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Department of Forensic Pathology, University of Foggia, School of Medicine, Ospedali, Riuniti, Via L. Pinto, no. 1, 71100 Foggia, Italy
b
Department of Cardiology, University of Siena, School of Medicine, Policlinico Le Scotte, Siena, Italy
Received 20 May 2005; received in revised form 16 July 2005; accepted 24 July 2005
Available online 27 October 2005
Abstract
The documented cardiovascular effects of an electrical shock include acute myocardial necrosis, myocardial ischemia with or without
necrosis, heart failure, arrhythmias, haemorrhagic pericarditis, acute hypertension with peripheral vasospasm and anomalous, non specific
ECG alterations. Studies documenting the development of acute left ventricular failure and pulmonary oedema sustain that the observed ECG
changes are secondary to myocardial injury. The cause of death of victims of instantly fatal electrical accidents is ventricular fibrillation, but it
is not clear if this fibrillation is due to purely electrophysiological changes or to identifiable structural abnormalities in the heart. Little is
known about the morphological changes in the heart, as differing anatomical alterations are described. Data from such studies may aid in a
more accurate comprehension of clinical and morphological alterations of the heart and in the development of therapeutic strategies that could
counterbalance such effects.
D 2005 Elsevier Ireland Ltd. All rights reserved.
Keywords: Electrocution; Heart morphology; Myocardial ischemia; Ventricular fibrillation
1. Introduction
It is a well known fact that an electrical shock may
cause death or any degree of damage to various organs
and systems according to the type, voltage and intensity
of the electrical current and to the location of the
damage.
The electrical shock may strike the victims central
nervous system, the cardiovascular apparatus, the skeletal
muscular tissue, the lungs, the skin and other internal
organs [1]. Electricity causes its physiologic effect, as
opposed to its heat effect, by causing cells to depolarize or
to in effect lose the resting membrane potential across the
cell membrane. The amount of current required to cause
damage depends on the kind of cell and where it is in the
body [2].
2. Clinical reports
Fish describes the pathophysiology of electric injury and
discusses the cause of direct myocardial damage as
reviewed in existing clinical literature [5] (Table 1).
Ventricular fibrillation is possible from 70 mA up to
approximately 4 A. For more sensitive subjects, the current
in milliamperes at 60 Hz required to cause ventricular
fibrillation is 116 mA times the square root of the duration
of the shock in seconds [1,16].
Lichtenberg, subsequent to his observation of 19
patients struck by lightning, sustains that the type of
cardiovascular damage is related to the type of lightning
(direct, splash and ground strike): the direct effect can
result in myocardial injury (evaluated through the
significant increase in CPK-MB), depression of the ST-T
tract, alterations of the ventricular kinetics detected through
an echocardiography, and lengthening of the QT interval; in
one case haemorrhagic pericarditis was observed, resulting
in death, but the lack of a post-mortem examination
excludes any definitive hypothesis. According to the
author, the other two types of electrical shock (splash and
ground strike), usually determine specific ECG alterations
of the ST-T tract [17].
Cardiac arrhythmias and conduction disturbances are
among the most serious clinical manifestations of electrical
accidents. After low voltage injuries (< 350 V) arrhythmias
and conduction disturbances have been found in 11 39% of
the patients [18].
Kleiner confirms that ventricular fibrillation may also be
induced by lightning but does not establish whether this
arrhythmia is a direct effect of lightning, (i.e., discharge
during the vulnerable period of the cardiac cycle), or a
secondary effect of prolonged hypoxia. He describes
another cardiovascular effect of lightning, transient hypertension and tachycardia, considered to be secondary to
adrenal stimulation with excess catecholamine release [19].
A 23-year-old male, victim of injury due to electrical
shock, is described to present intermittent episodes of nonsustained ventricular tachycardia, recurrent ventricular
premature complexes, atrial fibrillation, supraventricular
tachycardia and ST changes indicating pericarditis [20].
Chandra examined patients with high voltage electrical
injury and myocardial damage who did not present
indicative cardiac signs, symptoms, or dysrhythmias [21].
These patients may develop left ventricular dysfunction, but
Table 1
Effects of electric current on humans (modified from Fish, 1993)
Minimum current level,
milliamperes, 60 Hz
Effects
0.5 to 2
1 to 4
6 to 22
100 mA
2000 (2 A)
Tingling sensation
Pain
Inability to let go, tetanic contractions
Ventricular fibrillation
Ventricular standstill
3. Morphologic findings
Xenopoulos [30] describes the case of a 19-year-old
male, hospitalized after an electrocution, who, after attempts
at cardiopulmonary resuscitation, presented an ECG suggestive of massive anterior IMA with a notable increase in
CPK, LDH and SGOT; a bidimensional echocardiography
revealed a moderate dilatation of the LV with hypo-akinesia
of the septum, anterior wall, and apex. The EF was 35%;
there was absence of pericardial effusion. The patient died
three days after the clinical presentation. At the post-mortem
exam, coronary arteries with minimal traces of atheroma,
haemorrhagic foci in the anterior myocardial wall and the
septum, widespread contraction band necrosis, myocytolysis with coagulative modifications, loss of striations and
nuclear disappearance were observed. Microscopically,
sections of the coronary arteries presented minimal vacuo-
Table 2
Morphologic findings about direct electrical cardiac damage
Authors
Number of cases
3 (survivors)
Clinical findings
1 (deceased)
21 (deceased)
Morphologic findings
Focal myocardial fibrosis (myocardial biopsy)
10
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injured patients predictive of myocardial injury? JAMA 1986;255(6):
764 8.
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