Related Subjects:
|Hyperkalaemia
|ECG - Hyperkalaemia
|Hypokalemia
|Hyperkalaemic and Hypokalaemic Periodic Paralysis
|Resuscitation - Advanced Life Support
|Action Potential
⚡ Hyperkalaemia is a medical emergency. Electrolyte abnormalities are part of the MLA.
Rising plasma [K⁺] causes partial membrane depolarisation → inactivation of Na⁺ channels → risk of cardioplegia, muscle paralysis, and death.
💉 Calcium gluconate is preferred (less irritating to veins than calcium chloride).
🚑 Emergency Management: K⁺ >6.5 mmol/L or >6.0 mmol/L with ECG changes |
- 📟 Telemetry + ECG + IV access. Resend bloods if unexpected (exclude haemolysis).
- 💉 30 mL 10% Calcium Gluconate IV slow (5–10 min). Repeat if ECG changes persist.
OR
- 💉 10 mL 10% Calcium Chloride IV slow (5–10 min). Repeat if ECG changes persist.
- 💉 10 U short-acting insulin (Actrapid) + 50 mL of 50% glucose IV over 15–30 min.
- 💊 Lokelma (SZC) 10 g TDS up to 72 h.
- 🌬️ Salbutamol 5–20 mg nebulised (caution: IHD/arrhythmia).
- 💧 IV fluids as appropriate. Always identify & treat the cause.
- 💧 Stop drugs containing K or K retaining
- 💧 Hypervolaemia: Consider IV Frusemide to remove K
- 🔁 If K⁺ remains high but not critical, repeat in 1–2 h.
- 💧 Consider haemodialysis ASAP if Renal failure
- 💉 Cardiac arrest: IV Sodium Bicarbonate 50 mL 8.4% (especially if metabolic acidosis)
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📉 ECG Changes (Act Fast!)
- ⚠️ Tented T waves → Broad QRS → Bradycardia → Sinewave → VT/VF → Asystole
- Flat/absent P waves often precede collapse.
🧠 Physiology
- High [K⁺] inactivates Na⁺ channels → ineffective action potentials → conduction block.
- IV calcium works by enhancing conduction through L-type Ca²⁺ channels (resistant to K⁺ effects).
- This restores excitability but does not lower K⁺.
📋 Aetiology (Check Drug Chart!)
- 🩺 CKD/AKI, missed dialysis
- 💊 Drugs: ACEi, ARBs, spironolactone, eplerenone, amiloride, NSAIDs, ciclosporin, trimethoprim, heparin
- 🧬 Addison’s, Type 4 RTA, congenital adrenal enzyme defects
- 🩸 Rhabdomyolysis, trauma, burns, tumour lysis, transfusion, haemolysis
- 🍫 High-K⁺ diet (chocolate, fruit juice, salt substitutes)
- ⚠️ Pseudohyperkalaemia: haemolysed sample, fist clenching, lab error
🧾 Clinical Features
- Often asymptomatic → 🫀 arrhythmias may be first sign
- Weakness, cramps, paraesthesia
- Hypotension, bradycardia → cardiac arrest
📊 Severity
- Mild: 5.5–5.9 mmol/L
- Moderate: 6.0–6.4 mmol/L
- Severe: ≥6.5 mmol/L or ECG changes → 🚨 emergency
🔬 Investigations
- FBC (haemolysis, anaemia), LDH
- CK (rhabdomyolysis)
- U&E, Ca, Mg; repeat if unexpected
- VBG/ABG (metabolic acidosis)
- ECG (tented T → sinewave → VT/VF)
⚕️ Management Summary
- Stop offending drugs 🚫
- IV access + fluids (unless overloaded)
- Calcium gluconate IV if ECG changes
- Insulin + glucose infusion
- Nebulised salbutamol
- Consider furosemide if volume status allows
- Resins (Lokelma) as bridge
- Repeat U&E q2h, ECG monitoring
- If refractory/severe → dialysis
💔 Hyperkalaemia in Cardiac Arrest
- Confirm K⁺ >6.5 mmol/L (blood gas)
- 10 mL 10% Calcium chloride IV bolus (can repeat)
- 10 U insulin + 25 g glucose IV bolus, then glucose infusion
- 50 mmol NaHCO₃ (50 mL 8.4%) IV if severe acidosis
- Dialysis if refractory
- Consider mechanical CPR device / ECLS if prolonged
📚 References
Cases — Hyperkalaemia
- Case 1: A 68-year-old man with CKD stage 4 and poorly controlled hypertension presents with muscle weakness. ECG shows tall, tented T-waves. Serum potassium is 6.8 mmol/L. Management: IV calcium gluconate for cardiac membrane stabilisation, IV insulin with dextrose to shift K⁺ intracellularly, nebulised salbutamol, and oral sodium zirconium cyclosilicate. Loop diuretic started, and his ramipril held.
Outcome: Potassium falls to 5.0 mmol/L over 6 hours, symptoms resolve, and he is discharged after nephrology review.
- Case 2: A 42-year-old man with poorly controlled type 1 diabetes presents with vomiting and dehydration. Labs show diabetic ketoacidosis with potassium 7.2 mmol/L. ECG: absent P-waves, widened QRS. Management: IV calcium gluconate, insulin/dextrose infusion, aggressive fluid resuscitation with normal saline, and close cardiac monitoring. Outcome: As acidosis corrects, K⁺ shifts intracellularly and falls rapidly; potassium replacement is later required to prevent hypokalaemia. He recovers fully after 4 days in hospital.
- Case 3: A 79-year-old woman on spironolactone and an ACE inhibitor for heart failure presents after a collapse. Potassium 8.1 mmol/L. She is bradycardic (HR 38), hypotensive, and her ECG shows sine-wave complexes. Management: Immediate IV calcium chloride, repeated insulin/dextrose, IV sodium bicarbonate (metabolic acidosis present), and IV furosemide. Emergency haemodialysis organised. Outcome: ROSC achieved after transient cardiac arrest during dialysis initiation. Survives to discharge after 2 weeks but ACE inhibitor permanently discontinued.
Teaching Commentary 🧑⚕️
Hyperkalaemia is life-threatening because of its effects on cardiac conduction. Early ECG changes (tall T-waves, PR prolongation) progress to sine-wave and arrest. Management principles:
1) Stabilise the myocardium (calcium salts),
2) Shift potassium into cells (insulin/dextrose, salbutamol, bicarbonate if acidotic),
3) Remove potassium (resins, diuretics, dialysis).
Case 1 shows chronic renal disease, Case 2 highlights acidosis-driven hyperkalaemia in DKA, and Case 3 demonstrates the deadly drug–renal interaction in elderly patients. Always treat both the serum potassium and the underlying cause.