5.3 Electrolyte Imbalances & Acid-Base Disorders

Electrolyte Imbalances & Acid-Base Disorders

Electrolyte abnormalities and acid-base disorders are among the most frequent acute clinical presentations in internal medicine. Systematic diagnostic algorithms based on physiological principles are necessary to prevent catastrophic management errors.

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Disorders of Sodium & Water Balance

Sodium concentration reflects water balance, not total body sodium content.

1. Hyponatremia Algorithm

• Step 1: Confirm Hypotonic Hyponatremia: Check measured serum osmolality. If normal ($280\text{--}295\,\text{mOsm/kg}$), suspect pseudohyponatremia (severe hyperlipidemia or hyperproteinemia). If elevated ($> 295\,\text{mOsm/kg}$), suspect hyperglycemia (corrected $\text{Na}^+ = \text{measured }\text{Na}^+ + 0.3 \times [\text{Glucose} - 5.5\,\text{mmol/L}]$).
• Step 2: Assess Volume Status:
  • Hypovolemic: Dehydration, vomiting/diarrhea (Urine $\text{Na}^+ < 20\,\text{mmol/L}$), or renal losses / diuretics (Urine $\text{Na}^+ > 20\,\text{mmol/L}$).
  • Euvolemic: Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH), secondary adrenal insufficiency, severe hypothyroidism, primary polydipsia.
  • Hypervolemic: Congestive heart failure, liver cirrhosis, nephrotic syndrome (Urine $\text{Na}^+ < 20\,\text{mmol/L}$).

Diagnostic Criteria for SIADH

1. Hypotonic hyponatremia (Serum osmolality $< 275\,\text{mOsm/kg}$).
2. Inappropriately concentrated urine (Urine osmolality $> 100\,\text{mOsm/kg}$).
3. High urine sodium concentration (Urine $\text{Na}^+ > 30\,\text{mmol/L}$) despite normal salt and water intake.
4. Euvolemic clinical examination (no edema, no orthostatic hypotension).
5. Normal thyroid, adrenal, and renal function.

Treatment & Safety Limits

• Severe Symptomatic Hyponatremia (seizures, coma, confusion): Administer $150\,\text{mL}$ of $3\%$ hypertonic saline IV over 20 minutes; repeat if necessary to raise serum $\text{Na}^+$ by $4\text{--}6\,\text{mmol/L}$ acutely.
• Correction Limit: Never exceed a rise of $8\text{--}10\,\text{mmol/L}$ in 24 hours ($< 18\,\text{mmol/L}$ in 48 hours). Overly rapid correction leads to Osmotic Demyelination Syndrome (Central Pontine Myelinolysis), manifesting with spastic quadriparesis, pseudobulbar palsy, and locked-in syndrome.

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Disorders of Potassium Balance

Potassium is primarily an intracellular cation ($98\%$ intracellular, $[\text{K}^+] \approx 140\,\text{mmol/L}$). Small shifts between intracellular and extracellular compartments produce drastic changes in serum concentration.

Hyperkalemia Management Protocol

Severe hyperkalemia ($[\text{K}^+] > 6.5\,\text{mmol/L}$) or hyperkalemia accompanied by ECG changes is a medical emergency requiring rapid sequential treatment.

Three-Step Emergency Treatment:

1. Myocardial Membrane Stabilization (Acts within 1–3 minutes; duration 30–60 minutes):
   • Calcium Gluconate 10%: $10\,\text{mL}$ IV over 2–5 minutes (or Calcium Chloride $10\%\,10\,\text{mL}$ via central access). Stabilizes resting membrane potential without lowering serum potassium.
2. Intracellular Potassium Shifting (Acts within 15–30 minutes):
   • Insulin & Dextrose: 10 units Actrapid insulin in $50\,\text{mL}$ of $50\%$ Dextrose IV. Drives $\text{K}^+$ into cells via $\text{Na}^+/\text{K}^+\text{-ATPase}$ stimulation.
   • Nebulized Salbutamol: $10\text{--}20\,\text{mg}$ nebulized. $\beta_2$-agonist action stimulates $\text{Na}^+/\text{K}^+\text{-ATPase}$.
   • Intravenous Sodium Bicarbonate: $8.4\%\,50\text{--}100\,\text{mL}$ IV (only if concomitant metabolic acidosis).
3. Potassium Elimination from the Body:
   • Cation Exchange Resins / Binders: Sodium Zirconium Cyclosilicate (Lokelma) or Patiromer.
   • Loop Diuretics: Furosemide $40\text{--}80\,\text{mg}$ IV (if renal function is preserved).
   • Hemodialysis: Definitive removal in renal failure.

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Systematic Approach to Acid-Base Disorders

Arterial Blood Gas (ABG) analysis follows a structured four-step procedure:

1. Step 1: Check pH (Acidemia $<7.35$ vs. Alkalemia $>7.45$).
2. Step 2: Identify Primary Process (Change in $\text{HCO}_3^-$ vs. $\text{pCO}_2$).
3. Step 3: Calculate Compensation (Winter's Formula for Metabolic Acidosis).
4. Step 4: Calculate Serum Anion Gap $= [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$.

Normal Reference Ranges (ABG):

• $\text{pH}$: $7.35\text{--}7.45$
• $\text{pCO}_2$: $4.7\text{--}6.0\,\text{kPa}$ ($35\text{--}45\,\text{mmHg}$)
• $\text{HCO}_3^-$: $22\text{--}26\,\text{mmol/L}$
• $\text{Base Excess}$: $-2\text{ to }+2\,\text{mmol/L}$

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Metabolic Acidosis & Anion Gap Calculation

Serum Anion Gap ($\text{AG}$) represents unmeasured anions in plasma:

$$\text{Anion Gap} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$$

• Normal Range: $8\text{--}12\,\text{mmol/L}$. (Correct for hypoalbuminemia: add $2.5\,\text{mmol/L}$ to AG for every $10\,\text{g/L}$ drop in serum albumin below $40\,\text{g/L}$).

Differential Diagnosis of Metabolic Acidosis

Winter's Formula for Respiratory Compensation

In metabolic acidosis, expected respiratory compensation ($\text{pCO}_2$) is calculated using Winter's formula:

$$\text{Expected }\text{pCO}_2 (\text{mmHg}) = 1.5 \times [\text{HCO}_3^-] + 8 \pm 2$$ $$\text{Expected }\text{pCO}_2 (\text{kPa}) = 0.2 \times [\text{HCO}_3^-] + 1.1 \pm 0.3$$

• If measured $\text{pCO}_2 > \text{expected } \text{pCO}_2$: Co-existing Respiratory Acidosis (e.g., respiratory depression, severe asthma/COPD).
• If measured $\text{pCO}_2 < \text{expected } \text{pCO}_2$: Co-existing Respiratory Alkalosis (e.g., salicylate toxicity, sepsis, pulmonary embolism).

Delta Ratio ($\Delta / \Delta$) for Mixed Disorders

In High Anion Gap Metabolic Acidosis, calculate the Delta Ratio:

$$\text{Delta Ratio} = \frac{\Delta \text{Anion Gap}}{\Delta \text{HCO}_3^-} = \frac{\text{Calculated AG} - 12}{24 - \text{Measured } \text{HCO}_3^-}$$

• $< 0.8$: Combined High Anion Gap and Normal Anion Gap Metabolic Acidosis (e.g., DKA + Diarrhea).
• $1.0\text{--}2.0$: Uncomplicated High Anion Gap Metabolic Acidosis.
• $> 2.0$: Combined High Anion Gap Metabolic Acidosis and Metabolic Alkalosis (e.g., DKA + Vomiting) or pre-existing chronic respiratory acidosis.

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Renal Tubular Acidosis (RTA) Differentiation