respiratory acidosis; hypercapnic acidosis

Introduction

Inadequate pulmonary excretion of CO2.

Etiology

• CNS depression (inhibition of medullary respiratory center)
  • CNS depressants
    • anesthesia, sedatives, opiates
  • infection
  • brain injury
    • head trauma
    • stroke
    • brain tumor
  • central hypoventilation syndrome
  • obesity-hypoventilation syndrome
  • central sleep apnea
  • hypercapnia
  • myxedema coma
• neuromuscular disorder (disorders of respiratory muscles)
  • myopathy
    • polymyositis
  • Guillain-Barre syndrome
  • myasthenic crisis
  • amyotrophic lateral sclerosis (ALS)
  • spinal cord injury
  • periodic paralysis
  • hypokalemia
  • hypophosphatemia
• musculoskeletal disorders
  • morbid obesity
  • kyphoscoliosis
• pulmonary diseases (disorders of gas exchange across alveolar capillaries)
  • chronic obstructive pulmonary disease
  • obstructive sleep apnea
  • asthma
  • interstitial lung disease
    • pulmonary fibrosis
  • pneumothorax, hemothorax
  • pulmonary edema
  • pulmonary embolism
  • pneumonia
  • ARDS
• increased carbon dioxide production
  • extreme exercise
  • seizures
  • heart failure (severe)
• increased wotk of breathing
• mechanical ventilation
  • hyperalimentation
• upper airway obstruction
  • tonsillar hypertrophy
  • vocal cord paralysis
  • foreign body aspiration
  • laryngospasm
  • tracheal stenosis
  • angioedema

Clinical manifestations

• acute
  • confusion
  • asterixis
  • papilledema
  • headache
  • somnolence
  • seizures
• chronic
  • memory loss
  • inattention
  • irritability, agitation
• cardiovascular
  • hypertension
  • tachycardia
  • heart failure
  • cardiac arrhythmias

Laboratory

• arterial blood gas (ABG)
  • decreased pH
  • increased pCO2
• serum bicarbonate:
  • compensatory metabolic alkalosis generally does not result in serum HCO3- > 35 meq/L
  • 1 meq/L acute increase in serum HCO3- for every 10 mm Hg increase in pCO2
  • 3.5 meq/L chronic increase in serum HCO3- for every 10 mm Hg increase in pCO2
  • 3-5 days for compensatory metabolic alkalosis

* Rules for predicting serum HCO3- compensation for pure respiratory acidosis

• acute: 1 meq increase in serum HCO3- for each 10 mm Hg increase in pCO2 (PaCO2, arterial)
• chronic: 3.5 meq increase in serum HCO3- for each 10 mm Hg increase in pCO2
• failure of serum HCO3- to increase by the expected value suggests complicating metabolic acidosis
• excessive increase in serum HCO3- suggests complicating metabolic alkalosis
• in calculating the anticipated HCO3- compensation use the midpoint of the reference interval 25-26 meq/L as the baseline

Complications

• acute respiratory acid associated with risk of hypoxemia rather than acidemia or hypercapnia
• uncompensated respiratory acidosis is associated with increased mortality in mechanically-ventilated patients with traumatic brain injury
  • compensated respiratory acidosis is not

Management

• therapy directed towards improving ventilation
  • correct hypoxia - oxygen as needed
  • excessive oxygen may blunt respiratory drive & worsen hypoventilation in patients with chronic respiratory acidosis
  • airway injury may necessitate endotracheal intubation to protect airway
• administration of bicarbonate
  • may be harmful since low pH is a stimulus for respiration
  • may be beneficial in patients with asthma on a ventilator
    • may improve response to beta-adrenergic agonists
    • may allow less vigorous ventilation reducing risk of barotrauma
  • may be indicated to maintain plasma pH above 7.1
• post-hypercapneic metabolic alkalosis can usually be corrected with saline & discontinuation of loop diuretics

More general terms

• acidosis