In this ECG Cases blog we learn from 9 patients with potential hyperkalemia

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. June 2020

Which of the following 9 patients had hyperkalemia? Can you estimate how high their serum potassium was based on the ECG?

Patient 1. 80yo from a nursing home with a few days of lethargy, decreased po intake

Patient 2. 50yo with acute epigastric pain

Patient 3. 60yo ESRD with weakness and presyncope. Old then new

Patient 4. 80yo on ARB and beta-blocker with syncope and nausea, HR 50 BP 90

Patient 5. 80yo DM/CKD with weakness and decreased po intake

Patient 6. 40yo ESRD with weakness, N/V

Patient 7. 80yo CKD with diarrhea, weakness

Patient 8. 90yo with weakness, on spironolactone. Old then new

Patient 9. 50yo IDDM with chest pain, SOB, weak

ECG findings in hyperkalemia

Hyperkalemia can result in a variety of presentations—including asymptomatic, dyspnea, nausea/vomiting, diarrhea, weakness, chest pain, missed dialysis or cardiac arrest. Most patients have risk factors including CKD, CHF, DM, or medications like ACE inhibitors or potassium-sparing diuretics [1].

Hyperkalemia has been called the great ECG mimicker. By poisoning the atria, hyperkalemia can produce bradycardia, and reduced P wave amplitude can mimic “regular” atrial fibrillation or junctional rhythm. By slowing conduction, hyperkalemia can produce AV blockade, fascicular or bundle branch blocks, or wide complex rhythms that mimic ventricular rhythms (but slower or wider than VT). By blocking sodium channels, hyperkalemia can produce Brugada phenocopy with ST elevation that can be mistaken for STEMI, and by altering the membrane potential hyperkalemia leads to peaked T waves that might be mistaken for ischemic hyperacute T waves—but the former are pinched, with a narrow base and sharp peak, while the latter are bulky, with a wide base and broader peak. Occasionally these peaked T waves are so narrow and tall that ECGs machines will confuse them with QRS complexes and double-count them, leading to a false label of tachycardia [2]. In paced rhythms, hyperkalemia can lead to failure to capture, increased latency from pacemaker to depolarization, and widening of the paced complexes [3].

With so much mimicry, it’s not surprising that hyperkalemic changes are not specific in isolation: one study found that 20% of normokalemic ECGs had one change that can be seen in hyperkalemia—including bradycardia, first degree heart block, wide QRS, or peaked T waves—but only 4% had more than one finding. On the other hand, each of these findings were more common with hyperkalemia, both individually and collectively: 39% of those with severe hyperkalemia (>7) had ECG changes, and 32% had more than one change. [4] In another study, 71% of those with K>6.5 had ECG changes and 43% had more than one. The greatest risk for adverse events was not only PR/QRS prolongation, but also bradycardia and junctional rhythm. Despite these abnormalities the median time from ECG to treatment was 85 minutes, independent of ECG changes, suggesting that physicians are waiting for potassium levels before starting treatment. As a consequence, 15% had adverse outcomes (unstable bradycardia, VT, CPR or death), all of whom had preceding ECG abnormalities (and 86% of whom had more than one), all prior to receiving calcium and all but one prior to potassium-lowering medication.[5]

ECG changes depend not only the potassium level but its rate of increase and associated metabolic abnormalities, and the clinical impact can be magnified by medications like AV-nodal blockers. The BRASH syndrome (Bradycardia, Renal Failure, AV node blockers, Shock and Hyperkalemia) can produce bradycardia and shock out of proportion to potassium level or ECG changes—because the synergy of AV blockers and hyperkalemia on bradycardia, which in turn worsens renal failure and reduces clearance of AV blockers and potassium. So serum levels don’t correlate well with ECG changes or clinical outcome, and patients can become clinically unstable even with narrow QRS. But multiple ECG changes and clinical instability can predict significant hyperkalemia and guide emergency treatment, including empiric calcium.

Back to the cases

Patient 1. moderate hyperkalemia (6.7) without ECG changes

  • HR: borderline sinus tachycardia
  • Electrical conduction: normal intervals/conduction
  • Axis: normal
  • R wave: normal
  • Tension: no hypertrophy
  • ST/T wave: nonspecific T wave flattening

No ECG signs of hyperkalemia, likely from gradual rise and concomitant hypernatremia. K 6.7, Na 164. Treated with calcium, normal saline, dextrose/insulin.

Patient 2. LAD occlusion, normal potassium

  • HR: NSR
  • Electrical: normal
  • Axis: normal
  • R wave: loss of R wave and small Q wave in V3
  • Tension: no hypertrophy
  • ST/T: hyperacute T waves V2-3 (broad base, larger than QRS complex in V3) and inferior reciprocal changes

Cath lab activated: LAD occlusion, normal potassium. ECG post-cath: resolution of hyperacute T waves

Patient 3. severe hyperkalemia (7.1) with subtle changes

  • HR: NSR (not a ventricular rate of 175 as the machine says)
  • Electrical: old first degree AV block, RBBB, LPFB
  • Axis: old right axis
  • R wave: normal
  • Tension: no hypertrophy
  • ST/T: compared with old the T waves are more peaked (narrower, taller and more pointy)

Potassium 7.1: treated with calcium, insulin/dextrose, and dialysis

Patient 4. Moderate hyperkalemia (6.2) and BRASH syndrome causing brady-asystolic arrest

  • HR: sinus bradycardia
  • Electrical: first degree heart block, narrow QRS
  • Axis: normal
  • R wave: normal
  • Tension: no hypertrophy
  • ST/T: peaked T waves

Potassium 6.2, treatment initiated with insulin/dextrose/fluids but not calcium because of narrow complex. Then patient developed narrow complex brady-asystole

Treated with calcium and more insulin/dextrose/fluids, with recovery and resolution of changes

Patient 5. severe hyperkalemia (8.6) causing wide complex rhythm

  • HR: normal rate (can’t be VT), no P waves
  • Electrical: LAFB and wide complex QRS
  • Axis: left
  • R wave: normal
  • Tension: no hypertrophy
  • ST/T: peaked T waves

Treated empirically with calcium, insulin/dextrose, fluids, ventolin. Repeat ECG: reappearance of P waves and narrow QRS, T waves still peaked.

Patient 6. Severe hyperkalemia (9.0) causing classic findings and brief sine wave

  • HR: NSR
  • Electrical: first degree AV block, LAFB, slightly wide QRS
  • Axis: left
  • R wave: delayed progression
  • Tension: no hypertrophy
  • ST/T: extremely peaked T waves

Brief sine wave

Empiric treatment with calcium, insulin/dextrose pending dialysis: reappearance of P waves and narrow QRS complex, ongoing peaked T waves

Post-dialysis resolution of all hyperkalemic changes:

Patient 8. Severe Hyperkalemia (7.1) causing wide complex bradycardia

  • HR: regular bradycardia without P waves
  • Electrical: wide complex QRS
  • Axis: normal
  • R wave: delayed progression
  • Tension: no hypertrophy
  • ST/T: peaked T wave

Treated empirically with calcium, insulin/dextrose, fluids. Repeat ECG: reappearance of p waves, resolution of broad complex bradycardia and peaked T waves

Patient 9. Severe hyperkalemia (7.1) causing subtle pacemaker changes

Compared with baseline, the new ECG has prolonged atrial and ventricular conduction. Potassium 7.1: treated with calcium, insulin/dextrose, fluids.

Patient 10. severe hyperkalemia (7.2) causing Brugada phenocopy and hyperkalemic ECG changes

  • HR: sinus tach
  • Electrical: wide QRS
  • Axis: right
  • R-wave: normal
  • Tension: no hypertrophy
  • ST/T: Brugada phenocopy and peaked T waves

Treated, with resolution of changes (ECG not available)

Take home points on ECG findings in hyperkalemia

  1. The ECG cannot rule out hyperkalemia, but significant hyperkalemia often produces multiple changes: survey every aspect of the ECG, especially heart rate (bradycardia, junctional rhythm), electrical conduction (PR prolongation or loss of P waves, QRS prolongation, pacemaker delays), and ST/T waves (Brugada phenocopy, peaked T waves that are narrow/pointy)
  2. Consider empiric calcium for multiple signs of hyperkalemia, especially unstable bradycardia, slow or regular “AF”, or “VT” which is slow or very wide

References for ECG Cases 10: Hyperkalemia

  1. Peacock F, Rafique Z, Clark C, et al. Real world evidence for treatment of hyperkalemia in the emergency department (REVEAL-ED): a multicenter, prospective, observational study. J of Emerg Med 2018:55(6):741-750
  2. Littman L and Gibbs M. Electrocardiographic manifestations of severe hyperkalemia. J of electrocardiol 2018;51:814-817.
  3. Barold SS and Herweg B. The effect of hyperkalaemia on cardiac rhythm devices. Europace 2014 Apr;16(4):467-76.
  4. Varga C, Kalman Z, Szakall A, et al. ECG alterations suggestive of hyperkalemia in normokalemic versus hyperkalemic patients. BMC Emerg Med 2019 Amy 31;19(1):33.
  5. Durfey N, Lehnhof B, Bergeson A, et al. Severe hyperkalemia: can the electrocardiogram risk stratify for short-term adverse events. West J of Emerg Med 2017 Aug;18(5):963-971/.
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