Internal Medicine & Nephrology & Family Medicine
Electrolytes: sodium, potassium, and chlorine
Electrolytes—ions dissolved in body fluids that can conduct an electric current—play a fundamental role in maintaining plasma osmolarity, acid-base balance, neuromuscular and cardiac excitability, and fluid distribution between fluid compartments. Basic electrolyte balance (sodium, potassium, chloride—often associated with bicarbonate and creatinine in the «blood ionogram» or «metabolic panel») is one of the most frequently ordered laboratory tests in primary care, emergency medicine, and inpatient settings. sodium (Na⁺) is the primary extracellular cation (normal value 136–145 mmol/L) — it determines effective plasma osmolarity and regulates the distribution of water between the intracellular and extracellular compartments; its regulation is ensured by the hypothalamic-pituitary axis (ADH — antidiuretic hormone — vasopressin) and the renin-angiotensin-aldosterone system (RAAS). The Potassium (K⁺) est le principal cation intracellulaire (98 % du potassium corporel total est intracellulaire — concentration intracellulaire ≈ 140 mmol/L vs plasmatique 3,5–5,0 mmol/L) — il détermine le potentiel de repos des cellules excitables (myocytes cardiaques, cellules musculaires squelettiques, neurones) et son gradient transmembranaire est le principal déterminant de l'excitabilité cellulaire ; sa régulation est assurée par l'aldostérone (excrétion rénale), l'insuline et les catécholamines (redistribution intracellulaire), et le pH (acidose → hyperkaliémie par shift extracellulaire du K⁺ ; alcalose → hypokaliémie). Le chloride (Cl⁻) is the main extracellular anion (normal range 98–107 mmol/L) — it passively follows sodium to maintain electroneutrality and plays a key role in acid-base balance (chloridemia inversely correlated with bicarbonatemia — hypochloremic metabolic alkalosis).
Sodium, potassium, and chlorine disorders
- Hyponatremia (Na⁺ <136 mmol/L) — classification by osmolality and volume status: Hyponatremia, hypo-osmolar (most frequent - plasma osmolarity <275 mosmkg) → classification par volémie : hypovolémique (pertes hydrosodées — diarrhées, vomissements, diurétiques, insuffisance surrénalienne na urinaire>20 mmol/L is renal cause, <20 si cause extrarénale) ; euvolémique (siadh — sécrétion inappropriée d'adh cancer pulmonaire à petites cellules, médicaments isrs, carbamazépine, cyclophosphamide, ains pathologie snc, hypothyroïdie, insuffisance corticosurrénalienne na urinaire>40 mmol/L + high urine osmolality + low plasma osmolality) ; hypervolemic (heart failure, cirrhosis, nephrotic syndrome — water and sodium retention predominates over water retention — urinary Na (20 mmol/L); iso-osmolar hyponatremia (pseudohyponatremia - hyperproteinemia, hyperlipidemia - measurement artifact due to dilution, corrected if ionogram using ion-selective electrode); hyperosmolar hyponatremia (hyperglycemia - correction: corrected Na = measured Na + 1.6 x [blood glucose - 5.6]/5.6 in mmol/L)
- Hypernatremia (Na⁺ >145 mmol/L) — free water deficit: free water loss > intake (always associated with hyperosmolarity); causes: deficit of water intake (unconscious patient, altered thirst — elderly, infants); extrarenal free water loss (osmotic diarrhea, cutaneous losses — fever, burns); central diabetes insipidus (ADH deficit — pituitary tumor, head trauma, meningitis) or nephrogenic (renal resistance to ADH — lithium, hypercalcemia, V2 receptor or aquaporin 2 mutation) → polyuria + polydipsia + low urinary osmolality (<300 mosmkg) ; symptômes : soif intense, sécheresse des muqueuses, confusion → convulsions coma si na>160 mmol/L or rapid installation
- Hypokalemia (K⁺ <3.5 mmol/L) - causes and consequences: renal losses (thiazide and loop diuretics - most common cause in practice; primary hyperaldosteronism - Conn's syndrome - HTN + hypokalemia + urinary K >30 mmol/d; renal tubular acidosis types I and II; Cushing's syndrome; low serum magnesium - Mg correction is mandatory); digestive losses (vomiting - associated metabolic alkalosis + hypochloremia; severe diarrhea - high fecal K); intracellular redistribution (insulin, beta-2 agonists - salbutamol, alkalosis, familial hypokalemic periodic paralysis - Ca²⁺ or K⁺ channel mutation); manifestations: muscle weakness → ascending flaccid paralysis; constipation, ileus; cramps; ECG: flattened T wave → U wave appearance → ST depression → prolonged QT → risk of arrhythmias (VT, VF - especially with heart disease or digitalis)
- Hyperkalemia (K⁺ >5.0 mmol/L) - potential emergency: Pseudo-hyperkalemia (hemolysis during blood draw — poorly handled tube, delay before centrifugation — most common cause of mild isolated hyperkalemia; thrombocytosis > 1,000,000/µL — release of K⁺ during coagulation); decreased renal excretion (CKD — most common cause of true hyperkalemia; oliguric-anuric AKI; medications: ACE inhibitors, ARBs, spironolactone, triamterene, heparin, TMP-SMX, NSAIDs, cyclosporine; adrenal insufficiency — Addison's disease — hypoaldosteronism); extracellular redistribution (metabolic acidosis — each 0.1 decrease in pH → increase in K⁺ of 0.5–0.7 mmol/L; cell lysis — rhabdomyolysis, tumor lysis syndrome, massive hemolysis; insulin deficiency — diabetic ketoacidosis); ECG: peaked, symmetrical T waves (K⁺ 6–7) → disappearance of P wave → widening of QRS → sine wave → VF/asystole (K⁺ >8–9) — absolute emergency
Investigation and treatment of major disorders
| Trouble / Treatment | Mechanism, balance sheet, and terms | Targets, duration, and precautions |
|---|---|---|
| Hyponatremia — Investigation and Treatment Stepwise approach — osmolality → volemia → urinary Na |
Initial assessment: plasma osmolality + urine osmolality + spot urine Na + urine K + creatinine + blood glucose + TSH + cortisol 8 AM + liver function tests + albumin + chest X-ray (lung cancer → SIADH); SIADH treatment (euvolemic): fluid restriction 800–1,000 mL/day (first-line) + oral salt if moderate to severe hyponatremia; vaptans (tolvaptan — Samsca 15–60 mg/day oral, conivaptan IV) — ADH V2 receptor antagonists → aquaresis (excretion of free water without Na) → reserved for refractory SIADH or if Na <125 mmol/L with symptoms; hypovolemic hyponatremia treatment: 0.9% NaCl % IV (correction of volume deficit); hypervolemic hyponatremia treatment: sodium and fluid restriction + loop diuretics (furosemide); hypertonic NaCl 3 % (150–300 mL over 20 min IV): reserved for severe symptomatic hyponatremia (seizures, coma, PRES) — goal: increase Na by 5 mmol/L in 1 hour | Threshold rule for absolute correction: never correct natremia by more than 8–10 mmol/L per 24 hours (and 18 mmol/L per 48h) in chronic hyponatremia (>48h) → risk of central pontine myelinolysis (osmotic demyelination syndrome — ODS) — dysarthria, dysphagia, quadriplegia, locked-in syndrome — irreversible; if accidental overcorrection (Na increases by >10 mmol/L/24h) → administer dextrose 5% % + desmopressin (DDAVP 2–4 µg SC) to slow correction; monitoring: Na every 2–4h during active treatment; acute hyponatremia (<48h)<48h — post-opératoire, potomanie aiguë, mdma) : correction plus rapide tolérée (risque d'œdème cérébral> SDO risk |
| Hypokalemia — oral and IV correction Always check the Mg before the K |
Etiological assessment: 24-hour urinary potassium (K) or spot urine K/creatinine ratio (TTKG) + serum magnesium (hypomagnesemia → refractory hypokalemia - Mg blocks K+ channels in the collecting duct) + arterial pH + aldosterone + renin + cortisol if hyperaldosteronism or Cushing's syndrome is suspected; oral potassium supplementation (K+ <3.0-3.5 mmol/L without severe manifestations): potassium chloride (KCl - Slow-K, K-Dur) 20-40 mEq/day orally in divided doses (maximum 40-60 mEq per dose - nausea, gastric irritation); K-rich foods: banana, avocado, orange, tomato, potato; IV supplementation (K+ <3.0 mmol/L + cardiac or neurological manifestations or NPO patient): IV KCl - maximum rate 10 mEq/h in a peripheral vein (risk of phlebitis) or 20-40 mEq/h via central line with continuous ECG monitoring; correct serum magnesium if <0.7 mmol/L → IV MgSO4 2 g over 15-30 min then 6 g over 24h | Never administer KCl IV as a bolus (cardiac arrest) — always diluted and as a slow infusion; target K⁺: >3.5 mmol/L (≥4.0 mmol/L if ischemic heart disease, heart failure, or digitalis treatment); continuous ECG monitoring if K⁺ <2.5 mmol/L or if arrhythmias; thiazide diuretics cause hypokalemia in 30–50 % of long-term cases → preventive supplementation + K⁺-rich diet or combination with a potassium-sparing diuretic (spironolactone, amiloride); caution with digitalis (digoxin): hypokalemia potentiates digitalis toxicity → maintain K⁺ ≥4.0 mmol/L in all patients on digoxin |
| Hyperkalemia — treatment by severity ECG required — emergency if K >6.5 or ECG changes |
First, exclude pseudohyperkalemia (hemolysis — repeat collection on a green heparin tube or arterial sample); immediate ECG if K⁺ > 5.5 mmol/L; stepwise treatment: (1) cardiac membrane stabilization — calcium gluconate 10 % 1 g IV over 2–3 min (effect in 2–5 min — duration 30–60 min — CI if digitalis toxicity) — indicated if peaked T waves, QRS widening, or sine wave; (2) intracellular redistribution — regular insulin 10 IU IV + dextrose 50 % 50 mL (effect in 20–30 min — K⁺ decrease of 0.5–1.5 mmol/L) + nebulized salbutamol 10–20 mg (effect in 30–60 min — K⁺ decrease of 0.5–1 mmol/L) + sodium bicarbonate 50–100 mEq IV if concomitant metabolic acidosis (pH <7.2); (3) K⁺ elimination — furosemide 40–80 mg IV (forced diuresis) + Kayexalate (ion-exchange resin — 15–30 g orally or as enema — delay 2–6h) + patiromer (Veltassa 8.4 g/day orally — new resin — better tolerance) + urgent hemodialysis if severe CKD or oligo-anuria | Action thresholds: K⁺ 5.0–5.5 mmol/L → eliminate pseudohyperkalemia + identify cause + review medications (ACE inhibitors, ARBs, spironolactone); K⁺ 5.5–6.5 mmol/L without ECG changes → insulin-glucose + K⁺ dietary restriction + kayexalate/patiromer; K⁺ >6.5 mmol/L or ECG changes → IV calcium gluconate + insulin-glucose + salbutamol + emergency/resuscitation call; K⁺ >7 mmol/L or sine wave → urgent hemodialysis; medications to stop urgently: ACE inhibitors (ramipril, lisinopril), ARBs (losartan, valsartan), spironolactone, amiloride, triamterene, TMP-SMX (aldosterone antagonist effect), NSAIDs, heparin; dietary restriction (K <40–50 mEq/day — avoid bananas, citrus, tomatoes, legumes, chocolate, salt substitutes) is a key element of long-term treatment in renal insufficiency |
| Chloride imbalance — metabolic alkalosis and acidosis Cl⁻ - indirect acid-base marker |
Hypochloremia (Cl⁻ 7.45 + bicarbonates >26 mmol/L + urinary Cl 20 mmol/L (chloro-resistant — hyperaldosteronism, Bartter syndrome); hyperchloremia (Cl⁻ >107 mmol/L): secondary to normal anion gap metabolic acidosis (hyperchloremic acidosis) — diarrhea (loss of digestive HCO₃⁻ → compensation by renal reabsorption of Cl⁻); renal tubular acidosis (type I, II, IV); excessive administration of isotonic NaCl (0.9% NaCl % — iatrogenic); pancreatic or ileal fistula | Anion gap (AG) = Na⁺ − (Cl⁻ + HCO₃⁻) — normal value 8–12 mmol/L (or 10–16 mmol/L if uncorrected albuminemia); high AG (>12) → high AG acidosis (mnemonic GOLDMARK: Glycols, Oxoproline, L-lactate, D-lactate, Methanol, Aspirin, Renal uremic, Ketoacidosis); normal AG + hyperchloremia → hyperchloremic acidosis (diarrhea, RTA, excess IV NaCl); correction of hypochloremia with alkalosis: 0.9% NaCl % + IV KCl according to kaliemia (hypochloremic metabolic alkalosis does not resolve without Cl⁻ and K⁺ intake – «chloride-dependent»); osmolar gap = measured osmolality − calculated osmolality [2 × Na + glycemia + urea] — normal <10 mOsm/kg — high osmolar gap → ethanol, methanol, ethylene glycol, propylene glycol intoxication |
| Hypernatremia - careful correction Free water deficit — slow rehydration |
Bilan : osmolalité plasmatique (élevée — >295 mOsm/kg) + osmolalité urinaire + Na urinaire + glycémie + créatinine + test de restriction hydrique + test à la desmopressine (DDAVP) si diabète insipide suspecté (DI central → osmolalité urinaire double après DDAVP ; DI néphrogénique → pas de réponse) ; calcul du déficit en eau libre : déficit H₂O (L) = 0,6 × poids (kg) × [(Na mesuré / 140) − 1] ; correction : eau libre per os ou SNG si patient conscient et coopérant (1re intention) ; dextrose 5 % IV ou NaCl 0,45 % IV si voie orale impossible ; vitesse de correction : ne pas corriger plus de 10–12 mmol/L per 24h In chronic hypernatremia (>48 hours) → risk of cerebral edema due to too rapid osmotic restoration (intracellular water shift); central DI: nasal or SC desmopressin (DDAVP) — rapid response | Monitor serum sodium every 4–6 hours during treatment. Elderly patients, infants, and patients with swallowing difficulties are at high risk of hypernatremia due to insufficient intake. Prevention: Ensure adequate fluid intake (30–35 mL/kg/day in elderly adults—minimum 1,500 mL/day). For hospitalized patients receiving enteral or parenteral nutrition, monitor sodium daily and adjust fluid intake. Lithium is the most common medication cause of nephrogenic diabetes insipidus. Thiazides are paradoxically effective (↓ GFR → ↓ collecting duct flow → ↑ proximal water reabsorption) along with sodium restriction and amiloride if lithium cannot be discontinued. |
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Urinary anion gap (UAG) and diagnostic orientation in hyperchloremic acidosis: The UAG = urinary Na⁺ + urinary K⁺ − urinary Cl⁻. In a normal anion gap metabolic acidosis, the UAG helps distinguish a renal cause from a digestive cause: negative UAG (typically −20 to −50 mmol/L) → increased renal excretion of NH₄⁺ → digestive cause (diarrhea — loss of digestive HCO₃⁻) or excessive NaCl intake; positive or near-zero UAG → impaired renal excretion of NH₄⁺ → renal tubular acidosis (types I, II, or IV). This distinction is essential for quickly guiding the etiological investigation of hyperchloremic acidosis without resorting to expensive tests.
Urgent - Critical values requiring immediate action
Consult immediately to the emergency room you compose the 911 if a patient presents with: K⁺ >6.5 mmol/L with ECG changes (peaked T waves, widened QRS, sinusoidal wave) - risk of imminent cardiac arrest; ; Na⁺ < 120 mmol/L with confusion, seizures, or coma (symptomatic severe hyponatremia — urgent IV NaCl 3 %); ; Na⁺ >160 mmol/L with altered consciousness (severe hypernatremia); ; K⁺ <2.5 mmol/L with significant muscle weakness or arrhythmias.
Visit Pseudo-hyperkalemia (pre-analytical hemolysis) must always be excluded before any therapeutic intervention — repeat the collection in a heparin tube if K⁺ >5.5 mmol/L without an obvious clinical cause and without ECG changes.
Consult at Clinique Omicron
The doctors at Clinique Omicron prescribe and interpret electrolyte panels, evaluate hydroelectrolytic imbalances, adjust medications that may disrupt electrolyte balance (diuretics, ACE inhibitors, ARBs, spironolactone), and monitor patients with chronic kidney disease, heart failure, or those requiring regular electrolyte monitoring. Tests are available at our service points in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content of this page is for informational purposes only and does not substitute for advice from a qualified healthcare professional. Any severe or symptomatic electrolyte disturbance requires urgent medical evaluation.
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