Small changes in extracellular levels of potassium can have pro- found effects on the function of the cardiovascular and neuromus- cular systems. As about 98% of total body potassium (around 3500 mmol) is intracellular, serum potassium concentration (nor- mally 3.5–5 mmol/L) is a poor indicator of total body potassium and there is no absolute formula to determine potassium deficit.
Serial monitoring of serum potassium is necessary to guide the appropriate management of potassium disturbances.
Acidosis reduces Na + /K + -ATPase activity and results in a net efflux of potassium from cells and hyperkalaemia.
Conversely, alkalosis results in an influx of potassium into cells and hypokalae- mia.
These abnormalities are exacerbated by renal compensatory mechanisms that correct the acid–base balance at the expense of potassium homeostasis.
Hyperkalaemia (K >5.5 mmol/L)
This is a potentially life-threatening condition that can be caused by exogenous administration of potassium, the release of 1 Fluid and electrolyte balance • 15 potassium from cells (transcellular shift) as a result of tissue dam- age or changes in the Na + /K + -ATPase function (e.g., acidosis), or impaired renal excretion.
Mild hyperkalaemia (K+ <6 mmol/L) is often asymptomatic, but as serum levels rise there is progressive slowing of electrical con- duction in the heart and the development of significant cardiac arrhythmias.
All patients suspected of having hyperkalaemia should have an electrocardiogram (ECG) for this reason.
Tall ‘tented’ T-waves in the precordial leads are the earliest ECG changes observed, but as hyperkalaemia progresses more signif- icant ECG changes occur, with flattening (or loss) of the P waves, a prolonged PR interval, widening of the QRS complex and, even- tually, asystole.
Severe hyperkalaemia (K + >7 mmol/L) requires immediate treatment to prevent this (Table 1.13).
Hypokalaemia (<3.0 mmol/L)
This is a common disorder in surgical patients.
Dietary intake of potassium is normally 60–80 mmol/day.
Under normal conditions, the majority of potassium loss (>85%) is via the kidneys and maintenance of potassium balance largely depends on normal renal tubular regulation.
Potassium depletion sufficient to cause a fall of 1 mmol/L in serum levels typically requires a loss of 100–200 mmol of potassium from total body stores.
Potassium excretion is increased by metabolic alkalosis, diuresis, increased aldosterone release and increased losses from the gastrointestinal tract—all of which occur commonly in the surgical patient.
Muscle weakness, paralytic ileus and flattening of T waves with prominent U waves on ECG are diagnostic features.
In hypokalaemia, for every three potassium ions that come out from the intracellular compartment, one hydrogen and two sodium ions are exchan- ged, causing extracellular alkalosis and intracellular acidosis.
Oral or nasogastric potassium replacement is safer than intrave- nous replacement and is the preferred route in asymptomatic patients with mild hypokalaemia.
Severe (K+ <2.5 mmol/L) or symptomatic hypokalaemia requires intravenous replacement.
While replacement rates of up to 40 mmol/h may be used (with cardiac monitoring) in an emergency, there is a risk of serious cardiac arrhythmias and rates exceeding 20 mmol/h should gen- erally be avoided.
Potassium solutions should never be adminis- tered as a bolus. A useful rule of thumb is: not more than 40 mmol of potassium chloride in 500 mL and not more than 15 mmol/h (outside a critical care setting).