From the Guidelines
Chronic respiratory acidosis should be managed by treating the underlying cause, with a focus on non-invasive ventilation (NIV) and careful titration of supplemental oxygen therapy to prevent worsening hypercapnia and improve quality of life 1.
Definition and Causes
Chronic respiratory acidosis is a condition characterized by persistently elevated carbon dioxide levels in the blood (hypercapnia) with a compensatory increase in bicarbonate, resulting in a pH that is below normal but relatively stable. The primary causes include chronic obstructive pulmonary disease (COPD), severe obesity hypoventilation syndrome, neuromuscular disorders, and chest wall deformities.
Management
Management focuses on treating the underlying cause rather than the acidosis itself. For COPD patients, this includes:
- Bronchodilators such as albuterol (2-4 puffs every 4-6 hours)
- Long-acting agents like tiotropium (18 mcg once daily)
- Inhaled corticosteroids when appropriate Supplemental oxygen therapy is crucial but must be carefully titrated, typically 1-2 L/min via nasal cannula, to maintain oxygen saturation between 88-92% without worsening hypercapnia.
Non-Invasive Ventilation
Non-invasive ventilation, particularly BiPAP with settings of 10-12 cmH2O inspiratory pressure and 4-6 cmH2O expiratory pressure, may be necessary for severe cases, especially during sleep 1. Bilevel NIV may be considered in COPD patients with an acute exacerbation to prevent acute respiratory acidosis, prevent endotracheal intubation, or as an alternative to invasive ventilation 1.
Monitoring and Treatment of Underlying Conditions
Regular monitoring of arterial blood gases is important to assess compensation and detect acute-on-chronic respiratory failure. Weight loss is essential for obesity hypoventilation syndrome, while specific treatments for neuromuscular disorders vary by condition. Unlike metabolic acidosis, bicarbonate administration is generally avoided as it may suppress respiratory drive and worsen hypercapnia. The body compensates for chronic respiratory acidosis by increasing renal bicarbonate reabsorption, which helps stabilize pH despite elevated CO2 levels.
Key considerations in managing chronic respiratory acidosis include:
- Early recognition and treatment of underlying causes
- Careful titration of supplemental oxygen therapy
- Use of non-invasive ventilation to prevent worsening hypercapnia and improve quality of life
- Regular monitoring of arterial blood gases to assess compensation and detect acute-on-chronic respiratory failure.
From the Research
Definition of Chronic Respiratory Acidosis
- Chronic respiratory acidosis is defined as a sustained increase in arterial partial pressure of carbon dioxide, resulting in renal adaptation and a more marked increase in plasma bicarbonate 2.
- It can result from numerous processes, including increased carbon dioxide production, alveolar hypoventilation, abnormal respiratory drive, abnormalities of the chest wall and respiratory muscles, and increased dead space.
Mechanisms of Chronic Respiratory Acidosis
- The principal effects of respiratory acidosis are on the central nervous and cardiovascular systems 2.
- Mechanisms of respiratory acidosis include:
- Increased carbon dioxide production
- Alveolar hypoventilation
- Abnormal respiratory drive
- Abnormalities of the chest wall and respiratory muscles
- Increased dead space
Management of Chronic Respiratory Acidosis
- Treatment for respiratory acidosis may include invasive or noninvasive ventilatory support and specific medical therapies directed at the underlying pathophysiology 2.
- In patients with chronic obstructive pulmonary disease (COPD), treatment with tiotropium has been shown to be effective in preventing exacerbations 3.
- Combination therapy with tiotropium and salmeterol has been shown to provide clinically meaningful improvements in airflow obstruction and dyspnea, as well as a reduction in reliever medication 4, 5.
- Tiotropium and salmeterol/fluticasone combination do not cause oxygen desaturation in COPD patients 6.