Electrocardiographic manifestations following electric injury

International

Journal

of

cardiology ELSEVIER

International Journal of Cardiology 57 (1996) 100-101

Electrocardiographic manifestations f&swing

electric injury

Kavita R. Arya*, Girish K. Taori, Sanjeev S. Khanna Department of Medicine, K. B. Bhabha Hospital, Bandra, Bombay -

4ooO50, India

Received 25 April 1996; revised 17 July 1996; accepted 17 July 1996

Abstract A 23-year-old man admitted with electric injury had intermittent episodes of non-sustained ventricular tachycardia, recurrent ventricular premature complexes, atria1 fibrillation, supraventricular tachycardia and ST changes suggestive of pericarditis. The non-sustained ventricular tachycardia and ventricular premature complexes responded to intravenous lidocaine, atria1 fibrillation and supraventricular tachycardia to intravenous digoxin. Keywords: Electrical injury; Electrocardiogram; Arrhythmias

1. Introduction

2. Case report

Electrical injury can result in a variety of cardiac arrhythmias like sinus tachycardia, sinus bradycardia, atrial premature contractions, atria1 fibrillation,ventricular premature contractions and conduction disturbances. Rarely, sudden death due to ventricular fibrillation and asystole occur. Transitional ST-T changes and myocardial infarction have also been reported [ 11. We report a young patient who developed various arrhythmias, ST segment changes suggestive of acute pericarditis (Fig. l), MP-CK elevations and hemoptysis due to lung trauma following electrical injury.

A 23-year-old healthy steward was admitted at 18:OOh, 1 h after sustaining electrical injury from a deep freezer. He was unconscious for 10 mm; subsequently, was restless and complained of blindness. On admission, he was disoriented, had a pulse of 96/n& blood pressureof 130190mmHg, respiration rate of 24/min, no cyanosis. He had diminished breath sounds on the entire left side. Cardiovascular and neurological systems were normal. The entry wound was a contact abrasion over the right arm. Exit wound was a small black dysesthetic burn on the left heel. The electrocardiogram (ECG) showed sinus tachycardia, chest radiograph showed a non homogeneous opacity in the entire left lung. At 19:00 h his vision returned to normal. An hour later, he had massive hemoptysis, requiring 350 ml of blood transfusion. At 23%) h he developed frequent

*Corresponding author, 23 Sopan Baug Cooperative Housing Society, Pune - 411001, India.

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incidence of cardiac complications in electrical injuries has been lo-40%. Hughes [3] has described that type of irregularity is related to currents to which the heart is exposed. Upto 25 mA, rhythm is unchanged. At 25-75 mA, the heart stops momentarily and resumes an irregular heart beat. At 75 mA to 4 A there is ventricular fibrillation which persists unless stopped by defibrillation. Beyond 4 A, the heart locks in spasm, but resumes a normal beat provided the current is discontinued. In our patient the current was probably above 4 A. A current passing from the right hand to either foot would be more dangerous to the heart than one passing through the right to left hand [4]. In our patient, the entry wound on the right arm and exit wound on the left heel explains the extensive cardiac involvement. Also, alternating current is more dangerous than direct current [5], as in our case. In various reports, no more than two arrhythmias were seen in one patient. In our patient, many types of arrhythmias were seen within a 4 h span. Most electrocardiographic changes have been reported to return to normal.

Acknowledgments Fig. 1. Surface electrocardiogram (rhythm strip) showing various arrhythmias in order of appearance.

ventricular premature contractions and episodic non sustained ventricular tachycardia, requiring a lidoCaine bolus and drip at 4 mg/min. At midnight he had episodes of supraventricular tachycardia and atrial fibrillation which returned to normal sinus rhythm with intravenous digoxin. He remained hemodyanamically stable thereafter. Next morning, at 10:00 h, ECG changes suggestive of acute pericarditis were observed. Serum enzymes were elevated - CPK (423 IU/L), LDH (572 IU/L) and SGOT (104 IU/L). Hemoglobin increased from 10 to 12 g%. The ECG normalised within 48 h. Chest radiograph cleared completely. The patient was discharged.

3. Discussion Lynn et al. have reported abnormal ECG in 36% of 64 patients with electrical injury [2]. Overall

We thank Dr Satyavan Sharma, MD, DM, Consultant Cardiologist, Bombay Hospital, Bombay, India, for his suggestions and guidance.

References [l] Crawley IS. Effect of noncardiac drugs, electricity and poisons on the heart. In: Hurst JW, editor. The Heart, arteries and veins, 7th edn. New York McGraw Hill Inc., 1990; 1571-1583. [2] Solem L. The natural history of electrical injury. J Trauma 1977; 17: 487-500. [3] Hughes JBW. Electrical shock and associated injuries. Br Med J 1957; 1: 852-856. [4] Morgan ZV, Headley RN, Alexander EA, Savyer CG. Atria1 fibrillation and epidurrd hematoma associated with lightning stroke. N Engl J Med 1958; 259: 956-958. [5] Wallace JF. Electrical injuries. In: Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, editors. Harrison’s principles of internal medicine, 13th edn. New York: McGraw Hill Inc., 1994; 2480-2482.