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Hyperkalemia Masked by Pseudo-Stemi Infarct Pattern and Cardiac Arrest Shareez Peerbhai1 , Luke Masha2, Adrian Dasilva-Deabreu1 and Abhijeet Dhoble1,2*

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Hyperkalemia Masked by Pseudo-Stemi Infarct Pattern and Cardiac Arrest Shareez Peerbhai1 , Luke Masha2, Adrian Dasilva-Deabreu1 and Abhijeet Dhoble1,2* View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Springer - Publisher Connector Peerbhai et al. International Journal of Emergency Medicine (2017) 10:3 International Journal of DOI 10.1186/s12245-017-0132-0 Emergency Medicine CASEREPORT Open Access Hyperkalemia masked by pseudo-stemi infarct pattern and cardiac arrest Shareez Peerbhai1 , Luke Masha2, Adrian DaSilva-DeAbreu1 and Abhijeet Dhoble1,2* Abstract Background: Hyperkalemia is a common electrolyte abnormality and has well-recognized early electrocardiographic manifestations including PR prolongation and symmetric T wave peaking. With severe increase in serum potassium, dysrhythmias and atrioventricular and bundle branch blocks can be seen on electrocardiogram. Although cardiac arrest is a worrisome consequence of untreated hyperkalemia, rarely does hyperkalemia electrocardiographically manifest as acute ischemia. Case presentation: We present a case of acute renal failure complicated by malignant hyperkalemia and eventual ventricular fibrillation cardiac arrest. Recognition of this disorder was delayed secondary to an initial ECG pattern suggesting an acute ST segment elevation myocardial infarction (STEMI). Emergent coronary angiography performed showed no evidence of coronary artery disease. Conclusions: Pseudo-STEMI patterns are rarely seen in association with acute hyperkalemia and are most commonly described with patient without acute cardiac symptomatology. This is the first such case presenting concurrently with cardiac arrest. A brief review of this rare pseudo-infarct pattern is also given. Keywords: Cardiac arrest, Hyperkalemia, Myocardial infarction, STEMI, ECG Background Case presentation Hyperkalemia that manifests with electrocardiographic A 27-year-old Caucasian male with a past medical his- findings of an ST segment elevation myocardial infarc- tory of hypertension presented to the emergency room tion (STEMI) is very rare. A handful of cases describing (ER) for evaluation of a cardiac arrest. He had a one- this phenomenon have been described [1–5]. Although month history of unexplained progressive fatigue and de- the mechanism is poorly understood, it is proposed that creased oral intake. He experienced a witnessed collapse high potassium may, at times, shorten the action potential at home from a seated position, and emergency medical in phase three repolarization and thus lead to ST segment services (EMS) were called. No bystander cardiopulmo- elevation. Such presentations may delay necessary therapy nary resuscitation (CPR) was given prior to EMS arrival, particularly if dramatic cardiac complications of hyperka- and ECG in the field found the patient to be in acute ven- lemia are also present. We raise awareness of such occur- tricular fibrillation. He was defibrillated emergently which rences by presenting a case of symptomatic acute resulted in immediate asystole. CPR was performed, and hyperkalemia and cardiac arrest masked by an ECG sug- return of spontaneous circulation (ROSC) was achieved. gesting an acute anterior STEMI. The rhythm strip at this time revealed significant ST seg- ment elevations in V1–V2, AVL, and AVR; Q waves in V1–V2; as well as diffuse ST depressions in II, III, AVF, and V3–V6 (Fig. 1). These findings were relayed to the co- ordinating ER, and a STEMI protocol to allow for urgent * Correspondence: [email protected] cardiac catherization was initiated. 1Department of Internal Medicine, McGovern Medical School, The University On route to the hospital, the patient again developed of Texas Health Science Center at Houston, 6431 Fannin, MSB 1.150, Houston acute asystole. CPR was initiated and was in process at 77030, TX, USA 2Department of Internal Medicine, Section of Cardiology, The University of arrival to the ER. On exam, the patient was pale, cold, Texas Health Science Center at Houston, Houston, USA markedly cachectic, and severely volume depleted. Central © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Peerbhai et al. International Journal of Emergency Medicine (2017) 10:3 Page 2 of 4 Fig. 1 Pre-hospital ECG showing antero-septal Q wave MI venous access could not be achieved, and peripheral ven- patient was transferred to the coronary care unit (CCU) ous access allowed for the infusion of medications and re- for initiation of therapeutic hypothermia and further care. suscitation fluids but not for withdrawal of blood for Upon arrival to the CCU, laboratory testing began to re- laboratory testing due to marked venous collapse. veal several marked laboratory abnormalities (Table 1) in- Advanced cardiovascular life support (ACLS) was con- cluding profound hyperkalemia with a serum potassium of tinued for approximately 40 min. During this time, it was 9.8 mEq/L and disseminated intravascular coagulation noted that asystole consistently converted spontaneously (INR of >5, D-dimer >20 μg/mL, and fibrinogen <60 mg/ to ventricular tachycardia/fibrillation, and defibrillation dL). Emergent hemodialysis to correct his metabolic abnor- would consistently result in asystole. The patient received malities was performed, and fresh frozen plasma was ad- epinephrine, vasopressin, bicarbonate, and normal saline ministered to correct his coagulopathy. After hemodialysis, during this period. ROSC was achieved, and all vasopres- his ECG normalized (Fig. 3). sin, dopamine, and norepinephrine were required to The remainder of his hospitalization was complicated maintain a perfusing blood pressure. At this time, an by aspiration pneumonia, shock liver, acute kidney in- initial in-hospital ECG was acquired (Fig. 2). jury, and mild anoxic brain injury all due to prolonged Given the findings and presentation, the patient was resuscitation. However, he slowly recovered with sup- then taken emergently to the cardiac catheterization lab portive care. The etiology of his severe volume depletion for coronary angiography. Blood samples for laboratory and profound renal failure was never identified. He was testing were then drawn from femoral access catheters, transferred from the hospital to a rehabilitation facility and coronary angiography was performed. The coronary with a need for intermittent scheduled hemodialysis and arteries were found to be fully patent. Echocardiography eventually discharged home. revealed normal cardiac systolic function without wall motion abnormalities or pericardial effusion. Conclusions A right femoral angiogram revealed an extremely small Hyperkalemia is a common electrolyte abnormality with right common femoral artery, which was nearly com- protean manifestations. It may present as almost any dys- pletely occluded by the utilized 6-french catheter. Distal rhythmia including sinus bradycardia, atrioventricular pulses were absent, and the patient’s foot was cold to blockade of various degrees, intermittent bundle branch touch. The catheter was removed promptly, and the blocks, ventricular tachycardia, and ventricular fibrillation Fig. 2 Post ROSC ECG showing marked peaked T waves Peerbhai et al. International Journal of Emergency Medicine (2017) 10:3 Page 3 of 4 Table 1 Laboratory studies upon admission [6]. PR prolongation and symmetric T wave peaking are Lab data Results well-recognized early manifestations of mild to moderate White blood cell count 27.1 K/mm3 hyperkalemia. QRS widening is a harbinger of impending Complete blood count 7.66 M/mm3 cardiac arrest. It is poorly recognized however that acute hyperkale- Hemoglobin 22.4 g/dL mia on ECG may resemble an acute STEMI as descrip- Hematocrit 72.1% tions of this in the literature are rare. The mechanism is Sodium 164 meq/L unclear but may be related to shortening of phase three Potassium 9.8 meq/L repolarization where potassium efflux is the predomin- Chloride 101 meq/L ant ionic shift. A potassium current channel (Ikr) located Bicarbonate 14 meq/L on myocyte cell membranes is responsible for most po- tassium efflux during phase two and phase three of the Blood urea nitrogen 120 mg/dL cardiac action potential and increases potassium efflux Creatinine 19.1 mg/dL when extracellular potassium is elevated [7]. This leads Glucose 208 mg/dL to the shortening of phases two and three of the action Anion gap 58.8 meq/L potential in the setting of hyperkalemia and therefore Magnesium 6.8 mg/dL shortening of repolarization. Similar ST segment eleva- Phosphorus 33 mg/dL tions may be seen in other conditions of shortened phases two and three repolarization including genetic Total protein 11.1 g/dL benign early repolarization and acute hypercalcemia [8]. Albumin 2.7 g/dL Approximately 28 case descriptions of acute hyperka- Alanine transaminase (ALT) 85 U/L lemia mimicking acute STEMI have been described in Aspartate aminotransferase (AST) 63 U/L the literature at this time. One review [9] notes that 80% Alkaline phosphatase 167 U/L of case descriptions involve an antero-septal pseudo- – Total bilirubin 1.1 mg/dL infarct pattern with Q waves present in V1 V2 and ST segment elevation in AVR. The mean serum potassium Lipase 1430 U/L in this series was 8.1 meq/L [9]. Patterns of isolated in- Serum arterial pH 6.84 ferior and antero-lateral infarcts have
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