Electrolytes and Bradycardia

This EKG displays a couple of significant pathologies. The EKG is from a female patient complaining of diffuse bilateral chest pain and hypoperfusion. It is notable that she presents at a local dialysis clinic. 

The most obvious EKG characteristic is probably the slow rate. She presents with a bradycardia that the monitor software initially diagnosed as atrial fibrillation. A quick check on the R-to-R intervals reveals that every interval is precisely 45 mm. Since atrial fib is always chaotically irregular, it is unlikely that this is the right diagnosis. The QRS complexes are narrow, meaning that the pacemaker for this rhythm is supraventricular, but there are no discernable P waves present. We have excluded a ventricular-based rhythm with the narrow QRS complexes, we have excluded a sinus rhythm because of the absence of P waves, and we have excluded atrial fib because of the regularity. This is, by exclusion, a junctional rhythm.

 We should also designate this as a junctional escape rhythm because of its slow rate. The slow junctional rate indicates that the junction has assumed the pacemaker function because the SA node is not firing at its faster, intrinsic rate. This patient is in sinus failure and that alone warrants a stat  cardiology consult. Looking at the rhythm further may reveal clues as to why the patient is in this state.

In addition to narrow, slow QRS complexes, this EKG diplays unusual T wave morphology. T waves are not typically as tall as their corresponding QRS complexes as they are here in at least half the leads. They aren’t usually this pointed either. Tall, pointy T waves can indicate hyperkalemia. This T wave abnormality, along with the inclusion of dialysis in the history paints a very strong case for hyperkalemia. 

Hyperkalemia can be classified into three stages, each with their own characteristic EKG changes. 

Early EKG changes of hyperkalemia, typically seen at a serum potassium level of 5.5-6.5 mEq/L, include the following:

Tall, peaked T waves with a narrow base, best seen in precordial leads

Shortened QT interval

ST-segment depression

At a serum potassium level of 6.5-8.0 mEq/L, the EKG typically shows the following:

Peaked T waves

Prolonged PR interval

Decreased or disappearing P wave

Widening of the QRS

Amplified R wave

At a serum potassium level higher than 8.0 mEq/L, the EKG shows the following:

Absence of P wave

Progressive QRS widening

Intraventricular/fascicular/bundle branch blocks

As the potassium level approaches 6.5-8.0 it is common to see sinus arrest like that seen in the example EKG. If the potassium goes much farther beyond that you begin to see ventricular dysfunction with wide QRS complexes, “sine wave” V tach, and rapid progression to cardiac arrest. The patient with hyperkalemia is not playing around. This is a deadly electrolyte imbalance. When the penal system executes death row inmates, it uses potassium to do the job. This patient’s initial K was 8.0 mEq/L.

Your first clue for hyperkalemia is probably going to be history. If you do not have access to lab values, you will have to pick up on clues like the tall, peaked T waves, the prolongation of PR intervals, and the vanishing P wave to gauge the severity of problem.  Field treatment can include administration of calcium to correct cardiotoxicity, bicarbonate to correct metabolic acidosis, and a beta-agonist like albuterol to stimulate increase intracellular potassium uptake. ED treatment may also include the administration of glucose and insulin or administration of emergency dialysis. In the meantime, if the patient is symptomatic of the dysrhythmias, i.e. bradycardia, it may be necessary to treat for that problem as well.

Doug Morris

No Stress Training

nostresstraining@outlook.com