Noradrenaline-induced ventricular tachycardia in a patient with severe Parkinson's disease with denervation supersensitivity

DOI 3 References Open Access
  • Miyamoto Kazuyuki
    Department of emergency medicine, Tokyo Rosai hospital Department of emergency and critical care medicine, Showa University
  • Tanaka Kotaro
    Department of emergency medicine, Tokyo Rosai hospital Department of emergency and critical care medicine, Showa University
  • Tanaka Toshio
    Department of emergency and critical care medicine, Showa University
  • Ide Ryota
    Department of emergency and critical care medicine, Showa University
  • Hagiwara Yoshihiro
    Department of emergency and critical care medicine, Showa University
  • Fukuda Kenichiro
    Department of emergency and critical care medicine, Showa University
  • Miyake Yasufumi
    Department of emergency and critical care medicine, Showa University
  • Aruga Tohru
    Department of emergency and critical care medicine, Showa University

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Other Title
  • 除神経過敏へのノルアドレナリン投与で心室頻拍をきたした重症パーキンソン病の1例
  • Noradrenaline-induced ventricular tachycardia in a patient with severe Parkinson's disease with denervation supersensitivity

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Parkinson's disease (PD) is a multiple system degenerative disease that involves autonomic failure as well as dysmobility. Recently, denervation supersensitivity of cardiac sympathetic nerves was proven to be present in patients with PD. However, it is not well understood how to use cardiovascular agents in such cases. A 78-year-old male (Hoehn-Yahr 5) presented at our hospital with severe lower abdominal pain and a high fever. He had experienced severe constipation for more than five days. Upon arrival, he was in a shock state, and his colon was markedly enlarged due to the presence of a large amount of stool and gas, as observed on an abdominal CT scan. Septic shock induced by intestinal pseudo-obstruction was suspected. Transanal anal drainage, fluid resuscitation based on early goal-directed therapy and antimicrobial treatment were performed immediately, although the patient’s MAP gradually decreased. Therefore, noradrenaline (NA) was administered, after which frequent premature ventricular contraction (PVC) appeared and the MAP failed to increase. After increasing the dose of NA, unsustained ventricular tachycardia (VT) occurred, and the MAP further reduced, in contrast to our aim. The cardiovascular agent was therefore changed from NA to vasopressin (VP), as a diagnosis of denervation supersensitivity was highly suspected. Thereafter, the arrhythmia significantly decreased, and the patient’s hemodynamic status improved. Cardiac sympathetic nerves begin to degenerate in the early phase of PD in association with increases in the number of cardiac adrenergic receptors and the induction of denervation supersensitivity. VP is a vasopressor that acts on V1a receptors. The administration of VP should be considered in PD patients with denervation supersensitivity of the cardiac sympathetic nerves.

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