Acid-Base Disorders: Clinical Examples and Management Approach
Respiratory Acidosis
Respiratory acidosis occurs when CO2 accumulates due to inadequate ventilation, resulting in PaCO2 >46 mmHg and pH <7.35. 1
Clinical Examples:
- COPD exacerbation with acute-on-chronic respiratory failure, where patients develop hypercapnia and acidosis (pH <7.26 predicts poor outcome) 2
- Pediatric septic shock where patients progress from initial respiratory alkalosis to respiratory acidosis due to parenchymal lung disease, inadequate respiratory effort from altered mental status, or increased work of breathing 2
- Neuromuscular disease requiring mechanical ventilation, where inadequate tidal volumes lead to CO2 retention 2
Management Algorithm:
- Restore adequate ventilation immediately—this is the primary treatment, NOT alkali therapy 3
- For impending respiratory failure: intubate based on clinical assessment (increased work of breathing, hypoventilation, altered mental status) without waiting for confirmatory labs 2
- Use ketamine with atropine for intubation to maintain cardiovascular stability; never use etomidate as it increases mortality in septic shock 3
- For mechanical ventilation in obstructive disease: use tidal volumes 6-8 mL/kg, respiratory rate 10-15, I:E ratio 1:2-1:4 to prolong expiratory time 2
- Employ permissive hypercapnia (target pH >7.2) when peak airway pressure exceeds 30 cm H2O to avoid ventilator-induced lung injury 2
- Never give sodium bicarbonate for pure respiratory acidosis—it generates CO2 that cannot be eliminated and worsens the condition 3
Respiratory Alkalosis
Respiratory alkalosis results from hyperventilation causing excessive CO2 elimination, leading to elevated pH and decreased PaCO2. 1
Clinical Examples:
- Early septic shock where patients develop centrally-mediated hyperventilation before progressing to acidosis 2
- Anxiety/hyperventilation syndrome in the emergency department (diagnosis of exclusion) 4
- Mechanically ventilated patients with excessive minute ventilation settings 3
Management Algorithm:
- Identify and treat the underlying cause of hyperventilation 3
- For mechanically ventilated patients: adjust ventilator settings to reduce minute ventilation by decreasing respiratory rate or tidal volume 3
- For hyperventilation syndrome: treat anxiety and provide reassurance after excluding organic causes 3
- Avoid bicarbonate-containing fluids which worsen alkalosis 3
- Monitor for metabolic complications including hypokalemia, hypophosphatemia, hypocalcemia, and mild lactic acidosis 4
- Avoid overly rapid correction to prevent new acid-base imbalances 3
Metabolic Acidosis
Metabolic acidosis is characterized by pH <7.35, serum bicarbonate <22 mmol/L, elevated lactate, and increased base deficit. 5
Clinical Examples:
- Septic shock with lactic acidosis from tissue hypoperfusion and inadequate oxygen delivery (lactate >2 mmol/L indicates tissue hypoxia) 5
- Diabetic ketoacidosis with increased anion gap from ketoacid accumulation 6
- Renal tubular acidosis with normal anion gap from bicarbonate loss 6
- Traumatic hemorrhagic shock where base deficit independently predicts mortality 5
Management Algorithm:
- Restore tissue perfusion and oxygen delivery first—this is the primary intervention for lactic acidosis 3
- Maintain hemoglobin ≥10 g/dL to optimize oxygen delivery 3
- Monitor lactate, base deficit, and pH serially to assess shock severity and treatment response 3
- Sodium bicarbonate is reserved for severe acidosis (pH <7.20) and only after establishing effective ventilation 3
- When bicarbonate is indicated: give 2-5 mEq/kg IV over 4-8 hours, targeting total CO2 of ~20 mEq/L (not full correction) on day 1 to avoid overshoot alkalosis 7
- Never give bicarbonate before establishing effective ventilation—it generates CO2 requiring elimination 3
- Never mix bicarbonate with vasoactive amines or calcium 3
- Avoid hypothermia, hypocalcemia, and worsening acidosis during resuscitation as these exacerbate coagulopathy 3
Metabolic Alkalosis
Metabolic alkalosis is characterized by elevated pH, increased serum bicarbonate, and results from H+ loss or alkali ingestion. 8
Clinical Examples:
- Chronic respiratory acidosis with renal compensation where bicarbonate retention produces compensatory metabolic alkalosis 1
- Gastric H+ loss from vomiting (saline-responsive, urinary chloride <10 mEq/L) 8
- Diuretic therapy causing chloride and potassium depletion 8
- Hyperaldosteronism (saline-resistant, moderate urinary chloride) 8
Management Algorithm:
- Determine urinary chloride to guide therapy: 8
- Avoid bicarbonate-containing fluids in volume-depleted patients 3
- For mechanically ventilated patients with chronic CO2 retention: reduce bicarbonate buffering capacity through relative hyperventilation to reset central respiratory drive 2
- Consider carbonic anhydrase inhibitors cautiously (unpredictable effects from central respiratory stimulation) 2
- Avoid inappropriate fluid therapy that worsens alkalosis 3
Critical Pitfalls to Avoid Across All Disorders
- Never correct acid-base disorders too rapidly in critically ill patients 3
- Never use sodium bicarbonate by endotracheal route 3
- In COPD with respiratory acidosis: power nebulizers with compressed air, not oxygen, to prevent worsening hypercapnia 2
- Monitor for patient-ventilator asynchrony by examining pressure/flow waveforms, not just vital signs 2
- Recognize that attempting full correction of metabolic acidosis within 24 hours often causes unrecognized alkalosis due to delayed ventilatory readjustment 7