Acid–Base Disorders 

🔹 1. Overview

What Are Acid–Base Disorders?

The body keeps blood pH within a narrow range (7.35–7.45) to allow enzymes and cellular functions to work properly.
This balance is maintained by two main systems:

• Lungs → control CO₂ (acid component)

• Kidneys → control HCO₃⁻ (base component)

So,

• Too much H⁺ or CO₂ → acidosis

• Too little H⁺ or too much HCO₃⁻ → alkalosis

Important distinction:

• “Acidosis” = the process that tends to lower pH.

• “Acidemia” = the actual low blood pH (<7.35).
  If compensation restores pH to near-normal, you can have an acidosis without acidemia.

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🔹 2. The Chemistry Behind It: Henderson–Hasselbalch Equation

[
pH = 6.1 + \log \frac{[HCO₃⁻]}{0.03 × PCO₂}
]

This shows that:

• pH is proportional to [HCO₃⁻] (metabolic component)

• pH is inversely proportional to PCO₂ (respiratory component)

So:

• ↓ HCO₃⁻ or ↑ PCO₂ → ↓ pH (acidemia)

• ↑ HCO₃⁻ or ↓ PCO₂ → ↑ pH (alkalemia)

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🔹 3. Types of Acid–Base Disorders

Disorder	Primary Change	Compensatory Change
Metabolic Acidosis	↓ HCO₃⁻	↓ PCO₂ (hyperventilation)
Metabolic Alkalosis	↑ HCO₃⁻	↑ PCO₂ (hypoventilation)
Respiratory Acidosis	↑ PCO₂	↑ HCO₃⁻ (renal retention)
Respiratory Alkalosis	↓ PCO₂	↓ HCO₃⁻ (renal excretion)

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🔹 4. Diagnosis: Step-by-Step Approach

Step 1 — Check pH

• pH < 7.35 → acidemia

• pH > 7.45 → alkalemia

Step 2 — Identify Primary Disorder

Use PCO₂ and HCO₃⁻:

• ↓ pH + ↓ HCO₃⁻ → metabolic acidosis

• ↓ pH + ↑ PCO₂ → respiratory acidosis

• ↑ pH + ↑ HCO₃⁻ → metabolic alkalosis

• ↑ pH + ↓ PCO₂ → respiratory alkalosis

Step 3 — Determine Compensation

Each disorder triggers an opposite mechanism to buffer pH.
If actual compensation ≠ expected → there is a mixed disorder.

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🔹 5. Compensation Formulas (Memorize!)

Primary Disorder	Expected Compensation	Interpretation
Metabolic Acidosis	Winter formula: PCO₂ = (1.5 × HCO₃⁻) + 8 ± 2	If measured PCO₂ higher → added resp. acidosis; if lower → added resp. alkalosis
Metabolic Alkalosis	PCO₂ = 0.7 × (HCO₃⁻ − 24) + 40 ± 2	—
Respiratory Acidosis (acute)	HCO₃⁻ ↑ 1 mEq/L for every 10 ↑ in PCO₂	—
Respiratory Acidosis (chronic)	HCO₃⁻ ↑ 3.5 mEq/L per 10 ↑ in PCO₂	—
Respiratory Alkalosis (acute)	HCO₃⁻ ↓ 2 mEq/L per 10 ↓ in PCO₂	—
Respiratory Alkalosis (chronic)	HCO₃⁻ ↓ 4 mEq/L per 10 ↓ in PCO₂	—

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🔹 6. Metabolic Acidosis — Deep Dive

Step 1: Calculate Anion Gap (AG)

[
AG = [Na⁺] - ([Cl⁻] + [HCO₃⁻])
]

• Normal = 6–12 mEq/L

• Correct for albumin: add 2.5 mEq/L for every ↓1 g/dL in albumin below 4.

Step 2: Interpret

• High AG Metabolic Acidosis: accumulation of unmeasured acids (e.g., lactate, ketones).

• Normal AG Metabolic Acidosis: direct loss of HCO₃⁻ replaced by Cl⁻ (hyperchloremic).

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a. High Anion Gap Metabolic Acidosis

Mnemonic MUDPILES:

Cause	Mechanism
M – Methanol	→ formic acid accumulation
U – Uremia (renal failure)	→ retention of organic acids
D – DKA	→ ketoacids
P – Paraldehyde / Propylene glycol	→ lactic acidosis
I – Isoniazid / Iron	→ lactic acidosis, mitochondrial toxicity
L – Lactic acidosis	→ tissue hypoxia, sepsis, shock
E – Ethylene glycol	→ oxalic acid
S – Salicylates	→ mixed metabolic acidosis + resp. alkalosis

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b. Normal (Non–Anion Gap) Metabolic Acidosis

Mnemonic FUSEDCARS:

Cause	Mechanism
F – Fistulas (biliary, pancreatic)	Loss of bicarbonate-rich fluid
U – Ureterogastric conduit	HCO₃⁻ loss
S – Saline infusion	Dilutional acidosis
E – Endocrine (Addison’s disease)	↓ aldosterone → ↓ H⁺ excretion
D – Diarrhea	Bicarbonate loss
C – Carbonic anhydrase inhibitors (acetazolamide)	↓ HCO₃⁻ reabsorption
A – Ammonium chloride	H⁺ load
R – Renal tubular acidosis	Defective acid secretion/reabsorption
S – Spironolactone	↓ aldosterone effect

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Step 3: Calculate Delta Gap

To check for mixed disorders:
[
\Delta \text{AG} / \Delta \text{HCO₃⁻} = \frac{(AG - 12)}{(24 - HCO₃⁻)}
]

• ≈1 → pure high AG acidosis

• <1 → concurrent normal AG acidosis

• 2 → concurrent metabolic alkalosis

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🔹 7. Metabolic Alkalosis — Deep Dive

Usually due to loss of H⁺ or gain of HCO₃⁻.

Step 1: Check Urine Chloride

Urine Cl⁻	Type	Common Causes
<25 mEq/L	Chloride-responsive	Vomiting, NG suction, diuretics (early), volume depletion
>40 mEq/L	Chloride-resistant	Hyperaldosteronism, Cushing’s, Bartter/Gitelman, Liddle, licorice

Mechanisms

• Loss of gastric acid → ↑ HCO₃⁻

• Diuretics → volume contraction → ↑ HCO₃⁻ reabsorption

• Mineralocorticoid excess → ↑ H⁺ and K⁺ secretion

Compensation

Hypoventilation increases PCO₂ slightly — but limited by hypoxia.

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🔹 8. Respiratory Disorders — Deep Dive

a. Respiratory Acidosis

→ Hypoventilation → CO₂ retention

Acute:
CNS depression (opiates, head injury, stroke), airway obstruction, severe asthma, pneumonia.

Chronic:
COPD, neuromuscular disease (MG, ALS, GBS).

Compensation:
Kidneys ↑ H⁺ excretion and ↑ HCO₃⁻ reabsorption (slow, 3–5 days).

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b. Respiratory Alkalosis

→ Hyperventilation → CO₂ washout

Causes:

• Hypoxemia (PE, pneumonia, high altitude)

• Pain, anxiety, panic attacks

• Fever, sepsis

• Salicylate overdose (early)

• Pregnancy, liver failure, thyrotoxicosis

Compensation:
Kidneys ↓ HCO₃⁻ reabsorption.

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🔹 9. GI-Related Acid–Base Disturbances

Disorder	Mechanism	Result
Severe diarrhea	Loss of bicarbonate-rich intestinal fluid	Metabolic acidosis (normal AG)
Vomiting / NG suction	Loss of gastric acid (H⁺)	Metabolic alkalosis

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🔹 10. Treatment Principles

Disorder	Management
Metabolic Acidosis	Treat cause; if severe (pH < 7.1) → IV NaHCO₃
Metabolic Alkalosis	Correct volume with isotonic saline if Cl⁻-responsive; acetazolamide if resistant
Respiratory Acidosis	Improve ventilation, clear airway, reverse drug effects
Respiratory Alkalosis	Treat underlying cause (pain, anxiety, hypoxemia)

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🧠 Key Memory Aids

• SMORE rule:

  • Same direction of PCO₂ and pH → Metabolic

  • Opposite direction → Respiratory

• MUDPILES → High AG metabolic acidosis

• FUSEDCARS → Normal AG metabolic acidosis

• Chloride <25 → responsive, >40 → resistant