12.2 Electrolyte Imbalances: Potassium, Sodium, Calcium & Magnesium

Electrolyte Imbalances: Potassium, Sodium, Calcium & Magnesium

Statutory Nursing Safety Principle: Electrolyte disturbances represent frequent, high-risk clinical presentations across Irish medical and surgical wards. Because electrolyte shifts destabilize cardiac rhythmicity, neuromuscular conductivity, and cerebral cell volume, registered nurses must understand both emergency pharmacological interventions and statutory medication safety limits. In both the theoretical examination and OSCE simulation circuits, candidates are tested on ECG interpretation, clinical diagnostic signs, and life-saving drug administration sequences.

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Potassium Homeostasis (Normal Reference: 3.5 – 5.0 mmol/L)

Potassium (K+) is the primary intracellular cation, maintained at ~140–150 mmol/L inside cells and only 3.5–5.0 mmol/L in the extracellular plasma. This massive chemical gradient across the cell membrane is actively maintained by the energy-dependent Na+/K+ ATPase pump. Potassium governs the resting membrane potential (Em) of cardiac myocytes and neuromuscular cells. Deviations in extracellular potassium profoundly affect myocardial excitability.

Hyperkalaemia (K+ > 5.0 mmol/L; Severe ≥ 6.5 mmol/L)

Etiology

• Reduced Renal Excretion: Acute Kidney Injury (AKI), Chronic Kidney Disease (CKD Stage 4–5), Addison's disease (hypoaldosteronism).
• Pharmacological Agents: Potassium-sparing diuretics (spironolactone, eplerenone, amiloride), Angiotensin-Converting Enzyme Inhibitors (ACEi, e.g., ramipril), Angiotensin Receptor Blockers (ARBs, e.g., losartan), NSAIDs, trimethoprim, calcineurin inhibitors (tacrolimus).
• Extracellular Shifts: Severe metabolic acidosis (excess extracellular H+ ions enter cells, driving K+ out into plasma to preserve electrical neutrality), insulin deficiency / hyperglycaemia.
• Cellular Breakdown / Tissue Lysis: Rhabdomyolysis, severe crush injuries, massive burns, tumour lysis syndrome, major haemolytic reactions.
• Pseudohyperkalaemia: In vitro haemolysis during traumatic phlebotomy, prolonged tourniquet application, fist clenching, or delayed laboratory analysis. Always verify with an urgent repeat sample or arterial blood gas (ABG) if clinical findings do not correlate.

Electrocardiographic (ECG) Progression

As extracellular potassium rises, cardiac repolarization accelerates and resting membrane potential becomes progressively hypopolarized, creating distinctive serial ECG anomalies:

+-----------------------------------------------------------------------------+
|                     ECG PROGRESSION IN HYPERKALAEMIA                        |
+-----------------------------------------------------------------------------+
| 1. Serum K+ 5.5 - 6.5 mmol/L:                                               |
|    - Tall, peaked, symmetrical 'tented' T waves (narrow base; precordial    |
|      leads V2-V4)                                                           |
|                                                                             |
| 2. Serum K+ 6.5 - 7.5 mmol/L:                                               |
|    - Prolongation of the PR interval                                        |
|    - Flattening and eventual disappearance (loss) of P waves                |
|                                                                             |
| 3. Serum K+ 7.5 - 8.5 mmol/L:                                               |
|    - Marked widening of the QRS complex (> 0.12 seconds)                    |
|    - ST-segment depression                                                  |
|                                                                             |
| 4. Serum K+ > 8.5 mmol/L:                                                   |
|    - QRS widens and merges with the elevated T wave -> 'SINE WAVE' PATTERN  |
|    - Pre-terminal arrest: Ventricular Fibrillation, Extreme Bradycardia,    |
|      or Asystole                                                            |
+-----------------------------------------------------------------------------+

Emergency Three-Pronged Resuscitation Protocol

When severe hyperkalaemia (K+ ≥ 6.5 mmol/L) or hyperkalaemia with any ECG changes is identified, the nurse must activate the emergency medical team and follow the standardized three-phase treatment protocol:

+-----------------------------------------------------------------------------+
|              THREE-PHASE EMERGENCY HYPERKALAEMIA PROTOCOL                   |
+-----------------------------------------------------------------------------+
| PHASE 1: MYOCARDIAL MEMBRANE STABILISATION (Minutes 0 - 5)                  |
| - Medication: 10% Calcium Gluconate (10 mL IV over 5 to 10 minutes)        |
| - Onset: 1 to 3 minutes; Duration: 30 to 60 minutes                         |
| - CRITICAL SAFETY RULE: Calcium gluconate protects the myocardium against   |
|   ventricular arrhythmias; IT DOES NOT LOWER SERUM POTASSIUM!               |
| - Repeat dose after 5-10 minutes if ECG anomalies persist.                  |
+-----------------------------------------------------------------------------+
| PHASE 2: INTRACELLULAR POTASSIUM SHIFT (Minutes 15 - 30)                    |
| - Medication: 10 units Soluble Insulin (Actrapid) in 50 mL 50% Glucose (or  |
|   100 mL 20% Glucose) IV over 15 to 30 minutes                              |
| - Action: Stimulates Na+/K+ ATPase, driving K+ into intracellular spaces    |
| - Onset: 15 to 30 minutes; Peak: 60 minutes; Duration: 4 to 6 hours         |
| - Nursing Action: Monitor bedside capillary blood glucose at 15, 30, 60,    |
|   90, and 120 minutes to prevent fatal iatrogenic hypoglycaemia!            |
| - Synergistic Therapy: Nebulised Salbutamol (10 to 20 mg in 4 mL saline via |
|   oxygen-driven nebuliser; stimulates beta-2 receptors to shift K+ into     |
|   cells). Avoid if patient has severe tachyarrhythmias.                     |
+-----------------------------------------------------------------------------+
| PHASE 3: TOTAL BODY POTASSIUM ELIMINATION (Hours 1 - 6)                     |
| - Cation Exchange Resins: Calcium Polystyrene Sulfonate (Calcium Resonium,  |
|   15 g PO TDS or 30 g PR) or Sodium Zirconium Cyclosilicate (Lokelma).      |
| - Loop Diuretics: Furosemide (40 to 80 mg IV) to promote kaliuresis if      |
|   patient has preserved renal perfusion.                                    |
| - Renal Replacement Therapy: Emergency Haemodialysis is the definitive gold |
|   standard for refractory severe hyperkalaemia or anuric renal failure.     |
+-----------------------------------------------------------------------------+

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Hypokalaemia (K+ < 3.5 mmol/L; Severe < 2.5 mmol/L)

Etiology

• Gastrointestinal Losses: Severe vomiting, nasogastric continuous suction, profuse diarrhoea, laxative abuse, high-output enterocutaneous fistulae or ileostomies.
• Renal Losses: Loop diuretics (furosemide, bumetanide) and thiazide diuretics (bendroflumethiazide), hyperaldosteronism (Cushing's, Conn's syndrome), renal tubular acidosis.
• Intracellular Shifts: Exogenous insulin administration without adequate potassium supplementation, beta-2 agonists (salbutamol), refeeding syndrome, alkalosis (H+ exits cells, K+ enters).
• Concurrent Hypomagnesaemia: Low magnesium disinhibits renal potassium wasting; hypokalaemia is completely refractory to replacement until magnesium is replenished.

Clinical & ECG Features

• Neuromuscular: Generalized skeletal muscle weakness, fatigue, diminished deep tendon reflexes (hyporeflexia), painful muscle cramps, ascending flaccid paralysis, respiratory muscle hypoventilation.
• Gastrointestinal: Decreased smooth muscle motility leading to constipation, abdominal distension, and paralytic ileus.
• ECG Abnormalities: Flattened or inverted T waves, ST-segment depression, prominent U waves (an extra upward deflection following the T wave), prolonged PR and QT/QU intervals, atrial fibrillation, polymorphic ventricular tachycardia, and risk of Ventricular Fibrillation.

+-----------------------------------------------------------------------------+
|                 ECG TRACING CHARACTERISTICS IN HYPOKALAEMIA                 |
+-----------------------------------------------------------------------------+
|                                                                             |
|      Baseline Normal Complex       vs        Hypokalaemia Complex           |
|                                                                             |
|              R                                     R                        |\n|             /|                                    /|                        |\n|            / |                                   / |                        |\n|           /  |      T                           /  |    T (Flat)   U Wave   |\n|          /   |    +---+                        /   |   +------+   +----+    |\n|   P     /    |   /     |                  P   /    |  /        | /      |   |\n|  +-+   /     |  /       |                +-+ /     | +          +        +  |\n| /   +-+      +-+         +              /   v      |                        |\n|        Q      S                              Q     +-+ (ST depression)      |\n|                                                     S                       |\n|                                                                             |\n+-----------------------------------------------------------------------------+\n```\n\n#### Treatment & High-Alert Medication Safety Rules
- **Mild to Moderate (3.0 – 3.4 mmol/L)**: Oral potassium chloride (e.g., Sando-K effervescent tablets, 2 to 4 tablets daily dissolved in water after meals to prevent gastric mucosal irritation).
- **Severe (<2.5 mmol/L) or Symptomatic**: Intravenous Potassium Replacement.

> [!CAUTION] **STRICT STATUTORY MEDICATION SAFETY WARNING: IV POTASSIUM:**
> 1. **NEVER administer Potassium Chloride as an IV Push or Undiluted Bolus.** Direct IV injection causes instantaneous hyperkalaemic cardiac arrest and is a fatal sentinel error.
> 2. **Use Pre-Mixed Manufacturer Bags Only.** On acute Irish hospital wards, nurses must never manually dilute concentrated potassium ampoules into fluid bags; only commercially prepared, clearly labelled pre-mixed bags may be stocked and infused.
> 3. **Mandatory Electronic Infusion Pump.** All IV potassium infusions must be delivered using a dedicated volumetric infusion pump with anti-free-flow protection. Gravity drip administration is strictly forbidden.
> 4. **Infusion Rate Limit**: Standard peripheral infusion rate must **never exceed 10 to 20 mmol of potassium per hour**.
> 5. **Peripheral Concentration Limit**: Maximum concentration infused via a peripheral cannula is **40 mmol/L** (e.g., 40 mmol KCl in 1,000 mL 0.9% NaCl). Higher concentrations (e.g., 20 mmol in 100 mL mini-bags) cause severe local chemical burning and thrombophlebitis; they require a central venous catheter (CVC) and continuous cardiac telemetry in a high-dependency setting.

Sodium Homeostasis (Normal Reference: 135 – 145 mmol/L)

Sodium (Na+) is the principal extracellular cation and the primary determinant of plasma osmolality (275–295 mOsm/kg). Water moves across semi-permeable cell membranes via osmosis to equilibrate osmolality between the ICF and ECF. Therefore, sodium disorders are fundamentally disorders of water balance that alter brain cell volume.

Hyponatraemia (Na+ < 135 mmol/L; Severe < 120 mmol/L)

When plasma sodium falls, extracellular fluid becomes hypotonic relative to brain cells. Water shifts down the osmotic gradient into cerebral neurons, precipitating cerebral edema.

Diagnostic Classification by Volume Status

To manage hyponatraemia, the nurse must assist in determining the patient's extracellular volume status:

1. Hypovolaemic Hyponatraemia (Deficit of both sodium and water; sodium deficit > water deficit):

   • Causes: Renal losses (diuretics, mineralocorticoid deficiency) or Extra-renal losses (severe vomiting, diarrhoea, excessive sweating, high-output stomas).
   • Bedside signs: Hypotension, tachycardia, dry mucous membranes, flat neck veins, oliguria.
   • Treatment: Volume restoration with intravenous 0.9% Sodium Chloride.

2. Euvolaemic Hyponatraemia (Normal body sodium, excess free water retention):

   • Causes: Syndrome of Inappropriate Antidiuretic Hormone (SIADH) — caused by small cell lung carcinoma, head trauma, stroke, CNS infections, pneumonia, and medications (SSRIs, carbamazepine, PPIs, antipsychotics). Other causes include severe hypothyroidism and psychogenic polydipsia.
   • Bedside signs: Clinically normal volume status; no edema, normal blood pressure, normal JVP.
   • Diagnostic criteria for SIADH: Plasma osmolality < 275 mOsm/kg, inappropriate urinary concentration (Urine Osmolality > 100 mOsm/kg), and high urine sodium (Urine Na+ > 30 mmol/L) despite hyponatraemia.
   • Treatment: Strict Fluid Restriction (typically 500 to 1,000 mL/24 hours); discontinue offending medications; oral urea or vasopressin receptor antagonists (vaptans).

3. Hypervolaemic Hyponatraemia (Excess sodium and water; water excess >> sodium excess — 'dilutional hyponatraemia'):

   • Causes: Congestive heart failure, liver cirrhosis with ascites, nephrotic syndrome, acute or chronic renal failure.
   • Bedside signs: Peripheral pitting edema, ascites, elevated JVP, pulmonary crackles.
   • Treatment: Fluid Restriction, sodium restriction, and loop diuretics (furosemide).

Neurological Symptoms & Emergency Hypertonic Saline

• Mild/Moderate: Anorexia, nausea, headache, malaise, lethargy, cognitive slowing, muscle cramps, gait instability.
• Severe (Na+ < 120 mmol/L or rapid drop): Confusion, delirium, seizures, coma, respiratory arrest, and fatal uncal herniation.
• Acute Symptomatic Emergency: In patients presenting with active seizures, stupor, or signs of herniation, an immediate bolus of hypertonic 3% Sodium Chloride (100 to 150 mL IV over 10–20 minutes) is administered to rapidly raise serum sodium by 4–6 mmol/L, relieving intracranial pressure.

[!WARNING] THE FATAL DANGER OF RAPID CORRECTION: CENTRAL PONTINE MYELINOLYSIS: When hyponatraemia develops chronically (>48 hours), brain cells adapt by pumping out intracellular osmolytes (myoinositol, taurine, glutamate) to protect against swelling. If the clinician corrects chronic hyponatraemia too quickly, the sudden hypertonic plasma pulls water violently out of brain cells, causing dehydration of cerebral tissue, disruption of the blood-brain barrier, and destruction of myelin sheaths in the pons. This produces Central Pontine Myelinolysis (Osmotic Demyelination Syndrome - ODS), resulting in irreversible spastic quadriparesis, pseudobulbar palsy, dysphagia, and 'locked-in syndrome'.

STRICT CEILING RULE: The rate of sodium correction in chronic hyponatraemia must NEVER exceed 8 to 10 mmol/L in any 24-hour period (and < 18 mmol/L in 48 hours). Serum sodium must be monitored every 4 to 6 hours during active correction.

Hypernatraemia (Na+ > 145 mmol/L; Severe > 155 mmol/L)

Hypernatraemia creates a hypertonic extracellular state, pulling water out of neurons and shrinking brain tissue.

• Etiology: Deficient water intake (frail, elderly, or unconscious patients lacking access to water; defective thirst mechanism), unreplaced water losses (febrile illness, hyperventilation, osmotic diuresis in DKA/HHS), Diabetes Insipidus (central: deficient ADH from pituitary surgery/trauma; nephrogenic: renal ADH insensitivity due to lithium or hypercalcaemia).
• Clinical Presentation: Intense unquenchable thirst, dry flushed skin, dry parched tongue, restlessness, irritability, ataxia, delirium, hyperreflexia, spasticity, coma, and intracerebral haemorrhage due to tearing of bridging cerebral veins.
• Correction Strategy: Slow correction over 48 hours using oral free water or intravenous 5% Dextrose. The rate of sodium reduction must not exceed 10 mmol/L in 24 hours; lowering sodium too quickly causes water to rush into brain cells, inducing fatal cerebral edema and convulsions.

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Calcium & Magnesium Homeostasis

Calcium Homeostasis (Total: 2.15 – 2.55 mmol/L; Ionised: 1.15 – 1.35 mmol/L)

Approximately 40% to 50% of circulating total serum calcium is bound to plasma proteins (predominantly albumin). The remaining fraction is the biologically active ionised calcium (Ca2+). If albumin is abnormal, nurses must calculate the corrected calcium:

Corrected Calcium (mmol/L) = Total Calcium (mmol/L) + 0.02 × (40 - Serum Albumin [g/L])

Hypocalcaemia (Corrected Calcium < 2.15 mmol/L)

• Etiology: Iatrogenic hypoparathyroidism following thyroidectomy or radical neck dissection (inadvertent excision or vascular compromise of parathyroid glands), severe vitamin D deficiency, hypomagnesaemia, acute pancreatitis (calcium saponification in retroperitoneal fat), chronic kidney disease, massive red blood cell transfusion (citrate anticoagulant binds circulating ionised calcium).
• Clinical Features: Neuromuscular excitability: perioral tingling/numbness, paresthesias in fingertips and toes, muscle cramps, hyperreflexia, laryngospasm/stridor, bronchospasm, seizures, and prolonged QT interval on ECG (predisposing to Torsades de Pointes).
• Classic Physical Diagnostic Signs:
  1. Chvostek's Sign: Tapping the facial nerve immediately anterior to the ear tragus (over the parotid gland) elicits unilateral involuntary twitching of the ipsilateral facial muscles (corner of mouth, nose, eye).
  2. Trousseau's Sign: Inflating a sphygmomanometer blood pressure cuff on the upper arm to >20 mmHg above the patient's systolic blood pressure for 3 minutes occludes the brachial artery, causing localized ischaemia in irritable motor nerves. This precipitates characteristic carpopedal spasm: flexion of the wrist and metacarpophalangeal joints, hyperextension of the interphalangeal joints, and adduction of the thumb ('obstetrician's hand'). Highly sensitive and specific for hypocalcaemia.
• Emergency Treatment: Symptomatic severe hypocalcaemia requires 10% Calcium Gluconate (10 to 20 mL IV in 50–100 mL 5% Dextrose over 10 to 20 minutes) with continuous ECG monitoring.

+-----------------------------------------------------------------------------+
|                        TROUSSEAU'S SIGN CLINICAL TEST                       |
+-----------------------------------------------------------------------------+
| 1. Apply standard blood pressure cuff to upper arm.                         |
| 2. Inflate cuff to 20 mmHg ABOVE patient's baseline systolic blood pressure.|
| 3. Maintain continuous inflation for 3 FULL MINUTES.                       |
| 4. POSITIVE RESULT: Ischaemia triggers acute carpopedal spasm               |
|    - Adduction of thumb across palm                                         |
|    - Flexion of metacarpophalangeal (MCP) joints                            |
|    - Extension of interphalangeal (IP) joints                               |
|    - Flexion of wrist ('Obstetrician's Hand' / Main d'accoucheur)           |
+-----------------------------------------------------------------------------+

Hypercalcaemia (Corrected Calcium > 2.55 mmol/L; Severe > 3.0 mmol/L)

• Etiology: Over 90% of cases are caused by Primary Hyperparathyroidism (parathyroid adenoma; dominant in outpatient clinic settings) or Malignancy (bony metastases in breast/prostate, multiple myeloma, or secretion of Parathyroid Hormone-Related Protein [PTHrP] by squamous cell carcinomas; dominant in acute hospital wards).
• Clinical Signs ('Bones, Stones, Groans, and Psychiatric Overtones'):
  • Bones: Bone pain, osteopenia, pathological fractures.
  • Stones: Nephrolithiasis (renal calculi), nephrocalcinosis, polyuria, polydipsia (nephrogenic DI).
  • Groans: Anorexia, nausea, vomiting, severe constipation, abdominal pain, peptic ulcers, pancreatitis.
  • Psychiatric Overtones: Lethargy, fatigue, depression, cognitive impairment, delirium, coma.
  • ECG: Shortened QT interval, widened T wave, bradycardia, heart block.
• Emergency Management:
  1. Aggressive IV Rehydration: Infuse 0.9% Sodium Chloride (3 to 4 litres over 24 hours) to expand circulating volume and promote urinary calcium excretion (calciuresis).
  2. Intravenous Bisphosphonates: Pamidronate (30 to 90 mg IV) or Zoledronic acid (4 mg IV over 15 minutes) to inhibit osteoclastic bone resorption (takes 48–72 hours to achieve peak effect).
  3. Subcutaneous Calcitonin: Rapid temporary reduction in serum calcium while awaiting bisphosphonate action.

Magnesium Homeostasis (Normal Reference: 0.7 – 1.0 mmol/L)

Magnesium (Mg2+) is the second most abundant intracellular cation, serving as an essential enzymatic cofactor for over 300 biochemical reactions, including ATP hydrolysis and the Na+/K+ ATPase pump.

Hypomagnesaemia (Mg2+ < 0.7 mmol/L)

• Etiology: Chronic alcohol dependence (poor dietary intake and renal tubular wasting), chronic malnutrition, malabsorption syndromes (Crohn's, coeliac), chronic diarrhoea, loop and thiazide diuretics, prolonged use of Proton Pump Inhibitors (PPIs, e.g., omeprazole), and nephrotoxic drugs (aminoglycosides, amphotericin, cisplatin).
• Clinical Manifestations: Neuromuscular hyperactivity: tremors, choreiform movements, muscle fasciculations, hyperreflexia, tetany (positive Chvostek's and Trousseau's signs), cardiac arrhythmias, and distinctive ECG findings: prolonged PR and QT intervals, ventricular ectopics, and fatal Torsades de Pointes (polymorphic ventricular tachycardia).

[!IMPORTANT] THE REFRACTORY ELECTROLYTE TRAP: RESISTANT HYPOKALAEMIA & HYPOCALCAEMIA: If an acute hospital patient has hypokalaemia or hypocalcaemia that fails to correct despite aggressive intravenous potassium or calcium administration, the nurse must check the magnesium level!

• Magnesium is required to keep renal potassium secretory channels (ROMK) closed. In hypomagnesaemia, the channels stay wide open, causing massive renal potassium dumping.
• Magnesium is also required for the release and receptor sensitivity of Parathyroid Hormone (PTH). Low magnesium induces PTH resistance, locking calcium out of the circulation. Clinical Rule: You CANNOT correct hypokalaemia or hypocalcaemia until hypomagnesaemia is treated. Administer IV Magnesium Sulfate (e.g., 2 g / 8 mmol in 100 mL 5% Dextrose over 20–60 minutes).