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Textbook
1. Anatomy
2. Microbiology
3. Physiology
4. Pathology
4.1 General pathology
4.2 Central and peripheral nervous system
4.3 Cardiovascular system
4.4 Respiratory system
4.4.1 Benign tumors of the respiratory tract
4.4.2 Malignant tumors of the respiratory tract
4.4.3 Obstructive lung disease
4.4.4 COPD, chronic bronchitis, and emphysema
4.4.5 Restrictive lung disease
4.4.6 Silicosis
4.4.7 Respiratory failure and ARDS
4.4.8 Miscellaneous topics
4.4.9 Pleural effusion
4.4.10 Additional information
4.5 Hematology and oncology
4.6 Gastrointestinal pathology
4.7 Renal, endocrine and reproductive system
4.8 Musculoskeletal system
5. Pharmacology
6. Immunology
7. Biochemistry
8. Cell and molecular biology
9. Biostatistics and epidemiology
10. Genetics
11. Behavioral science
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4.4.7 Respiratory failure and ARDS
Achievable USMLE/1
4. Pathology
4.4. Respiratory system

Respiratory failure and ARDS

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Respiratory failure is failure of gas-exchange and can either be hypoxemic or hypercapnic. Acute respiratory failure may be type I or type II. In some patients, both types may co-exist.

Types of acute respiratory failure

Type Features
Type I or hypoxemic PaO2 <60 mmHg; PaCO2 normal or low; most common type; presence of V/Q mismatch and shunt; increased A-a gradient; hypoxemia can be corrected by 100% oxygen in V/Q mismatch but not in shunts; seen in primarily lung diseases like pulmonary edema, pneumonia, pulmonary hemorrhage, COPD.
Type II or hypercapnic PaCO2 >50 mmHg; PaO2 low; Normal A-a gradient; seen in chest wall and muscle diseases like myasthenia gravis, poliomyelitis, Guillain-Barre syndrome, asthma, kyphoscoliosis, flail chest, COPD, drug overdose, CNS depression.

Acute deterioration in a patient with chronic respiratory failure is termed acute-on-chronic respiratory failure. It is seen in COPD in the presence of respiratory infections, bronchoconstriction, non-compliance to therapy etc.

ABG and history will help to differentiate between acute and chronic causes of respiratory failure.

Acute respiratory distress syndrome (ARDS)

  • Development of severe, acute respiratory failure within 1 week of an inciting lung injury, not due to cardiac causes
  • CxR shows bilateral, diffuse opacities
  • Characteristically, PCWP* <18 mmHg
  • PaO2/FiO2 <300 mmHg in the presence of PEEP of >5cmH2O
  • Mild, moderate or severe types
  • Mild: PaO2/FiO2 200-300 mmHg
  • Moderate:PaO2/FiO2 100 to <200 mmHg
  • Severe: PaO2/FiO2 <100 mmHg
  • Causes: pneumonia, inhalation of toxic fumes, lung contusion, aspiration of gastric contents, drowning, multiple transfusions, burns, pancreatitis, sepsis, drug overdose
  • Increased vascular permeability and endothelial damage seen causing fluid buildup in alveoli
  • Apoptosis of alveolar epithelial cells seen
  • Presents with tachypnea, dyspnea, hypoxemia, cyanosis
  • Extracorporeal membrane oxygenation and higher PEEP helps severe cases.

*PCWP or pulmonary capillary wedge pressure of > 18mmHg suggests cardiac origin of pulmonary edema and excludes ARDS (in some cases both conditions may co-exist).

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