Identifying and managing hyperkalaemia in the prehospital environment
Abstract
Hyperkalaemia is defined as a high level of potassium within the blood. Potassium concentration is normally tightly regulated at 3.5–5.5 mmol/litre. Hyperkalaemia can have major consequences for muscle, nerve and cardiac function, leading to arrhythmias and cardiac arrest. It has many causes, including disease states, trauma and medication; a tourniquet can lead to pseudohyperkalaemia. Some patients are at a greater risk of developing it. Hyperkalaemia is most accurately identified through blood tests but results of these may not be available prehospitally. Paramedics need to take a thorough history and carry out an electrocardiogram (ECG) to diagnose hyperkalaemia. ECG results can indicate the severity of the condition, and a guide to the ECG changes corresponding to serum potassium levels could help paramedics in diagnosis. Nebulised salbutamol is recommended as the first-line management of hyperkalaemia in several healthcare areas but there are no protocols that enable UK paramedics to provide this, even though emergency vehicles carry the drug and paramedics administer it for other conditions. Establishing such protocols would allow paramedics to treat patients effectively at the scene and en route to hospital.
After completing this module, the paramedic will be able to:
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Hyperkalaemia is classified as a high level of potassium within the blood and can be defined as a serum potassium level of more than 5.5 mmol/litre (Nyirenda et al, 2009; Nair and Peate, 2013).
Potassium is the commonest positive ion in the human body and is essential for muscle contraction through the conduction of nerve impulses via action potentials. Approximately 2% of the body's potassium is in extracellular fluid, with the largest concentration being within intracellular fluid.
Potassium is tightly regulated at 3.5–5.5 mmol/litre; this is maintained by a complex process involving the transfer of potassium between intracellular and extracellular fluid by the sodium-potassium pump (Simon et al, 2020). This pump is stimulated by beta agonists, insulin and theophyllines taking potassium into cells. Conversely, acidosis and cell damage decrease the activity of the pump causing an extracellular shift in potassium ions, thereby increasing concentration. The action of aldosterone within the kidneys increases the excretion of potassium, maintaining homeostasis in the long term, with an increase in potassium concentration stimulating the release of aldosterone (Kumar and Clark, 2017). These mechanisms ensure serum potassium levels are maintained at a level within the normal range even though daily potassium intake varies.
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