Aetiology
Respiratory acidosis is due either to:
An acute reduction in alveolar ventilation (cannot breathe or will not breathe)
A dramatic increase in carbon dioxide production
A failure to increase alveolar ventilation in association with increased production.
While patients with COPD have chronic hypercapnia, their pH is usually between 7.35 and 7.4.
The causes of respiratory acidosis are diverse and may result from disorders of many different organ systems. The differential diagnosis of respiratory acidosis can be formulated based on the acuity of the acidosis (acute or chronic) or by organ system. Determination of the acuity of an acidosis can be complicated by other underlying acid-base disorders. Therefore, an approach to the differential diagnoses from an organ-based perspective is useful.
Parenchymal lung disease
Both intrinsic lung disease and pulmonary vascular pathology can impair carbon dioxide excretion.
Common causes are COPD and pneumonia.[3] Cardiogenic pulmonary oedema rarely causes hypercapnia, and it is a late complication of acute respiratory distress syndrome due to a combination of the use of positive end-expiratory pressure and increased dead space.
Acute lung injury is an uncommon but serious cause.
Airway obstruction
Often dramatic and acute, airway obstruction is a life-threatening emergency.
Causes include foreign body aspiration, laryngospasm, status asthmaticus, and angio-oedema.
Laryngospasm, status asthmaticus, and angio-oedema are uncommon causes of respiratory acidosis except in the last stages when patients present with hypoxaemia or respiratory distress.
Central nervous system
Central nervous system (CNS) depression leads to alveolar hypoventilation.
Often associated with altered mental status.
Common causes include intentional or accidental drug ingestion.
Serious causes include CNS infarct, haemorrhage, and infection.
Oxygen therapy administered to patients with COPD, resulting in hyperoxia, has been associated with hypercapnia. The mechanism is multifactorial, but probably results from a combination of respiratory depression and increased alveolar dead space consequent to reversal of hypoxic pulmonary vasoconstriction.[4]
Impaired chest wall mobility
Characterised by restriction of the normal chest wall excursion.
Pleural disease (effusion, empyema, pneumothorax, haemothorax, fibrothorax) may impair normal lung parenchymal expansion.
Common causes include obesity, pleural effusions, and empyema.
Serious causes include flail chest, pneumothorax, haemothorax, and empyema.
Skeletal disease such as kyphoscoliosis and ankylosing spondylitis minimises normal chest expansion.
Neuromuscular disorders
Neuromuscular disorders can affect any component of the nerve-muscle complex.
Other neuromuscular abnormalities are typically present.
Common causes include electrolyte derangements (hypokalaemia and hypophosphataemia).
Serious causes include progressive neurological diseases (Guillain-Barre syndrome, amyotrophic lateral sclerosis), high cord trauma/lesion, organophosphate ingestion, tetanus, and botulism.
Systemic illnesses such as myasthenia gravis and hypothyroidism can be associated with hypoventilation, although hypothyroidism is an uncommon cause of respiratory acidosis except in the last stages when patients present with hypoxaemia.
Overproduction of carbon dioxide
Systemic illnesses can lead to increased carbon dioxide production sufficient to overwhelm the normal respiratory system, but overproduction of carbon dioxide is a rare cause of respiratory acidosis.
Some causes are malignant hyperthermia, sepsis, heat exhaustion, thyrotoxicosis, and overfeeding with parenteral nutrition.
Other
Inadequate mechanical ventilation and insufflation of carbon dioxide into a body cavity (laparoscopic surgery) should be considered in the appropriate clinical setting.
The causes of respiratory acidosis associated with inadequate mechanical ventilation are diverse, and specific testing should focus on the history and examination findings.
Low tidal volume ventilation will commonly cause respiratory acidosis due to intentional hypoventilation as part of a lung-protective ventilation strategy.
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