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Anesth Analg 2009; 108:379-380
© 2009 International Anesthesia Research Society
doi: 10.1213/ane.0b013e31818c0d06
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LETTER TO THE EDITOR

Dexmedetomidine Sedation (and Cardiac Perforation, Pericardial Tamponade, Cardiac Arrest, and Cardiopulmonary Resuscitation) Leading to Refractory Cardiogenic Shock

Michael P. Hutchens, MD, MA, and Per Thorborg, MD, PhD

Department of Anesthesiology and Perioperative Medicine Oregon Health and Science University; Portland, Oregon; hutchenm{at}ohsu.edu

To the Editor:

Sichrovsky et al.1 report a death attributed in part to dexmedetomidine. The patient had polycythemia vera and coronary artery disease. He suffered a cardiac arrest due to pericardial tamponade. After pericardiocentesis, the patient was resuscitated with vasoconstrictors but cardiogenic shock recurred. The authors argue that the recurrent shock was due to sympatholysis and coronary vasospasm induced by dexmedetomidine.

As the authors point out, dexmedetomidine is usually well tolerated. Although the authors report a high dose infusion during the first 45 min (2.2 µg · kg–1 · h–1), we have reported a case series in which up to 60 µg · kg–1 · h–1 was tolerated.2 Bradycardia and cardiac arrest have been reported with dexmedetomidine use3 but, in this case, the bradycardia may be explained by tamponade with Bezold-Jarish reflex.4 Postresuscitation rhythms included sinus, ventricular fibrillation, and pulseless electrical activity, but not bradycardia, suggesting the bradycardia was of mechanical origin.

Cardiogenic shock following resuscitation from cardiac arrest is well described and results from myocardial stunning.5 The polycythemia vera and left ventricular hypertophy reduced myocardial perfusion, increased the area at risk of stunning, and increases the likelihood of cardiac death.6 These phenomena were exacerbated by the necessary administration of vasoconstrictors. The autopsy finding of diffuse myocardial necrosis is consistent with catecholamine excess rather than sympatholytic failure. Finally, the patient's cerebral ischemic insult suggests there was prolonged whole body ischemia, which reduced myocardial performance.

This patient had mechanical, ischemic, and chemical insults, which explain his death. We believe it is unnecessary to invoke dexmedetomidine.

REFERENCES

  1. Sichrovsky TC, Mittal S, Steinberg JS. Dexmedetomidine sedation leading to refractory cardiogenic shock. Anesth Analg 2008;106:1784–6[Abstract/Free Full Text]
  2. Jorden VS, Pousman RM, Sanford MM, Thorborg PA, Hutchens MP. Dexmedetomidine overdose in the perioperative setting. Ann Pharmacother 2004;38:803–7[Abstract/Free Full Text]
  3. Ingersoll-Weng E, Manecke GR Jr, Thistlethwaite PA. Dexmedetomidine and cardiac arrest. Anesthesiology 2004;100:738–9[Web of Science][Medline]
  4. Campagna JA, Carter C. Clinical relevance of the Bezold-Jarisch reflex. Anesthesiology 2003;98:1250–60[Web of Science][Medline]
  5. Kern KB. Postresuscitation myocardial dysfunction. Cardiol Clin 2002;20:89–101[Medline]
  6. Soo LH, Gray D, Hampton JR. Pathological features of witnessed out-of-hospital cardiac arrest presenting with ventricular fibrillation. Resuscitation 2001;51:257–64[Web of Science][Medline]




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2009 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press