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International Journal of Cardiology 111 (2006) 6 11

www.elsevier.com/locate/ijcard

Review

Electric shock: Cardiac effects relative to non fatal injuries


and post-mortem findings in fatal cases
Vittorio Fineschi a,*, Sabina Di Donato a, Sergio Mondillo b, Emanuela Turillazzi a
a

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].

* Corresponding author. Tel.: +390881733835; fax: +390881732180.


E-mail address: vfinesc@tin.it (V. Fineschi).
0167-5273/$ - see front matter D 2005 Elsevier Ireland Ltd. All rights reserved.
doi:10.1016/j.ijcard.2005.07.060

Electrical injuries have been reported to result in


numerous cardiovascular complications. The most
severe of these are usually manifested at the onset
of injury [3]; however, serious arrhythmias have also
been reported in the immediate post injury period
[4].
The documented cardiovascular effects of an electrical
shock include acute myocardial necrosis, myocardial
ischemia without necrosis, heart failure, arrhythmias,
haemorrhagic pericarditis, acute hypertension with peripheral vasospasm and anomalous non specific ECG changes
[5,6]. Electrical injury, particularly alternating current,
may lead to disease of the conducting tissue [7] and
related symptoms are described to occur several months
after the accident [8]. Evidence for myocardial injury or
infarction is usually confirmed by compatible history,
ECG evidence (including diagnostic Q waves, ST-T
abnormalities and echocardiographic or scintigraphic
abnormalities), presence of abnormal cardiac isoenzyme
levels [9 15].

V. Fineschi et al. / International Journal of Cardiology 111 (2006) 6 11

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

ST elevation rarely occurs because myocardial necrosis is


usually not transmural.
Lewin sustains that electric injury sometimes produces
patchy necrosis of the myocardium [22]. However, the ECG
findings are non-diagnostic because the pattern of myocardial injury is patchy rather than following the distribution of
a coronary artery.
Vianello describes a hospitalized patient with retrosternal
pain accompanied by ECG signs of depression of the ST tract,
approximately two weeks after experiencing an electrical
shock. A coronary arteriography immediately performed
reveals a 90% eccentric occlusion of the descendent anterior
artery. The author suggests that the electrical injury might
cause coronary occlusive thrombosis [23].
Ku describes a 20-year-old subject, electrocuted through
alternating current, who, during the clinical course, developed ventricular tachycardia and ventricular fibrillation.
After treatment, the ECG revealed acute anterolateral
myocardial infarction (Q wave in D1, avL and from V4 to
V6). The echocardiogram revealed a left ventricular apical
hypokinesia and the coronary arteriography confirmed
undamaged coronaries. These findings prove that the cause
of myocardial dysfunction is inconclusive to which the
author provides three hypotheses: first, direct injury to the
myocardium with resulting damage; second, myocardial
contusion during cardiopulmonary resuscitation with subsequent haematoma formation in small coronary arteries
possibly producing a myocardial infarction with normal
coronary arteries; third, coronary spasm induced by
electricity with resulting myocardial infarction [24].
Guinard has studied 10 patients, 9 of which were struck
by high voltage electricity, one by lightning, all survived.
All subjects presented alterations in the ECG, one showed
increase of the CPK-MB. In a long term follow-up, 5
patients had one or more abnormalities in their cardiac
conduction system and function, with or without symptoms;
one patient developed cardiac failure; in three patients ECG
anomalies persisted and anomalies in the left ventricular
functions were revealed through an echocardiography. The
authors thus conclude that high voltage electrocution is
associated with a high incidence of cardiac abnormalities,
which may persist [25].
Zeana describes a 65-year-old subject, electrocuted,
whom during the two weeks of hospitalization experienced
precordial pain, serous enzymes of negative myocardial
necrosis, evolved ECG inverse to the T wave, elevated ST-T
segment in the derivations D1 and avL, while T waves were
diphasic in D2, D3, avF indicating subepicardial ischemia
inferior and antero-lateral (two years later, negative ECG
and stress test). These findings suggest the possibility of
widespread pericardial or myocardial lesions from diffused
and reversible coronary insufficiency [26].
The arrhythmogenic stimulus induced by cardiac damage
due to electrocution is described in other clinical reports.
Jensen describes three cases: two patients developed
tachycardia and ventricular fibrillation; one developed

V. Fineschi et al. / International Journal of Cardiology 111 (2006) 6 11

ventricular parasystolia. In all three patients there was an 8 to


12 h time lapse from the electrical damage to the onset of the
symptoms. The myocardial biopsy revealed focal myocardial
fibrosis. In one patient, after a few days, transitory alterations
of the ST-T tract and T waves appeared, negative in the DI,
DII, DIII and V4 V6 derivations (the enzymes of myocardial
necrosis and the stress test; a thallium 201 scintigraphy and an
echocardiography were negative). The Author hypothesizes
that the delayed arrhythmia can be associated to the
development of patchy necrosis after electrical injury and to
an increased Na K pump concentration [27].
McGill and collaborators describe a 27-year-old male who
survived a high-voltage chest injury and regained complete
recovery of left ventricular function, but had persistent right
heart dysfunction on serial clinical evaluations [28].
Seven patients with high-tension electrical injury have
been studied by Iino et al. [29]. They suggest that even in
patients without definite evidence of severe cardiac complications in conventional examinations, radionuclide imaging reveals significant damage due to high-tension electrical
injury, in which sympathetic nerve dysfunction could be less
than myocardial cell damage.

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-

Fig. 1. Square nuclei (arrows) in the hyper contracted myocells.

Fig. 2. Non-eosinophilic bands of hyper contracted sarcomeres alternating


with stretched, often apparently separated sarcomeres (arrows).

lization between the endothelium and the elastic internal


membrane. The author hypothesized that these findings may
indicate direct myocardial damage by reperfusion and
coronary spasm due to electrocution, in the absence of
thrombosis and coronary atherosclerosis.
Homma [31] describes two cases: a 25-year-old male,
with ECG changes of scarce progression of the R wave in
V1 V6, apical and inferior vascular perfusion defect
detected through thallium scintigraphy. The post-mortem
examination revealed extended left ventricular subendocardial infarction, contraction band necrosis and eosinophilia of
the myocytes. The epicardial coronary arteries were normal,
while diffused thrombosis of the intra-myocardial vessels
was detected. The other patient demonstrated, together with
an inversion of the T waves in many electrocardiographic
derivations, severe biventricular hypokinesia with dyskinesia at the left ventricular apex; thallium imaging revealed a
fixed apical defect consistent with scar. The author
hypothesized two mechanisms: thermic damage or a more
probable ischemic injury precipitated by arrhythmiainduced hypotension.
James [32] describes 4 cases of males who died following
electrical accidents. Coronary arteries were grossly normal
but there were focally distributed areas of contraction band
necrosis within the tunica media of both large and small
coronary arteries, focal degeneration of smooth muscle fibres
and, in one case, a focal fibro muscular dysplastic narrowing
of small coronary arteries. The authors hypothesize that
during the period immediately following electrocution, the
greatest hazard for surviving victims is represented by
cardiac electrical instability. Victims of these acute events
may develop congestive heart failure immediately following
the electrocution, or after some time. Subsequent to recovery,
focal fibrosis could repair the sites of severe injury. Zack
describes the case of a 27-year-old male, deceased days after
he was struck by lightning. The clinical characteristics
illustrated an inversion of the T wave and ST depression in
the ECG, increase of the enzymes (CPK, CPK-MB,
myoglobin) and comatose state. Macroscopic examination
of the heart showed disseminated focal thermally damaged

V. Fineschi et al. / International Journal of Cardiology 111 (2006) 6 11

regions besides haemorrhagic areas in the myocardium of


both atria and ventricles. The coronary arteries appeared
normal, exhibiting no signs of thrombosis. Histological
examination revealed a mixture of necroses, mainly striated
haemorrhages, inflammatory reactions, eosinophilia of some
myocytes and contraction bands: the author maintains that
histological findings on the heart were the same of those for
severe acute myocardial infarction [33].
Fineschi et al. describe morphological findings in 21 fatal
electrocution cases [34]. Examination of the conduction
system was unremarkable but the Authors describe a
morphologic modification of the heart characterized by a
break-up of myocardial fibres (MFB) [35]. They use the
term myofiber break-up (MFB) to include the following
histological patterns: (a) bundles of distended myocardial
cells alternating with hyper contracted ones. In the latter
group of cells there is also widening or rupture (segmentation) of the intercalated discs. Myocardial nuclei in the

hyper contracted cells assume a square aspect rather than


the ovoid morphology seen in distended myocytes (Fig. 1);
(b) hyper contracted myocytes alternated with hyper
distended cells that are often divided by a widened disc;
(c) non-eosinophilic bands of hyper contracted sarcomeres
alternating with stretched, often apparently separated
sarcomeres (Fig. 2). They hypothesize that the MFB
described could be interpreted as the morphologic counterpart of a terminal dysfunction ending in ventricular
fibrillation, giving a structural background to the chaotic
electrical asynchronous activity [35]. The frequency of
MFB they found was maximal in cases of electrocution
(90%), in respect to control groups. They conclude that in
rapid death due to electrical shock, typical cardiac lesions
exist, characterized by a break-up of myocardial fibres
(MFB) that could provide the structural substrate necessary
to initiate chaotic, electrical asynchronous activity, possibly
induced by the passage of abnormal electrical currents.

Table 2
Morphologic findings about direct electrical cardiac damage
Authors

Number of cases

Jensen et al. [27]

3 (survivors)

Homma et al. [31]

James et al. [32]

Clinical findings

2 cases had tachycardia and ventricular


fibrillation;
one case had ventricular parasystolia
2 (a, deceased; b survivor) (a) Scarce progression of the R wave in
V1 V6; apical and inferior perfusion defect.
(b) Inversion of the T waves (ECG); severe
biventricular hypokinesia with dyskinesia
at the left ventricular apex.
Fixed apical defect consistent with scar
(thallium imaging)
4 (deceased)

Xenopoulos et al. [30] 1 (deceased)

Zack et al. [33]

1 (deceased)

Fineschi et al. [34]

21 (deceased)

Morphologic findings
Focal myocardial fibrosis (myocardial biopsy)

(a) Extended left ventricular subendocardial


infarction, contraction band necrosis and
eosinophilia. Normal epicardial coronary arteries;
thrombi in many of the intra-myocardial vessels

Undamaged coronaries, foci of contraction band


necrosis, fibre rupture with intercellular dehiscence,
within the tunica media of both large and small
coronary arteries, focal degeneration of smooth
muscle fibres, contraction band necrosis. In one case,
focal fibro muscular dysplasia of the tunica media
Massive anterior IMA (ECG); notable
Patient coronary arteries with minimal traces of
increase in CPK, LDH and SGOT;
atheroma, haemorrhagic areas in the anterior
moderate dilatation of the VS with
myocardial wall and the septum, widespread
hypo-akinesia of the septum, anterior wall
contraction band necrosis, myocytolysis, coagulative
and apex. FE at 35%
changes, loss of striations and nuclear disappearance
Comatose state; inversion of the T wave
Disseminated focal thermally damaged regions
and ST depression in the EKG, increase
besides haemorrhagic areas in the myocardium of
of the enzymes (CPK, CPK-MB, myoglobin) both atria and both ventricles. Normal coronary
arteries. Mixture of necroses, mainly striated
haemorrhages, inflammatory reactions, eosinophilia
of some myocytes and contractions bands
(a) Bundles of distended myocardial cells alternating
with hyper contracted ones. In the latter group of
cells there is also widening or rupture (segmentation)
of the intercalated discs. Myocardial nuclei in the
hyper contracted cells assume a square aspect
rather than the ovoid morphology seen in distended
myocytes; (b) hyper contracted myocytes alternated
with hyper distended cells that are often divided
by a widened disc; (c) non-eosinophilic bands of
hyper contracted sarcomeres alternating with stretched,
often apparently separated sarcomeres. Examination of
the conduction system was unremarkable.

10

V. Fineschi et al. / International Journal of Cardiology 111 (2006) 6 11

The morphologic findings described are summarized in


Table 2.

4. Conclusions and future directions


The importance of understanding the mechanism that
electric shock plays in modifying the cardiac function is
obvious. Ventricular fibrillation is the main cause of death
following electric shock (low voltage alternating current).
The impendence of the body influences the passage of the
electrical current and is therefore the main physical factor
determining the degree of damage [36].
A specific therapy does not exist however, victims with
cardiac arrest from electrical shock or lightning strike
require prompt, aggressive resuscitation [37]. Treatment of
myocardial necrosis requires drugs to reduce platelet
aggregation and heparin; Ca-antagonist (in no heart failure
cases) and nitrate may be helpful to reduce coronary spasm.
Hypertension, heart failure or conduction abnormalities
required standard therapeutic regimens [38]. However, in
managing apparent acute myocardial infarction, the possibility that injury is not of ischemic origin must be
considered [39].
Future researches are therefore urgently required to better
understand processes described in this review. Imaging
techniques (nuclear medicine, magnetic resonance, echocardiography) are useful in the acute clinical phase and
during the follow-up of electrocuted victims. Data from
such studies may aid in the more accurate comprehension of
clinical and morphologic alterations of the heart, and in the
development of therapeutic strategies that can counterbalance these effects [40,41].

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