Pathophysiology

Pathophysiology

II-17. Respiratory acid-base disorders: respiratory acidosis & alkalosis

呼吸性酸塩基平衡障害：呼吸性アシドーシスとアルカローシス

Respiratory Acidosis

Definition & parameters

  • CO₂ accumulates due to type 2 respiratory failure (pO₂ <60 mmHg, pCO₂ >50 mmHg) → hypercapnia
  • pH < 7.4
  • pCO₂ > 40 mmHg (→ low pH)
  • Standard [HCO₃⁻] unchanged (24 mM)

Causes

  • Intrinsic lung disease with significant V/Q mismatch (COPD, ARDS, pneumothorax)
  • Lesions along the neuromuscular pathway from brain to respiratory muscles (opioid overdose, myopathy)

Metabolic (renal) compensation

  • Kidneys raise plasma HCO₃⁻ via reabsorption of filtered HCO₃⁻ and formation of “new HCO₃⁻”, closely linked to NH₃ generation/excretion
  • Glutamine deamination in the proximal tubule → NH₃ secreted into lumen, new HCO₃⁻ reabsorbed, and ammoniagenesis upregulates as needed (glutamine from skeletal-muscle protein catabolism → muscle loss)
  • Time course: acid excretion rises gradually over days; maximal compensation needs multiple days

Clinical presentation & management

  • Underlying cause dominates (paralysis, chest-wall injury, COPD). CO₂ retention → drowsiness → further depresses respiratory drive
  • Treat the underlying disease: raise pO₂ (>60 mmHg) while avoiding further pCO₂ rise
  • Acute type II respiratory failure = emergency, distinguish:
    • High ventilatory drive but cannot move air → consider upper-airway obstruction (stridor) → Heimlich, intubation or emergency tracheostomy
    • Reduced respiratory effort (more common — COPD, asthma, ARDS, tension pneumothorax) → high-concentration O₂, nebulized salbutamol, ventilatory support
    • Monitor arterial blood gases regularly

Respiratory Alkalosis

Definition & parameters

  • Hyperventilation → ↓pCO₂ → ↑plasma pH
  • pH > 7.4
  • pCO₂ < 40 mmHg (→ high pH)
  • Standard [HCO₃⁻] unchanged (24 mM)

Causes

  • Hyperventilation: anxiety states (short-lived), high altitude (low pO₂)
  • Prolonged: pregnancy (progesterone), pulmonary embolism + pneumonia (hypoxia), chronic liver disease, salicylates (stimulate brainstem respiratory centers)

Clinical presentation & management

  • Hyperventilation obvious in panic disorder
  • Hypocalcemia features: perioral and digital tingling (↑Ca²⁺ binding to albumin in alkalotic ECF). In severe cases Trousseau & Chvostek signs, tetany or seizures
  • With hypoxia → O₂ therapy. With normal pO₂ → correct the cause, reduce anxiety, rebreathing into a closed bag to raise CO₂

一問一答

▶What are the blood gas parameters of respiratory acidosis?

pH <7.4, pCO₂ >40 mmHg (hypercapnia), with standard [HCO₃⁻] initially unchanged (24 mM).

▶What defines type 2 respiratory failure?

pO₂ <60 mmHg and pCO₂ >50 mmHg → hypercapnia (the basis of respiratory acidosis).

▶What are the causes of respiratory acidosis?

Intrinsic lung disease with significant V/Q mismatch (COPD, ARDS, pneumothorax) and lesions along the neuromuscular pathway from brain to respiratory muscles (opioid overdose, myopathy).

▶How do kidneys compensate for respiratory acidosis?

They raise plasma HCO₃⁻ by reabsorbing filtered HCO₃⁻ and forming "new HCO₃⁻," closely linked to NH₃ generation/excretion.

▶How does ammoniagenesis in respiratory acidosis cause muscle loss?

Glutamine deamination in the proximal tubule generates NH₃ and new HCO₃⁻; the glutamine comes from skeletal-muscle protein catabolism, causing muscle loss.

▶What is the time course of renal compensation for respiratory acidosis?

Acid excretion rises gradually over days; maximal compensation requires multiple days.

▶Why does CO₂ retention create a vicious cycle in respiratory acidosis?

CO₂ retention → drowsiness → further depresses respiratory drive → more CO₂ retention.

▶How is acute type II respiratory failure with reduced respiratory effort managed?

(More common — COPD, asthma, ARDS, tension pneumothorax) high-concentration O₂, nebulized salbutamol, and ventilatory support, with regular arterial blood gas monitoring.

▶How is acute type II respiratory failure with high ventilatory drive but no air movement managed?

Suspect upper-airway obstruction (stridor) → Heimlich, intubation, or emergency tracheostomy.

▶What is the treatment goal in respiratory acidosis?

Treat the underlying disease and raise pO₂ (>60 mmHg) while avoiding a further rise in pCO₂.

▶What are the blood gas parameters of respiratory alkalosis?

pH >7.4, pCO₂ <40 mmHg, with standard [HCO₃⁻] initially unchanged (24 mM) — due to hyperventilation.

▶What are the acute (short-lived) causes of respiratory alkalosis?

Hyperventilation from anxiety states and high altitude (low pO₂).

▶What are the prolonged causes of respiratory alkalosis?

Pregnancy (progesterone), pulmonary embolism + pneumonia (hypoxia), chronic liver disease, and salicylates (stimulate brainstem respiratory centers).

▶Why does respiratory alkalosis cause hypocalcemia symptoms?

Alkalotic ECF increases Ca²⁺ binding to albumin, lowering free calcium → perioral and digital tingling, and in severe cases Trousseau & Chvostek signs, tetany, or seizures.

▶How is respiratory alkalosis managed depending on oxygenation?

With hypoxia → O₂ therapy; with normal pO₂ → correct the cause, reduce anxiety, and rebreathe into a closed bag to raise CO₂.

▶Why is acute type II respiratory failure a medical emergency?

Rapid CO₂ retention with hypoxemia can quickly depress consciousness and respiratory drive, requiring urgent intervention.

▶How do salicylates affect acid-base balance?

They stimulate brainstem respiratory centers, causing hyperventilation and respiratory alkalosis (and can also cause a high anion gap metabolic acidosis).

▶Why does high altitude cause respiratory alkalosis?

Low ambient pO₂ stimulates hyperventilation, which lowers pCO₂ and raises pH.

▶What is the source of "new HCO₃⁻" generated by the kidney?

Ammoniagenesis — glutamine deamination in the proximal tubule generates NH₃ (excreted) and produces new bicarbonate that is reabsorbed.

▶Why does pregnancy cause a chronic respiratory alkalosis?

Progesterone stimulates ventilation, lowering pCO₂ and raising pH.