Hyperkalemia Intro
- Potassium is primarily an intracellular ion responsible for maintenance of the resting membrane potential for normal cell conduction.
- Serum measured potassium is typically between 3.5 and 5.0 mEq/L.
- Serum K greater than 5.0 mEq/L is generally considered the threshold for hyperkalemia.
- Potassium is mostly excreted via the kidneys, and the “classic” hyperkalemia patient is one who has missed several dialysis appointments complaining of paralysis or diffuse weakness.
Causes of HyperK
- Most commonly, renal failure.
- Transcelluar shift
- DKA
- Acidosis
- Other acid-base disturbances
- Medications
- RAAS or ACE inhibitors
Effects of HyperK
- Most drastically affect cardiac myocytes
- Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased.
- Leads to ominous “sine wave” pattern on ECG.
- Arrythmogenic
- May produce classic tall, “peaked” T waves on ECG.
- Conduction between myocytes is depressed, leading to slower conduction and widened QRS complexes, however, the rate of repolarization is increased.
- Stepwise ECG changes in hyperkalemia:
- 5.5-6.5 mEq/L – Peaked T Waves
- 6.5-7.5 mEq/L – P waves amplitude becomes smaller and PR intervals prolong
- 7.5-8.0 mEq/L – QRS becomes wide
- ECGs are not always sensitive for hyperkalemia. Patients may have a critical K with no changes on the ECG.
- Skeletal muscle tissue is also sensitive to hyperkalemia, and patients may present with weakness or paralysis as a result.
- Nondescript symptoms such as muscle cramps, diarrhea, vomiting, nausea, and focal paralysis may also be present – but are also not reliable findings.
Management
- Prioritized by a strategy of:
- Stabilization of cardiac cell membranes
- Shifting potassium back into the cells
- Eliminating potassium
- Calcium (Chloride or gluconate) administered to stabilize cell membranes
- Stabilizing effect is transient and relatively short lived
- Calcium Chloride contains roughly 3 times the amount of elemental calcium as compared to Ca gluconate, but is associated with severe complications if extravasation occurs.
- Effects (narrowing of QRS complex, return of more hemodynamic stability) occurs within minutes
- Calcium Chloride – generally, 1 gram is administered over 3 minutes.
- Calcium Gluconate – 1 gram over 2-3 minutes
- Repeat either q5min
- Albuterol / Beta 2 agonists
- These act on beta 2 receptors to assist in moving potassium back into the intracellular space
- Albuterol – 10-20mg (inhalation), with most effect noted in 30 minutes
- IV Insulin
- Drives K back into the cells (shift)
- Generally administered with dextrose unless the patient’s BGL is below 250mg/dL
- 10 units IVP followed by 25G dextrose
- Incidence of hypoglycemia is high, and this therapy should be administered cautiously
- Dialysis
- Treating reversible cause
- d/c RASS or ACE inhibiting medicaitions
- Volume administration
Now for the Podcast!
References
Jaber, S., Paugam, C., Futier, E., Lefrant, J. Y., Lasocki, S., Lescot, T., … Kipnis, E. (2018). Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial. The Lancet, 392(10141), 31–40. https://doi.org/10.1016/S0140-6736(18)31080-8
Panchal, A. R., Berg, K. M., Hirsch, K. G., Kudenchuk, P. J., Del Rios, M., Cabañas, J. G., … Donnino, M. W. (2019). 2019 American Heart Association Focused Update on Advanced Cardiovascular Life Support: Use of Advanced Airways, Vasopressors, and Extracorporeal Cardiopulmonary Resuscitation During Cardiac Arrest: An Update to the American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. https://doi.org/10.1161/CIR.0000000000000732
Hyperkalemia Master Class with Joel Topf MD – The Curbsiders. (n.d.). Retrieved November 18, 2019, from https://thecurbsiders.com/podcast/137-hyperkalemia-master-class
Treatment of hyperkalemia in the ED. (n.d.). Retrieved November 18, 2019, from https://emcrit.org/emcrit/hyperkalemia/
Weisberg, L. S. (2008). Management of severe hyperkalemia. Critical Care Medicine. Lippincott Williams and Wilkins. https://doi.org/10.1097/CCM.0b013e31818f222b
Wrenn, K. D., Slovis, C. M., & Slovis, B. S. (1991). The ability of physicians to predict hyperkalemia from the ECG. Annals of Emergency Medicine, 20(11), 1229–1232. https://doi.org/10.1016/S0196-0644(05)81476-3
Abuelo, J. G. (2018). Treatment of Severe Hyperkalemia: Confronting 4 Fallacies. Kidney International Reports. Elsevier Inc. https://doi.org/10.1016/j.ekir.2017.10.001Durfey, N., Lehnhof, B., Bergeson, A., Durfey, S. N. M., Leytin, V., McAteer, K., … Valiquet, J. (2017). Severe hyperkalemia: Can the electrocardiogram risk stratify for short-term adverse events? Western Journal of Emergency Medicine, 18(5), 963–971. https://doi.org/10.5811/westjem.2017.6.33033