long QT interval in a patient after out-“>American Journal of Emergency Medicine 31 (2013) 1722.e1-1722.e3

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Case Report

Long QT interval in a patient after out-of-hospital cardiac arrest with hypocalcaemia, undergoing therapeutic hypothermia?

Abstract

A 53-year-old woman was hospitalized after out-of-hospital cardiac arrest due to ventricular fibrillation. Initial electrocardioagram showed sinus rhythm of 117 beats per minute, 452 ms QTc interval, ST-segment depression up to 1 mm in V₂-V₆, and ST-elevation in Lead aVR. Patient was treated with primary coronary angioplasty and therapeutic hypothermia, during which QTc interval prolonged up to 616 ms and Osborn wave was seen in lead V₄, along with elevation of ST-segment in I, II, III, aVF, V₅ and V₆; Negative T waves in I, II, aVL, aVF, and V₂-V₆. Laboratory test results showed hypocalcaemia. After rewarming and ion correction QT abnormalities resolved.

We present a case of a 53-year-old woman with no previous history of cardiovascular disease hospitalized after out-of-hospital cardiac arrest due to ventricular fibrillation. She was resuscitated and successfully defibrillated by emergency medical services. On admission she was unconscious in a poor general condition (Glasgow Coma Scale [GCS] score 4), blood pressure 180/100 mm Hg, heart rate 130 beats per minute (bpm). In arterial blood gas results we saw acidosis high lactates level (pH 7.26 [norm 7.25-7.45]; PO₂ 104 mmHg [norm 83-108 mmHg], pCO2 36.5 mmHg [norm 35-45 mmHg], K⁺ 3.6 mmol/L [norm 3.6-5.0 mmol/L], lactates 3.7 mmol/L [norm 0.5-1.6 mmol/L]). Troponin I level was 1.55 ng/mL (12.5 ng/mL, 8.22 ng/mL), and creatine kinase-MB 32.2 ng/mL (166 ng/mL, 140 ng/mL). In laboratory results low calcium level (1.81 mmol/L [norm 2.15-2.60]) drew attention. Performed head CT showed no signs of trauma, bleeding or ischemia. Patient was started on therapeutic hypothermia protocol and transported to catheterization laboratory, where performed angioplasty showed critical occlusion of proximal part of left anterior ascending artery. Everolimus eluting stent was implanted into anterior ascending artery and distal part of the left coronary, with good effect (TIMI flow 3). Echocardiography showed akinesis of medial and apical segments of left ventricle (Philips iE 33 and 2.5-3.5 MHz transthoracic probe; Philips Medical Systems, USA). Several 12-lead Electrocardiograms were performed in this patient, showing peculiar findings. On admission, when patient had body temperature of 36.2?C ECG showed sinus rhythm of 117 bpm, incomplete Right bundle branch block, and left atrium abnormalities. Also ST-segment depression up to 1 mm was seen in V₂-V₆, with ST- elevation in aVR. QTc interval was 452 ms (Fig. A). Another ECG performed, when patient’s body temperature reached 33.0?C showed sinus rhythm of 69 bpm, with QTc interval of 616 ms, with depression of ST interval. Elevation of ST-segment up to 1 mm was seen in lead I, II, III, aVF, V₅ and V₆. Negative T waves were seen in I, II, aVL, aVF, and V₂-V₆ leads. Osborn wave was seen in lead V₄ (Fig. B).

? Conflict of interest: The authors have no conflicts of interest to disclose.

Standard pharmacotherapy for myocardial infarction was intro- duced along with calcium supplementation. After patient’s calcium level was corrected, and hypothermia protocol was successfully completed (at temperature of 36.0?C), we observed sinus rhythm of 87 bpm, QTc interval of 397 ms, and negative T waves in I, II, aVL, aVF, and V₄-V₆ leads. Osborn wave resolved along with shortening the QTc interval (Fig. C). In third day of hospitalization patient was in good general condition, breathing on her own, with GCS score of 15, blood pressure 120/70 mmHg, heart rate 86 bpm, temperature 37.1?C, and calcium level of 2.31 mmol/L. The patient was finally discharged home without any complications.

Cardiac arrest is often, as in our patient’s case, first manifestation of cardiovascular disease. Though constant development in medicine, prognosis after cardiac arrest remains poor. Patients afflicted with the event require immediate diagnosis, and management of them must be constantly improved to meet more, and more strict standards [1]. One of the newer and more effective developments of the last decades is therapeutic hypothermia. The method helped improve survival rates and neurological outcome but enforced on cardiologist a need to learn several ECG abnormalities which may occur during therapeutic hypothermia [2]. Findings most commonly occurring in ECG of hypothermic patients include Osborn waves, prolongation of PR, QRS or QT intervals, varied T-waves abnormalities, and atrial or ventricular arrhythmias [3]. Hypothermia can also make us miss common, usually easy to spot ECG findings diagnostic of conditions, like acute coronary syndrome or pericarditis [4].

Osborn wave is a late delta wave at the end of the QRS complex (or as a small secondary R wave (R?). Osborn waves can occur in condition other than hypothermia, like hypercalcaemia. They often have different morphology, for example, their height usually reflects degree of the hypothermia. The waves are not always easy to spot, first of all they can be mimicked by for example atrioventricular conduction delays, or have low voltage and be limited to few leads.

In our patients case Osborn wave occurred only in lead V₄. This fact may be partially due to hypocalcaemia. As mentioned before Osborn waves may be induced by high calcium levels, so probably in our case the opposite situation reduced Osborn waves despite hypothermia [5]. Another finding in our patient’s ECG was extensively prolonged QTc interval, even up to 616 ms on ECG taken at body temperature of 33.0?C. In spite of genetic predispositions, variety of Environmental factors can cause prolongation of the QT interval. Cardiac, endocrine, or neurologic conditions, as well as multiple types of drugs give QT prolongation [6]. This condition may be very dangerous, result in Life-threatening arrhythmias like Torsade de pointes. In our patient’s case this severe prolongation was a result of very low Blood calcium level. Hypocalcae- mia, like many other ion abnormalities can result in impaired cardiac contractibility and cause ventricular arrhythmias, or QT prolongation

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1722.e2 F.M. Szymanski et al. / American Journal of Emergency Medicine 31 (2013) 1722.e1-1722.e3

Fig. Series of ECGs performed: on admission - at body temperature of 36.4?C (A), on the intensive care unit-at body temperature of 33.0?C (B), on the intensive care unit-at body temperature of 36.0?C (C).

[7]. It often occurs due to primary aldosteronism and hyperparathy- roidism, congestive heart failure, acute and chronic hyperadrenergic stressor states, high dietary sodium, and low dietary calcium intake with hypovitaminosis D [8]. Another component of the prolongation, was probably as previously mentioned the hypothermia.

Presented case highlights how important is close inspection of ECG results. In this case it was particularly difficult, due to plenty of different findings. First of all we saw first acute, than progressing diffused myocardial infarction of anterolateral heart wall, accompanied by incomplete right bundle branch block, then significant QT prolongation making us look for ion abnormalities, and finally discreet Osborn wave.

Filip M. Szymanski MD, PhD Grzegorz Karpinski MD

Anna E. Platek Bartosz Puchalski MD, PhD

Krzyszof J. Filipiak MD, PhD

Department of Cardiology Medical University of Warsaw, Warsaw, Poland E-mail address: [email protected]

http://dx.doi.org/10.1016/j.ajem.2013.07.026

References

1. Ewy GA, Sanders AB. Alternative approach to improving survival of patients with out-of-hospital primary cardiac arrest. J Am Coll Cardiol 2013;61:113-8.
2. Szymanski FM, Karpinski G, Platek AE, Opolski G. Osborn waves during therapeutic hypothermia in young ST-ACS patient after out-of-hospital cardiac arrest. Kardiol Pol 2013;71:88-90.
3. Lebiedz P, Meiners J, Samol A, et al. Electrocardiographic changes during therapeutic hypothermia. Resuscitation 2012;83:602-6.

   F.M. Szymanski et al. / American Journal of Emergency Medicine 31 (2013) 1722.e1-1722.e3 1722.e3

   Chhabra L, Spodick DH. Hypothermia masquerading as pericarditis: an unusual electrocardiographic analogy. J Electrocardiol 2012;45:350-2.

4. Hoffmayer KS, Goldschlager N. Apparent Osborne waves. J Electrocardiol 2009;42:423.
5. Ackerman MJ. Molecular basis of congenital and acquired Long QT syndromes. J Electrocardiol 2004;37(Suppl.):1-6.
6. Digby GC, Perez Riera AR, Barbosa Barros R, et al. Acquired long QT interval: a case series of multifactorial QT prolongation. Clin Cardiol 2011;34:577-82.
7. Yusuf J, Khan MU, Cheema Y, Bhattacharya SK, Weber KT. Disturbances in calcium metabolism and cardiomyocyte necrosis: the role of calcitropic hormones. Prog Cardiovasc Dis 2012;55:77-86.