Clin. Cardiol. 14, 165-168 (1991)
Cardiac Conduction Defects Associated with Hyponatremia M. MOUALLEM. M.D., E. FRIEDMAN, M.D., Y .
SHEMESH, M.D..*
H. MAYAN, M.D.. R. PAUZNER, M.D.,
z. FARFEL,M.D.
Departments of Internal Medicine E, and *Cardiology, Chaim Sheba Medical Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
Summary: Cardiac conduction defects have not been previously described in association with hyponatremia, although in patients with congestive heart failure the frequency of ventricular premature beats was found to correlate to the severity of' hyponatremia. We describe three patients with second-degree or complete atrioventricular (AV) block which occurred during or shortly after an episode of severe hyponatremia. The first had thiazide-induced hyponatremia while on amiodamne. In the second, definite etiology for hyponatremia which was associated with longstanding 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 after diuretics use. Although it is usually difficult to single out hyponatremia as the cause of conduction defects which usually occur in the presence of cardiac disease, potent medications or other electrolyte abnormalities, we suggest that hyponatremia may play a role in the pathogenesis of conduction defects in the diseased heart.
Key wards: heart block, hyponatremia Introduction Hyponatremia, the most common electrolyte disorder in hospitalized patients is usually asymptomatic. I When clinical manifestations of hyponatremia do occur they are usually related to central nervous system dysfunction: confusion, convulsions, coma, and death. The pathophysio-
Address for reprints: Zvi Farlel, M.D. Department of Internal Medicine E Sheba Medical Center Tel Hashomer 5262 I Israel Received: April 2, 1990 Accepted with revision: July I , 1990
logical basis for these is serum hypo-osmolality which in turn causes neuronal cell swelling and dysfunction.* Clinical cardiac toxicity associated with hyponatremia has not been described, although in patients with congestive heart failure it was shown that the number of ventricular premature beats (VPBs) correlated to the same degree with the severity of either hyponatremia or hypokalemia. In this report we describe three patients who developed reversible cardiac conduction defects temporally associated with hyponatremia or its correction.
Patient 1 A 75-year-old woman with hypertension and paroxysmal atrial fibrillation was treated by digoxin 0.25 mg and amiodarone 200 mg daily. One week prior to admission Kaluril (hydrochlorothiazide 50 mg, amiloride 5 mg) was started. She was admitted because of progressive weakness. On examination she was oriented. The pulse was regular at 68/min, and blood pressure was 130/90 mmHg. Cardiac examination was unremarkable and the rest of the physical examination was normal. Electrocardiogram showed first-degree atrioventricular (AV) block with PR interval of 0.24 s and complete left bundle-branch block (CLBBB). A few hours later she became confused. Blood pressure was unchanged and on ECG complete AV block appeared, requiring insertion of a temporary pacemaker. Pacemaker insertion did not alter mental status. Serum sodium concentration at that time was 120 mmol/l and potassium 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 no electrocardiographic or enzymatic evidence of myocardial infarction. Serum digoxin concentration on admission was 0.3 ng/ml. Comment
The patient presents a case of thiazide-induced hyponatremia, which typically occurs in elderly women
Clin. Cardiol. Vol. 14. Fcbruary 1991
166
TABLEI Coursc of electrolyte and electrocardiographic changes in two patients Hospitalization day
Serum sodium (mmol/l)
Serum potassium (mmol/l)
Serum bicarbonate (minol/l)
ECC
Patient I 1
I 2
120 117
5 .O 5.3
3
126 131 128 137 14 I
4.8 5.1 5.I 4.9 5.3
108
4.1
I29 134
4.7 4.2 4.2 4.1 4.0 4.2
4 5 6
7 Patient 2 I
I39
147 142 140 Ahbreviutions:
18
24 22 24
20 20 16
14 20
CLBBB, and first-degree A V block (P-R 0.24S ) Completc AV block Complete A V block alternating with CLBBB 2:l A V block. CLBBB Normal sinus rhythm Normal sinus rhythm Normal sinus rhythm Normal sinus rhythm
First-degree A V block (P-R 0.44 S ) P-R 0.34s Wcnkebach type AV block Normal sinus rhythm Nomial sinus rhythm Normal sinus rhythm Normal sinus rhythm
CLBBB=complete left bundle-branch block, AV =atrioventricular.
a few days after thiazide therapy is ~ t a r t e d . The ~ unusual appearance of conduction defects could not be explained solely by a diseased conduction system, myocardial ischemia, or by amiodarone or digoxin therapy. The close temporal association between the totally reversible conduction defect and hyponatremia strongly suggests that hyponatremia played a role in the pathogenesis of the conduction defect.
Patient 2 A 33-year-old man was admitted because of confusion. The patient sustained traumatic quadriplegia at age 20, and because of an indwelling permanent urinary catheter he used to drink large quantities of water. Five days prior to admission he developed diffuse abdominal pains, nausea, vomiting, and diarrhea, and later became drowsy and dysarthric. On admission he was confused, his rectal temperature was 33"C, blood pressure was 110/60 mmHg, pulse rate was 52 beatdmin, hemoglobin concentration was 90 g/l and serum sodium concentration was 108 mmol/l. ECG showed sinus bradycardia with first-degree A V block, P-R interval of0.44 s, and J waves. Hyponatremia was corrected by hypertonic saline, and serum sodium concentration of 129 mmol/l was measured after 22 h (Table I). The patient became more oriented, his temperature rose to 36"C, and the P-R intcrval shortened (0.34 s), however, 8 h later he became confused again. Serum
sodium, blood pressure, and body temperature wcrc all normal. Wenkebach type second-dcgrce AV block appeared on ECG. This electrocardiographic abnormality as well as the sinus bradycardia and the first-degree AV block spontaneously disappeared after 24 h (Table I). His confusion lasted a few more days until complete recovcry ot mental function. Serum cortisol and thyroxine concentrations as well a5 chest x-rays were normal. The EECi showed diffuse abnormality compatible with the severe electrolyte disturbance. Cerebral computerized tomography and examination of the ccrebrospinal fluid were normal. Thus, no definite cause for the hyponatrcniia could be established. It was attributed partially at least to cxcessive drinking.'j
Comments The cause of the hyponatremia in this paticnt was not definitively established. Theoretically, a viral disease could account for most or all clinical manifestations: myocarditis, encephalitis, and concomitantly and indirectlyhyponatremia.' No known virus could be dernonstratcd in blood or cerebro spinal fluid (CSF) and thc EEG findings argue against herpes encephalitis. Alternativcly, thc hypothermia observed could have contributed to the ECG changes. Hypothermia-associated ECG abnormalitics include bradycardia, atrial fibrillation, prolonged Q-T interval, first-degree AV block, and the pathognomonic J waves. 8 . 9 However, these changes are usually associatcd
M. Mouallem et d . : Cardiac conduction defects and hyponatremia
with prolonged and profound hypothermia (
Cardiac Conduction Defects Associated with Hyponatremia M. MOUALLEM. M.D., E. FRIEDMAN, M.D., Y .
SHEMESH, M.D..*
H. MAYAN, M.D.. R. PAUZNER, M.D.,
z. FARFEL,M.D.
Departments of Internal Medicine E, and *Cardiology, Chaim Sheba Medical Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
Summary: Cardiac conduction defects have not been previously described in association with hyponatremia, although in patients with congestive heart failure the frequency of ventricular premature beats was found to correlate to the severity of' hyponatremia. We describe three patients with second-degree or complete atrioventricular (AV) block which occurred during or shortly after an episode of severe hyponatremia. The first had thiazide-induced hyponatremia while on amiodamne. In the second, definite etiology for hyponatremia which was associated with longstanding 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 after diuretics use. Although it is usually difficult to single out hyponatremia as the cause of conduction defects which usually occur in the presence of cardiac disease, potent medications or other electrolyte abnormalities, we suggest that hyponatremia may play a role in the pathogenesis of conduction defects in the diseased heart.
Key wards: heart block, hyponatremia Introduction Hyponatremia, the most common electrolyte disorder in hospitalized patients is usually asymptomatic. I When clinical manifestations of hyponatremia do occur they are usually related to central nervous system dysfunction: confusion, convulsions, coma, and death. The pathophysio-
Address for reprints: Zvi Farlel, M.D. Department of Internal Medicine E Sheba Medical Center Tel Hashomer 5262 I Israel Received: April 2, 1990 Accepted with revision: July I , 1990
logical basis for these is serum hypo-osmolality which in turn causes neuronal cell swelling and dysfunction.* Clinical cardiac toxicity associated with hyponatremia has not been described, although in patients with congestive heart failure it was shown that the number of ventricular premature beats (VPBs) correlated to the same degree with the severity of either hyponatremia or hypokalemia. In this report we describe three patients who developed reversible cardiac conduction defects temporally associated with hyponatremia or its correction.
Patient 1 A 75-year-old woman with hypertension and paroxysmal atrial fibrillation was treated by digoxin 0.25 mg and amiodarone 200 mg daily. One week prior to admission Kaluril (hydrochlorothiazide 50 mg, amiloride 5 mg) was started. She was admitted because of progressive weakness. On examination she was oriented. The pulse was regular at 68/min, and blood pressure was 130/90 mmHg. Cardiac examination was unremarkable and the rest of the physical examination was normal. Electrocardiogram showed first-degree atrioventricular (AV) block with PR interval of 0.24 s and complete left bundle-branch block (CLBBB). A few hours later she became confused. Blood pressure was unchanged and on ECG complete AV block appeared, requiring insertion of a temporary pacemaker. Pacemaker insertion did not alter mental status. Serum sodium concentration at that time was 120 mmol/l and potassium 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 no electrocardiographic or enzymatic evidence of myocardial infarction. Serum digoxin concentration on admission was 0.3 ng/ml. Comment
The patient presents a case of thiazide-induced hyponatremia, which typically occurs in elderly women
Clin. Cardiol. Vol. 14. Fcbruary 1991
166
TABLEI Coursc of electrolyte and electrocardiographic changes in two patients Hospitalization day
Serum sodium (mmol/l)
Serum potassium (mmol/l)
Serum bicarbonate (minol/l)
ECC
Patient I 1
I 2
120 117
5 .O 5.3
3
126 131 128 137 14 I
4.8 5.1 5.I 4.9 5.3
108
4.1
I29 134
4.7 4.2 4.2 4.1 4.0 4.2
4 5 6
7 Patient 2 I
I39
147 142 140 Ahbreviutions:
18
24 22 24
20 20 16
14 20
CLBBB, and first-degree A V block (P-R 0.24S ) Completc AV block Complete A V block alternating with CLBBB 2:l A V block. CLBBB Normal sinus rhythm Normal sinus rhythm Normal sinus rhythm Normal sinus rhythm
First-degree A V block (P-R 0.44 S ) P-R 0.34s Wcnkebach type AV block Normal sinus rhythm Nomial sinus rhythm Normal sinus rhythm Normal sinus rhythm
CLBBB=complete left bundle-branch block, AV =atrioventricular.
a few days after thiazide therapy is ~ t a r t e d . The ~ unusual appearance of conduction defects could not be explained solely by a diseased conduction system, myocardial ischemia, or by amiodarone or digoxin therapy. The close temporal association between the totally reversible conduction defect and hyponatremia strongly suggests that hyponatremia played a role in the pathogenesis of the conduction defect.
Patient 2 A 33-year-old man was admitted because of confusion. The patient sustained traumatic quadriplegia at age 20, and because of an indwelling permanent urinary catheter he used to drink large quantities of water. Five days prior to admission he developed diffuse abdominal pains, nausea, vomiting, and diarrhea, and later became drowsy and dysarthric. On admission he was confused, his rectal temperature was 33"C, blood pressure was 110/60 mmHg, pulse rate was 52 beatdmin, hemoglobin concentration was 90 g/l and serum sodium concentration was 108 mmol/l. ECG showed sinus bradycardia with first-degree A V block, P-R interval of0.44 s, and J waves. Hyponatremia was corrected by hypertonic saline, and serum sodium concentration of 129 mmol/l was measured after 22 h (Table I). The patient became more oriented, his temperature rose to 36"C, and the P-R intcrval shortened (0.34 s), however, 8 h later he became confused again. Serum
sodium, blood pressure, and body temperature wcrc all normal. Wenkebach type second-dcgrce AV block appeared on ECG. This electrocardiographic abnormality as well as the sinus bradycardia and the first-degree AV block spontaneously disappeared after 24 h (Table I). His confusion lasted a few more days until complete recovcry ot mental function. Serum cortisol and thyroxine concentrations as well a5 chest x-rays were normal. The EECi showed diffuse abnormality compatible with the severe electrolyte disturbance. Cerebral computerized tomography and examination of the ccrebrospinal fluid were normal. Thus, no definite cause for the hyponatrcniia could be established. It was attributed partially at least to cxcessive drinking.'j
Comments The cause of the hyponatremia in this paticnt was not definitively established. Theoretically, a viral disease could account for most or all clinical manifestations: myocarditis, encephalitis, and concomitantly and indirectlyhyponatremia.' No known virus could be dernonstratcd in blood or cerebro spinal fluid (CSF) and thc EEG findings argue against herpes encephalitis. Alternativcly, thc hypothermia observed could have contributed to the ECG changes. Hypothermia-associated ECG abnormalitics include bradycardia, atrial fibrillation, prolonged Q-T interval, first-degree AV block, and the pathognomonic J waves. 8 . 9 However, these changes are usually associatcd
M. Mouallem et d . : Cardiac conduction defects and hyponatremia
with prolonged and profound hypothermia (
