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 
