Pathophysiology

Pathophysiology

II-12. Acute respiratory failure; effects of hyperventilation

急性呼吸不全の症状；過換気の影響

Acute Respiratory Failure

Life-threatening: blood lacks O₂ or has excess CO₂. Normal: pO₂ 85–95 mmHg, pCO₂ 36–45 mmHg.

Types

  • Type 1 (partial): lung disease (pneumonia, asthma, COPD, restrictive) → V/Q mismatch/diffusion/shunt. Dyspnea + hypoxemia → hyperventilate → normal/low pCO₂. pO₂ <60, pCO₂ <46 (hypoxemia, no hypercapnia).
  • Type 2 (systemic): alveolar hypoventilation (healthy lung, pump failure — neuromuscular, morphine, respiratory center injury). pO₂ <60, pCO₂ >46 (hypercapnia + ↓O₂).
  • Type 3 (mixed): both; usually type 1 → type 2 as respiratory muscles fatigue. Severe hypoxemia + mild hypercapnia (e.g. COVID pneumonia).

Body’s Response to Acute Hypoxemia

  1. Hyperventilation (dyspnea drive; alveolar ventilation up to 6×). pCO₂ changes drive ventilation even more than hypoxemia — even mild hypercapnia → hyperventilation.
  2. Neurohormonal: SYM-adrenal activation.
  3. Cardiac: positive chrono/inotropic effect → ↑CO; heart most burdened by acute respiratory failure (chronic disease patients risk respiratory muscle exhaustion → death).

Cerebral Effects (by O₂ saturation)

  • 80–100%: ↓visual sensitivity; 70–80%: cognitive impairment; 60–70%: altered judgment/coordination; 40–60%: unconscious in hours; 20–40%: minutes; 0–20%: seconds. Death usually = brain death.

Diffusion Disorders

  • RBC contact time with alveolar O₂ = 0.75 s; normally 0.25 s suffices (wide gradient, thin membrane).
  • Fibrosis/interstitial edema: thicker membrane → O₂ needs full 0.75 s; not hypoxemic at rest.
  • Exercise: ↑CO/HR → ↓contact time → cyanosis, dyspnea, syncope, ↑lactate (anaerobic metabolism).

Tissue O₂ Extraction

  • Delivery ~1000 ml/min, 25% extracted → consumption 250 ml/min (cannot be reduced). In failure, periphery extracts more (up to 550 ml delivery); below that → supply-dependent consumption → syncope, ↑lactate.

Treatment

  • Administer O₂ (check if hypoxemia improves), bronchodilator, anti-inflammatory (systemic steroids), fluid/electrolyte replacement, maintain normotension + sinus rhythm (cardiac failure in 30% of elderly).

一問一答

▶What defines acute respiratory failure and the normal blood gas values?

A life-threatening lack of O₂ or excess CO₂ in blood; normal pO₂ 85–95 mmHg, pCO₂ 36–45 mmHg.

▶What characterizes type 1 (partial) respiratory failure?

Lung disease (pneumonia, asthma, COPD, restrictive) → V/Q mismatch/diffusion/shunt; hypoxemia drives hyperventilation. pO₂ <60, pCO₂ <46 (hypoxemia without hypercapnia).

▶What characterizes type 2 (systemic) respiratory failure?

Alveolar hypoventilation with a healthy lung (pump failure — neuromuscular, morphine, respiratory center injury). pO₂ <60, pCO₂ >46 (hypercapnia + low O₂).

▶What is type 3 (mixed) respiratory failure?

Both types together — usually type 1 progressing to type 2 as respiratory muscles fatigue; severe hypoxemia + mild hypercapnia (e.g. COVID pneumonia).

▶What are the three components of the body's response to acute hypoxemia?

1) Hyperventilation (dyspnea drive, up to 6× alveolar ventilation), 2) neurohormonal sympatho-adrenal activation, 3) cardiac positive chrono/inotropic effect → ↑CO.

▶Why is the heart the most burdened organ in acute respiratory failure?

It must increase cardiac output (positive chrono/inotropic effect) to compensate; in chronic disease, respiratory muscle exhaustion can lead to death.

▶Which is a stronger ventilatory drive — hypoxemia or hypercapnia?

pCO₂ changes drive ventilation even more than hypoxemia — even mild hypercapnia triggers hyperventilation.

▶How do cerebral effects relate to O₂ saturation?

80–100%: ↓visual sensitivity; 70–80%: cognitive impairment; 60–70%: altered judgment/coordination; 40–60%: unconscious in hours; 20–40%: minutes; 0–20%: seconds (death ≈ brain death).

▶How long is the RBC contact time with alveolar O₂, and how much is normally needed?

Contact time is 0.75 s, but normally only 0.25 s is needed (wide gradient, thin membrane).

▶Why are patients with diffusion disorders often not hypoxemic at rest but become so with exercise?

A thicker membrane (fibrosis/edema) needs the full 0.75 s for O₂ transfer; exercise raises CO/HR, shortening contact time → cyanosis, dyspnea, syncope, ↑lactate.

▶What is the normal tissue oxygen delivery, extraction, and consumption?

Delivery ~1000 ml/min, 25% extracted → consumption ~250 ml/min (which cannot be reduced).

▶What is supply-dependent oxygen consumption?

When delivery falls below ~550 ml/min (after maximal extraction), consumption becomes supply-dependent → syncope and ↑lactate.

▶What is the treatment of acute respiratory failure?

Oxygen (check if hypoxemia improves), bronchodilator, anti-inflammatory (systemic steroids), fluid/electrolyte replacement, and maintaining normotension + sinus rhythm.

▶What causes type 2 respiratory failure despite healthy lungs?

Alveolar hypoventilation from pump failure — neuromuscular disease, morphine, or respiratory center injury.

▶How much can alveolar ventilation increase during the hyperventilation response to hypoxemia?

Up to about 6-fold.

▶Why does type 1 failure feature hypoxemia without hypercapnia?

Hyperventilation (driven by hypoxemia) removes CO₂ effectively, keeping pCO₂ normal or low while O₂ stays low.

▶What metabolic consequence occurs when tissue O₂ delivery is critically low?

Anaerobic metabolism with rising lactate, plus syncope.

▶How do the lab values of type 1, type 2, and type 3 failure compare?

Type 1: pO₂ <60, pCO₂ <46. Type 2: pO₂ <60, pCO₂ >46. Type 3: severe hypoxemia + mild hypercapnia.

▶Why does type 1 often progress to type 2 in mixed failure?

The respiratory muscles fatigue from sustained high work of breathing, leading to hypoventilation and CO₂ retention.

▶Why is maintaining cardiac function important in respiratory failure management?

Cardiac failure occurs in ~30% of elderly patients, and the heart bears the main burden of compensating; normotension and sinus rhythm must be maintained.