the most widespread antiarrhythmic used following heart transplant and is effective in treating acute arrythmias. Chronic amiodarone use is avoided as cyclosporine levels are affected. Digoxin is less effective at delaying AV conduction in the denervated heart. Adenosine is effective at blocking AV nodal conduction but exhibits a supersensitivity response. Thus, the initial dose should be reduced to 1 mg.

Denervation will affect the activity of some anaesthesia drugs [1, 3, 4]. Tachycardia associated with pancuronium is not seen, and bradycardia in response to succinylcholine, neostigmine and with some synthetic opioids (e.g. fentanyl) is absent. The advent of sugammadex has offered an alternative for reversing neuromuscular blockade with rocuronium, and it has been used without adverse effect in heart transplant patients [23].

This must be extensive and should provide a detailed picture on the individual patients existing limitations and assessment of the implications of these to intraoperative and postoperative functions [1, 3, 4]. In the elective setting, this is best done by directly accessing the last comprehensive transplant review (cardiac transplant “MOT”). Transplant physicians methodically review heart transplant patients at least annually or more frequently pending complications. Thus, the patients have regular assessment of cardiac function and any associated organ dysfunction that may exist (e.g. renal function with cyclosporine use). The transplant team is an invaluable source of information and should be in regular contact when a patient presents for a noncardiac procedure.

Transthoracic echocardiography imaging provides a good snapshot of biventricular systolic function, diastolic performance, existence of valvular comorbidities and frequent information on pulmonary pressures. Coronary artery imaging is paramount given the silent nature of any myocardial ischaemia. Electrophysiology evaluation should include a current ECG to uncover ischaemia and arrhythmias, and pacemaker advice should be thought if present ensuring an up-to-date pacemaker check is available.

Cardiac history is also informative regarding any lasting symptoms of the original heart failure condition with residual cardiorenal alterations and hepatic dysfunction due to end-stage RV failure [24]. Patient journey, especially significant complications of cardiac allograft implantation, primary graft failure, bridging or salvage mechanical support, frequent rejections and documented development of accelerated atherosclerosis, should ring alarm bells for concerns.

All patients should be carefully assessed for any significant change in performance status or the occurrence of any new symptoms covering the period from the last transplant review. Should these generate any suspicion for change of status, elective procedures should be postponed and patient referred back to the transplant unit.

Review and plans for immunosuppression should constitute a central part of preoperative workup [25]. Review of rejection episodes should provide an indication for compliance with and efficiency of immunosuppressive regimes. Up to date report and advice should be directly sought from the principal transplant physician taking into consideration the extent of surgery, suitability of oral or intravenous administration and multiple factors that may influence plasma levels and depth of immunosuppression [1, 2]. The signs of chronic complications attributable to chronic immunosuppression such as worsening hypertension, diabetes, renal function, neurotoxicity with calcineurine inhibitors or bone marrow depression with azathioprine and MMF resulting in anaemia/leucopenia and reduced platelet counts should be carefully acknowledged [1, 3, 4]. Not only these side effects bare direct relevance to the conduct of anaesthesia, but also they may indicate the patient’s heightened response to normal immunosuppression or overzealous immunosuppressed state. A detailed plan for continuing or temporarily suspending some immunosuppression medications, monitoring drug levels and provisions for the postoperative period with different scenarios have to be documented.