Hypokalemia
last authored: Feb 2013, David LaPierre
last reviewed:
Introduction
main article: potassium
Potassium (K) is the most abundant cation within cells, and its deficiency can cause a host of problems. These range from benign to life-threatening, most importantly related to arrhythmias.
Hypokalemia is defined as plasma [K] of less than 3.5 mM/L. Moderate hypokalemia is from 2.5-3 mM/L, with severe hypokalemia defined as less than 2.5 mM/L.
Normal potassium regulation is mediated by the kidney. The majority of cases of hypokalemia are caused by dieuretic therapy.
However, as the majority (over 98%) of potassium is intracellular, hypokalemia can occur in concert with normal total body stores and a further shift of potassium from the extracellular to intracellular space. This flux is regulated by pH as well as circulating hormones, including aldosterone, insulin, and catecholamines lead to potassium shift.
The Case of Jane R
Jane is a 66 year-old woman who comes to her family doctor complaining of fatigue. As a component of the investigation, lab results show a serum potassium of 2.6 mM.
- what other symptoms could this low potassium be causing?
- what could be causing the hypokalemia?
- how should it be treated?
Causes and Risk Factors
There are a number of causes of hypokalemia, related to different mechanisms. These include:
cellular redistribution:
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GI losses
renal losses
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poor intake
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Pathophysiology
Hypokalemia increases the cell's resting potential by disruption of the Na/K transporter, leading to a lengthened refractory period. Hyperpolarization lead
Effects on the Heart
Hypokalemia can be very dangerous when combined with digoxin. Digitalis binds to the K site on the Na/K pump. less K will increase digoxin binding.
Normally, volume loss = decreased distal flow, decreasing K secretion.
Potassium deficiency is often seen alongside magnesium deficiency.
Signs, Symptoms, and Diagnosis
Obtain an ECG immediately.
Diagnosis is facilitated through understanding of blood pressure, acid-base status, and measurement of urinary chloride.
- history
- physical exam
- ECG changes
- lab investigations
History
Symptoms of hypokalemia can be vague, and can include:
- weakness
- paralysis
- palpitations
- abdominal cramping and constipation (ileus)
- muscle pain
- cardiac ischemia
A careful history, with emphasis on diet and use of medications and laxatives, should be obtained.
Chronic hypokalemia stimulates thirst and can cause nephrogenic diabetes insipidus.
Physical Exam
The most prominent abnormalities involve the cardiovascular system, as discussed in ECG changes.
Signs of hypokalemia include:
- polyuria
- impaired muscle contraction
- peritoneal distention
- dyspnea
- paralysis
ECG changes
ECG changes are more clincially important than K levels. Changes include:
- U waves (most important; represents delayed ventricular repolarization)
- flattened or inverted T waves
- depressed ST segment
- prolonged QT interval
Prolonged QT interval, prolonging action potential duration, and increasing spontaneous firing can lead to arrhythmias, including:
- supraventricular tachycardia
- atrial fibrillation
- ventricular tachycardia
- Torsades des pointes
Lab Investigations
Lab investigations should include:
- CBC (to examine for leukemia or other leukocytic conditions that could cause spurious results
- electrolytes
- kidney function (BUN, creatinine)
- magesium levels
- venous pH or arterial blood gas
- serum and urine electrolytes and osmolality
- if urinary K is >20 mEq/day, plasma renin and aldosterone should be assayed to assess causes of hyperaldosteronism
Treatments
Identify and treat the underlying cause.
Patients with a potassium below 2.5 mEq/L should be hospitalized and monitored during treatment.
If hypomagnesemia is also present, this too needs to be replaced.
Potassium repletion
Note: be very cautious in potassium replacement in the elderly, or patients with renal impairment or diabetes; life-threatening hyperkalemia can result.
The net deficit can be difficult to determine, given the role of intracellular stores and shift. However, a decrease in serum K of 1 mEq is approximately 300 mEq total body loss.
For mild deficiency, oral supplementation should be used if possible, at a rate of at approximately 20-40 mEq every 4 hours. Higher doses can lead to gastrointestinal irritation. Sources can include food, tablets, or liquid. Potassium bicarbonate can be used if phosphate deficiency is present.
For more significant deficiency, IV replacement is warranted. IV potassium should not exceed 10-20 mEq/hour, and concentration should not exceed >40 mEq/L for periperal lines or 60 mmol/L for central lines, to prevent irritation. Avoid dextrose-containing fluids to prevent intracellular shift via insulin release.
Prevention
K-sparing diuretics such as spironolactone, amiloride, or triamterene can prevent renal loss.
Consequences and Course
Life-threatening cardiac arrhythmias are the most significant consequence of hypokalemia, and begin to be worrisome below 2.7 mEq.
Other consequences can include:
- weakness and paralysis
- paralytic ileus
- rhabdomyolsis
Resources and References
Kjeldsen K. 201. Hypokalemia and sudden cardiac death. Exp Clin Cardiol. 15(4):e96-9.
Slovis C, Jenkins R. 2002. Conditions not primarily affecting the heart. BMJ. 324:1320.1
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