Hyperkalemia

last authored: July 2012, David LaPierre
last reviewed:

 

 

 

Introduction

Hyperkalemia, or elevated serum potassium, is a common electrolyte abnormality that is associated with adverse clinical outcomes (Weisberg, 2008) and can be life-threatening through the emergence of cardiac arrhythmias.

 

Hyperkalemia is defined as potassium greater than 5.5 mmol/L. It occurs during 1-10% of hospital admissions.

• 5.5 - 6.0 mmol/L - Mild
• 6.1 - 7.0 mmol/L - Moderate
• 7.0 mmol/L and greater - Severe

 

 

 

The Case of John B.

John is a 44 year-old man admitted with pneumonia. On admission, his bloodwork reveals a potassium of 6.6 mmol/L.

• What might be the causes of this?
• Should you be concerned?
• What consequences could a high potassium lead to?
• How do you treat John?

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Causes and Risk Factors

Increased Intake diet KCl medication (oral or IV)	Cellular Release hemolysis rhabdomyolysis trauma and tissue damage burns insulin deficiency hyperosmolar states (ie hyperglycemia) metabolic acidosis (not keto/lactic acidosis tumour lysis syndrome cocaine use significant exercise mannitol drugs: beta blockers, digoxin	Decreased Excretion decreased GFR or renal failure low effective circulating volume NSAIDs ACE inhibitors spironolactone hypoaldosteronism Addison disease type IV renal tubular acidosis	Factitious Serum K can be falsely elevated due to the following reasons: sample hemolysis prolongued tourniquet extreme leukocytosis or thrombocytosis
Medications cyclosporin NSAIDs digoxin heparin ACE inhibitors ARBs some beta blockers, eg carvedilol ethinyl estradiol penicillin succinylcholine tacrolimus trimethoprim	Herbal products (from Evans et al, 2005) alfalfa ginseng dandilion nettles milkweed hawthorne berries oleander foxglove

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Pathophysiology

Potassium regulation is described in detail here.

 

Regulation

Potassium is injested and absorbed, and is moved intracellularly through the action of insulin.

 

The ratio of intracellular to excellular potassium is the major determinant of cell membrane resting potential. This resting potential is largely responsible for cardiac, nerve, and skeletal muscle function.

 

Small changes in extracellular [K] have a large impact on the cellular ratio, and as such, tight control of extracellular [K] is normally maintained. This is accomplished via the following factors:

• insulin
• catecholamines (ie epinephrine and nor-epinephrine)
• acid-base status
• tonicity
• aldosterone (mediated by kidney renin release)

These all increase K uptake by the Na/K pump.

 

Excretion by the kidneys is very dynamic in order to maintain effective K levels. This occurs at the level of the distal nephron - the connecting tubule and the collecting duct. The main factors are flow of sodium and chloride through the distal nephron, as well as action of aldosterone. Increased flow leads to increased secretion, which explains the mechanism of loop dieuretic drugs like furosemide leading to hypokalemia.

 

 

Effect on the Body

As homeostatic mechanisms are overwhelmed, extracellular potential increases. The excitable cells becomes partially depolarized, and the ability to generate action potentials is diminished.

Cardiac depolarization leads to slowed ventricular conduction and decreased action potential duration. Cardiac disturbances and ECG changes do not correlate well with K levels; rather, the rate of change in potassium levels appear to be very important in regards to cardiac consequences.

Neuromuscular depolarization can also lead to poor action potentials, with accompanying paresthesias and weakness.

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Signs, Symptoms, and Diagnosis

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Treatments

WARNING: the following information should not be used without verifying with an experienced clinician, or referring to other resources.

 

Treatment depends on symptoms, ECG changes, and level of elevation, and rate of rise. The actual [K] and ECG changes do not absolutely depict risk, and thus defining 'emergency' hyperkalemia is difficult. However, as lethal consequences can be unpredictable, and as treatment is normally safe, intervention should be provided without any great delay if concern is present.

 

In general, consider admission with a K of >6 mmol/L.

 

Hold exogenous K and any medications which are K-retaining.

 

Cardiac Stabilization

The most rapid way of reversing cardiac membrane potential is to give calcium gluconate (1-2 amps, 10 mL of 10% solution). Calcium lowers the resting potential of cardiac cells, and in so permits normal function, even with hyperkalemia in place.

This is short lived (30-60 minutes), however, and does not lower serum [K]. It must therefore be followed by other therapies to shift K into the cells and decrease extracellular potassium concentration. ECG should be monitored.

Note: use extreme caution if digoxin toxicity is suspected.

If the patient is hyponatremic, they may also benefit from use of IV infusion of hypertonic (3%) saline.

 

Transcellular shifting

K can be moved into cells via many mechanisms:

• insulin R 10-20 units IV, given with 25g of D50W bolus and then dextrose infusion
  • onset ~15 min; duration 1-2h
• salbutamol 10 mg inhaled, 0.5 mg IV: stimulates Na/K ATPase
  • onset 30-90 min; caution with heart disease
  • can lower by 0.5-1.5
• bicarbonate 1-3 amps
  • onset 15-30 min, transient and less useful; not usually used

 

Enhance K removal

Renal excretion can be enhanced by giving furosemide >40 mg IV; consider IV NS to avoid hypovolemia, which with further worsen hyperkalemia.

Sodium bicarbonate infusion given over 4-6 hours may enhance urinary excretion through alkalination (Weisberg, 2008).

Gut excretion can be increased by cation-exchange resins: calcium or Kayexalate (sodium polystyrene sulfonate); this is effective in 1-4 hours, and may be faster, though less effective, if given rectally. Constipation is very common, and intestinal necrosis is a rare, but serious, complication (Weisberg, 2008).

Dialysis can be done in renal failure or if life-threatening hyperkalemia is unresponsive to therapy. However, it may also induce ventricular arrhythmias, therefore requiring careful use and constant monitoring.

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Consequences and Course

In muscle, decreased action potentials leads to muscle weakness and paralysis.

 

Effects on the Heart

As plasma levels rise above 6 mM, T waves become symmetrically tented, with a sharp peak. The P-R interval lengthens and the P wave becomes smaller. Sinus bradycardia and conduction defects can also occur.

Above 8 mM, the P wave disappears and the QRS complex widens and merges with the T wave.

At higher concentrations, ventricular fibrillation can result and death can result.

The cell will have an easier time depolarizing if [K]i/[K]o is reduced .

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Resources and References

Evans KJ, Greenberg A. 2005. Hyperkalemia: a review. J intensive care medicine. 20:272-90.

Hollander-Rodriguez JC, Calvert JF. 2006. Hyperkalemia. Americal Family Physician. 73:283-90.

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