51. Partial or complete 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, 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.