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Low Potassium (Hypokalemia)
In normal circumstances more than 90 per cent of the total body potassium is intracellular the remaining is in the extracellular fluid and blood plasma.
As the normal daily dietary intake of potassium varies widely and can be as much as 100 millimoles a day. the body must quickly and precisely react to keep blood potassium levels within the normal limits. This is achieved by two 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. Hypokalemia is defined as a serum potassium concentration lower than 3 points 5 millivolts per litre
What Causes Hypokalemia (Low Blood Potassium)?
Hypokalemia may result from increased excretion inadequate intake or shift to potassium from the extracellular fluid into the cells poor intake or intracellular shift alone rarely causes the disease but may be a contributing factor.
Most commonly hypokalemia is caused by excessive loss of potassium in the urine from the GI tract or skin the cause is usually apparent by the patient's history of predisposing diseases or medication. Urine potassium levels are measured to differentiate between renal and non-renal causes
Depending on the level of severe symptoms may include muscle weakness, cramping, tremor intestinal obstruction, hypotension, respiratory depression and abnormal heart rhythm. As potassium levels decrease in the extracellular space the magnitude of the potassium gradient across the cell membrane is increased causing hyperpolarization.
This moves the membrane voltage further from the threshold and a greater than normal stimulus is required to generate an action potential.
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The result is reduced excitability or responsiveness of the neurons and muscles.
In the heart however hyperexcitability is observed this is because hyper-polarization enhances the funny currents in cardiac pacemaker cells resulting in a faster phase for depolarization and thus a faster heart rate. The effect is greatest in Purkinje fibres as these are more sensitive to potassium levels as compared to the SA node
Increased automaticity of the Purkinje fibres may lead to the development of one or more ectopic pacemaker sites in the ventricles causing ventricular, premature beats, tachycardia and fibrillation. Reduced extracellular potassium paradoxically also inhibits the activity of some potassium channels
Slowing down potassium efflux during repolarization and thus delays ventricular repolarization. As hypokalemia becomes more severe especially in patients with other heart conditions the inward current may exceed the outward current.
Resulting in early, after depolarization and consequently extra heartbeats prolonged repolarization may also promote re-entrant arrhythmias. Early ECG changes in hypokalemia are mainly due to delayed ventricular repolarization these include flattening or inversion of T wave increasingly prominent new wave ST-segment depression and prolonged qu interval
Hypokalemia induced arrhythmias require immediate potassium replacement oral administration is safer but may not be effective in severe cases. If potassium infusion is indicated continuous cardiac monitoring and hourly serum potassium determination must be performed to avoid hyperkalemia complications
In the long term, the underlying causes must be addressed.
What Causes Hyperkalemia (High Potassium)?
Hyperkalemia is defined as a serum potassium concentration higher than 5 millivolts per litre. Hyperkalemia may result from decreased excretion excessive intake or shift of potassium from inside the cells to extracellular 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. The 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 the excitability of monocytes, 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-waves p-wave widens and flattens PR interval lengthens QRS complex widens and eventually blends with T wave and practice. This pattern is present only a fraction of hyperkalemia patients and does not always correlate with potassium levels this makes a diagnosis on the basis of ECG alone very difficult.
Severe hyperkalemia is treated in three 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 in the case of digoxin toxicity. insulin is administered to stimulate the sodium-potassium pump,
Promoting the intracellular 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.
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