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I have completed bits of my EM training from India. Currently I am boarded with credentials from Christian Medical College, Vellore and also from the prestigious Royal College of Emergency Medicine, UK.  I am currently working in London as an A&E doctor, trying to appreciate the differences in the practise and culture of Emergency Medicine across different healthcare systems. I have always been an avid FOAMed supporter because FOAMed played an indispensable role during the days of my initial training. Through this blog, I aspire to disseminate knowledge and stay up to date with the EM literature. 

Monday, August 10, 2015

Hyperkalemia Revisited

This week lets review a topic, parts of which have been covered in the past.
Hyperkalemia is a life threatening electrolyte imbalance. Prompt recognition and treatment of severe hyperkalemia is crucial to avoid potential cardiac arrhythmias. Hyperkalemia (K>5.5 mEq/L) can be the result of:

1.    Transcellular Shift (Acidosis, Rhabdomyolysis, Tumor Lysis, Transfusions, Medications)
2.    Impaired renal excretion of potassium (CRF, Adrenal Insufficiency)
3.    Ex vivo hemolysis (pseudohyperkalemia) – Obtain a repeat sample

If the source of the hyperkalemia is unclear, a spot urine K can be useful. A high urine K(>30 mEq/L) suggests a transcellular shift, and a low urine K(<30 mEq/L) indicates impaired renal excretion.

Clinical Features of Hyperkalemia
ECG Abnormalities: Often ECG is used as the first investigation when hyperkalemia is suspected. The classic teaching of sequential ECG changes with progressive hyperkalemia does not always hold true. Threshold for ECG changes can vary widely. ECG can be bang normal with severe HyperK OR the first cardiac manifestation of hyperkalemia may be ventricular fibrillation. So overall, ECG has got a poor sensitivity to diagnose hyperK. Nevertheless, It is important to be aware of the important ECG findings of HyperK:
  • Peaked T waves, Prolonged PR, flattening of P waves, widenced QRS, Sine wave, VF
  • Bradycardia, BBB, AV Blocks, ST Elevation
Here, I am not saying that you should not use ECG for suspected HyperK. But if the ECG turns out to be normal don't have that false sense of reassurance. On the other hand, if you see hyperkalemic changes of EKG, go ahead with potassium correction. Since the treatment for hyperK is almost harmless, but hyperK itself is lethal, it makes sense to have a low threshold for treating hyperK.

So, ECG changes should not be considered necessary for treating emergent hyperK.

Neuromuscular Effects: Hyperkalemia may result in paraesthesias and weakness progressing to a depressed DTRs, flaccid paralysis.

Severe hyperkalemia is defined as a serum K>6.5 mEq/L, or any serum Kassociated with ECG changes. We have 3 goals here:
1.    Cardiac membrane Stabilisation (Calcium, Hypertonic Saline)
2.    Redistribution of K (Insulin, Beta agonists)
3.    K Elimination (Diuretics, Kayexylate, NaHCO3, HD)

Some medications that can cause HyperK are listed below:
  •    Acute Digitalis Toxicity 
  •     Succinylcholine 
  •     Beta blockers
  •     ACE/ARBC
  •     K Sparing diuretics
  •     NSAIDS
  •     Heparin
  •     Cotrimoxazole
Is Calcium safe for those on digoxin?
Though  the traditional teaching was "Calcium must be used cautiously in patients receiving digoxin because hypercalcemia aggravates digitalis cardiotoxicity. It appears that Ca is safe in those with hyperK on digoxin.

Which one is preferred, Ca gluconate or Ca Chloride?
Use what you are more familiar with 
Ca Gluconate: less likely to cause necrosis
Ca Chloride: needs central venous access, contains 3 times more calcium than gluconate

Hypertonic Saline: Restrict use to HypoNa with HyperK

Insulin and Dextrose: Always watch for hypoglycaemia and skip the dextrose when treating hyperK with hyperglycaemia. 

Kayexylate: Use this only if you don't have nephrology back up, otherwise stay away from this drug. Read the post on Kayexylate to find out more on this.

What is the appropriate dose of Beta 2 agonists to treat hyperK?
The dose of inhaled β2- agonists needed to produce a significant drop in serum Kis at least 4 times the therapeutic dose, and this can produce unwanted side effects (e.g., tachycardia). As many as 40% seem to be resistant to the hypokalemic effect of albuterol due to unknown reasons. Therefore, beta 2 agonists should never be used as a single agent for the treatment of hyperkalemia.

Sodium bicarbonate seems to have no effect to shift K into cells, even after several hours. It is likely to be effective in combination with a diuretic drug. I tend to use it when they have acidosis in addition to hyperK. Bicarbonate can also  form complexes with calcium antagonising the membrane stabilising effects of Ca.

Key Points:
  • Don't be reassured with a normal ECG in hyperkalemia.
Have a low threshold to administer Calcium for hyperK.
  • Calcium appears to be safe for treating hyperK patients who are on digoxin.
  • When using beta 2 agonists, give 10-20mg news and avoid using beta 2 agnostic alone for treating hyperkalemia.


  • Weisberg L. Management of severe hyperkalemia. Crit Care Med 2008; 36:3246–3251.
  • Levine, Michael, Heikki Nikkanen, and Daniel J. Pallin. "The effects of intravenous calcium in patients with digoxin toxicity." The Journal of emergency medicine 40.1 (2011): 41-46.
  • Alfonzo AVM, Isles C, Geddes C, Deighan C. Potassium disorders—clinical spectrum and emergency management. Resusc 2006; 70:10–25.
  • Schaefer TJ, Wolford RW. Disorders of potassium. Emerg Med Clin North Am 2005; 23:723–747, viii–ix.
  • Tran HA. Extreme hyperkalemia. South Med J 2005; 98:729–732. 

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