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EverydayEBM:EKGChallenge#3CaseConclusionMindyourp'sandK's.
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An educational blog by the Emergency Medicine residents at
Washington University in St.Louis. #FOAMed
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SUNDAY,NOVEMBER9,2014
EKGChallenge#3CaseConclusionMindyourp'sandK's.
You are working on a busy night in TCC when an elderly lady is
brought in by EMS with acomplaint of dizziness. The paramedic looks
a bit more stressed than you expect for theaverage old lady with a
case of the dizzies and rightly so. As he reports her vital signs,
youare shocked to hear that her HR has been steadily below 30 with
a systolic blood pressurein the 80s and youre even more shocked to
hear that shes awake! She reports feelinggenerally weak and thinks
she has the stomach flu. As the nurses get down to businessplacing
the patient on the monitor and obtaining IV access, the tech hands
you this EKG.
You note the absence of P waves, widened QRS and prominent T
wave. You place thepatient on an external pacer and run through
your differential. Did she overdose on herantihypertensives? 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 gluconateas you set up for internal pacing. As
youre ready to pass the pacer, you hear that herwhole blood
potassium is nearly 7. You aggressively treat her hyperkalemia
withinsulin/dextrose, albuterol, IV fluids and give renal a call.
To your relief, her pulse and BPimprove dramatically.
Given the importance of recognizing the EKG changes of acute
hyperkalemia (indeed, youwill save a life by doing so), you decide
to take a moment to review the breadth of EKGfindings associated
with hyperkalemia, the sensitivity/specificity of these findings,
and a
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2/6/2015
EverydayEBM:EKGChallenge#3CaseConclusionMindyourp'sandK's.
http://wueverydayebm.blogspot.in/2014/11/ekgchallenge3caseconclusionmind.html
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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 prolongationof the PR interval [Ref 1]. But
beware, these classics are not the only EKG abnormalitiesobserved
in hyperkalemia! As serum potassium increases, p wave amplitude
decreasesuntil p waves disappear entirely and intraventricular,
fascicular and bundle branch blockscan occur in severe
hyperkalemia. At extremes, QRS widening becomes so pronouncedand a
sine-wave pattern develops and eventually deteriorates to VF and
asystole. It isimportant to note that while common and widely
recognized, T waves can appearreassuringly normal in a patient with
LVH and chronically inverted lateral T waves to
havepseudonormalization of their T waves during an acute
hyperkalemic episode.
But what about sensitivity and specificity of EKG changes as a
rapid assessment forhyperkalemia? Unfortunately, they are not
great. A retrospective case study found asensitivity of only 52%
for ANY EKG change in hyperkalemia [Ref 2]. Additionally
thepresence of new or resolving peaked T waves was not
significantly associated with serumpotassium concentration. When
evaluating an EKG with a prominent T wave it isimportant 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 wavesare tall in all these conditions, there
are some morphological differences that can helpyou distinguish
between them:
- 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 ofnormal 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, andasymmetric (can sometimes be symmetric). The T
waves are often associated withreciprocal ST segment depression in
other leads. The R wave also increases in amplitudeand 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 witheventual QRS complex
widening. Sometimes in severe hyperkalemia with QRS
complexwidening, there may also be some ST elevation that simulate
an infarction pattern. It hasalso been observed that a terminal
slur in the QRS complex or an S wave in lead I or V6without gross
QRS widening is commonly associated with hyperkalemic T waves.
- Benign Early Repolarization (BER): This is a variant of the
normal ECG, found in people
Figure Modified from Reference 3 with additional tracings
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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 diffusedistribution of
ST-segment elevation on the ECG; and (6) relative temporal
stability." (Ref3). Click here for a review by Amal Mattu on the
differences between EKG findings of BERand endocarditis.
Unfortunately, many of the discussed features above are not
exclusive to certainconditions. 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 mustalso
consider age, comorbidities, and presenting complaint and overall
clinical picture.
Throwback to Medical School: Why does hyperkalemia result in a
peaked T on the EKG?
First, lets think a little bit about potassium. The normal
extracellular potassiumconcentration (what we ask the lab guys to
measure) is around 4 4.5mEq/L, but thisrepresents only a tiny
fraction of total body potassium as 95% is intracellular. The
kidneystake 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 thatpotassium and sodium are the major role players.
Potassium is concentratedintracellularly and sodium is hanging out
extracellularly. The good old Sodium-Potassiumpump is keeping the
peace, the peace being a negative resting membrane potential.
Theconcentration gradient across this membrane plays an important
role in maintaining thisaction potential. As the extracellular
potassium concentration increases, the restingmembrane potential
gets less negative. This is important because the resting
membranepotential (the flat part before the action potential gets
going) directly impacts the numberof voltage-gated sodium channels
available to generate the action potential. Fewersodium channels
means slower impulse conduction and prolonged
membranedepolarization. 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 waverepresents repolarization, or phase 3 of
the cardiac action potential when the calciumchannels have closed
and the potassium channels remain open. For some crazy reasonNot
well understood per the literature, increased extracellular
potassium leads thesechannels to pump more potassium out of the
cell, shortening repolarization, producingthe 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 forhyperkalemia. -Common findings
include peaked T waves, PR prolongation, P wave flattening,
QRSwidening all eventually producing sine wave ECG, Vfib and
asystole.-Underlying conduction abnormalities and history of CKD
can impact the EKGmorphology at various K levels. - The "tall T
wave" has a differential diagnosis. T wave morphology can give
youimportant 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.
ElectrocardiographicManifestations of Hyperkalemia, American
Journal of Emergency Medicine. 2000; 18:721-729.
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Posted by Wash U EM Residency at 8:49 PM
Labels: EKG challenge
[2]Montague, B et al, Retrospective review of the Frequency of
ECG changes inHyperkalemia, Clinical Journal of the American
Society of Nephrology. 2008. (3); 324-330.
[3]Somers MP, Brady WJ, Perron AD, Mattu A. The prominent T
wave:Electrocardiographic differential diagnosis. American Journal
of Emergency Medicine2002;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
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