Respiratory Alkalosis - The Big Gasp
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Pathophysiology - How We Blow It Off
- Primary Defect: Excessive elimination of $CO_2$ from the lungs due to alveolar hyperventilation, causing hypocapnia.
- Mechanism: A drop in arterial $PCO_2$ (< 35 mmHg) shifts the carbonic acid-bicarbonate buffer equation to the left: $H^+ + HCO_3^- \leftarrow H_2CO_3 \leftarrow CO_2 + H_2O$. This consumes free $H^+$ ions, directly raising the blood pH (> 7.45).
- Compensation (Metabolic): Kidneys respond by decreasing $H^+$ secretion and reducing $HCO_3^-$ reabsorption, effectively excreting bicarbonate. This is a slow process, taking 2-3 days to maximize.
⭐ Clinical Pearl: Alkalosis increases albumin's binding to calcium, causing a drop in ionized calcium. This can lead to perioral numbness, paresthesias, and even carpopedal spasm, mimicking hypocalcemia.

Compensation - Kidneys to the Rescue
Renal compensation is a slow process, taking 2-3 days to manifest. The goal is to decrease serum bicarbonate to correct the pH.
- Primary Mechanism: Triggered by low pCO₂, leading to intracellular alkalosis in renal tubule cells.
- Reduced activity of carbonic anhydrase.
- Decreased H⁺ secretion into the tubular lumen.
- Results in ↓ HCO₃⁻ reabsorption and ↑ HCO₃⁻ excretion.
- Urine becomes alkaline (pH > 6.0).

- Expected Change:
- Acute: For every 10 mmHg ↓ in pCO₂, [HCO₃⁻] ↓ by 2 mEq/L.
- Chronic: For every 10 mmHg ↓ in pCO₂, [HCO₃⁻] ↓ by 4-5 mEq/L.
⭐ In a fully compensated chronic state, for every 10 mmHg ↓ in pCO₂, the [HCO₃⁻] will decrease by approximately 4-5 mEq/L. This demonstrates appropriate renal compensation.
Clinical Features & Dx - Spotting the Signs
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Key symptoms stem from cerebral vasoconstriction (neurologic signs) & hypocalcemia (↓ ionized $Ca^{2+}$, neuromuscular irritability):
- Neurologic: Lightheadedness, dizziness, confusion, syncope, due to ↓ cerebral blood flow.
- Neuromuscular: Perioral/digital paresthesias, muscle cramps, carpopedal spasm (Trousseau's), facial twitching (Chvostek's), tetany.
- Cardiovascular: Tachycardia, palpitations, arrhythmias.
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Diagnostic cornerstone is Arterial Blood Gas (ABG):
- Primary finding: ↑ pH > 7.45 with a primary ↓ PaCO₂ < 35 mmHg.
- Check serum electrolytes & anion gap to narrow the differential diagnosis.
⭐ Alkalosis increases albumin's affinity for calcium, causing a drop in its ionized form. This leads to neuromuscular excitability (tetany, Chvostek's sign) even when total serum calcium is normal.

High‑Yield Points - ⚡ Biggest Takeaways
- Respiratory alkalosis is driven by hyperventilation, causing a primary ↓ in PaCO₂.
- Key triggers include hypoxemia (e.g., high altitude, PE), anxiety/panic attacks, and salicylate toxicity.
- Acute compensation is minimal, relying on intracellular H⁺ buffering.
- Chronic renal compensation (2-3 days) involves ↓ H⁺ excretion and ↑ HCO₃⁻ excretion, markedly lowering serum HCO₃⁻.
- Clinical signs like tetany and paresthesias result from decreased ionized calcium.
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