Everyday EBM - EKG Challenge #3 Case Conclusion - Mind Your P's and K's

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Everyday EBM
An educational blog by the Emergency Medicine residents at Washington University in St.Louis. #FOAMed
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SUNDAY,NOVEMBER9,2014

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EKGChallenge#3CaseConclusionMindyourp'sandK's.
You are working on a busy night in TCC when an elderly lady is brought in by EMS with a
complaint of dizziness. The paramedic looks a bit more stressed than you expect for the
average old lady with a case of the dizzies and rightly so. As he reports her vital signs, you
are shocked to hear that her HR has been steadily below 30 with a systolic blood pressure
in the 80s and youre even more shocked to hear that shes awake! She reports feeling
generally weak and thinks she has the stomach flu. As the nurses get down to business
placing the patient on the monitor and obtaining IV access, the tech hands you this EKG.

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You note the absence of P waves, widened QRS and prominent T wave. You place the
patient on an external pacer and run through your differential. Did she overdose on her
antihypertensives? Is she having an MI? Does she have heart block? Something else?
You ask your nurse to get a whole blood potassium and give the patient calcium gluconate
as you set up for internal pacing. As youre ready to pass the pacer, you hear that her
whole blood potassium is nearly 7. You aggressively treat her hyperkalemia with
insulin/dextrose, albuterol, IV fluids and give renal a call. To your relief, her pulse and BP
improve dramatically.

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Given the importance of recognizing the EKG changes of acute hyperkalemia (indeed, you
will save a life by doing so), you decide to take a moment to review the breadth of EKG
findings associated with hyperkalemia, the sensitivity/specificity of these findings, and a

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EverydayEBM:EKGChallenge#3CaseConclusionMindyourp'sandK's.

little about the electrophysiology of why these changes happen.


EKG findings of hyperkalemia: Remember, Hyper-K is the syphilis of EKGs.
Classic EKG findings of hyperkalemia are peaked Twaves, QRS widening and prolongation
of the PR interval [Ref 1]. But beware, these classics are not the only EKG abnormalities
observed in hyperkalemia! As serum potassium increases, p wave amplitude decreases
until p waves disappear entirely and intraventricular, fascicular and bundle branch blocks
can occur in severe hyperkalemia. At extremes, QRS widening becomes so pronounced
and a sine-wave pattern develops and eventually deteriorates to VF and asystole. It is
important to note that while common and widely recognized, T waves can appear
reassuringly normal in a patient with LVH and chronically inverted lateral T waves to have
pseudonormalization of their T waves during an acute hyperkalemic episode.
But what about sensitivity and specificity of EKG changes as a rapid assessment for
hyperkalemia? Unfortunately, they are not great. A retrospective case study found a
sensitivity of only 52% for ANY EKG change in hyperkalemia [Ref 2]. Additionally the
presence of new or resolving peaked T waves was not significantly associated with serum
potassium concentration. When evaluating an EKG with a prominent T wave it is
important to remember than other important disease processes can induce tall T waves,
including acute MI and benign early repolarization (BER) [Ref 3]. Eventhough the T waves
are tall in all these conditions, there are some morphological differences that can help
you distinguish between them:

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Figure Modified from Reference 3 with additional tracings

- Normal T waves are symmetric. The amplitudes are usually greatest in leads II and V4,
are greater in men than women, and decrease with age. Generally accepted upper limits of
normal T-wave amplitude are 0.50 mV in the limb leads and 1.0 mV in precordial leads.
- Hyperacute T waves of acute MI:The T waves are typically broad, prominent, and
asymmetric (can sometimes be symmetric). The T waves are often associated with
reciprocal ST segment depression in other leads. The R wave also increases in amplitude
and the J point (end of QRS and beginning of ST segment) may be elevated.
- Peaked T waves of hyperkalemia: Often described as tall, peaked, symmetric T waves.
With further progression of hyperkalemia, the T wave tends to become taller with
eventual QRS complex widening. Sometimes in severe hyperkalemia with QRS complex
widening, there may also be some ST elevation that simulate an infarction pattern. It has
also been observed that a terminal slur in the QRS complex or an S wave in lead I or V6
without gross QRS widening is commonly associated with hyperkalemic T waves.

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- Benign Early Repolarization (BER): This is a variant of the normal ECG, found in people

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EverydayEBM:EKGChallenge#3CaseConclusionMindyourp'sandK's.

of all ages, but more common in young men. In BER, there is "(1) ST-segment elevation;
(2) upward concavity if the initial portion of the QRS complex; (4) widespread or diffuse
distribution of ST-segment elevation on the ECG; and (6) relative temporal stability." (Ref
3). Click here for a review by Amal Mattu on the differences between EKG findings of BER
and endocarditis.

BLOGDISCLAIMER

Unfortunately, many of the discussed features above are not exclusive to certain
conditions. These T wave changes can also been seen in LVH, pre-excitation syndromes,
bundle branch block, and acute pericarditis. When evaluating an ECG, the physician must
also consider age, comorbidities, and presenting complaint and overall clinical picture.

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Throwback to Medical School: Why does hyperkalemia result in a peaked T on the EKG?

Comments

First, lets think a little bit about potassium. The normal extracellular potassium
concentration (what we ask the lab guys to measure) is around 4 4.5mEq/L, but this
represents only a tiny fraction of total body potassium as 95% is intracellular. The kidneys
take the lead in potassium regulation, with the gut getting rid of only about 10%.
If we shift our focus over to the cardiac myocyte in particular well remember that
potassium and sodium are the major role players. Potassium is concentrated
intracellularly and sodium is hanging out extracellularly. The good old Sodium-Potassium
pump is keeping the peace, the peace being a negative resting membrane potential. The
concentration gradient across this membrane plays an important role in maintaining this
action potential. As the extracellular potassium concentration increases, the resting
membrane potential gets less negative. This is important because the resting membrane
potential (the flat part before the action potential gets going) directly impacts the number
of voltage-gated sodium channels available to generate the action potential. Fewer
sodium channels means slower impulse conduction and prolonged membrane
depolarization. How do we see this? QRS widening, P wave prolongation, PR widening.
What about the peaked T?! This is where it gets a little weird. Remember that the T wave
represents repolarization, or phase 3 of the cardiac action potential when the calcium
channels have closed and the potassium channels remain open. For some crazy reason
Not well understood per the literature, increased extracellular potassium leads these
channels to pump more potassium out of the cell, shortening repolarization, producing
the much talked about peaked T. Check out the Figure below from Parham et al. (Ref 4).

Fig. 3 Illustration of a normal action potential (solid line) and the action potential as seen in the setting of hyperkalemia (interrupted
line). The phases of the action potential are labeled on the normal action potential. Note the decrease in both the resting membrane
potential and the rate of phase 0 of the action potential (Vmax) seen in hyperkalemia. Phase 2 and 3 of the action potential have a
greater slope in the setting of hyperkalemia compared with the normal action potential.

Take home points:


- While EKG findings are common, they have poor sensitivity and specificity for
hyperkalemia.
-Common findings include peaked T waves, PR prolongation, P wave flattening, QRS
widening all eventually producing sine wave ECG, Vfib and asystole.
-Underlying conduction abnormalities and history of CKD can impact the EKG
morphology at various K levels.
- The "tall T wave" has a differential diagnosis. T wave morphology can give you
important clues to your diagnosis.
Submitted by Sara Manning, PGY-3 and Steven Hung, PGY-2.
Faculty Reviewed by Doug Char
References:
[1] Amal Mattu, William J Brady and David A Robinson. Electrocardiographic
Manifestations of Hyperkalemia, American Journal of Emergency Medicine. 2000; 18:
721-729.

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EverydayEBM:EKGChallenge#3CaseConclusionMindyourp'sandK's.

[2]Montague, B et al, Retrospective review of the Frequency of ECG changes in


Hyperkalemia, Clinical Journal of the American Society of Nephrology. 2008. (3); 324330.
[3]Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T wave:
Electrocardiographic differential diagnosis. American Journal of Emergency Medicine
2002;20(3):243-251
[4] Walter A Parham, Ali A Mehdirad, Kurt M Biermann and Carey S Fredman.
Hyperkalemia Revisited. Texas Heart Institute Journal. 2006; 33(1): 40 47
Posted by Wash U EM Residency at 8:49 PM
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