13.2 Acid-Base and Electrolyte Disorders

Acid-Base and Electrolyte Disorders

PANCE High-Yield Focus: Electrolyte and acid-base disturbances are core components of the PANCE renal blueprint. You must be able to rapidly identify the primary acid-base disorder on an arterial blood gas (ABG) and calculate the anion gap. For sodium disorders, focus on the risk of osmotic demyelination syndrome during rapid correction. For potassium disorders, memorize the classic ECG changes (peaked T waves vs. U waves) and the sequential steps of hyperkalemia management, emphasizing the role of calcium gluconate.

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Acid-Base Disorders

Arterial blood gas (ABG) interpretation requires a systematic, three-step approach:

1. Assess the pH: Normal range is 7.35-7.45. A pH < 7.35 indicates acidemia; a pH > 7.45 indicates alkalemia.
2. Identify the Primary Process: Compare pH changes with pCO2 (normal 35-45 mmHg) and HCO3- (normal 22-26 mEq/L). If pH and pCO2 move in opposite directions, the primary disorder is respiratory. If pH and HCO3- move in the same direction, the primary disorder is metabolic.
3. Determine Compensation: Compensation is the physiological response to restore pH. In metabolic acidosis, respiratory compensation (hyperventilation to blow off CO2) is evaluated using Winters' Formula: Expected pCO2 = (1.5 * [HCO3-]) + 8 +/- 2
   • If the actual pCO2 is within the expected range, there is appropriate respiratory compensation.
   • If the actual pCO2 is higher than expected, there is a superimposed respiratory acidosis (hypoventilation).
   • If the actual pCO2 is lower than expected, there is a superimposed respiratory alkalosis (hyperventilation).

1. Metabolic Acidosis

Metabolic acidosis is classified by the presence or absence of an elevated anion gap.

• Anion Gap (AG): Calculated as Na+ - (Cl- + HCO3-). The normal anion gap is 8-12 mEq/L.
• High Anion Gap Metabolic Acidosis (HAGMA): Occurs when unmeasured anions accumulate in the serum. The classic mnemonic MUDPILES outlines the causes:
  • Methanol (formic acid accumulation)
  • Uremia (renal failure preventing acid excretion)
  • Diabetic Ketoacidosis (beta-hydroxybutyrate and acetoacetate accumulation)
  • Propylene glycol
  • Isoniazid or Iron toxicity
  • Lactic acidosis (hypoxia, hypoperfusion, metformin toxicity)
  • Ethylene glycol (glycolic and oxalic acid accumulation causing calcium oxalate crystals)
  • Salicylates (aspirin toxicity; typically causes a mixed respiratory alkalosis and HAGMA)
• Normal Anion Gap Metabolic Acidosis (NAGMA): Occurs due to bicarbonate loss or decreased renal acid excretion. Also known as hyperchloremic metabolic acidosis.
  • Causes: Severe diarrhea (bicarbonate loss in stool) or Renal Tubular Acidosis (RTA).
    • Type 1 (Distal) RTA: Impaired distal H+ secretion; urine pH > 5.5. Associated with hypokalemia and nephrolithiasis.
    • Type 2 (Proximal) RTA: Impaired proximal HCO3- reabsorption; urine pH < 5.5 once systemic bicarbonate is low. Associated with hypokalemia and Fanconi syndrome.
    • Type 4 RTA: Hypoaldosteronism or aldosterone resistance; characterized by hyperkalemia and urine pH < 5.5.

2. Metabolic Alkalosis

Metabolic alkalosis is characterized by a high pH and elevated HCO3-. It is clinically classified using urine chloride (U_Cl) concentration:

• Saline-Responsive (U_Cl < 20 mEq/L): Caused by extracellular volume depletion (e.g., severe vomiting, nasogastric suction, or prior diuretic use). Volume depletion stimulates aldosterone, which increases renal H+ and K+ excretion.
  • Treatment: Intravenous normal saline (0.9% NaCl) to restore volume, which removes the stimulus for aldosterone.
• Saline-Unresistant (U_Cl > 20 mEq/L): Associated with normotension or hypertension, driven by mineralocorticoid excess (e.g., primary hyperaldosteronism, Cushing's syndrome).
  • Treatment: Target the underlying cause (e.g., aldosterone antagonists like spironolactone).

3. Respiratory Acidosis & Alkalosis

• Respiratory Acidosis: Caused by alveolar hypoventilation leading to CO2 retention. Causes include COPD, acute asthma, neuromuscular disorders (e.g., Myasthenia Gravis), and opioid overdose.
• Respiratory Alkalosis: Caused by alveolar hyperventilation leading to excessive loss of CO2. Causes include acute anxiety/panic attacks, pain, early sepsis, pulmonary embolism, and early salicylate toxicity.

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Sodium Disorders

1. Hyponatremia

Hyponatremia is defined as a serum sodium level < 135 mEq/L. The workup must follow a logical sequence:

1. Measure Serum Osmolality:
   • Hypertonic (> 295 mOsm/kg): Most commonly due to hyperglycemia. Glucose acts as an active osmole, pulling water into the extracellular space. Correct the sodium level by adding 1.6 mEq/L for every 100 mg/dL rise in blood glucose above 100 mg/dL.
   • Isotonic (280-295 mOsm/kg): Pseudohyponatremia due to hyperlipidemia or hyperproteinemia.
   • Hypotonic (< 280 mOsm/kg): True hyponatremia.
2. Assess Volume Status in Hypotonic Hyponatremia:
   • Hypovolemic: Renal losses (diuretics; U_Na > 20) or extrarenal losses (vomiting, diarrhea; U_Na < 10). Treatment is normal saline.
   • Euvolemic: Typically SIADH. Characterized by urine osmolality > 100 mOsm/kg and urine sodium > 20 mEq/L. Treatment is fluid restriction.
   • Hypervolemic: Volume overload (heart failure, cirrhosis, nephrotic syndrome). Treatment is fluid and sodium restriction, plus loop diuretics.
3. Safe Correction Guidelines:
   • The Trap: Correcting chronic hyponatremia too rapidly causes water to shift out of brain cells, resulting in Osmotic Demyelination Syndrome (ODS) (central pontine myelinolysis).
   • Rule: Do not exceed 8-10 mEq/L of sodium correction in any 24-hour period.
   • Symptomatic Hyponatremia (Seizures/Coma): Administer a bolus of hypertonic (3%) saline to raise the sodium level by 4-6 mEq/L rapidly to alleviate cerebral edema, then slow the rate of correction.

2. Hypernatremia

Hypernatremia (Na+ > 145 mEq/L) represents a relative free water deficit.

• Causes: Inadequate water intake, osmotic diuresis, or diabetes insipidus.
• Management: Calculate the free water deficit and replete with hypotonic fluids (D5W or oral water). Correct slowly (no more than 10 mEq/L per day) to avoid cerebral edema (water rushing into brain cells).

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Potassium Disorders

1. Hyperkalemia

Hyperkalemia (K+ > 5.0 mEq/L) is a medical emergency due to its risk of lethal cardiac conduction abnormalities.

• Etiology: Advanced CKD, ACEi/ARB therapy, aldosterone deficiency (Addison's disease), or intracellular shifts (acidosis, rhabdomyolysis, tumor lysis syndrome).
• ECG Changes (High Yield Sequence):
  1. Peaked T waves (narrow, symmetric, and tall).
  2. Prolonged PR interval and flattening of P waves.
  3. QRS complex widening.
  4. Sine wave pattern.
  5. Ventricular fibrillation/asystole.
• Management (Three-Phase Protocol):
  1. Stabilization: Calcium gluconate IV (stabilizes the cardiac membrane; does not affect serum potassium).
  2. Shifting: Regular insulin (10 units IV) + Dextrose (50% D50W) to shift potassium into cells. Inhaled albuterol and IV sodium bicarbonate also shift potassium.
  3. Elimination: Loop diuretics (furosemide), gastrointestinal potassium binders (sevelamer, lokelma, patiromer), or hemodialysis (definitive for renal failure).

2. Hypokalemia

Hypokalemia (K+ < 3.5 mEq/L) increases neuromuscular and cardiac irritability.

• ECG Changes: Flattened T waves, ST-segment depression, and U waves (positive deflection after the T wave).
• Management: Replacement with oral potassium chloride (preferred for mild/asymptomatic cases). For IV replacement, limit the rate to 10 mEq/h through peripheral lines.
• The Magnesium Rule: Refractory hypokalemia that does not respond to potassium supplementation is almost always due to coexisting hypomagnesemia. Low magnesium increases renal potassium excretion via ROMK channels. Replete magnesium first to correct the potassium.