Electrocardiogram
Electrocardiographic Pattern of Anteroseptal Myocardial Infarction
Mimicked by Hyperkalemia-Induced Disturbance of Impulse Conduction
Morton F. Arnsdorf, MD
In a patient with renal failure and
shortness of breath, Q waves transiently
appeared in the right precordial leads of
the electrocardiogram (ECG) during epi-
sodes of hyperkalemia, without a substan-
tial change in mean electrical axis. With
restoration of the plasma potassium
levels to normal, R waves reappeared in
these leads. It is concluded that the tran-
sient development of Q waves in the right
precordial leads during hyperkalemia
resulted from a hyperkalemia-induced
conduction disturbance. Hyperkalemia,
by affecting conduction in Purkinje fibers
or ventricular muscle, or both, disturbed
the normal sequence of septal and ante-
rior wall depolarization and resulted in an
ECG pattern that mimicked that of antero-
septal myocardial infarction. Clinically,
hyperkalemia-induced conduction distur-
bances of this type must be included in
the differential diagnosis of the ECG that
suggests an anteroseptal myocardial in-
farction.
(Arch Intern Med 136:1161-1163, 1976)
Received for publication Oct 27, 1975; accepted
Feb 18, 1976.
From the Section of Cardiology, Department
of Medicine, Pritzker School of Medicine, Univer-
sity of Chicago.
Reprint requests to Department of Medicine,
University of Chicago Hospitals and Clinics, 950
E 59th St, Box 423, Chicago, IL 60637.
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in Hyperkalemia
in the magnitude or
Disturbances
forces
in the sequence of electromotive
generated by the septum, apex,
and anterior free left
right ventricle,
ventricular wall may produce Q waves
in the right precordial leads of the
electrocardiogram (ECG).' The pres¬
ent case is, to my knowledge, the first
-
description of a transient hyperka-
lemia-induced conduction disturbance
that mimics the electrocardiographic
pattern of anteroseptal myocardial
infarction.
REPORT OF A CASE
A 43-year-old man was first seenat the
University of Chicago Hospitals and Clin¬
ics in 1973 because of renal failure.
Although the cause of his renal disease was
never fully defined, it was believed to be an
immune-complex glomerulopathy that per¬
haps was related to heroin abuse. At this
time, a chronic peritoneal dialysis program
was initiated. Associated problems in¬
cluded hypertension, which was controlled
by methyldopa; cardiac disease with left
ventricular hypertrophy, congestive heart
failure, which was treated with digitalis
and diuretics, and pericardial effusions;
anemia; acid-base abnormalities; and elec¬
trolyte imbalance.
He was admitted to the hospital on May
1, 1974 for peritoneal dialysis; he had
hyperkalemia and increasing shortness of
breath. An ECG taken three weeks prior to
this admission on April 10 (Figure, upper
panel), at which time his plasma potassium
level was 4.2 mEq/liter, showed a normal
sinus rhythm at a rate of 75 beats per
minute; an axis of 0°; a PR interval of 0.16
seconds; a QRS interval of 0.10 seconds; a
QT interval of 0.42 seconds; a prominent Q
wave in aV,.; small Q waves in I, Vr„ and V,;
R waves in V, through V:); left atrial
enlargement; left ventricular enlargement;
and ST-T wave abnormalities. The admis¬
sion ECG on May 1 (Figure, middle panel),
at which time the plasma potassium level
was 6.2 mEq/liter, showed a normal sinus
rhythm at a rate of 65 beats per minute; an
axis of -5°; a PR interval of 0.18 seconds; a
QRS interval of 0.12 seconds; and a QT
interval of 0.44 seconds. Compared to the
tracing of April 10, the voltage had
decreased, and Q waves had appeared in
the right precordial leads V, through V;l.
Further, a terminal rightward conduction
disturbance of a right bundle-branch type
had appeared. There may have been some
positional difference in the placement of
the right precordial leads compared to that
of April 10, but this would not change the
interpretation of a substantial alteration
in the initial depolarization vectors, since
the Q wave is apparent even in V.,. It should
be noted that the initial depolarization
vectors changed little in the frontal plane.
The decreased voltage was attributed to a
pericardial effusion that was verified by
echocardiographic findings.
Following peritoneal dialysis on May 2,
the plasma potassium level was 4.5 mEq/
liter, and the ECG that is shown in the
lower panel of the Figure was obtained.
The normal sinus rate was 72 beats per
 TU
[K+]
(mEq/L)
4.2
Date 4/10/74
6.2
Date 5/1/74
itetaff^:
4.5 ^IS^^á-rrT
Dote 5/2/74
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Electrocardiograms prior to admission (upper panel), during hyperkalemia (middle
panel), and following correction of hyperkalemia by peritoneal dialysis (lower panel).
minute; the axis was essentially un¬
changed; the duration of the PR and QRS
intervals decreased to 0.15 and 0.10
seconds, respectively; the QT interval was
0.38 seconds; and R waves reappeared in V,
through V3. Again, little change in the
initial depolarization vectors was seen in
the frontal plane.
A similar sequence of events occurred
during another admission, when, at a
plasma potassium level of 5.8 mEq/liter, Q
waves appeared in V, and V.,, without a
substantial shift in electrical axis. When
the plasma potassium level was reduced to
4.2 mEq/liter by peritoneal dialysis, R
waves reappeared in these leads. There
was no enzymatic evidence for myocardial
infarction during either of these two
episodes. In late 1974, the patient was
referred to another hospital nearer his
home for continued care.
COMMENT
The effect of hyperkalemia on
cardiac electrophysiologic characteris¬
tics and the ECG has long interested
both the basic investigator and the
clinician. Recently, the subject has
been extensively reviewed.,T Slowing
of impulse conduction in the special¬
ized conduction system and in ventric¬
ular muscle during hyperkalemia has
been demonstrated by several investi-
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aVR aVL aVF V,
Uffl
Ll
Has
Fr
gâtions in the experimental animal,714
as has hyperkalemia-incuced prolon¬
gation of the His-ventricular time in
man.1' The mechanism for the de¬
creased conductivity has been eluci¬
dated by Domínguez and Fozzard,
who examined the influence of extra¬
cellular potassium ion concentration
on cable properties and conduction
velocity in isolated cardiac Purkinje
fibers by microelectrode techniques.14
They observed conduction velocity to
decrease as the extracellular potas¬
sium concentration was increased
from 4.0 to 7.0 mEq/liter and
attributed this to hyperkalemia-
induced depolarization of the Purkinje
fiber membrane, which resulted in
less inward sodium current being
available. Purkinje fibers are respon¬
sible for the normally rapid conduc¬
tion through the His-bundle-branch-
terminal Purkinje system. Previously
described cases of bundle-branch and
trifascicular block during hyperka¬
lemia315"18 presumably resulted from a
notable decrease or abolition of con¬
ductivity through these tissues sec¬
ondary to hyperkalemia-induced al¬
terations in fundamental membrane
properties, such as those described by
V2 V3 V4 V9 V6
1 m
a
tt hÍm
J:-í :í¡L
11 HH^ «
Domínguez and Fozzard."
The development of reversible right
precordial Q waves in our patient,
resulting in an electrocardiographic
pattern mimicking anteroseptal myo-
cardial infarction, seems to have
resulted from abnormalities of im¬
pulse conduction. The septal vector of
the heart arises from activation of the
middle third of the septum from left
to right and initiates the R wave seen
by the right precordial ECG leads. The
remainder of the R wave is produced
by activation of the lower two thirds
of the septum, the apex, and portions
of the right ventricular and free left
ventricular wall, with the process
completed in 0.03 to 0.04 seconds.'-
The normal sequence of septal and
anterior wall depolarization, then,
depends on an orderly sequence of
wave-front propagation through the
septofascicular branch of the left
bundle, the terminal Purkinje fiber
network, and finally the ventricular
tissue itself. In this patient, the devel¬
opment of reversible Q waves strongly
suggested an alteration in this normal
depolarization sequence.
Recently, Gambetta and Childers
have observed the development of
 rate-related Q in the right
waves
precordial leads, which they at¬
tributed to reversible septofascicular
block.1" Frequently, right bundle-
branch block accompanied this pat¬
tern. They contended that previously
described cases of transient right
precordial Q wave development dur¬
ing episodes of chest pain without
evidence of infarction-"LM and during
aberrant conduction2--' represented
instances of intermittent septofascic¬
ular block. As in the cases of Gambet-
ta and Childers, the electrocardio-
graphic manifestation of abnormal
septal and anterior depolarization in
our patient were more apparent in the
horizontal plane, as reflected by the
precordial leads, than in the frontal
1. Chou T, Helm RA, Kaplan S: Clinical
Vectorcardiography.New York, Grune & Strat-
ton Inc, 1974.
2. Massie E, Walsh TJ: Clinical Vectorcardiog-
raphy and Electrocardiography. Chicago, Year
Book Medical Publishers Inc, 1960.
3. Fisch C: Relation of electrolyte disturbances
in cardiac arrhythmias. Circulation 47:408-419,
1973.
4. Surawicz B: Relationship between electro-
cardiogram and electrolytes. Am Heart 73:814\x=req-\
J al: Electrophysiologic changes in hyperkalemia,
834, 1967.
5. Vanderark CR, Ballantyne F, Reynolds EW
Jr: Electrolytes and the electrocardiogram. Car-
diovasc Clin 6:269-294, 1973.
6. Surawicz B: Electrolytes and the electrocar-
diogram. Postgrad Med 55:123-129, 1974.
7. Ettinger PO, Oldewurtel HA, Khan MI:
Ventricular conduction delay and asystole during
systemic hyperkalemia. Am J Cardiol 33:876-886,
1974.
8. Bammer H, Rothschuh EE: Uber die Erre-
gungs leitung in Froschherzeriten Substanzen.
Z Gesamte Exper Med 119:402-412, 1952.
9. Surawicz B, Gettes L: Two mechanisms of
cardiac arrest produced by potassium. Circ Res
12:415-421, 1963.
10. de Carvalho AP: Role of potassium ions in
Downloaded From: http://archinte.jamanetwork.com/ by a New York University User on 06/13/2015
plane. The development of right
bundle-branch block in our patient
suggests that other Purkinje fibers
were also influenced by hyperkalemia.
Given the relative resistance of Pur¬
kinje fibers, as compared to ventricu¬
lar muscle to hyperkalemia-induced
conduction disturbances,24 it is proba¬
ble that intraventricular conduction
delays were present as well.
In conclusion, it seems reasonable to
suppose that the transient develop¬
ment of Q waves in the right precor¬
dial leads during hyperkalemia, which
was noted on two occasions in our
patient, resulted from a hyperka¬
lemia-induced conduction disturbance,
presumably in the presence of under¬
lying cardiac disease. Hyperkalemia,
References
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septal and anterior wall depolariza¬
tion, resulting in an electrocardio-
graphic pattern mimicking that of
anteroseptal myocardial infarction.
Clinically, hyperkalemia-induced con¬
duction disturbances of this type must
be included in the differential diag¬
nosis of an electrocardiographic pat¬
tern that is suggestive of anteroseptal
myocardial infarction.
This study was supported in part by Public
Health Service grant HL 17648-01 SCOR IHD
III-l, Research Career Development award PHS
1 K04-HL-00196-01, and a grant-in-aid from the
Chicago Heart Association (A76-14).
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