Acid-Base Disorders

Approach to Acid-Base Disorders

Acid-base disorders are a frequent and critical challenge in the intensive care unit (ICU), often complicating the management of critically ill patients. This survey note provides a detailed, structured overview of the approach to diagnosing and managing these disorders, drawing from recent medical literature and critical care resources. The content is designed to mimic a professional article, offering a strict superset of the information in the direct answer section, with additional depth for medical professionals.

Introduction

Acid-base imbalances, such as acidosis and alkalosis, are ubiquitous in ICU settings, contributing significantly to morbidity and mortality. These disorders can be metabolic, respiratory, or mixed, requiring a systematic evaluation to identify the primary disturbance and any compensatory mechanisms. The traditional approach, centered on arterial blood gas (ABG) analysis and anion gap (AG) calculation, is widely adopted, while the quantitative (Stewart) approach offers a more detailed physicochemical analysis for complex cases. This note outlines the step-by-step process, common disorders, and management strategies, with an emphasis on evidence-based practice.

Stepwise Approach to Diagnosis

1. Initial Assessment with Arterial Blood Gas (ABG)

The first step involves obtaining an ABG to measure key parameters:

• pH: Normal range is 7.35–7.45. Values below 7.35 indicate acidosis, and above 7.45 indicate alkalosis.

• PaCO₂: Reflects respiratory component; elevated in respiratory acidosis, decreased in respiratory alkalosis.

• HCO₃⁻: Reflects metabolic component; decreased in metabolic acidosis, increased in metabolic alkalosis.

This analysis helps classify the primary disorder as respiratory or metabolic, with pH guiding the direction (acidotic or alkalotic).

2. Assessing Compensation

The body often compensates for primary acid-base disorders. Expected compensatory responses are:

• Metabolic Acidosis: Expected PaCO₂ = 1.5 × [HCO₃⁻] + 8 ± 2 (Winter’s formula).

• Metabolic Alkalosis: Expected PaCO₂ = 0.7 × [HCO₃⁻] + 20 ± 1.5.

• Respiratory Acidosis:

  • Acute: [HCO₃⁻] increases by 1 mEq/L for every 10 mmHg increase in PaCO₂.

  • Chronic: [HCO₃⁻] increases by 4 mEq/L for every 10 mmHg increase in PaCO₂.

• Respiratory Alkalosis:

  • Acute: [HCO₃⁻] decreases by 2 mEq/L for every 10 mmHg decrease in PaCO₂.

  • Chronic: [HCO₃⁻] decreases by 5 mEq/L for every 10 mmHg decrease in PaCO₂.

If the measured values deviate from expected compensation, a mixed disorder may be present, requiring further investigation.

3. Calculating and Interpreting the Anion Gap (AG)

The anion gap is calculated as:

• AG = [Na⁺] - ([Cl⁻] + [HCO₃⁻])

• Normal range: 8–12 mEq/L, though some sources suggest 7 ± 4 mEq/L.

Adjustments are necessary for hypoalbuminemia, using the formula:

• Adjusted AG = Observed AG + 2.5 × [normal albumin - measured albumin (g/dL)], where normal albumin is typically 4 g/dL.

• High AG Metabolic Acidosis: Indicates unmeasured anions, such as lactate, ketones, or toxins, and is common in ICU settings (e.g., lactic acidosis, diabetic ketoacidosis).

• Normal AG Metabolic Acidosis: Suggests bicarbonate loss (e.g., diarrhea) or chloride gain (e.g., saline infusion), often seen in early renal failure or gastrointestinal losses.

4. Differential Diagnosis Using Mnemonics

To aid in recalling causes, mnemonics are particularly useful:

• High AG Metabolic Acidosis (GOLDMARKeT):

  • Glycols (ethylene glycol, propylene glycol)

  • Oxoproline (from acetaminophen toxicity)

  • L-Lactate (lactic acidosis, common in sepsis, shock)

  • D-Lactate (short gut syndrome)

  • Methanol

  • Aspirin (salicylates)

  • Renal failure

  • Ketoacidosis (diabetic ketoacidosis, alcoholic ketoacidosis)

  • Toxin (e.g., toluene)

• Normal AG Metabolic Acidosis (BLVD PLACE):

  • Bicarbonate loss (diarrhea, pancreatic fistula)

  • Lactic acidosis (early, before AG increases)

  • Volume contraction (dehydration, contraction alkalosis context)

  • Drugs (acetazolamide, spironolactone)

  • Parenteral nutrition

  • Adrenal insufficiency

  • Cation exchange resins (e.g., Kayexalate)

  • Endocrine (hyperparathyroidism, hyperthyroidism)

• Metabolic Alkalosis (RAGES):

  • Renal (diuretics, post-hypercapnia)

  • Acid loss (vomiting, nasogastric suction)

  • Gastrointestinal (vomiting, NG suction)

  • Endocrine (hyperaldosteronism, Cushing's syndrome)

  • Salt (contraction alkalosis)

Respiratory disorders include:

• Respiratory Acidosis: Hypoventilation (e.g., COPD, neuromuscular disorders, sedation).

• Respiratory Alkalosis: Hyperventilation (e.g., anxiety, pain, sepsis, salicylate toxicity).

Management Strategies

1. Treating the Underlying Cause

Management prioritizes addressing the root cause:

• For lactic acidosis, treat circulatory shock, sepsis, or underlying conditions like hepatic insufficiency.

• For ketoacidosis, administer insulin for diabetic ketoacidosis or glucose for alcoholic ketoacidosis, with volume and electrolyte replacement.

• For toxic alcohols (e.g., ethylene glycol, methanol), consider fomepizole or hemodialysis.

• For metabolic alkalosis, correct volume depletion with saline and address hypokalemia.

2. Correcting Electrolyte Imbalances

Electrolyte imbalances, such as hypokalemia, hypocalcemia, or hypernatremia, must be addressed, as they can exacerbate acid-base disorders. For example, in chloride-responsive metabolic alkalosis, chloride replacement (e.g., saline) is mandatory.

3. Adjunctive Therapies

• Bicarbonate Therapy: Considered for severe metabolic acidosis (pH < 7.1), calculated as HCO₃⁻ deficit = 0.6 × weight (kg) × (15 - measured HCO₃⁻), targeting 15 mEq/L to avoid alkalosis. However, its role is controversial due to risks like intracellular acidosis, volume expansion, and overshoot alkalosis.

• Severe Metabolic Alkalosis: In rare cases (pH > 7.55, HCO₃⁻ > 40 mEq/L), dilute HCl infusion (0.1N, central vein, ≤0.2 mEq/kg/hr) or acetazolamide (5-10 mg/kg) may be used.

• Alternatives like Carbicarb, THAM, or dichloroacetate have limited evidence and are less commonly used.

4. Monitoring and Reassessment

Repeat ABG analysis as needed to evaluate response to treatment, ensuring adjustments are made based on clinical improvement and laboratory trends.

Additional Considerations

Quantitative (Stewart) Approach

The quantitative, or Stewart, approach uses three independent variables: PCO₂, strong ion difference (SID), and total weak acids (Aₜₒₜ). It quantifies causative ions, offering a deeper understanding of acid-base disorders, particularly in complex cases. While less commonly used in routine practice, it is valuable for research and in-depth analysis, with studies showing its utility in identifying unmeasured acids and predicting outcomes (e.g., strong ion gap >5 mEq/L in trauma linked to mortality).

Incidence and Epidemiology

Research indicates metabolic acidosis incidence varies widely (27%–100% across studies), with lactic acidosis, hyperchloremic acidosis, and strong ion gap acidosis being prevalent. A proposed classification system defines metabolic acidosis as standard base excess (SBE) below -2 mEq/L, with subtypes based on predominant anions (lactate, unmeasured ions, chloride). Outcomes may differ by type, with lactic acidosis often associated with worse prognosis, though results are controversial due to variations in measurement techniques and fluid administration