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Respiratory failure: Difference between revisions
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== Compensatory mechanisms == | == 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. | 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. | ||
<noinclude>[[Category:Pathophysiology]]</noinclude> | |||
== 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 CO<sub>2</sub> level drives the ventilatory drive. However, people with COPD have a decreased sensitivity to CO<sub>2</sub>, so for these persons, a lower O<sub>2</sub> 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 CO<sub>2</sub> 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 CO<sub>2</sub> weaker than deoxyhaemoglobin. For this reason will oxygen supplementation displace CO<sub>2</sub> from haemoglobin. This causes an increase in pCO<sub>2</sub> even though the actual total CO<sub>2</sub> 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. <noinclude> | |||
[[Category:Pathophysiology]] | |||
</noinclude> | |||