Internal Diseases and Therapy · MU Sofia

3. Respiratory failure – pathophysiology, and clinical features

Explains respiratory failure as a failure of gas exchange, with its blood-gas definition, then sets out a four-type classification by gas exchange and an acute, chronic and acute-on-chronic time course. It goes on to the mechanisms of hypoxaemia and hypercapnia, with tables of causes, the clinical features, and an extended section on ARDS including the Berlin definition. It closes with oxygen targets, a device table and ventilation options.

Inside: 7 sections · 1 labelled picture · 4 tables · 16 flashcards · 11 min

Topic 3 of 139 in the MU Sofia syllabus for Internal Diseases and Therapy (Medicine, Years 4 and 5). The free AceMed note covers it in 7 sections, about 1,246 words (11 min of reading), with 16 flashcards.

In this note

  1. Definition
  2. Classification
  3. Pathophysiology
  4. Clinical features
  5. Diagnosis
  6. Acute respiratory distress syndrome (ARDS)
  7. Principles of treatment

Definition

Respiratory failure is the inability of the respiratory system to maintain adequate gas exchange — to oxygenate the arterial blood and/or to eliminate CO2 — so that it no longer meets the metabolic demands of the body. It is defined by arterial blood gases on room air at rest:

  • Hypoxaemia: PaO2 < 60 mmHg (8 kPa) (SaO2 < 90%).
  • Hypercapnia: PaCO2 > 45–50 mmHg (6–6.7 kPa).

Classification

By gas exchange

By time course

  • Acute: develops over minutes to hours; in hypercapnia, pH falls (acute respiratory acidosis, bicarbonate still normal). Life-threatening.
  • Chronic: develops over days to months; the kidneys retain bicarbonate → compensated respiratory acidosis (near-normal pH, ↑ HCO3−); polycythaemia, pulmonary hypertension, cor pulmonale. Typical of advanced COPD, neuromuscular and chest wall disease.
  • Acute-on-chronic: a sudden worsening in chronic failure (e.g. COPD exacerbation): high PaCO2, high bicarbonate and a low pH.

Pathophysiology

The five mechanisms of hypoxaemia

  • Alveolar–arterial (A–a) O2 gradient = PAO2 − PaO2, where PAO2 = FiO2 × (760 − 47) − PaCO2/0.8 (≈ 150 − 1.25 × PaCO2 on room air at sea level). Normal < 10–15 mmHg in the young (roughly age/4 + 4). A normal gradient with hypoxaemia means the lungs are healthy and the cause is hypoventilation or low inspired O2.
  • Low mixed venous O2 (low cardiac output, anaemia, high O2 consumption) worsens hypoxaemia when V/Q mismatch or shunt is present.

Hypercapnia (ventilatory failure)

PaCO2 is inversely proportional to alveolar ventilation (PaCO2 ∝ VCO2 / VA). It rises when the respiratory pump cannot cope with the load: low drive ("won't breathe"), weak pump ("can't breathe"), or a load too high (airway obstruction, stiff lungs or chest wall, ↑ CO2 production, ↑ dead space).

Anatomical approach to acute hypoxaemic failure

  • Airways: asthma, COPD, mucus plugging.
  • Air spaces (alveolar filling): pulmonary oedema, pneumonia, ARDS, pulmonary haemorrhage, alveolar proteinosis.
  • Interstitium: pulmonary fibrosis, hypersensitivity pneumonitis, atypical (viral) pneumonia.
  • Vessels/heart: pulmonary embolism, intracardiac or intrapulmonary shunt, heart failure.
  • Pleura: pneumothorax, pleural effusion.

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