Initial Treatment of Respiratory Acidosis and Alkalosis
Respiratory Acidosis Management
For acute hypercapnic respiratory acidosis with pH <7.35 and pCO2 >6.5 kPa despite optimal medical therapy, initiate non-invasive ventilation (NIV) immediately as the primary intervention, targeting oxygen saturation of 88-92% rather than normalization of blood gases. 1
Ventilator Strategy for Respiratory Acidosis
Non-Invasive Ventilation (First-Line)
- Start bilevel positive airway pressure with inspiratory pressure 12-20 cm H2O and expiratory pressure 4-5 cm H2O 2
- Maximize NIV use in first 24 hours depending on tolerance 1
- Reassess arterial blood gases at 1-2 hours; if pH and respiratory rate worsen, escalate to invasive mechanical ventilation 1
- Continue NIV until pH normalizes and pCO2 improves, then taper over 2-3 days 1, 2
Invasive Mechanical Ventilation (When NIV Fails)
For obstructive disease (COPD, asthma):
- Tidal volume: 6-8 mL/kg predicted body weight 1
- Respiratory rate: 10-15 breaths/minute 1
- I:E ratio: 1:2 to 1:4 (prolonged expiratory time to prevent gas trapping) 1
- Accept permissive hypercapnia with target pH >7.20 if peak airway pressure exceeds 30 cm H2O 1
For neuromuscular disease/chest wall deformity:
- Tidal volume: 6 mL/kg 1
- Respiratory rate: 15-25 breaths/minute 1
- I:E ratio: 1:1 to 1:2 1
- Higher inspiratory pressures (10-15 cm H2O for neuromuscular, higher for chest wall deformity) 1
Oxygen Management
- Target SpO2 88-92% using controlled oxygen therapy (24-28% or 1-2 L/min nasal cannula) 1, 2
- Avoid high-flow uncontrolled oxygen as it worsens hypercapnia in chronic CO2 retainers 2
- Recheck arterial blood gases 30-60 minutes after any oxygen adjustment 2
Pharmacotherapeutic Agents
Doxapram (Limited Role)
- For chronic obstructive pulmonary disease with acute hypercapnia: mix 400 mg in 180 mL solution (2 mg/mL concentration) 3
- Infusion rate: start 1-2 mg/minute, maximum 3 mg/minute 3
- Maximum duration: 2 hours only; additional infusions beyond single 2-hour period not recommended 3
- Monitor arterial blood gases every 30 minutes during infusion 3
- Discontinue if blood gases show deterioration 3
Sodium Bicarbonate (Generally NOT Recommended)
- No randomized controlled trial evidence supports bicarbonate for respiratory acidosis 4
- Consider only for severe acidosis (pH <7.15) with hemodynamic instability 5
- Potential risks include increased CO2 production, volume overload, and negation of permissive hypercapnia benefits 4
Carbonic Anhydrase Inhibitors
- May be used cautiously in chronic hypercapnia to reduce bicarbonate buffering capacity 1
- High doses produce unpredictable effects through central respiratory stimulation 1
Critical Decision Points
Proceed to intubation if: 2
- Worsening pH or respiratory rate despite NIV after 1-2 hours
- Inability to protect airway or excessive secretions
- Hemodynamic instability
- Patient exhaustion or decreased consciousness
- NIV intolerance
Respiratory Alkalosis Management
Respiratory alkalosis treatment focuses on identifying and correcting the underlying cause rather than directly manipulating ventilator settings, as the condition itself is rarely life-threatening. 6
Ventilator Adjustments for Respiratory Alkalosis
For Mechanically Ventilated Patients
- Reduce minute ventilation by decreasing respiratory rate or tidal volume 6
- Increase dead space if hyperventilation persists (add tubing between ventilator circuit and endotracheal tube)
- Switch to pressure support or assist-control modes to allow patient-triggered breathing 6
- Ensure adequate sedation/analgesia if patient is fighting ventilator 6
For Spontaneously Breathing Patients
- Address underlying cause (pain, anxiety, hypoxemia, metabolic acidosis compensation) 6
- For hyperventilation syndrome: reassurance, rebreathing techniques, anxiolytics if severe 6
- Correct hypoxemia if present (may be driving compensatory hyperventilation) 6
Pharmacotherapeutic Agents
- Treat underlying etiology: analgesics for pain, anxiolytics for anxiety, antibiotics for sepsis 6
- Sedation for mechanically ventilated patients with patient-ventilator dyssynchrony 6
- Do NOT attempt to "correct" respiratory alkalosis with CO2 administration or hypoventilation if it represents appropriate compensation for metabolic acidosis 6
Environmental Interventions
For Respiratory Acidosis
- Position patient upright (30-45 degrees) to optimize diaphragmatic function and reduce work of breathing 1
- Ensure adequate humidification of inspired gases to facilitate secretion clearance 1
- Implement airway clearance techniques: assisted cough, mechanical insufflation-exsufflation for neuromuscular disease 1
- Minimize sedation when possible to preserve respiratory drive 1
- Avoid excessive PEEP in obstructive disease as it may worsen hyperinflation 1
For Respiratory Alkalosis
- Calm, quiet environment for hyperventilation syndrome 6
- Normalize room temperature (fever increases respiratory drive) 6
- Adequate pain control environment 6
Nutritional Interventions
For Respiratory Acidosis
- Reduce carbohydrate load to minimize CO2 production (carbohydrates produce more CO2 per calorie than fats) 7
- Increase proportion of calories from fat (40-50% of total calories) while reducing carbohydrates to 30-40% 7
- Avoid overfeeding (increases metabolic CO2 production and respiratory burden) 7
- Target 25-30 kcal/kg/day in acute phase 7
- Ensure adequate protein (1.2-1.5 g/kg/day) to maintain respiratory muscle function 7
- Monitor for refeeding syndrome in malnourished patients, as hypophosphatemia impairs respiratory muscle function 7
For Respiratory Alkalosis
- Correct any underlying metabolic acidosis that may be driving compensatory hyperventilation through appropriate nutritional support 6, 7
- Ensure adequate caloric intake to prevent catabolism-induced metabolic acidosis 7
- Standard macronutrient distribution unless specific metabolic derangements present 7
Common Nutritional Pitfalls
- Avoid high-carbohydrate enteral formulas in respiratory acidosis (increases CO2 production by 20-30%) 7
- Do not restrict nutrition in attempt to reduce CO2 production; this worsens respiratory muscle weakness 7
- Monitor electrolytes closely, particularly phosphate, potassium, and magnesium, as abnormalities impair respiratory muscle function 7