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A man in his mid-80s with a past medical history of diabetes and stage 5 chronic kidney disease was brought to the hospital by medics with two days of nausea, vomiting, and generalized weakness. He said he had no chest pain, difficulty breathing, fever, chills, abdominal pain, diarrhea, melena, or other symptoms.

He already had a functioning dialysis fistula but had not yet started dialysis. His medications included losartan, amlodipine, furosemide, sitagliptin, and clopidogrel, and he was normotensive, with a heart rate in the low 30s.

His extremities were warm and well perfused with a palpable thrill in the left arm. He was not confused, and he also had faint crackles in the lung bases bilaterally with trace lower extremity edema.

An ECG was done, and the computer read it as a rate of 64 bpm, an uncertain irregular rhythm, and an intraventricular conduction delay. What is the most likely cause of the ECG findings in this patient? BRASH syndrome, hyperkalemia, acute coronary syndrome, or hypocalcemia?

The ECG showed an atrial rate in the low 40s with a long PR interval that became a bit longer before dropping a QRS. The ventricular rate was about 30, but the computer appeared to be counting the peaked T-waves as a QRS and was therefore reading a rate of 64 bpm. The rhythm was most consistent with a Mobitz type I second-degree heart block. Bradycardia, AV block, and peaked T-waves are all potentially concerning for hyperkalemia, but together they are especially suggestive. The PR interval increased only slightly before the dropped beat, so it appeared to mimic Mobitz type II.

Complete or third-degree heart block occurs when depolarization cannot be conducted via the atrioventricular (AV) node to the ventricle, and a ventricular automaticity foci escape rhythm is generated at or below the bundle of His. A complete block that involves the proximal AV node leaves the distal AV node to produce a junctional escape rhythm and therefore may result in a narrow QRS complex.

Origination in the bundle of His also is narrow. Complete block of the entire AV node or bundle of His leaves only the ventricle to produce an escape rhythm and therefore generates a wide QRS complex. Complete or third-degree heart block on an ECG presents as complete atrioventricular dissociation in which P-waves are not associated with QRS complexes.

Second-degree AV block has two subtypes. Like third-degree, or complete, heart block, a Mobitz type II block occurs at or below the AV node and therefore is not responsive to atropine. Depolarizations in Mobitz type II block are only intermittently blocked. Mobitz type II can be identified by a series of normal P-QRS cycles (representing normal conduction between the atria and the ventricles) followed by nonconducted or blocked depolarizations below the AV node.

A P-wave is not followed by a QRS complex when this occurs. The PR interval remains constant in Mobitz type II (also termed Wenckebach), where the block occurs within the AV node. This block presents as progressively prolonging PR intervals until an atrial conduction is completely blocked at the level of the AV node, resulting in a dropped QRS complex. The AV node is innervated by the parasympathetic nervous system, so a Mobitz type I block may respond to atropine. First-degree AV block also occurs when conduction through the AV node is delayed but ultimately conducted, resulting in a prolonged PR interval (>0.2 s). It is also responsive to atropine, like a Mobitz type I block.

This patient had hyperkalemia. His troponin was <0.03 ng/mL with a potassium of 6.7 mmol/L and a pH of 7.1. Transcutaneous pacer pads were placed, and he received calcium gluconate, insulin, dextrose, albuterol, furosemide, and one amp of sodium bicarbonate. He remained normotensive with intact mentation throughout.

Nephrology was consulted for emergency dialysis, and he was started on a dopamine drip during dialysis and admitted to the intensive care unit. His hyperkalemia resolved, but he remained in heart block, so a permanent pacemaker was placed.

Hyperkalemia may present in various forms on the ECG, including peaked T-waves or a slow wide complex rhythm, and it is critically important to recognize. Bradycardia occurs because the atrioventricular node is sensitive to hyperkalemia. The His-Purkinje cells are also suppressed by hyperkalemia and are unable to generate reliable escape rhythms. Hyperkalemia is often caused by end-stage renal disease. Other acute etiologies include cell lysis (rhabdomyolysis, tumor lysis syndrome) and digoxin toxicity.

BRASH syndrome (Bradycardia, Renal failure, AV nodal blockage, Shock, and Hyperkalemia) may occur if the patient is on a beta blocker or nondihydropyridine calcium channel blocker (verapamil, diltiazem). BRASH syndrome may occur at lower potassium ranges, from 5.5 to 7 mmol/L.

Tenets of critical hyperkalemia management include calcium to stabilize the cardiac membrane and insulin, albuterol, and furosemide to shift potassium intracellularly. If a patient becomes hemodynamically unstable, an epinephrine drip can be initiated to increase the heart rate and stimulate beta-2 receptors to further shift potassium intracellularly.

This case report was written by Julia Sobel, MD, a third-year emergency medicine resident at the University of California San Diego, and was peer-reviewed by Stephen W. Smith, MD, of Dr. Smith's ECG Blog (https://bit.ly/306xAeq ) and Dr. Pregerson.

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Dr. Pregersonis an emergency physician with Palomar and Tri-City medical centers in San Diego. He is the author of the Emergency Medicine 1-Minute Consult, the 8-in-1 Emergency Department Quick Reference, the A-to-Z Emergency Pharmacopoeia & Antibiotic Guide, and Think Twice: More Lessons from the ER. Follow him on Twitter@EM1MinuteGuru , and visit his websiteshttps://www.erpocketbooks.com/ andhttps://em1minuteconsult.com . Read his past columns athttp://bit.ly/BradyCardiaEMN .

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