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 you’re 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.
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 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.
- Benign Early Repolarization (BER): This is a variant of the normal ECG, found in people 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.
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.
Throwback to Medical School: Why does hyperkalemia result in a peaked T on the EKG?
First, let’s 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 we’ll 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.
[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); 324-330.
[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
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