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Cardiac Conduction Defects Associated With Hyponatremia: A 75-Year-Old Woman With Hypertension and Paroxys
Cardiac Conduction Defects Associated With Hyponatremia: A 75-Year-Old Woman With Hypertension and Paroxys
Summary: Cardiac conduction defects have not been previ- logical basis for these is serum hypo-osmolality which in
ously described in association with hyponatremia, although turn causes neuronal cell swelling and dysfunction.*
in patients with congestive heart failure the frequency of Clinical cardiac toxicity associated with hyponatremia
ventricular premature beats was found to correlate to the has not been described, although in patients with conges-
severity of' hyponatremia. We describe three patients with tive heart failure it was shown that the number of ventric-
second-degree or complete atrioventricular (AV) block ular premature beats (VPBs) correlated to the same degree
which occurred during or shortly after an episode of se- with the severity of either hyponatremia or hypokalemia.
vere hyponatremia. The first had thiazide-induced In this report we describe three patients who developed
hyponatremia while on amiodamne. In the second, definite reversible cardiac conduction defects temporally associated
etiology for hyponatremia which was associated with long- with hyponatremia or its correction.
standing polydipsia could not be established. The third had
ischemic heart disease and intermittent conversion of his
first-degree to second-degree AV block while hyponatremic Patient 1
after diuretics use. Although it is usually difficult to single
out hyponatremia as the cause of conduction defects which A 75-year-old woman with hypertension and paroxys-
usually occur in the presence of cardiac disease, potent mal atrial fibrillation was treated by digoxin 0.25 mg and
medications or other electrolyte abnormalities, we suggest amiodarone 200 mg daily. One week prior to admission
that hyponatremia may play a role in the pathogenesis of Kaluril (hydrochlorothiazide 50 mg, amiloride 5 mg) was
conduction defects in the diseased heart. started. She was admitted because of progressive weak-
ness. On examination she was oriented. The pulse was
regular at 68/min, and blood pressure was 130/90 mmHg.
Key wards: heart block, hyponatremia
Cardiac examination was unremarkable and the rest of the
physical examination was normal. Electrocardiogram
Introduction showed first-degree atrioventricular (AV) block with P-
R interval of 0.24 s and complete left bundle-branch block
Hyponatremia, the most common electrolyte disorder (CLBBB). A few hours later she became confused. Blood
in hospitalized patients is usually asymptomatic. I When pressure was unchanged and on ECG complete AV block
clinical manifestations of hyponatremia do occur they are appeared, requiring insertion of a temporary pacemaker.
usually related to central nervous system dysfunction: con- Pacemaker insertion did not alter mental status. Serum so-
fusion, convulsions, coma, and death. The pathophysio- dium concentration at that time was 120 mmol/l and potas-
sium was 5 mmol/l (Table I). When serum sodium reached
126 mmol/l, the patient became oriented and the ECG
showed 2: 1 AV block. A day later ECG showed normal
sinus rhythm and CLBBB. The CLBBB disappeared when
serum sodium level rose above 130 mmol/l. There was
Address for reprints: no electrocardiographic or enzymatic evidence of my-
Zvi Farlel, M.D.
ocardial infarction. Serum digoxin concentration on ad-
Department of Internal Medicine E mission was 0.3 ng/ml.
Sheba Medical Center
Tel Hashomer 5262 I Comment
Israel
Received: April 2, 1990 The patient presents a case of thiazide-induced
Accepted with revision: July I , 1990 hyponatremia, which typically occurs in elderly women
166 Clin. Cardiol. Vol. 14. Fcbruary 1991
Patient I
1 CLBBB, and first-degree
A V block (P-R 0.24S )
I 120 5 .O Completc AV block
2 117 5.3 18 Complete A V block
alternating with CLBBB
3 126 4.8 24 2:l A V block. CLBBB
4 131 5.1 22 Normal sinus rhythm
5 128 5.I Normal sinus rhythm
6 137 4.9 24 Normal sinus rhythm
7 14 I 5.3 Normal sinus rhythm
Patient 2
I 108 4.1 First-degree A V block
(P-R 0.44 S )
I29 4.7 20 P-R 0.34s
134 4.2 20 Wcnkebach type AV block
I39 4.2 16 Normal sinus rhythm
147 4.1 14 Nomial sinus rhythm
142 4.0 Normal sinus rhythm
140 4.2 20 Normal sinus rhythm
Ahbreviutions: CLBBB=complete left bundle-branch block, AV =atrioventricular.
with prolonged and profound hypothermia ( <30°C),and development of second-degree AV block. This defect was
to the best of our knowledge second-degree AV block has not documented in previous hospitalizations when he was
never been associated with the mild degree of hypother- not hyponatremic, or in the last weeks of his life, when
mia observed in our patient. It is more plausible, there- he was only mildly hyponatremic. It is interesting that dur-
fore, that hyponatremia was involved in the conduction ing the period of moderate to severe hyponatremia, the
system abnormalities, since the latter were noted on ad- second-degree AV block was only intermittent. This may
mission and improved upon correction of hyponatremia. further indicate that hyponatremia was not the only ab-
The delayed appearance of Wenkebach type AV block is normality responsible for the conduction defect.
interesting, since it may represent a delayed type of dys-
function, analogous to the cerebral dysfunction encoun-
tered after correction of hyponatremia. l o Discussion
that hyponatremia may aggravate or cause cardiac con- 5 . Friedman E, Shadel M , Halkin H, Farfel Z:Thiazidc-induced
duction defects in a diseased heart. hyponatremia: Reproducibility by single dose rcchallenge in-
cluding an analysis of pathogenesis. Ann Intcwi Mrd 110. 24
In the specific hyponatremic patient, ascribing conduc-
( 1989)
tion defect to hyponatremia is usually complicated by other 6. Leehey DJ, Picache AA, Robertson GL: Hyponatremia in quad-
coexisting conditions which may have a direct deleteri- riplegic patients. CIin Sci 75, 441 (1988)
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mia). The clinical course of the three patients herein 8. Clements SD, Hurst JW: Diagnostic value of electrocardio-
graphic abnormalities in subjects accidentally exposed t o cold.
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The association between cardiac conduction defects and (1971)
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