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Decreased heart rate and blood pressure in a recent cardiac transplant patient after spinal anesthesia

[Baisse de la fréquence cardiaque et de la tension artérielle après rachianesthésie chez un patient qui a récemment reçu une greffe cardiaque]

From the Department of Anaesthesia, Royal Victoria Hospital, McGill University Health Centre, Montreal, Quebec, Canada.

Address correspondence to: Dr. Steven B. Backman, Department of Anaesthesia, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec H3A 1A1, Canada. Phone: 514-842-1231, ext. 34883; E-mail: steven.backman{at}muhc.mcgill.ca

Purpose: To describe the cardiovascular effects of neuraxial blockade in a heart transplant patient.

Clinical features: A 69-yr-old 70-kg male underwent orthotopic heart transplant (bicaval anastomosis technique) for ischemic cardiomyopathy. Five months after transplantation, the patient underwent a transurethral bladder tumour resection under spinal anesthesia. Two millilitres of bupivacaine 0.75% (15 mg) were injected intrathecally at L_3–4 and the patient remained seated for approximately 20 sec prior to assuming the lithotomy position. Subsequently, both blood pressure (BP) and heart rate (HR) diminished gradually (BP and HR immediately pre-spinal: 113 mmHg (mean arterial pressure) and 92 beats·min^–1, respectively; nadir BP and HR: 94 mmHg (16.8% decrease) 30 min postspinal and 73 beats·min^–1 (20.7% decrease) 40 min postspinal, respectively). HR and mean BP were highly correlated (r = 0.9410, P < 0.0001, R² = 0.8854). The dermatome level of neuraxial anesthesia, determined by sensitivity to pin prick, was T₈ (five minutes) and T₆ (ten minutes) postinjection of spinal anesthetic. Control patients (n = 10) undergoing elective urological procedures with identical anesthesia management demonstrated very similar cardiovascular responses.

Conclusions: Although cardiac transplant patients may tolerate neuraxial anesthesia admirably, a fall in HR may ensue which theoretically could have important physiological consequences. It is argued that the change in HR in the transplanted patient was mediated by mechanisms intrinsic to the transplanted heart and/or by reduced catecholamine secretion from the adrenal medulla. It is emphasized that HR changes observed in cardiac transplant patients do not necessarily imply reinnervation of the transplanted organ.