R.E.B.E.L. EM – ECG Changes of Hyperkalemia
Originally published at R.E.B.E.L. EM on April 17, 2014. Reposted with permission.
Follow Dr. Salim R. Rezaie on twitter @
Hyperkalemia is an electrolyte abnormality seen in the emergency department as well as in hospitalized patients and it can be associated with adverse clinical outcomes and death if not treated appropriately. It is important to remember that the electrophysiologic effects of hyperkalemia are directly proportional to both the absolute plasma potassium and its rate of rise. However, neither the ECG nor the plasma potassium alone are an adequate index of the severity of hyperkalemia, and therefore providers should have a low threshold to initiate therapy. Classic teaching of the chronological ECG changes of hyperkalemia include:
- Peaked T waves
- Prolongation of PR interval
- Widening QRS Complex
- Loss of P wave
- “Sine Wave”
Where did the evidence for order of ECG changes of hyperkalemia come from?
The order of ECG changes of hyperkalemia have been defined in the experimental setting, but no uniform order has been documented in animal models (Ettinger, Regan, and Oldewurtel 1974)*. The relationship between serum potassium and cardiac manifestations is even less clear in the clinical setting (Acker et al. 1998)*.
How good are ECGs at predicting hyperkalemia? (Wrenn, C M Slovis, and B S Slovis 1991)*
- 87 patients admitted from the ED with hyperkalemia
- ECG read by 2 EM physicians blinded to potassium level
- Sensitivity: 34 – 43%
- Specificity: 85 – 86%
- When only patients with potassium > 6.5 mmol/L were analyzed: Sensitivity 55 – 62%
- Conclusion: Based on this study the ECG has a poor correlation with detection of hyperkalemia
Any studies looking at the frequency of ECG changes with hyperkalemia? (Montague, Ouellette, and Buller 2008)*
What is the treatment regimen for hyperkalemia? (Weisberg 2008)*
Additional Treatment Pearls:
- 1 g Calcium Chloride (CaCl) = 3 g Calcium Gluconate: Bryan Hayes (@PharmERToxGuy) had a great post on Academic Life in EM on myths associated with different calcium regimens. There was also a Google+ conversation on this topic on theREBEL EM Community.
- Hypertonic (3%) Saline: Should be restricted to patients with hyponatremia and concurrent hyperkalemia. Its effects have not been established in eunatremic patients.
- Insulin: 10 Units of regular insulin + dextrose (25 g as 50% solution) lowers plasma potassium by about 0.6 mmol/L. Be careful as a single bolus of 25 g of dextrose has been shown to be inadequate ion prevention of hypoglycemia at 60 minutes.
- Beta Agonists: 10 mg and 20 mg of inhaled albuterol decreased serum potassium by 0.6 mmol/L and 1 mmol/L, respectively. Mild tachycardia is most common side effect.
- Bicarbonate: Bolus injection of sodium bicarbonate has not been studied. The dogma of bolus bicarbonate was derived from studies using a prolonged (4 – 6 hr) infusion of bicarbonate which does not reduce plasma potassium in patients with dialysis-dependent renal failure. Infusion sodium bicarbonate over 4 – 6 hours may have some benefit in excretion of serum potassium in the setting of metabolic acidosis.
- Exchange Resin: The onset of action is very long (2 hours to onset, and 6 ours to maximum effect) and there have been case reports of patients developing colonic necrosis. Also there have been studies that show no statistical benefit at 4, 8, and 12 hours (Gruy-Kapral et al. 1998)*.
- Hemodialysis: Definitive treatment of hyperkalemia. Watch out for rebound hyperkalemia which can occur in 30% of patients an hour after dialysis.
Clinical Bottom Line: Neither the ECG nor the plasma potassium alone are an adequate index of the severity of hyperkalemia, and providers should have a low threshold to initiate cardiac membrane stabilization in the setting of hyperkalemia and no ECG changes.