Pediatric Respiratory Acidosis

Overview

• Respiratory Acidosis: Occurs when arterial partial pressure of CO2 (Pa CO2) > 44 mmHg, leading to blood pH < 7.35.
• Diagnosis: Requires measurement of Pa CO2 and pH.
• Causes: Imbalance between CO2 production and excretion due to inadequate minute ventilation.
• Types:
  • Acute: Life-threatening if associated with severe hypoxemia and acidemia.
  • Chronic: Characterized by gradual increase in Pa CO2.

Pathophysiology

• Pa CO2: Directly proportional to CO2 production, inversely proportional to alveolar ventilation.
• Inadequate CO2 removal: Central respiratory drive depression, respiratory muscle paralysis, lung and airway diseases, increased dead space.
• Compensation:
  • Cellular Buffers: Proteins and phosphates.
  • Hemoglobin: Important blood buffer.
  • Renal Compensation: Begins in 6-12 hours, maximizes in 3-5 days.
• Effects:
  • Neurologic: Confusion, headache, possible hypercapnic encephalopathy.
  • Respiratory: Predicts hypoxemia development.
  • Cardiovascular: Epinephrine and norepinephrine release, potential cardiac effects.

Etiology

• CNS-Related: Trauma, infection, neoplasm, stroke, hypoxia, overdose.
• Nerve-Related: Spinal muscular atrophy, Guillain-Barré syndrome.
• Neuromuscular Junction: Myasthenia gravis, botulism.
• Airway Issues: CNS control loss, congenital lesions, asthma.
• Lung Injury: Pneumonia, pulmonary edema.
• Chronic Lung Disease: Cystic fibrosis, COPD.
• Chest Wall Restriction: Flail chest, pneumothorax.
• Increased CO2 Production: Malignant hyperthermia, extensive burns.

Prognosis

• Severity Factors: Duration, underlying disease, arterial saturation.
• Outcomes: Acute events reversible without sequelae if no hypoxemia; may indicate chronic or progressive disease.

References

• Studies and clinical observations detailing effects and treatment strategies related to respiratory acidosis.