Respiratory failure

Respiration is sufficient when it is able to provide enough oxygen to and remove enough carbon dioxide from the tissues. If this is not the case, there is respiratory failure. There are two types of respiratory failure, partial and global.

Partial respiratory failure, also called hypoxaemic respiratory failure or type I respiratory failure, is characterised by hypoxaemia (decreased pO2 < 60 mmHg) but no hypercapnia (elevated pCO2).

Complete respiratory failure, also called hypercapnic respiratory failure or type II respiratory failure, is characterised by both hypoxaemia and hypercapnia. This is more severe and also causes respiratory acidosis.

Respiratory can develop acutely or chronically, depending on whether the etiology is acute or chronic.

Etiology

Hypoxaemic respiratory failure

Hypoxaemic respiratory failure occurs due to problems with gas exchange in the lungs or due to mild V/Q mismatching. This is because CO2 exchanges much more easily in the lungs than O2.

Impaired gas exchange

Impairment of gas exchange, usually due to disorder of the lungs, can cause hypoxaemic respiratory failure.

• Interstitial lung disease
• Emphysema

Mild V/Q mismatching

Ventilation/perfusion mismatching can cause hypoxaemic respiratory failure, but if severe enough, hypercapnic respiratory failure occurs.

• Too high V/Q ratio (not enough perfusion compared to ventilation)
  • COPD
  • Bronchiectasis
  • Pulmonary hypertension
  • Interstitial lung disease
• Too low V/Q ratio (not enough ventilation compared to perfusion)
  • Pneumonia
  • Pulmonary oedema
  • Acute respiratory distress syndrome
  • Atelectasis
  • Pulmonary arteriovenous fistula

Hypercapnic respiratory failure

Hypercapnic respiratory failure may occur due to (alveolar) hypoventilation or due to increased dead space.

Hypoventilation

Physiological ventilation requires a normal respiratory drive from the CNS, normal conduction of nerve impulses from the CNS to the respiratory muscles, normal function of the chest wall and respiratory muscles, normal conduction of air through the upper airways, and normal functioning of the lungs.

As such, hypoventilation may occur due to problems in several different organ systems. Problems with the central nervous system can impair the normal drive to ventilate, problems with the peripheral nervous system, respiratory muscles, chest wall, or upper airways may make the patient unable to breathe despite the respiratory drive, and problems with the lung can impair gas exchange to such a degree that any amount of ventilation is insufficient for gas exchange.

• Problems with the CNS
  • Medications which decrease respiratory drive (benzodiazepines, alcohol, opioids)
  • Stroke
  • Encephalitis
• Impaired neuromuscular transmission
  • Injury to the cervical spine between C3 and C5
  • Neuromuscular disorders (ALS, GBS, MG)
  • Tetanus
  • Botulism
  • Electrolyte disorders
• Impaired function of chest wall
  • Severe kyphosis or scoliosis
  • Pectus excavatum
• Impaired airways (rarely causes hypoventilation by itself)
  • Acute exacerbation of COPD or asthma
  • Foreign body aspiration
  • External airway obstruction (goitre, tumour)

Increased dead space (V/Q mismatch)

Increased dead spacing occurs when there is a ventilation/perfusion mismatch (V/Q mismatch) where regions of the lung are not perfused. When a part of the lung receives no perfusion, the alveoli in the area effectively become dead space (due to not having blood to exchange gas to). This can occur in case of:

• Pulmonary embolism (severe)
• Interstitial lung disease (severe)

Pathophysiology

Hypoxaemia

Oxygen is essential for the body, and so hypoxaemia may cause a variety of complications, the severity of which depend on the severity of the hypoxaemia, the current oxygen requirement of the organs, and the patients habitual blood oxygen level.

Hypercapnia

Hypercapnia is problematic mainly because it causes respiratory acidosis and because it affects the brain. CO₂ increases glutamine and GABA transmission, depressing consciousness. Carbon dioxide is also a cerebral vasodilator, increasing cerebral blood flow and potentially increasing intracranial pressure. The depressive effects of CO₂ on the brain can cause so-called CO₂ narcosis.

Clinical features

Hypoxaemia causes symptoms of respiratory distress, including dyspnoea, tachypnoea, and anxiety. A compensatory tachycardia may occur. Severe hypoxaemia causes cyanosis, initially on the lips and tips of the body, called acrocyanosis. Eventually, altered mental status, confusion, and restlessness can occur.

Hypercapnia causes depressed consciousness, which may range from sluggishness to somnolence to coma.

Compensatory mechanisms

Symptoms are less severe for chronic than for acute respiratory failure. In chronic cases, compensatory mechanisms like polyglobulia for hypoxaemia and increased bicarbonate reabsorption in the kidney for respiratory acidosis decreases the physiological impacts of respiratory failure.