Respiratory acidosis: Difference between revisions
No edit summary |
No edit summary |
||
| (6 intermediate revisions by the same user not shown) | |||
| Line 1: | Line 1: | ||
<section begin="A&IC" /><section begin="clinical biochemistry" />{{Infobox medical condition | |||
| name = Respiratory acidosis | |||
| definition = A process decreasing pH due to abnormal ventilation | |||
| cause = Benzodiazepine or opioid overdose. Neuromuscular disorders. Emphysema. Interstitial lung disease. | |||
| symptoms = Depressed consciousness | |||
| treatment = Treatment of underlying cause. Non-invasive or invasive ventilation. | |||
}} | |||
'''Respiratory acidosis''' is an acid-base disorder characterised by a respiratory pathological process which decreases the pH of the blood. If the acidosis is severe, it can overcome the body's defense against acidosis, causes the pH in the blood to fall below 7.35. This is called [[acidaemia]]. | '''Respiratory acidosis''' is an acid-base disorder characterised by a respiratory pathological process which decreases the pH of the blood. If the acidosis is severe, it can overcome the body's defense against acidosis, causes the pH in the blood to fall below 7.35. This is called [[acidaemia]]. | ||
| Line 7: | Line 15: | ||
== Etiology == | == Etiology == | ||
Respiratory acidosis occurs due to hypercapnic respiratory failure. | Respiratory acidosis occurs due to hypercapnic respiratory failure. | ||
{{#lst:Respiratory failure|etiology}} | {{#lst:Respiratory failure|etiology}} | ||
== Pathophysiology == | == Pathophysiology == | ||
=== Compensatory mechanism === | === Compensatory mechanism === | ||
The body cannot compensate for respiratory acidosis by stimulating ventilation, as ventilation is the problem in the first place. However, kidney compensation occurs similarly as for metabolic acidosis. Kidneys respond to acidosis by increasing urinary excretion of acids and decreasing urinary excretion of bicarbonate. This mechanism is slow, taking a few days to kick in. | The body cannot compensate for respiratory acidosis by stimulating ventilation, as ventilation is the problem in the first place. However, kidney compensation occurs similarly as for metabolic acidosis. Kidneys respond to acidosis by increasing urinary excretion of acids and decreasing urinary excretion of bicarbonate. This mechanism is slow, taking a few days to kick in. | ||
== Clinical features == | == Clinical features == | ||
Hypercapnia causes depressed consciousness, which may range from sluggishness to somnolence to coma. | Hypercapnia causes depressed consciousness, which may range from sluggishness to somnolence to coma. | ||
== Diagnosis and evaluation == | == Diagnosis and evaluation == | ||
[[Arterial blood gas]] is essential in the evaluation of acid-base disorders. It will give the pH, bicarbonate level, pCO2, pO2, and lactate levels. In respiratory acidosis, the pCO<sub>2</sub> level is elevated (> 45 mmHg). If there is acidaemia, the pH is < 7.35. | [[Arterial blood gas]] is essential in the evaluation of acid-base disorders. It will give the pH, bicarbonate level, pCO2, pO2, and lactate levels. In respiratory acidosis, the pCO<sub>2</sub> level is elevated (> 45 mmHg). If there is acidaemia, the pH is < 7.35. | ||
When kidney compensation has kicked in, bicarbonate levels start to increase. Appropriate compensation causes an increase of approximately 4 units of bicarbonate per 10 mmHg elevation in pCO<sub>2</sub>. | When kidney compensation has kicked in, bicarbonate levels start to increase. Appropriate compensation causes an increase of approximately 4 units of bicarbonate per 10 mmHg elevation in pCO<sub>2</sub>.<section end="clinical biochemistry" /> | ||
== Management == | == Management == | ||
{{#lst:Respiratory failure|management}} | {{#lst:Respiratory failure|management}} | ||
<noinclude>[[Category:Pathophysiology]]</noinclude> | == Complications == | ||
Severe acidaemia can cause fatal [[Ventricular arrhythmias|ventricular arrhythmia]] and depression of cardiac contractility, which may cause heart failure. The usually co-present hypoxaemia may also cause similar complications.<section end="A&IC" /><noinclude> | |||
[[Category:Pathophysiology]] | |||
</noinclude> | |||
Latest revision as of 18:29, 27 October 2024
| Respiratory acidosis | |
|---|---|
| Definition | A process decreasing pH due to abnormal ventilation |
| Symptoms | Depressed consciousness |
| Causes | Benzodiazepine or opioid overdose. Neuromuscular disorders. Emphysema. Interstitial lung disease. |
| Treatment | Treatment of underlying cause. Non-invasive or invasive ventilation. |
Respiratory acidosis is an acid-base disorder characterised by a respiratory pathological process which decreases the pH of the blood. If the acidosis is severe, it can overcome the body's defense against acidosis, causes the pH in the blood to fall below 7.35. This is called acidaemia.
Metabolic acidosis is similar but is rather due to a metabolic problem. Respiratory alkalosis is sort of the opposite of respiratory acidosis.
Respiratory acidosis occurs due to impaired ventilation (hypoventilation), which causes pCO2 to increase (hypercapnia). This is called hypercapnic respiratory failure.
Etiology
Respiratory acidosis occurs due to 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
- 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
Compensatory mechanism
The body cannot compensate for respiratory acidosis by stimulating ventilation, as ventilation is the problem in the first place. However, kidney compensation occurs similarly as for metabolic acidosis. Kidneys respond to acidosis by increasing urinary excretion of acids and decreasing urinary excretion of bicarbonate. This mechanism is slow, taking a few days to kick in.
Clinical features
Hypercapnia causes depressed consciousness, which may range from sluggishness to somnolence to coma.
Diagnosis and evaluation
Arterial blood gas is essential in the evaluation of acid-base disorders. It will give the pH, bicarbonate level, pCO2, pO2, and lactate levels. In respiratory acidosis, the pCO2 level is elevated (> 45 mmHg). If there is acidaemia, the pH is < 7.35.
When kidney compensation has kicked in, bicarbonate levels start to increase. Appropriate compensation causes an increase of approximately 4 units of bicarbonate per 10 mmHg elevation in pCO2.
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.
Complications
Severe acidaemia can cause fatal ventricular arrhythmia and depression of cardiac contractility, which may cause heart failure. The usually co-present hypoxaemia may also cause similar complications.