51. Partial or complete respiratory failure

Page created on October 28, 2018. Last updated on January 1, 2023 at 20:38

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, we have respiratory failure. We have two types of respiratory failure, partial and global.

Partial respiratory failure

Partial respiratory failure is also called hypoxaemic normocapnic or type I respiratory failure. In partial respiratory failure is the pO₂ in the arteries lower than 60 mmHg, meaning there is hypoxaemia. However, pCO₂ is normal.

This type of respiratory failure often occurs due to diffusion problems or mild V/Q mismatching. The most frequent causes are:

• V/Q mismatching
  • Only in moderate cases, type II failure in severe cases
  • Pulmonary embolism
• Disorders of alveolo-capillary diffusion
  • Pulmonary fibrosis
  • Pulmonary oedema
  • Emphysema
  • Pneumonia
  • Atelectasis
  • Wet lung
  • Hepatopulmonary syndrome
• Pneumothorax
• High altitude

Recall that CO₂ diffuses much easier across the respiratory membrane than O₂ does. In cases where diffusion is impaired can CO₂ therefore still diffuse sufficiently while O₂ can’t, leading to hypoxaemia but normocapnia.

The consequence of partial respiratory failure can be hypoxaemic hypoxia of peripheral tissues. Because pCO₂ is normal is it possible that ventilation doesn’t increase to compensate for the hypoxaemia.

Global respiratory failure

Global respiratory failure, or hypoxaemic – hypercapnic or type II respiratory failure is characterized by not only hypoxaemia (pO₂ < 60 mmHg) but hypercapnia (pCO₂ > 50 mmHg) as well.

Type II failure is always caused by alveolar hypoventilation. Its most frequent causes are:

• Alveolar hypoventilation
  • Opioids (Morphin)
  • Neuromuscular disorders affecting the respiratory muscles
  • Kyphoscoliosis
  • Obesity (Pickwick syndrome)
  • Sleep apnoea syndrome
  • Severe form of COPD
  • Guillane barre syndrome
• Right-to-left shunting

The consequences of global respiratory failure are as follows (and are important!).

• Reduced air flow
  • → pO₂ decreased
    • → pulmonary vasoconstriction → pulmonary hypertension → cor pulmonale chronicum
    • → erythropoietin increases → polyglobulia → blood viscosity increases → blood pressure increases
  • → pCO₂ increased
    • → reflex systemic vasoconstriction → total peripheral resistance increases → blood pressure increases
    • → cerebral vasodilation → intracranial pressure increases → Cushing reflex activates → blood pressure increases and bradycardia
    • → CO₂ sensitivity of respiratory centre decreases → insufficient response to hypercapnia → ventilation may be driven by hypoxia
    • → respiratory acidosis
      • → reflex systemic vasoconstriction → blood pressure increases
      • → myocardial contractility decreases → heart failure
      • → capillary permeability increases → pulmonary oedema

Respiratory failures most commonly develop over a long period of time rather than acutely. However, both forms are important.

Chronic respiratory failure

The disorders causing chronic respiratory failure to develop slowly and over a long time. However the body also has more time to compensate for the failure. Polyglobulia can develop to compensate for hypoxaemia and respiratory acidosis can be counterbalanced by increasing bicarbonate reabsorption.

The most important causes are:

• COPD
• Neuromuscular disorders
• Chest abnormalities
• Pulmonary fibrosis
• Obesity
• Sleep apnoea syndrome

Acute respiratory failure

Disorders causing acute respiratory failure can only partially or hardly be compensated by enhancing the circulation. Common causes include:

• Cardiogenic or hydrostatic oedema
  • Left ventricular failure
  • Acute ischaemia
• Acute respiratory distress syndrome (ARDS)
• Sepsis
• Aspiration of foreign body
• Toxic gas inhalation (like chlorine)

Acute respiratory distress syndrome

Acute respiratory distress syndrome or (ARDS) is a restrictive lung disorder where pulmonary oedema and shunting (V/Q mismatching) occurs due to non-cardiological causes. The pulmonary oedema doesn’t develop due to high pulmonary pressure but rather because the capillary permeability is increased, leading to the term “low pressure oedema”. ARDS initially leads to partial respiratory failure but later global, and often occurs less than two hours from when the triggering event began. It’s usually caused by:

• Circulatory shock
• Sepsis
• Disseminated intravascular coagulation
• Inhalation of toxic gases
• Inhalation of gastric content
  • Gastro-oesophageal reflux disease (GERD)
• Pulmonary embolism
• Diabetic ketoacidosis
• Uraemia

Patients with ARDS usually present with rapidly worsening tachypnoea, dyspnoea and hypoxaemia. Their skin is also cyanotic.

In the progressive phase of circulatory shock will there be a lactic acidosis. Lactic acidosis leads to hyperventilation. However the gas tensions were normal, so the hyperventilation just causes hypocapnia.

The tissue damage in the later phases of circulatory shock will cause activation of neutrophils. The neutrophils will increase the capillary permeability in the lungs by releasing reactive oxygen species, inflammatory cytokines and lysosomal enzymes. The increased capillary permeability increases the flow of fluid from the capillaries into the interstitium, causing oedema.

The inflammation also decreases the production of surfactant, leading to atelectasis. Because some alveoli are collapsed (atelectasis) will the V/Q ratio in that area become 0 (there’s no ventilation), meaning that there is shunt formation. There will be vasoconstriction to move blood away from atelectic areas to areas that are well ventilated. The pulmonary vasoconstriction can lead to pulmonary hypertension.

The protein-rich oedema will cause fibrin to deposit in the alveoli, forming hyaline membranes, which further worsens the diffusion. The hypoxia, acidosis and pulmonary hypertension damage the endothelium, which predisposes to thrombosis.

If the patient survives the acute phase can the proteins in the oedema fluid organize and form pulmonary fibrosis, which causes long-term problems.