Third-degree atrioventricular block associated with severe acute hyponatraemia

Background

Third-degree, or complete, atrioventricular (AV) block is a condition in which no atrial impulses from the sinoatrial node are conducted to the ventricles via the AV node.1 Third-degree AV block may occur because of anatomic disruptions to the electrical conduction system such as in congenital heart block conditions and in conditions which cause scarring or infiltration to the conduction system like myocardial ischaemia, amyloidosis, sarcoidosis, malignancy and myocarditis.2 It may also be caused by functional disorders of the conduction system induced by electrolyte derangements such as in severe hyperkalaemia and hypermagnesaemia, profound hypothyroidism, increased vagal tone, increased intracranial pressure,3 and AV nodal blocking medications such as beta blockers and calcium channel blockers.2 Third-degree AV block is rarely associated with severe acute hyponatraemia but has been described in three cases in a review of the literature.4–6

Case presentation

A man in his early 70s with history of hypertension, emphysema with 23 pack-year tobacco usage and hyperlipidaemia presented to the emergency department after a fall when he got up from his recliner. He felt weakness in his arms and legs as he stood, lost consciousness and then struck his head against the floor. Prior to this admission, the patient did not have any history of presyncope or syncopal episodes. All vitals were stable on admission. On initial examination, the patient’s cognitive status, coordination and sensation were intact, but he was found to have moderately decreased lower extremity motor strength against resistance. He was also found to have dry mucous membranes with delayed capillary refill of 3 s, indicating dehydrated status, though the patient stated that he had been drinking several bottles of water daily for the last 4 days.

Three days after his admission, the patient became delirious and encephalopathic, oriented only to person and place. His heart rate was found to be in the 30–40 s, which was refractory to atropine, so the patient was transferred to the intensive care unit (ICU) for further evaluation and management.

Investigations

On admission, laboratory workup was unremarkable save for mild acute hyponatraemia of 126 mEq/L with corresponding serum osmolality 256 mOsm/kg, urinary sodium 27 mEq/L and urine osmolality 104 mOsm/kg. Thyroid and adrenal function tests were undertaken to rule out hypothyroidism and adrenal insufficiency as causes of hyponatraemia and bradycardia and were normal to be within normal limits.

CT head on admission revealed 13 mm extra-axial focal subdural haematoma over right parietal convexity. CT cervical spine revealed chronic degenerative changes without acute fracture. Repeat CT head images attained 1 day and 3 days after admission showed interval decrease in size of haematoma to 11 mm and 7 mm, respectively.

On transfer to the ICU, sodium acutely dropped to 115 mEq/L from 134 mEq/L the day prior with serum osmolality 244 mOsm/kg, urine sodium 26 mEq/L and urine osmolality 345 mOsm/kg. Electrocardiography (ECG) revealed new-onset third-degree AV block. Transthoracic echocardiography (TTE) revealed left ventricular global hypokinesis with mid-range ejection fraction of 49% and grade I diastolic dysfunction without regional wall motion abnormalities. High-sensitivity troponin I was mildly elevated at 33 ng/L, which subsequently normalised.

Differential diagnosis

Patient’s bradycardia which was refractory to multiple doses of atropine led to transfer to the ICU. ECG revealed new-onset third-degree AV block which prompted further investigation into the patient’s electrolyte status, renal function, thyroid function, medications and cardiac function. Cardiac aetiology was ruled out with TTE and troponin testing. AV nodal blocking medications like beta blockers and calcium channel blockers were not used by the patient and the patient’s potassium, magnesium and thyroid levels were within normal limits.

Subdural haematoma itself is rarely a cause of third-degree AV block but has been described in individuals with large temporal subdural haematomas causing increased intracranial pressure.3 In this patient, there were no signs of increased intracranial pressure including lack of papilloedema on fundoscopic examination. Moreover, this patient’s subdural haematoma was small and in the parietal region.

As the patient’s hyponatraemia resolved with treatment, the patient soon thereafter returned to his intrinsic normal sinus rhythm with heart rate in the 70s as was prior to his admission. The cause of the patient’s hyponatraemia was thought to be multifactorial related to syndrome of inappropriate antidiuretic hormone (SIADH) with superimposed polydipsia and mild dehydration. Though the patient’s volume status was mildly hypovolaemic on admission with dry mucus membranes, the patient stated that he had been drinking a large amount of water for the last 4 days prior to admission. This amount of water diluted the patient’s urine leading to a lower urinary sodium and osmolality on admission. When the patient’s sodium acutely declined to 115 mEq/L, his urinary osmolality was found to be higher than his serum osmolality consistent with SIADH related to his subdural haematoma. These compounding factors led to labile sodium levels which impacted the patient’s AV nodal system leading to third-degree AV block.

Hyponatraemia-induced third-degree AV block was initially not considered due to the rarity of its finding. Since other usual causes were ruled out including other electrolyte abnormalities, thyroid disease and myocardial infarction, the patient’s third-degree AV block was established to be induced by his acute severe hyponatraemia.

Treatment

Neurosurgery recommended no intervention for the patient’s small acute right subdural haematoma, so the patient was monitored for acute neurological changes.

In the ICU, the patient’s bradycardia was initially treated with multiple atropine dosages as per advanced cardiac life support (ACLS) protocol without improvement. After ECG revealed third-degree AV block, a transvenous pacer was placed into the patient’s right internal jugular vein which was paced at 70 bpm in ventricular-paced ventricular-sensed inhibition-response (VVI) mode.

The patient’s acute severe hypo-osmolar multifactorial hyponatraemia was treated initially with hypertonic saline infusion for 1 day and then the patient was transitioned to salt tablets with 1.5 L fluid restriction. The sodium increased at a slow rate of 5 mEq/24 hours to prevent osmotic demyelination syndrome in the context of this patient’s acute right subdural haematoma. No desmopressin boluses were needed for overcorrection.

Outcome and follow-up

The patient’s sodium returned to 130 mEq/L 3 days after transfer to the ICU. As the patient’s sodium approached normalisation over those 3 days, the patient required fewer paced beats so the transvenous pacer was gradually decreased to 65–60 bpm in VVI. It was discontinued when his sodium returned to normal as he no longer had any paced beats and he returned to his intrinsic normal sinus rhythm with heart rate in the 70s. The patient was kept on telemetry after transfer from the ICU to a step-down unit, which revealed no further arrhythmias. Cardiology removed the transvenous pacer and did not recommend permanent pacemaker placement as the third-degree AV block was found to be associated entirely with the patient’s sodium levels. They placed the patient on an extended cardiac Holter monitor with planned outpatient follow-up. The patient was discharged to acute rehabilitation to regain strength, and on discharge from the rehabilitation centre, he had no focal deficits secondary to his subdural haematoma or any arrhythmic episodes.