Limited time75% off all plans
Get the app

Acid-Base Disorders

On this page

Acid-Base Fundamentals - pH Balancing Act

  • pH: Measure of $H^+$ concentration; normal arterial range 7.35-7.45.
    • Acidemia: pH < 7.35.
    • Alkalemia: pH > 7.45.
  • Buffers: Resist pH shifts.
    • Bicarbonate system ($HCO_3^-/H_2CO_3$): Key extracellular buffer. $CO_2 + H_2O \leftrightarrow H_2CO_3 \leftrightarrow H^+ + HCO_3^-$.
  • Henderson-Hasselbalch Equation: $pH = 6.1 + \log([HCO_3^-] / (0.03 \times PCO_2))$. Links pH, $HCO_3^-$, and $PCO_2$.
  • Regulation:
    • Lungs: Control $PCO_2$ (respiratory component, rapid response).
    • Kidneys: Control $HCO_3^-$ and excrete $H^+$ (metabolic component, slower response).

⭐ The body maintains the $HCO_3^-$ to dissolved $CO_2$ (proportional to $PCO_2$) ratio at approximately 20:1 to keep pH at 7.4.

Metabolic Acidosis & Alkalosis - The Body's Chemistry Quiz

  • Metabolic Acidosis
    • Primary ↓ HCO₃⁻, ↓ pH. Compensation: ↓ PaCO₂ (hyperventilation).
    • Anion Gap (AG): $AG = Na⁺ - (Cl⁻ + HCO₃⁻)$. Normal: 8-12 mEq/L.
    • High AG (HAGMA):
      • 📌 MUDPILES: Methanol, Uremia, DKA, Paraldehyde, Iron/INH, Lactic acidosis, Ethylene glycol, Salicylates.
      • 📌 GOLDMARK: Glycols, Oxoproline, L/D-Lactate, Methanol, Aspirin, Renal failure, Ketoacidosis.
    • Normal AG (NAGMA) / Hyperchloremic:
      • 📌 HARDUPS: Hyperalimentation, Acetazolamide, RTA, Diarrhea, Uretero-enteric fistula, Pancreatic fistula, Saline (excess).

⭐ Assess respiratory compensation in metabolic acidosis using Winter's Formula.

Expected PaCO₂: $PaCO₂ = (1.5 \times HCO₃⁻) + 8 \pm 2$.

  • Metabolic Alkalosis
    • Primary ↑ HCO₃⁻, ↑ pH. Compensation: ↑ PaCO₂ (hypoventilation).
    • Types (based on Urine Chloride, UCl⁻):
      • Saline-Responsive: UCl⁻ < 10-20 mEq/L (e.g., Vomiting, NG suction, Diuretics - early).
      • Saline-Resistant: UCl⁻ > 20 mEq/L (e.g., Hyperaldosteronism, Cushing's, severe K⁺ depletion).

Respiratory Acidosis & Alkalosis - When Lungs Steer pH

Normal $PCO_2$: 35-45 mmHg. Primary change in respiratory disorders.

Respiratory Acidosis (↓pH, ↑$PCO_2$ > 45 mmHg)

  • Cause: Hypoventilation (COPD, opioids, ARDS, neuromuscular disease).
  • Compensation (Renal $HCO_3^-$ ↑):
    • Acute: ↑1 $HCO_3^-$ per 10 ↑$PCO_2$.
    • Chronic: ↑3-5 $HCO_3^-$ per 10 ↑$PCO_2$.

Respiratory Alkalosis (↑pH, ↓$PCO_2$ < 35 mmHg)

  • Cause: Hyperventilation (anxiety, hypoxia, salicylates, sepsis).
  • Compensation (Renal $HCO_3^-$ ↓):
    • Acute: ↓2 $HCO_3^-$ per 10 ↓$PCO_2$.
    • Chronic: ↓4-5 $HCO_3^-$ per 10 ↓$PCO_2$.

📌 ROME: Respiratory Opposite (pH & $PCO_2$ move oppositely).

⭐ > Chronic Resp. Acidosis (e.g., COPD): Kidneys compensate; for every 10 mmHg ↑$PCO_2$, $HCO_3^-$ ↑ by 3-5 mEq/L.

ABG Interpretation & Mixed Disorders - Decoding the Signals

Systematic ABG analysis:

  • Compensation Formulas:
    • Metabolic Acidosis (Winter's): $PCO_2 = \mathbf{1.5} \times [HCO_3^{-}] + \mathbf{8} \pm \mathbf{2}$.
    • Metabolic Alkalosis: $\Delta PCO_2 \approx \mathbf{0.7} \times \Delta [HCO_3^{-}]$.
    • Resp. Acidosis (Acute): For $\mathbf{10} \uparrow$ PaCO2, $HCO_3^{-} \uparrow \mathbf{1}$. (Chronic: $\uparrow \mathbf{3-4}$).
    • Resp. Alkalosis (Acute): For $\mathbf{10} \downarrow$ PaCO2, $HCO_3^{-} \downarrow \mathbf{2}$. (Chronic: $\downarrow \mathbf{4-5}$).
  • Mixed Disorders: Suspect if compensation inadequate/excessive or pH normal with abnormal PaCO2/HCO3.
    • Delta Gap: $(\text{AG} - \mathbf{12}) : (\mathbf{24} - [HCO_3^{-}])$. Ratio ~1: pure HAGMA.

    ⭐ In a patient with DKA (HAGMA), if the fall in bicarbonate is significantly more than the rise in anion gap (i.e., delta gap < 0.8 or delta ratio < 1), suspect a co-existing normal anion gap metabolic acidosis (NAGMA).

High‑Yield Points - ⚡ Biggest Takeaways

  • Anion gap (AG) is key for metabolic acidosis (MA) differential; calculate as Na - (Cl + HCO3).
  • Winter's formula predicts expected PCO2 for respiratory compensation in metabolic acidosis.
  • Delta-delta gap (ΔAG / ΔHCO3) helps detect mixed acid-base disorders.
  • Salicylate toxicity classically presents as mixed respiratory alkalosis and high AG metabolic acidosis.
  • Diarrhea leads to Normal AG Metabolic Acidosis (NAGMA) via HCO3- loss.
  • Vomiting or NG suction causes metabolic alkalosis due to H+ and Cl- loss.
  • Identify primary disorder first, then assess compensation using expected changes.

Continue reading on Oncourse

Sign up for free to access the full lesson, plus unlimited questions, flashcards, AI-powered notes, and more.

CONTINUE READING — FREE

or get the app

Rezzy — Oncourse's AI Study Mate

Have doubts about this lesson?

Ask Rezzy, your AI Study Mate, to explain anything you didn't understand

Enjoying this lesson?

Get full access to all lessons, practice questions, and more.

START FOR FREE