Hyperkalemia refers to abnormally high levels of potassium in the blood. In normal circumstances,
more than 90% of the total body potassium is intracellular; the remaining is in the
extracellular fluid and blood plasma. The ratio of intracellular to extracellular potassium is
important for generation of action potentials and is essential for normal functions of neurons,
skeletal muscles and cardiac muscles. This is why potassium levels in the blood are
strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal
daily dietary intake of potassium varies widely and can be as much as 100mmol a day,
the body must quickly and precisely react to keep blood potassium levels within the normal limits.
This is achieved by 2 mechanisms: - Excretion of potassium through
the kidneys and intestines; with the kidneys playing a predominant role.
- Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium
pump. The pump is mainly regulated by hormones such as insulin and catecholamines.
Hyperkalemia is defined as a serum potassium concentration HIGHER than 5mmol/L. Hyperkalemia
may result from decreased excretion, excessive intake, or shift of potassium from inside the
cells to extra-cellular space. Usually, a combination of factors is responsible. The
most common scenario is a renal insufficiency combined with excessive potassium supplements OR
administration of certain drugs. Impaired kidney function is most prominent; excessive intake or
extracellular shift is rarely the only cause. Mild hyperkalemia is often without symptoms,
although some patients may develop muscle weakness. Slow or chronic increase in
potassium levels is less dangerous, as the kidneys eventually adapt by
excreting more potassium. Sudden onset and rapid progression of hyperkalemia, on the other hand,
can be fatal. Primary cause of mortality is the effect of potassium on cardiac functions.
As potassium levels increase in the extracellular space, the magnitude of potassium gradient across
the cell membrane is reduced, and so is the absolute value of the resting membrane potential.
Membrane voltage becomes less negative, moving closer to the threshold potential,
making it easier to initiate an action potential. The effect this has on excitability of myocytes,
however, is complex. While initial changes seem to increase myocyte excitability;
further rise of potassium has the opposite effect. This is because the value of membrane
potential at the onset of an action potential determines the number of voltage-gated sodium
channels activated during depolarization. As this value becomes less negative in hyperkalemia,
the number of available sodium channels decreases, resulting in a slower influx of
sodium and subsequently slower impulse conduction. In experimental models, ECG changes produced by
hyperkalemia follow a typical pattern that correlates with serum potassium levels:
peaked T-wave, P wave widens and flattens, PR interval lengthens, QRS complex widens and
eventually blends with T-wave. In practice, however, this pattern is present only in a
fraction of hyperkalemia patients and does not always correlate with potassium levels. This
makes diagnosis on the basis of ECG alone very difficult. Given the dangerous nature of acute
hyperkalemia, it must be suspected in any patient having new bradycardia or conduction block,
especially in those with renal problems. Severe hyperkalemia is treated in 3 steps:
- Calcium infusion is given to rapidly reverse conduction abnormalities. Calcium antagonizes the
effect of potassium at the cellular level, stabilizing membrane potential. However,
it does not remove potassium, and should not be used in the case of digoxin toxicity.
- Insulin is administered to stimulate the sodium/potassium pump, promoting
intra-cellular shift of potassium. - Hemodialysis is performed to
remove potassium from the body. Longer term treatment for hyperkalemia
without conduction problems consists of reducing intake and increasing excretion.