What is the initial approach to managing acid-base disorders?

Initial Approach to Managing Acid-Base Disorders

Begin by obtaining arterial blood gas (ABG) with pH, PaCO2, and bicarbonate, along with serum electrolytes to calculate the anion gap—this systematic assessment identifies the primary disturbance and guides all subsequent management decisions. 1, 2, 3

Step 1: Obtain Essential Laboratory Data

• Draw ABG immediately to measure pH, PaCO2, and bicarbonate—these three values determine the primary acid-base disturbance 1, 2
• Obtain serum electrolytes (sodium, potassium, chloride, bicarbonate) to calculate the anion gap using the formula: AG = Na+ - (Cl- + HCO3-), with normal being 8-12 mEq/L 3, 4
• Measure serum glucose to identify diabetic ketoacidosis as a potential cause 1
• Check blood urea nitrogen and creatinine to assess renal function and identify uremic acidosis 1, 2
• Verify accuracy of lab values using the Henderson equation: H+ = 24 × (PaCO2/HCO3-) 3

Step 2: Identify the Primary Disturbance

• If pH < 7.35: Primary acidosis is present—determine if metabolic (low HCO3-) or respiratory (high PaCO2) 5, 6
• If pH > 7.45: Primary alkalosis is present—determine if metabolic (high HCO3-) or respiratory (low PaCO2) 5, 6
• Calculate expected compensation to identify mixed disorders: For metabolic acidosis, expected PaCO2 = 1.5 × (HCO3-) + 8 ± 2; deviations indicate additional processes 4, 5

Step 3: Categorize Metabolic Acidosis by Anion Gap

For metabolic acidosis, the anion gap distinguishes between two fundamentally different etiologies requiring different management approaches. 2, 5

Anion Gap Metabolic Acidosis (AG > 12 mEq/L):

• Calculate osmolal gap if toxic ingestion suspected: Osmolal gap = measured osmolality - calculated osmolality (2×Na+ + glucose/18 + BUN/2.8); gap >10 suggests toxic alcohol 5
• Perform gap-gap analysis: Δ AG / Δ HCO3- ratio helps identify concurrent metabolic alkalosis (ratio >2) or non-gap acidosis (ratio <1) 4, 6
• Common causes include: Lactic acidosis from sepsis or shock (most common in ICU), diabetic ketoacidosis, uremia, toxic ingestions (ethylene glycol, methanol, salicylates) 1, 2
• Treatment focuses on the underlying cause: Fluid resuscitation and insulin for DKA, source control for sepsis, extracorporeal removal for toxins 7, 1

Non-Anion Gap Metabolic Acidosis (Normal AG):

• Calculate urine anion gap: UAG = (Na+ + K+) - Cl- in urine; negative UAG suggests GI bicarbonate loss, positive UAG suggests renal tubular acidosis 5, 6
• Common causes include: Diarrhea, renal tubular acidosis, dilutional acidosis from excessive normal saline administration 2, 6

Step 4: Initiate Cause-Specific Treatment

For Diabetic Ketoacidosis (Most Common Anion Gap Acidosis):

• Fluid resuscitation first: Administer balanced electrolyte solutions at 15-20 mL/kg/h during the first hour 1
• Check potassium before insulin: Never start insulin if K+ <3.3 mEq/L due to fatal arrhythmia risk; replete potassium first 1
• Start insulin therapy: Give IV bolus of regular insulin 0.15 units/kg, then continuous infusion at 0.1 units/kg/h 1
• Add potassium to fluids: When K+ falls below 5.5 mEq/L, add 20-40 mEq/L to infusion 1
• Monitor every 2-4 hours: Recheck glucose, electrolytes, and venous pH; measure β-hydroxybutyrate directly rather than urine ketones 1
• Bicarbonate generally not recommended: Consider only if pH <6.9, as aggressive alkali therapy may worsen outcomes 1, 8

For Toxic Ingestions (Ethylene Glycol/Methanol):

• Initiate extracorporeal treatment (ECTR) when severe acidosis present with pH <7.1 or anion gap >24 mEq/L 7
• High-efficiency hemodialysis preferred over continuous renal replacement therapy for faster toxin and metabolite removal 7
• Continue ECTR until: Anion gap <18 mEq/L (strong recommendation), ethylene glycol <4 mmol/L, and all acid-base abnormalities corrected 7

For Metabolic Alkalosis:

• Measure urine chloride: Urine Cl- <25 mEq/L indicates chloride-responsive alkalosis (volume depletion); >40 mEq/L suggests chloride-resistant (mineralocorticoid excess) 5
• Volume resuscitation with normal saline for chloride-responsive alkalosis 2
• Replete potassium deficits: Hypokalemia perpetuates metabolic alkalosis and must be corrected 2

For Respiratory Acidosis:

• Optimize ventilation: In acute exacerbation of COPD with pH <7.35 and PaCO2 >6.5 kPa despite optimal medical therapy and controlled oxygen (target SpO2 88-92%), initiate non-invasive ventilation 7
• Permissive hypercapnia acceptable: In mechanically ventilated patients, allowing elevated PaCO2 to prevent barotrauma is standard of care 7, 2
• Bicarbonate not recommended for respiratory acidosis; treat the underlying ventilatory problem 2

For Respiratory Alkalosis:

• Identify and treat underlying cause: Common in sepsis, liver disease, pulmonary embolism, and anxiety 5
• No specific pH correction needed: Focus on treating the precipitating condition 2, 5

Critical Pitfalls to Avoid

• Never start insulin if potassium <3.3 mEq/L without first repleting potassium—this causes fatal arrhythmias 1
• Do not use bicarbonate routinely in metabolic acidosis; indicated only for severe acidemia (pH <6.9) and even then controversial 1, 8, 2
• Do not overlook mixed disorders: Calculate expected compensation for every primary disturbance; deviations indicate additional acid-base processes 4, 5, 6
• Do not rely on urine ketone testing alone in suspected DKA—it misses β-hydroxybutyrate, the predominant ketone 1
• Do not stop extracorporeal treatment prematurely in toxic ingestions—continue until anion gap normalizes and toxin levels are safe 7
• Avoid excessive normal saline administration: Large volumes cause hyperchloremic non-gap metabolic acidosis; use balanced crystalloids instead 2

Monitoring and Reassessment

• Recheck ABG and electrolytes every 2-4 hours during active treatment of severe acidosis 1
• Reassess for new disturbances: Worsening pH or respiratory rate despite treatment indicates need to change management strategy, consider different diagnosis, or escalate care 7
• Monitor for complications: Check for arrhythmias with ECG, especially when correcting potassium abnormalities 1