FEBRUARY 1975

The American Journal of CARDIOLOGY@

VOLUME 35

NUMBER 2

CLINICAL STUDIES

Atrioventricular and lntraventricular Conduction

in Hyperkalemia

TALI BASHOUR, MD, FACC Twelve patients exhibited electrocardiographic evidence of fascicuiar
IRENE HSU, MD block during hyperkaiemia. isolated left posterior hemibiock occurred
H. JOEL GORFINKEL, MD, FACC in four, isolated left anterior hemibiock in two, right bundle branch
RAJASEKARAN WICKRAMESEKARAN,
block with left anterior hemiblock in two, right bundle branch block
MD
with left posterior hemibiock in one, left bundle branch block with ab-
JORGE C. RIOS, MD
normal left axis deviation in two and advanced atrioventricuiar block in
Washington, D. C. one. in ail seven patients with sinus rhythm the P-R interval shortened
after correction of hyperkaiemia. Electrophysioiogic studies using His
bundle recording and atriai pacing in one patient revealed intraatrial
conduction delay and marked prolongation of conduction time in the
His-Purkinje system. it is concluded that conduction defects in the spe-
cialized intraventricuiar conduction system are common in hyperkaie-
mia and result in electrocardiographic patterns of fascicular block.

The electrocardiographic changes induced by hyperkalemia have re-

ceived considerable attention because of the potentially lethal nature
of this electrolytic abnormality. These changes may permit prompt
recognition of hyperkalemia and may indicate its severity. In this
communication we illustrate the spectrum of intraventricular con-
duction abnormalities associated with hyperkalemia and demonstrate
that disturbances in the specialized intraventricular conduction sys-
tem may play a significant role in these abnormalities.

Material and Methods

The electrocardiograms of 12 patients with hyperkalemia admitted to the
wards of the D. C. General Hospital and the George Washington University
Medical Center were studied. Tracings obtained during hyperkalemia and in
close temporal relation to measurement of the highest serum potassium lev-
els were analyzed and compared with tracings obtained after normalization
of serum potassium. A His bundle electrogram was recorded in one patient
From the Division of Cardiology, Department of who required temporary ventricular pacing because of repeated periods of
Medicine, The George Washington University sinus arrest. Atria1 pacing was accomplished during hyperkalemia and 5 days
Medical Center and The George Washington
later during normokalemia by placing the stimulating electrode against the
University Medical Division, D. C. General Hospi-
high lateral wall of the right atrium in the region of the right atrial-superior
tal, Washington, D. C. Manuscript accepted July
17, 1974.
vena caval junction. The acute nature of the illness in the other 11 patients
Address for reprints: Jorge C. Rios, MD, De- precluded electrophysiologic investigations.
partment of Medicine, George Washington Uni- The patients ranged in age between 14 and 82 years; seven were male and
versity Medical Center, 2150 Pennsylvania five were female. The clinical, laboratory and electrocardiographic data are
Ave., N.W., Washington, D. C. 20037. presented in Table I.

February 1975 The American Journal of CARDIOLOGY Volume 35 199

CARDIAC CONDUCTION IN HYPERKALEMIA-BASHOUR ET AL.

Results rhythm. Serum potassium values in these four pa-

Rhythm: Seven patients had sinus rhythm with tients ranged between 8.2 and 9.1 mEq/liter.
heart rates ranging from 46 to 150 beatslmin. Four Atrioventricular conduction: First degree atrio-
patients at the peak of their hyperkalemic state ex- ventricular (A-V) block was present in three pa-
hibited absence of P waves, suggesting either sino- tients, with P-R intervals ranging from 0.22 to 0.24
ventricular rhythm or junctional or idioventricular second. One patient had transient advanced A-V

FIGURE 1. Case IO. Rhythm strip of lead II

showing a period of advanced A-V block fol-
lowed by apparent sinus rhythm (rate 96/min).

TABLE I
Clinical and Electrocardiographic Data
-
Before Treatment

Electrocardiogram
___-
After Treatment
Cardiac
Serum Rhythm Serum
Electrocardiogram
K+ & Rate K+
Case Age (yr) (mEq/ (beats/ P-R QRS. lntraventricular (mEq/ P-R lntraventricular
no. & Sex Diagnosis liter) min) (msec) (msec) Conduction Other liter) (msec) Conduction Outcome
--
1 19M Overdose: methadone & 8.0 SR, 90 220 100 LPHB T 4.5 140 N Lived
secobarbital

2 26M Chronic renal failure, 5.7 SR, 92 230 80 LPHB T 4.7 150 N Lived
accelerated hyper-
tension

65M Chronic renal failure 8.8 ?SVR, ... 110 LAHB T 4.8 170 N Lived
90

28M Alcoholic cirrhosis, 7.7 SR, 88 190 125 LAHB, RBBB NSTC 4.2 130 N Died
bleeding esophageal
varices, uremia

55F COPD, CHF, progressive 8.4 ?SVR, ... 120 LPHB, T 4.6 200 Residual Died
renal failure 70 Inc. RBBB LAHB

56M Bronchogenic carcinoma 9.2 SR, 130 180 85 LAHB T, 5.1 140 N Died
with metastases, QS in
postoperative meta- VI-V3
bolic acidosis
14M Subarachnoid hemor- 7.9 SR, 110 180 80 LPHB T 5.5 160 N Lived
rhage, acute renal
failure
8 50M Hypertension, diabetes, 8.1 SR. 150 160 80 LPHB T 5.0 140 N Lived
ketoacidosis

9 82F Chronic renal failure, 9.1 ?SVR, ... 180 LAHB, RBBB T 5.1 170 N Lived
hypertension 75
10 33F Acute and chronic renal 8.2 ?SVR, ... 180 Transient ... 4.7 ... ... Died
tailure 98 advanced
A-V block

11 55F Chronic renal failure 7.9 AF, ... 140 LBBB 5.1 ... N Died
80-90
12 74M Chronic CHF with 6.8 SB, 46 240 180 LAHB, LBBB 3.6 210 LAHB Lived
azotemia

AF = atrial tibrillation; CHF = congestive heart failure; COPD = chronic obstructive pulmonary disease; Inc. = incomplete; LAHB =
left anterior hemiblock; LBBB = left bundle branch block; LPHB = left posterior hemiblock; N = normal; NSTC = nonspecific T
wave changes; RBBB = right bundle branch block; SB = sinus bradycardia; SR = sinus rhythm; SVR = sinoventicular rhythm; T =
peaked T waves.

200 February 1975 The American Journal of CARDIOLOGY Volume 35

 CARDIAC CONDUCTION IN HYPERKALEMtA-BASHOUR ET AL.

block (Fig, 1). In the patient whose His bundle elec-
trogram was recorded during a serum potassium level
of 6.8 mEq/Iiter (Case 12), the A-H interval was 142
msec and the H-V interval 100 msec, thus demon-
strating a conduction delay predominantly in the
His-Purkinje system (Fig. 2A). In the same patient a
delay in intraatrial conduction was demonstrated by
atria1 pacing, which revealed an abnormally pro-
longed latency between the pacemaker spike and the
onset of the A wave (Fig. ZB).
Intraventricular conduction: All 12 patients
demonstrated some form of reversible abnormality in
intraventricular conduction. Left posterior hemi-
block, manifested by right axis deviation of more
than +llO’ and clockwise inscription of the frontal
QRS loop, was present in five patients (Fig. 3); in one
it was accompanied by incomplete right bundle
branch block. Left anterior hemiblock, manifested by
a mean QRS axis of -45” or greater and a counter-
clockwise frontal loop, was also observed in five pa-
tients (Fig. 4); in two, it was associated with right
bundle branch block (Fig. 5) and in one with left
bundle branch biock. One of the patients who mani-
fested incomplete right bundle branch block and left

AH: 142 AH:128’

HV : 100 HV:55 II

‘-~:T--
I.
it
A H V t.,If.
!

K: 6.8 K:3.6 j’

FIGURE 2. Case 12. A, simultaneous surface leads I

and II and His bundle electrogram reveal marked pro-
longation of H-V interval during hyperkalemia. B, dur-
ing atria! pacing. The time interval between electrical
stimuli (S) and the resultant atriai activation (A) is
markedly prolonged during hyperkaiemia and shortens
after normalization of serum potassium. A-H, H-V and K: 6.8 K:3.6 :
S-A intervals in msec, potassium (K) in mEq/liter.

February 1975 The American Journal of CARDIOLOGY Volume 35 20-l

CARDIAC CONDUCTION IN HYPERKALEMIA-BASHOUR ET AL

aVR aVL aVF v5 v6

K=
8.0

K=
4.8

.
FIGURE 3. Case 1. Twelve lead electrocardiogram during hyperkalemia (K = 8.0 mEq/liter) reveals a + 120” frontal QRS axis consistent with
left posterior hemiblock. First degree atrioventricular block is also present (P-R interval 220 msec). With normalization of serum potassium, both
atrioventricular and intraventricular conduction defects were abolished.

III aVR aVL aVF VI v2 v3 v4 v5 v6

FIGURE 4. Case 8. Three serial 12 lead electrocardiograms. The first (top), recorded when serum potassium was 9.2 mEq/liter, reveals a mean
frontal QRS axis of -45’ with counterclockwise inscription of the initial forces consistent with lefi anterior hemiblock. The second tracing (mid-
dle), recorded when serum potassium was 6.3 mEq/liter, reveals almost complete normalization of the QRS axis and shortening of the P-R in-
terval. The third tracing (bottom) is entirely normal.

aVR aVL aVF Vl v2 V3 v4 V5 v6

FIGURE 5. Case 9. Two 12 lead e&trocardiograms. The first (top), recorded during severe hycerkalemia (K = 9.1 mEq/liter), shows’intraven-
tricular conduction defects manifested by right bundle branch block and left anterior hemiblock. After correction of hyperkalemia (bottom) all
conduction abnormalities were reversed.

202 February 1975 The American Journal of CARDIOLOGY Volume 35

 CARDIAC CONDUCTION IN HYPERKALEMIA-BASHOUR ET AL.

posterior hemiblock during hyperkalemia had a the pacing spike to the low atria1 sensing electrode
preexisting left anterior hemiblock that persisted (S-A interval) was much longer than normaliZ-l4 and
after correction of hyperkalemia. One patient had the prolongation was reversible after correction of
isolated left bundle branch block. hyperkalemia. Prolonged A-V nodal and especially
prolonged His-Purkinje conduction times reversible
Discussion after correction of hyperkalemia were also observed.
The electrocardiographic manifestations of hyper- In experimental hyperkalemia in the dog, multiple
kalemia are ascribed to shortening in the duration of areas of A-V block could be identified by His bundle
the transmembrane action potential, lowering of the recordings.i5
resting membrane potential and increased velocity of In an earlier study by one of us,16 it was noted that
phase 3.l The changes in the duration of action po- P-R intervals were often relatively prolonged during
tential and velocity of phase 3 are considered to be the hyperkalemic state and were consistently short-
the cause of the characteristic narrowing and peaking ened with correction of hyperkalemia. P wave
of the T wave and shortening of the Q-T interval ob- changes manifested by decreased P amplitude and
served when serum potassium exceeds 5.5 mEq/liter.s increased P duration were also reversed as hyperkale-
Further elevations of serum potassium decrease mia was corrected by hemodialysis. It was postulated
the rate of rise (dV/dt) of phase 0 and result in slower that the changes reflected conduction impairment in
ventricular depolarization,3 thus interfering with im- the atria1 myocardium due to hyperkalemia.
pulse conduction within the myocardial muscle fibers The present study illustrates the multifaceted na-
of both the atria and ventricles. Sensitivity to hyper- ture of the intraventricular conduction defects in hy-
kalemia is maximal in the atrium, less in the ventricle perkalemia and demonstrates by means of His bun-
and is least in the specialized conduction system.4,5 dle electrocardiography performed in one patient
Accordingly, impaired conductivity of the atria1 myo- that prolongation of the P-R interval may be caused
cardium may result in sinoventricular rhythm.697 In by conduction delay at any level within the conduc-
cases of severe hyperkalemia, abnormalities in ven- tion system.
tricular depolarization are due to impairment of im-
pulse transmission along the specialized ventricular Acknowledgment
conduction system as well as in the myocardial fibers. We express our appreciation to Mrs. Marlyn Baran for
The appearance in hyperkalemic patients of conduc- her patient typing of the manuscript.
tion defects that mimic fascicular blocks has been de-
scribed,8-11 but we are aware of only one previous His Addendum
bundle electrocardiogram obtained in a patient dur- Since submission of this manuscript, we have leareed of
ing hyperkalemialO; in that study a delay proximal to a study in which two patients with hyperkalemia manifest-
the His bundle was observed. In our patient intraatri- ed block above the bundle of His (Cohen H, Rosen K, Pick
al and His bundle electrograms indicated prolonged A: Disorders of impulse conduction and impulse formation
conduction times in the atria since the interval from caused by hyperkalemia in man. Am Heart J, in press).

References
1. Weidmann S: Shortening of cardiac action potential due to brief
injection of KCI following the onset of activity. J Physiol 132:
157-163, 1956
2. Surawicz B: The pathogenesis and clinical significance of pri-
mary T-wave abnormalities. In, Advances in Electrocardiogra-
phy (Schlant RC, Hurst JW, ed). New York, Grune & Stratton,
1972, p 387-388.
3. Fisch C: Relation of electrolyte disturbances to cardiac arrhyth-
mias. Circulation 47:408-419. 1973
4. Bellet S: Clinical Disorders of the Heart Beat. Philadelphia, Lee
8 Febiger, 1971, p 895
5. Surawlcz B: Relationship between electrocardiogram and elec-
trolytes. Am Heart J 73:814-834. 1967
6. Belfet S, Jedlicka J: Sinoventricular conduction and its relation
to sinoatrial conduction. Am J Cardiol 24:831-835. 1969
7. Vassalle M, Hoffman B: The spread of sinus activation during
potassium administration. Circ Res 17:285-295, 1965
8. Pryor R, Blount SG Jr: The clinical significance of true left axis
deviation. Left intraventricular blocks. Am Heart J 72:391-413,
1966
9. Ewy GA, Karllner J, Bedyneck JL Jr: Electrocardiographic axis
shift as a manifestation of hyperkalemia. JAMA 215429-432,
1971
10. Pick A, Cohen H, Rosen K, et al: Atrioventricular and intraven-
tricular block due to hyperkalemia in man (abstr). Circulation 46:
Suppl II: 11-109, 1972
11. Punja MM, Schneebaum R, Cohen J: Bifascicular block induced
by hyperkalemia. J Electrocardiol 6:71-76, 1973
12. Narula OS, Scherlag SJ, Samet P, et al: Atrioventricular block.
Am J Med 50:146-165, 1971
13. Damato AN, Lau SH, Patlon RD, et al: A study of atrioventricu-
lar conduction in man using premature atrial stimulation and His
bundie recordings. Circulation 40:61-69. 1969
14. Rosen KM, Loeb HS, Sinno MZ, et al: dardiac conduction in pa-
tients with symptomatic sinus node disease. Circulation 43:
836-844, 197 1
15. Cohen HC, GOZO EG Jr, Pick A: The nature and type of arrhyth-
mias in acute experimental hyperkalemia in the intact dog. Am
Heart J 82:777-785, 1971
16. Bastaroll J, Kremer A, Rio8 JC: Aftura de P, duration de P, y
duration del interval0 PR, en pacientes hiperpotasemicos trata-
dos con el rinon artificial. Rev Argent Cardiol 33: 1 l-14, 1966

February 1975 The American Journal of CARDIOLOGY Volume 35 203