Management of Acid-Base Disturbances
The management of acid-base disturbances requires systematic identification of the primary disorder through arterial blood gas analysis (pH, PaCO2, HCO3-) and anion gap calculation, followed by treatment directed at the underlying cause rather than aggressive pH correction in most cases. 1, 2
Systematic Diagnostic Approach
Initial Assessment
- Obtain arterial blood gas to determine pH (normal 7.35-7.45), PaCO2 (normal 35-45 mmHg), and HCO3- (normal 22-26 mEq/L) 1, 2
- Calculate anion gap using the formula: (Na+ + K+) - (Cl- + HCO3-) to differentiate types of metabolic acidosis 2, 3
- Assess compensation to identify simple versus mixed disorders - when bicarbonate and PaCO2 move in opposite directions, extreme pH shifts may occur 4, 5
Management by Disorder Type
Metabolic Acidosis
Anion Gap Metabolic Acidosis (pH <7.35, HCO3- <22 mEq/L, elevated anion gap)
- Treat the underlying cause - this is the primary intervention for lactic acidosis from sepsis, diabetic ketoacidosis, toxins, or renal failure 2, 4
- Consider sodium bicarbonate only for severe acidosis (pH <7.1-7.2 or base deficit >10), though its use remains controversial in lactic acidosis and diabetic ketoacidosis 6, 4
- For ethylene glycol poisoning specifically: Recommend extracorporeal treatment (hemodialysis preferred) if glycolate concentration >12 mmol/L or anion gap >27 mmol/L 6
- Stop dialysis when anion gap <18 mmol/L 6
Non-Anion Gap Metabolic Acidosis
- Identify the source: renal tubular disorders, gastrointestinal bicarbonate losses, dilutional acidosis from excessive IV fluids, or hydrochloric acid addition 2
- Prevent hyperchloremic acidosis by using balanced crystalloid solutions instead of normal saline for volume resuscitation 1
- Provide sodium bicarbonate for severe cases (pH <7.1) 4
Metabolic Alkalosis (pH >7.45, HCO3- >26 mEq/L)
This is the most common acid-base disorder in critically ill patients, typically developing after ICU admission from aggressive therapeutic interventions 2.
Chloride-Responsive Alkalosis
- Administer chloride salts (normal saline) to restore acid-base balance over several days 4
- Replete potassium deficits - essential for correction 4
- Use loop diuretics (e.g., sodium polystyrene 1 g/kg) if needed for mild hyperkalemia management 6
Chloride-Resistant Alkalosis
- Target the underlying disease rather than the alkalosis itself 4
- For severe alkalemia: Consider hydrochloric acid or hydrochloric acid precursor administration 4
Respiratory Acidosis (pH <7.35, PaCO2 >45 mmHg)
Acute Hypercapnic Respiratory Failure
- Initiate controlled oxygen therapy targeting saturation 88-92% to avoid worsening hypercapnia 6, 7
- Recheck arterial blood gases within 60 minutes 7
- Administer bronchodilators immediately: nebulized salbutamol 2.5-5 mg or ipratropium 0.25-0.5 mg every 4-6 hours, driven by compressed air (not oxygen) if PaCO2 elevated 7
- Give corticosteroids: prednisolone 30 mg daily orally or hydrocortisone 100 mg IV for 7-14 days 7
- Prescribe antibiotics if infection signs present (increased sputum purulence/volume) 7
Non-Invasive Ventilation (NIV)
- Initiate bilevel NIV when pH <7.35 persists after optimal medical therapy, particularly if pH <7.26 or PaCO2 >6.5 kPa with respiratory rate >23 breaths/min 6, 7
- Start NIV promptly - delays worsen outcomes 7
- Use BiPAP as preferred modality for acute-on-chronic respiratory acidosis 7
Invasive Mechanical Ventilation
- Consider intubation if pH remains <7.26 with rising PaCO2 despite NIV and optimal medical therapy 7
- Recognize hemodynamic risks: transition from negative to positive pressure ventilation can cause hypotension, atelectasis, and vagal stimulation 6
- Use permissive hypercapnia to prevent barotrauma - this is standard of care 2
- Do not use bicarbonate to correct acidemia from respiratory causes 2
Respiratory Alkalosis (pH >7.45, PaCO2 <35 mmHg)
- Reverse the root cause - there is no effective direct treatment for primary hypocapnia 4
- Avoid aggressive intervention unless severe symptoms present 4
Special Clinical Situations
Tumor Lysis Syndrome
- Initiate renal replacement therapy for persistent hyperkalemia, severe metabolic acidosis, volume overload unresponsive to diuretics, or overt uremic symptoms 6
- Use intermittent hemodialysis for effective removal of uric acid (clearance 70-100 mL/min) and phosphate 6
- Consider prophylactic dialysis before overt uremic symptoms in high-risk patients with progressive hyperuricemia and hyperphosphatemia 6
Cardiogenic Shock
- Optimize ventilation to handle systemic acidosis from shock state 6
- Use continuous renal replacement therapy (CRRT) over intermittent hemodialysis for hemodynamically unstable patients requiring management of electrolyte disturbances and acid-base disorders 6
Cardiac Arrest
- Prioritize restoration of spontaneous circulation - this is the best method of reversing acidosis 6
- Limit sodium bicarbonate use to severe acidosis (pH <7.1, base deficit <10) or special circumstances like hyperkalemia or tricyclic antidepressant overdose 6
- Recognize that arterial blood gas alone may be misleading - mixed venous samples may not accurately reflect myocardial or cerebral intracellular acid-base status 6
Critical Monitoring Parameters
- Monitor potassium closely during treatment - pH changes alter plasma potassium concentrations significantly 3
- For hyperkalemia >6 mmol/L: rapid insulin 0.1 units/kg plus 25% dextrose 2 mL/kg, calcium carbonate 100-200 mg/kg/dose, and sodium bicarbonate to stabilize myocardium and correct acidosis 6
- Perform ECG monitoring in hyperkalemic patients 6
- Assess for under-recognition of complex acid-base disturbances - this is a common deficiency in clinical practice 6
- Coordinate with ICU for patients requiring enhanced monitoring facilities beyond general ward capabilities 6