Hyperkalemia-induced pacemaker dysfunction
Correspondence / American Journal of Emergency Medicine 31 (2013) 873-885
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Narat Srivali MD Supawat Ratanapo MD
Menzin J, White LA, Friedman M, et al. Factors associated with failure to correct the international normalized ration following fresh frozen plasma administration among patients treated for warfarin-related major bleeding. Thromb Haemost 2012;107:662-72.
Hyperkalemia-induced pacemaker dysfunction??
To the Editor,
We read with great interest the article by Muck et al [1]. The authors reported a very interesting case surviving extreme hyperka- lemia. We also recently had a case of hyperkalemia-induced pace- maker dysfunction manifested as failure of pacemaker capture and leading to unnecessary invasive pacemaker evaluation.
An 86-year-old man with ischemic cardiomyopathy status post-Implantable cardioverter-defibrillator implantation and com- plete atrioventricular block requiring permanent pacemaker with the rate-responsive accelerometer-based (DDDR) mode admitted for implantation of a left ventricular lead for cardiac resynchro- nization therapy. After the procedure, the patient subsequently developed failure to capture of the pacemaker stimulus with a wide idioventricular rhythm on 12-lead Electrocardiography (Fig. 1).
He was asymptomatic with a normal blood pressure. However, because of the concern that the prior procedure might have inter- fered with his Pacemaker function, he was brought down to electro- physiology laboratory and the pacemaker pocket was re-explored. No problems with the pacemaker generator or pacemaker wire were identified. The patient was later found to have hyperkalemia with a potassium level of 7.1 mEq/dL. He was treated with Calcium gluconate, insulin with dextrose, and Kayexalate, and the potassium level decreased to 4.6 mEq/dL in 3 hours. His cardiac rhythm re- turned to a normal ventricular paced rhythm with full capture (Fig. 2). He remained hemodynamically stable and was discharged the following day.
Pacemaker dysfunction is usually due to mechanical problems such as lead fracture, lead dislodgement, or generator malfunction. However, hyperkalemia is an uncommon but easily correctable cause of pacemaker dysfunction, which can manifest as failure to capture [1,2], as in our patient. Hyperkalemia causes a decrease in Myocardial excitability, which eventually leads to a decreased response to pace- maker stimulus [3,4]. It is important to think about hyperkalemia before considering an invasive procedure to evaluate for technical or primary pacemaker dysfunction. Failure to recognize this can lead to a Delay in diagnosis, unnecessary invasive procedures, and poten- tially fatal Hemodynamic deterioration.
? Authors’ contributions: All authors had access to the data and a role in writing the manuscript.
Wisit Cheungpasitporn MD Daych Chongnarungsin MD Edward F. Bischof MD
Department of Medicine, Bassett Medical Center
Cooperstown, NY 13326, USA E-mail address: [email protected]
http://dx.doi.org/10.1016/j.ajem.2013.01.021
References
- Muck PM, Letterer S, Lindner U, Lehnert H, Haas CS. Beating the odds-surviving extreme hyperkalemia. Am J Emerg Med 2012;30(1):250.e1-4.
- Schiraldi F, Guiotto G, Paladino F. Hyperkalemia induced failure of pacemaker capture and sensing. Resuscitation 2008;79(1):161-4.
- Kahloon MU, Aslam AK, Aslam AF, Wilbur SL. Hyperkalemia induced failure of atrial and ventricular pacemaker capture. Int J Cardiol 2005;105(2): 224-6.
- Sestito A, Lanza GA, Montebelli MR, Zecchi P. Images in cardiovascular medicine. Pacemaker failure caused by hyperkalemia. Ital Heart J 2002;3(2): 141-2.
Reply to: Brain computed tomographic scan findings in Acute opium overdose patients
To the Editor,
I read with great interest a recent article published by Farkhondeh Jamshidi et al-“Brain computed tomographic scan findings in acute opium overdose patients” in the recent issue of American Journal of Emergency Medicine (Volume 31, issue 1, January 2013, Pages 50-53) [1].
As a practicing neurointensivist, I found this article very relevant to my practice as I often encounter such cases. The authors have tried to correlate the opium poisoning/overdose with computed tomographic (CT) scan changes. However, one is forced to stop and wonder about 2 vital questions.
The authors mention that “no other drug overdose in this study as per patient’s history.” This is a crucial question as polysubstance abuse is rule than exception. Furthermore, other substances of abuse could have varied effects on the central nervous system with potential changes in CT scan. I wonder if authors had the data for toxicology screens. Without these data, the conclusions are shaky, as the history may not be accurate in such population. Next, authors mention that “subjects with history of CNS disorders were excluded.” However, authors have not elaborated what criteria were used to exclude “Central Nervous system disorders,” as any preexisting illness would change the interpretation drasti- cally. Did authors have previous CT scan results to corroborate? Without these answers, I would be hesitant to apply these results in clinical practice.
Sankalp Gokhale, MD Department of Neurology (Neurocritical care and stroke) Duke University Hospital, Durham, NC, USA, 27710
E-mail address: [email protected]