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Hyperkalemia (Aetiology (Iatrogenic
Massive blood transfusion
Excess K+…
Hyperkalemia
Aetiology
Iatrogenic
Massive blood transfusion
Excess K+ therapy
Artefact (haemolysis, EDTA contamination, thrombocythaemia, delayed blood analysis)
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Pathophysiology
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Mechanism
Decreased membrane exciteability in all tissues
High levels cause myocardial exciteability,
VF then cardiac arrest; also neuromuscular depression
Defect
Reduced K excretion (renal problems): AKI, CKD, Addisons, RAAS enzymes
Inc K+ production: TLS, rhabdomyolysis, K+ supplements
K+ shifts: DKA
Pseudo: lysis of blood sample
Diagnosis
Examination
Neuro exam
Reduced tone, weakness, reduced reflexes,
seizures, confusion
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History
PMH
Known medical conditions (CKD, Addison's, DM),
recent surgery or inpatient treatment
DH
Meds (diuretics, ACEi's), allergies
PC/HPC
Palpitations, chest pain, weakness,
confusion, seizures, coma
FH
Endocrine disease, renal disease
SH
Living arrangements, occupation,
smoking, alcohol
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Investigations
Bedside
Obs (tachycardic)
ECG - tall tented T waves, small P waves,
wide QRS complexes, VF
Bloods
ABG (acidosis), FBC, U+E (high K), LFTs, TFTs,
CK (rhabdomyolsis)
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Management
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Definitive
Medical
K+ binders
Indication: definitive reduction of serum K+ levels
e.g. Ca resonium PO pls lactulose
MOA: binds K in gut, prevents absorption,
reduces K+ levels over a few days
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Cardioprotection
Indication: severe hyper-K (>6.5 or ECG change)
E.g. calcium gluconate, calcium chloride
MOA: cardioprotective (stabilises myocardium,
but does not reduce K+ levels; give 10mL 10% over 5m;
repeat 20m until ECG normalises
B-agonists
Indication: severe hyper-K
E.g. nebulised salbutamol
MOA: drives K+ into cells (does not reduce K+ levels)
Insulin + glucose
Indication: severe hyper-K+
MOA: insulin drives K+ into cells, glucose
prevents hypoglycaemia
Conservative
Information, advice, support
Identify and manage cause
Lifestyle (reduced K intake)
Meds review (stop causative meds)
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