II-16. Metabolic acid-base disorders: metabolic acidosis & alkalosis

代謝性酸塩基平衡障害：代謝性アシドーシスとアルカローシス

Acid-Base Background

Arterial pH normally 7.40 (range 7.35–7.45). Acidosis = below, alkalosis = above.
Buffers (weak acid + conjugate base) resist pH change. Regulated by: (1) blood/tissue buffers (bicarbonate, proteins, phosphate), (2) respiratory (CO₂ exhalation), (3) renal (acid excretion + HCO₃⁻ reabsorption).
Non-volatile acids: anaerobic metabolism (lactic, acetoacetic), protein catabolism (phosphoric, HCl); excreted by kidneys as ammonia (NH₃/NH₄⁺).
4 simple disorders: metabolic acidosis (most common, DKA), metabolic alkalosis (vomiting), respiratory acidosis (COPD), respiratory alkalosis (panic hyperventilation).
Respiratory compensation = immediate; metabolic = days–weeks. Possible symptom: Kussmaul breathing.

Metabolic Acidosis

Non-carbonic acid accumulates → ↓plasma HCO₃⁻. Parameters: pH <7.4, unchanged pCO₂, HCO₃⁻ <24 mM.
Anion gap (AG) = [Na⁺] − [Cl⁻ + HCO₃⁻]; normal ~12 mmol/L (unmeasured anions). ↑AG when acid accumulates.
↑AG metabolic acidosis: diabetic ketoacidosis, lactic acidosis (type 1 = tissue hypoxia/shock; type 2 = impaired liver metabolism), renal failure, poisoning (aspirin, methanol, ethanol).
Normal AG (hyperchloremic): diarrhea (HCO₃⁻ loss), renal tubular acidosis (urine pH >5.5; impaired HCO₃⁻ reabsorption/acid secretion).

Compensation

Respiratory (main, immediate): hyperventilation → ↓pCO₂ → ↑pH. Metabolic: renal acid excretion over days–weeks.
Ventilation driven by chemoreceptors: peripheral (pO₂, aorta/carotid) + central (pH, medulla). Hyperventilation more intense in acidosis than hypoventilation in alkalosis.

Example: Diabetic Ketoacidosis (DKA)

Labs: glucose >11.1 mmol/L, pH >7.3 or HCO₃⁻ <15, ketonemia/ketonuria.
Clinical: dehydration, tachycardia, Kussmaul breathing, acetone breath, nausea/vomiting, abdominal pain, drowsiness, confusion.
Mechanism: severe insulin deficiency + ↑glucagon/glucocorticoids/catecholamines → ↑gluconeogenesis + lipolysis → hyperglycemia + ketone body overproduction → ketonemia → acidosis (↓HCO₃⁻, hyperventilation, ketonuria).
Management: (1) fluid + electrolyte (IV saline + K⁺), (2) insulin (IV regular insulin until glucose 14 mmol/L → glucose infusion; sc insulin after resolution).

Metabolic Alkalosis

↑Plasma HCO₃⁻ → ↑pH. Parameters: pH >7.4, unchanged pCO₂, HCO₃⁻ >24 mM.
Hypovolemic (most common): lost gastric acid (vomiting → ↑HCO₃⁻), diuretics (urinary acid loss).
Normo/hypervolemic: hyperaldosteronism (↑H⁺ secretion), antacid overuse.

Compensation

Respiratory (main, immediate): hypoventilation → ↑pCO₂. Limited by hypoxia (alternative ventilation stimulus). Metabolic: ↓renal acid excretion over days–weeks.

Management

Hypovolemic: IV 0.9% saline + K⁺ (corrects hypokalemia, reverses secondary hyperaldosteronism → kidney excretes excess HCO₃⁻).
Normal/↑volume: treat underlying endocrine cause.

一問一答

▶What are non-volatile acids and how are they excreted?

Acids from anaerobic metabolism (lactic, acetoacetic) and protein catabolism (phosphoric, HCl); excreted by kidneys as ammonia (NH₃/NH₄⁺).

▶What is the normal arterial pH and its range?

7.40, with a normal range of 7.35–7.45; below is acidosis, above is alkalosis.

▶What are the four simple acid-base disorders with a typical cause for each?

Metabolic acidosis (DKA, most common), metabolic alkalosis (vomiting), respiratory acidosis (COPD), respiratory alkalosis (panic hyperventilation).

▶What defines a buffer and what are the major blood/tissue buffers?

A buffer is a weak acid plus its conjugate base that resists pH change; the major ones are bicarbonate, proteins, and phosphate.

▶What are the three lines of acid-base regulation?

1) Blood/tissue buffers (bicarbonate, proteins, phosphate), 2) respiratory (CO₂ exhalation), 3) renal (acid excretion + HCO₃⁻ reabsorption).

▶What are the blood gas parameters of metabolic acidosis?

pH <7.4, unchanged pCO₂, and HCO₃⁻ <24 mM (non-carbonic acid accumulates, lowering plasma HCO₃⁻).

▶How is the anion gap calculated and what is its normal value?

AG = [Na⁺] − ([Cl⁻] + [HCO₃⁻]); normal is ~12 mmol/L, representing unmeasured anions.

▶What are the causes of high anion gap metabolic acidosis?

Diabetic ketoacidosis, lactic acidosis (type 1 = tissue hypoxia/shock; type 2 = impaired liver metabolism), renal failure, and poisoning (aspirin, methanol, ethanol).

▶What are the causes of normal anion gap (hyperchloremic) metabolic acidosis?

Diarrhea (HCO₃⁻ loss) and renal tubular acidosis (urine pH >5.5; impaired HCO₃⁻ reabsorption/acid secretion).

▶How does the body compensate for metabolic acidosis?

Mainly respiratory (immediate): hyperventilation → ↓pCO₂ → ↑pH; metabolic compensation is renal acid excretion over days–weeks.

▶What are the diagnostic labs for diabetic ketoacidosis (DKA)?

Glucose >11.1 mmol/L, pH >7.3 or HCO₃⁻ <15, and ketonemia/ketonuria.

▶What is the clinical presentation of DKA?

Dehydration, tachycardia, Kussmaul breathing, acetone breath, nausea/vomiting, abdominal pain, drowsiness, and confusion.

▶What is the mechanism of DKA?

Severe insulin deficiency + ↑glucagon/glucocorticoids/catecholamines → ↑gluconeogenesis + lipolysis → hyperglycemia + ketone overproduction → ketonemia → acidosis (↓HCO₃⁻, hyperventilation, ketonuria).

▶What is the management of DKA?

1) Fluid + electrolytes (IV saline + K⁺), 2) insulin (IV regular insulin until glucose ~14 mmol/L, then glucose infusion; sc insulin after resolution).

▶What are the blood gas parameters of metabolic alkalosis?

pH >7.4, unchanged pCO₂, and HCO₃⁻ >24 mM.

▶What is the most common (hypovolemic) cause of metabolic alkalosis?

Loss of gastric acid (vomiting → ↑HCO₃⁻) and diuretics (urinary acid loss).

▶What are the normo/hypervolemic causes of metabolic alkalosis?

Hyperaldosteronism (↑H⁺ secretion) and antacid overuse.

▶How does the body compensate for metabolic alkalosis and what limits it?

Mainly respiratory (immediate): hypoventilation → ↑pCO₂, but it is limited by hypoxia (which is an alternative ventilation stimulus); metabolic compensation is reduced renal acid excretion over days–weeks.

▶How is hypovolemic metabolic alkalosis treated?

IV 0.9% saline + K⁺, which corrects hypokalemia and reverses secondary hyperaldosteronism so the kidney excretes excess HCO₃⁻.

▶Why is respiratory compensation faster than metabolic compensation?

Respiratory compensation (changing CO₂ exhalation) is immediate, whereas metabolic (renal) compensation takes days to weeks.