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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.

Mild V/Q mismatching

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

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.

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:

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.

Management

Treating the underlying cause is essential, but measures to improve hypoxaemia and hypercapnia are important as well, to prevent worsening. Oxygen supplementation, non-invasive ventilation, or invasive ventilation may be used.

Oxygen supplementation in COPD

Persons with COPD may occasionally require oxygen therapy, for example during a COPD exacerbation or pneumonia. However, administration of oxygen to some people with COPD causes hypercapnia. This has often been explained by the following mechanism:

In healthy people, a higher CO2 level drives the ventilatory drive. However, people with COPD have a decreased sensitivity to CO2, so for these persons, a lower O2 level drives the ventilatory drive instead. Administration of oxygen to such a person will then lead to a decreased ventilatory drive, causing hypoventilation. Because they are receiving oxygen supplementation, they won't become hypoxaemic, but they will become hypercapnic.

This mechanism does take place, but its contribution to increasing CO2 levels is minor. Hypercapnia rather occurs mainly due to the following two mechanisms:

  • Administration of oxygen reduces hypoxaemia-reduced pulmonary vasoconstriction, which would normally redirect blood flow from poorly-ventilated areas of the lung to well-ventilated areas. When oxygen supplementation reduces this vasoconstriction, this compensatory mechanism is lost, effectively causing a V/Q mismatch leading to hypercapnia.
  • Oxygenated haemoglobin (oxyhaemoglobin) binds CO2 weaker than deoxyhaemoglobin. For this reason will oxygen supplementation displace CO2 from haemoglobin. This causes an increase in pCO2 even though the actual total CO2 content of the blood increases. This is called the Haldane effect.

Regardless of mechanism, it's important to know that only some people with COPD develop hypercapnia in response to oxygen therapy, and that in most people who develop this effect, the hypercapnia is limited and not progressive.