Hyperkalaemia Nursing Guide

Hyperkalaemia Overview

Hyperkalaemia is defined as serum potassium >5.5 mmol/L. Severe hyperkalaemia (>6.5 mmol/L) is a cardiac emergency — can cause fatal ventricular fibrillation without warning.

Severity Classification

Level	K⁺ (mmol/L)	Urgency
Mild	5.5–6.0	Monitor; treat underlying cause; dietary restriction
Moderate	6.0–6.5	Active treatment needed; cardiac monitoring; check ECG
Severe	>6.5 OR any ECG changes	Emergency — immediate IV calcium + insulin/dextrose

Pseudohyperkalaemia: Check for haemolysis (traumatic venepuncture), prolonged tourniquet, delayed sample processing or extreme thrombocytosis/leucocytosis. Repeat sample from new venepuncture if unexpected result before treating.

ECG Changes — Progression

Know the progression: Peaked T waves → prolonged PR → wide QRS → sine wave → VF/asystole. Any ECG change = immediate treatment regardless of serum K⁺ level.

Sequential ECG Changes with Rising K⁺

K⁺ Level	ECG Change
5.5–6.5 mmol/L	Peaked (tall, narrow, symmetric) T waves — best seen V4–V6; "tent-shaped"
6.5–7.0 mmol/L	Prolonged PR interval; flattening/loss of P waves
7.0–7.5 mmol/L	Widened QRS complex (>0.12 seconds)
7.5–8.0 mmol/L	Sine wave pattern — QRS merges with T wave
>8.0 mmol/L	Ventricular fibrillation or asystole — cardiac arrest

Critical nursing action: Any ECG change (including peaked T waves alone) = treat as emergency regardless of serum K⁺ value. Start continuous cardiac monitoring; call senior immediately; prepare calcium gluconate.

Emergency Treatment — C-BIG-K-DROP

Mnemonic for systematic treatment of hyperkalaemia: Calcium, Bicarbonate, Insulin/dextrose, Glucose monitoring, Kayexalate (resonium), Dialysis, Remove cause, Oral/IV furosemide, Patrolling (continuous monitoring)

Step 1 — Cardiac Membrane Stabilisation (IMMEDIATE)

First and most urgent: Calcium gluconate 10% — 10 mL (1 g) IV over 5–10 minutes. Repeat if ECG does not improve after 5 minutes. Effect within 1–3 minutes, duration 30–60 minutes.

Mechanism: Does NOT lower serum K⁺ — temporarily stabilises cardiac membrane by raising threshold potential. Buys time for K⁺-lowering treatments to work
Calcium chloride 10%: Higher calcium content (3× more elemental calcium); use in cardiac arrest; MUST be via central line (causes tissue necrosis peripherally)
Calcium gluconate: Safer for peripheral IV; can be given via large peripheral vein
ECG monitoring: Continuous ECG during calcium administration; repeat dose if no improvement in 5 min

Step 2 — Shift K⁺ into Cells

Treatment	Dose	Onset	Duration	Mechanism
Insulin + Dextrose	10 units Actrapid IV + 50 mL 50% dextrose (or 250 mL 10% dextrose)	15–30 min	2–6 hrs	Insulin activates Na/K-ATPase pump, driving K⁺ intracellular
Salbutamol (nebulised)	10–20 mg via nebuliser (high dose)	15–30 min	2 hrs	Beta-2 activation → Na/K-ATPase → K⁺ into cells
Sodium bicarbonate IV	50 mmol (50 mL of 8.4%) over 5 min	30–60 min	1–2 hrs	Alkalinisation → H⁺ leaves cells, K⁺ enters in exchange. Less reliable in non-acidotic patients

MONITOR GLUCOSE every 15–30 minutes after insulin-dextrose — risk of hypoglycaemia. Have 50% dextrose at bedside. If BGL falls <5 mmol/L → further dextrose bolus.

Step 3 — Remove K⁺ from Body

Method	Time to effect	Notes
Furosemide (loop diuretic)	Hours	40–80 mg IV if patient not anuric; increases renal K⁺ excretion; ensure not dehydrated
Calcium resonium (sodium polystyrene sulphonate)	4–6 hrs	15 g orally TDS or 30 g PR; K⁺ exchange resin in gut — avoid in post-op (paralytic ileus risk); colonic necrosis risk
Patiromer (Veltassa)	7 hrs	Newer potassium binder; better tolerated than resonium; once daily oral
Sodium zirconium cyclosilicate (ZS-9)	1 hr	Rapid onset K⁺ binder; 10 g TDS for 2 days then maintenance; available in major GCC centres
Haemodialysis	Minutes	Most effective and fastest method; indicated for severe refractory hyperkalaemia, oliguria/anuria, or when other measures fail

Causes of Hyperkalaemia

Main Causes — MACHINE

Letter	Cause
M	Medications — ACE inhibitors, ARBs, K-sparing diuretics (spironolactone, amiloride), NSAIDs, heparin, trimethoprim, succinylcholine, digoxin toxicity
A	Acidosis (metabolic) — H⁺ enters cell, K⁺ exits to maintain electrical neutrality
C	Cellular destruction — rhabdomyolysis, haemolysis, tumour lysis syndrome, burns, major trauma
H	Hypoaldosteronism — Addison's disease, adrenal insufficiency, type 4 RTA
I	Intake excess — excessive dietary K⁺, K⁺ IV supplements, blood transfusions (old blood)
N	Nephrology — acute and chronic kidney disease (primary cause)
E	Endocrine — diabetic ketoacidosis (K⁺ shift), hyperosmolality

GCC-Specific Context

Hyperkalaemia in GCC

CKD/ESKD prevalence: GCC has among the world's highest rates of diabetic nephropathy and CKD — leading to hyperkalaemia as a chronic management challenge in dialysis-dependent patients
ACEi/ARB + K-sparing diuretic combinations: High prescribing in GCC for heart failure and DM nephropathy — dangerous combinations particularly in elderly with declining eGFR
Ramadan fasting: Dialysis patients who fast during Ramadan skip dialysis sessions → accumulate potassium. Pre-Ramadan potassium management education essential for dialysis nurses
Sickle cell disease: Hyperkalaemia from sickle cell haemolysis — particularly in Bahrain, Eastern Saudi, Oman populations
DKA: Pseudohyperkalaemia at DKA presentation (acidosis shifts K⁺ extracellular) — total body K⁺ depleted. Never give K⁺ before insulin in DKA with K⁺ >5.5

Exam Tips

Calcium gluconate first in hyperkalaemia — stabilises heart, does NOT lower K⁺
ECG: peaked T waves first → wide QRS → sine wave → VF
Insulin + dextrose: most reliable acute K⁺-lowering; monitor BGL every 15 min
Haemodialysis = most effective; indicated for K⁺ >7 or refractory cases
Calcium chloride goes via CENTRAL line only (peripheral causes necrosis)
Resonium (resonium) for gut K⁺ removal — avoid post-operatively

Exam MCQs — DHA / SCFHS / QCHP

Q1. A dialysis patient has K⁺ 7.2 mmol/L. ECG shows wide QRS complexes and no P waves. What is the FIRST drug to administer?

A) Insulin 10 units IV with 50% dextrose B) Calcium gluconate 10% — 10 mL IV over 5–10 minutes C) Sodium bicarbonate 50 mmol IV D) Furosemide 80 mg IV

✅ B — ECG changes (especially wide QRS) = imminent cardiac arrest risk. Calcium gluconate is the FIRST priority — it stabilises the cardiac membrane within 1–3 minutes. It does NOT lower K⁺ but prevents fatal arrhythmia while K⁺-lowering treatments take effect. Insulin-dextrose is given immediately after but calcium is the top priority.

Q2. Insulin 10 units IV has been administered with 50% dextrose for hyperkalaemia. What is the MOST IMPORTANT nursing action in the next 60 minutes?

A) Administer repeat insulin dose every 30 minutes B) Monitor blood glucose every 15–30 minutes — hypoglycaemia risk C) Check serum potassium immediately — insulin should normalise K⁺ within 5 minutes D) Restrict oral fluid intake to prevent fluid overload

✅ B — Insulin-dextrose carries significant hypoglycaemia risk. Blood glucose must be monitored every 15–30 minutes after insulin administration. Have 50% dextrose drawn up at the bedside. Insulin's K⁺-lowering effect peaks at 30–60 minutes but hypoglycaemia can occur earlier. Failure to monitor glucose in hyperkalaemia treatment is a critical nursing error.

Q3. What ECG change is typically the EARLIEST sign of hyperkalaemia?

A) Widened QRS complex B) Loss of P waves C) Peaked (tall, symmetric, narrow) T waves D) Sine wave pattern

✅ C — Peaked T waves (tall, narrow, symmetric, tent-shaped) are the earliest ECG manifestation of hyperkalaemia, typically appearing at K⁺ 5.5–6.5 mmol/L. The progression continues: peaked T waves → prolonged PR → loss of P waves → wide QRS → sine wave → VF. Any ECG change mandates immediate treatment.

Q4. A patient with hyperkalaemia requires calcium chloride 10% IV. Via which route should this be administered?

A) Any peripheral IV cannula — same as calcium gluconate B) Central venous catheter ONLY — calcium chloride causes severe tissue necrosis if extravasated peripherally C) Intramuscular injection if no IV access available D) Oral route is equivalent to IV for calcium chloride

✅ B — Calcium chloride 10% MUST be administered via central venous catheter. If extravasated peripherally, it causes severe tissue necrosis and chemical burns. Calcium gluconate is safer for peripheral administration. In a cardiac arrest scenario where no central access exists, calcium chloride may be given into a large antecubital vein as a last resort — but central access should be established as soon as possible.

⚡ Hyperkalaemia