- Typical symptoms associated with a rapid increase in pCO2 include anxiety, dyspnea, confusion, hallucination, and psychosis; this can progress to coma.
- A more gradual increase, as is seen with chronic respiratory acidosis, may cause memory impairment, sleep disturbances, personality changes, daytime somnolence, coordination impairment, tremors, myoclonic jerks, or asterixis.
- Decreased central respiratory drive (eg, sedative overdose, encephalitis, stroke, sleep apnea, obesity hypoventilation, hypothermia, starvation)
- Decreased respiratory, neuromuscular, or thoracic cage function (eg, primary spinal cord / lower motor neuron / muscle disorders, thoracic cage disorders, metabolic disorders, toxins / poisoning / drugs)
- Increased alveolar dead space
- Anatomic (eg, short, shallow breathing)
- Physiologic (eg, pulmonary embolism, pulmonary vascular disease, severe asthma, chronic obstructive pulmonary disease [COPD], end-stage interstitial lung disease)
- Increased carbon dioxide production (eg, fever, thyrotoxicosis, sepsis, steroids, overfeeding, exercise) – Unless a patient has limited pulmonary reserve, this will rarely result in clinically important hypercapnia.
- Upper airway disorders (eg, epiglottitis, foreign body aspiration, obstructive goiter) – These are rare causes of hypercapnia.
- Acute respiratory acidosis – Acute hypercapnia typically follows sudden obstruction of the airway or generalized bronchospasm. The acute compensatory response for respiratory acidosis is an increase in the serum bicarbonate concentration by 1 mEq/L for every 10 mm Hg elevation in pCO2.
- Chronic respiratory acidosis – Chronic hypercapnia (defined as respiratory acidosis persisting after 3-5 days) occurs in end-stage COPD, restrictive lung disease with ventilatory muscle fatigue, or advanced states of intrapulmonary and extrapulmonary restrictive lung disease. With chronic acidosis, the kidneys increase acid excretion, allowing for generation of additional HCO3, and the renal tubule increases HCO3 reabsorption, a process that takes 3-5 days to complete. The chronic response leads to a 4 mEq/L increase in the serum bicarbonate concentration per 10 mm Hg elevation in pCO2.
E87.2 – Acidosis
12326000 – Respiratory acidosis
- Severe asthma
- Acute respiratory distress syndrome
- Opioid / sedative overdose (see opioid toxicity)
- Stroke (see cerebral stroke)
- Infection (see sepsis)
- Neuromuscular disorders
- Obesity hypoventilation syndrome
- Secondary effects of mechanical ventilation
If a patient with a chronic respiratory acidosis presents with a moderate to severe acidemia, it is usually suggestive of a concurrent metabolic acidosis or superimposed acute respiratory acidosis. On the contrary, if a patient with a chronic respiratory acidosis presents with a pH ≥ 7.40, look for a concurrent metabolic alkalosis or acute respiratory alkalosis.