Acid Base Disorders

 

 Acid–base disorders are common clinical problems resulting from disturbances in hydrogen ion (H⁺) balance. Understanding them is essential for interpreting arterial blood gases (ABGs), managing critically ill patients, and identifying underlying systemic diseases.

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Acid–Base Physiology (Quick Review)

Normal arterial values

pH: 7.35–7.45

PaCO₂: 35–45 mmHg (respiratory component)

HCO₃⁻: 22–26 mEq/L (metabolic component)

Key relationship (Henderson–Hasselbalch concept):

pH depends on the ratio of HCO₃⁻ (kidney) to PaCO₂ (lungs)

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Classification of Acid–Base Disorders

There are four primary acid–base disorders:

1. Metabolic Acidosis

2. Metabolic Alkalosis

3. Respiratory Acidosis

4. Respiratory Alkalosis

Each primary disorder triggers a predictable compensatory response.

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1. Metabolic Acidosis

Definition

↓ pH, ↓ HCO₃⁻

Mechanisms

• Increased acid production

• Loss of bicarbonate

• Reduced acid excretion

Anion Gap (AG)

AG = Na⁺ − (Cl⁻ + HCO₃⁻)

Normal: 8–12 mEq/L

High Anion Gap Metabolic Acidosis (HAGMA)

Common causes (GOLD MARK):

• Glycols (ethylene, propylene)

• Oxoproline (chronic paracetamol use)

• L-lactate (shock, sepsis)

• D-lactate

• Methanol

• Aspirin

• Renal failure

• Ketoacidosis (DKA, starvation, alcohol)

Normal Anion Gap Metabolic Acidosis (NAGMA)

• Diarrhea

• Renal tubular acidosis

• Saline infusion

• Pancreatic fistula

Compensation (Winter’s Formula)

Expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2

If measured PaCO₂ differs → mixed disorder

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2. Metabolic Alkalosis

Definition

↑ pH, ↑ HCO₃⁻

Mechanisms

• Loss of hydrogen ions

• Gain of bicarbonate

• Volume depletion with chloride loss

Causes

• Vomiting, nasogastric suction

• Diuretics (loop, thiazide)

• Hyperaldosteronism

• Excess bicarbonate intake

Chloride-Based Classification

Chloride-responsive:

• Vomiting

• Diuretics

Responds to saline

Chloride-resistant:

• Primary hyperaldosteronism

• Cushing syndrome

Compensation

Expected PaCO₂ ≈ 0.7 × (HCO₃⁻ − 24) + 40 ± 5

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3. Respiratory Acidosis

Definition

↓ pH, ↑ PaCO₂

Mechanism

Alveolar hypoventilation → CO₂ retention

Causes

• COPD, asthma (severe)

• CNS depression (opioids, sedatives)

• Neuromuscular disorders

• Chest wall abnormalities

Acute vs Chronic

Acute:

• Small rise in HCO₃⁻ (no renal compensation yet)

Chronic:

• Significant ↑ HCO₃⁻ due to renal adaptation

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4. Respiratory Alkalosis

Definition

↑ pH, ↓ PaCO₂

Mechanism

Hyperventilation → excessive CO₂ loss

Causes

• Anxiety, panic attacks

• Hypoxemia (PE, pneumonia, high altitude)

• Sepsis (early)

• Pregnancy

• Liver disease

Compensation

Kidneys excrete bicarbonate over time

More pronounced in chronic states

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Stepwise Approach to ABG Interpretation

1. Look at pH

• Acidemia (<7.35) or alkalemia (>7.45)

2. Identify primary disorder

• PaCO₂ → respiratory

• HCO₃⁻ → metabolic

3. Check compensation

• Use formulas (Winter’s, expected PaCO₂/HCO₃⁻)

4. Calculate anion gap (if metabolic acidosis)

5. Look for mixed disorders

• pH near normal with abnormal PaCO₂ and HCO₃⁻

• Inappropriate compensation

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Mixed Acid–Base Disorders (Examples)

• Metabolic acidosis + respiratory alkalosis (sepsis)

• Metabolic alkalosis + respiratory acidosis (COPD + vomiting)

• DKA with vomiting (high AG acidosis + alkalosis)

Clues:

• Normal pH with abnormal values

• Compensation outside expected range

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Clinical Pearls

• Always interpret ABG in clinical context

• Normal pH does not exclude serious pathology

• Anion gap helps narrow diagnosis rapidly

• Compensation never overcorrects pH

• Mixed disorders are common in ICU patients

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Summary Table

Disorder pH PaCO₂ HCO₃⁻

Metabolic Acidosis ↓ ↓ (comp) ↓

Metabolic Alkalosis ↑ ↑ (comp) ↑

Respiratory Acidosis ↓ ↑ ↑ (chronic)

Respiratory Alkalosis ↑ ↓ ↓ (chronic)

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