Physiology · Renal, fluids and acid–base
Respiratory acidosis and alkalosis !
- Mechanism
- Exam priority: high
Breathing too little builds up CO₂ and acidifies the blood; breathing too much blows off CO₂ and makes it alkaline. The kidneys compensate over days.
Updated 2026-11-01
Also called: Hypercapnia, Hypocapnia
See it in 3D: Medulla oblongata · Diaphragm · Kidneys
What it is
Respiratory acid–base disorders start with a change in PaCO₂ from hypoventilation (acidosis) or hyperventilation (alkalosis). CO₂ is hydrated to carbonic acid, so moving PaCO₂ moves pH. Cell proteins and hemoglobin buffer first; then, over 2 to 5 days, the kidney adjusts HCO₃⁻.
How it works, step by step
- Alveolar ventilation falls: CO₂ produced by tissues accumulates and PaCO₂ rises.
- CO₂ + H₂O ↔ H₂CO₃ ↔ H⁺ + HCO₃⁻ (carbonic anhydrase): H⁺ rises and pH falls.
- Within minutes, hemoglobin and cell proteins buffer H⁺; HCO₃⁻ rises slightly.
- If it lasts days, the proximal tubule and collecting duct secrete more H⁺, excrete more NH₄⁺ and reclaim all HCO₃⁻, so HCO₃⁻ rises considerably.
- In respiratory alkalosis the reverse happens: the kidney excretes HCO₃⁻ and secretes less H⁺.
- CO₂ crosses the blood–brain barrier quickly, so PaCO₂ changes immediately alter CSF pH, cerebral blood flow and consciousness.
Equations
- carbonic anhydrase
- speeds the first step
Raising PaCO₂ pushes the reaction to the right.
- k (acidosis)
- ≈ 1 acute; ≈ 3.5 chronic
- k (alkalosis)
- ≈ 2 acute; ≈ 4–5 chronic
The rules in detail are on the Biochemistry page (acid–base compensation).
Comparison
| Feature | Respiratory acidosis | Respiratory alkalosis |
|---|---|---|
| Primary change | PaCO₂ ↑ (hypoventilation) | PaCO₂ ↓ (hyperventilation) |
| Renal compensation | Retains HCO₃⁻, excretes more H⁺ (days) | Excretes HCO₃⁻ (days) |
| Brain | Vasodilation, headache, drowsiness, CO₂ narcosis | Vasoconstriction, dizziness, paresthesias |
| Potassium and calcium | K⁺ slightly ↑ | Ionized Ca²⁺ ↓ (tetany), K⁺ ↓ |
| Typical causes | Opioids, COPD, neuromuscular disease | Anxiety, altitude, embolism, early sepsis, pregnancy |
Clinical notes
- Opioid overdose: slow breathing, high PaCO₂ and low pH; naloxone reverses the respiratory depression.
- In COPD with chronic hypercapnia, HCO₃⁻ is high. Ventilating abruptly down to a 'normal' PaCO₂ leaves a post-hypercapnic metabolic alkalosis.
- Asthma attack: respiratory alkalosis at first; a PaCO₂ that 'normalises' or rises signals fatigue and is a red flag.
- On arrival at altitude, hyperventilation causes alkalosis; over the following days the kidney excretes HCO₃⁻ (acclimatisation).
Test yourself
Think of the answer, then tap the question to see it.
PaCO₂ 60 mmHg and HCO₃⁻ 26 mEq/L: acute or chronic?
Acute. With a 20 mmHg rise, acute change raises HCO₃⁻ by ≈ 2 (≈ 26) and chronic by ≈ 7 (≈ 31). Renal compensation has not happened yet.
Why does anxiety-driven hyperventilation cause perioral tingling and carpopedal spasm?
Alkalosis increases calcium binding to albumin; ionized calcium falls and nerves become hyperexcitable.
Why can a normal PaCO₂ be a bad sign in an asthma attack?
Early on, the patient hyperventilates and PaCO₂ is low. If it rises to 'normal', the muscles are tiring and ventilation is no longer enough: respiratory failure is near.
Why does acute hypercapnia cause headache and drowsiness?
CO₂ crosses the blood–brain barrier, acidifies the CSF and dilates cerebral vessels: blood flow and intracranial pressure rise and the cortex is depressed.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Reading an arterial blood gas step by step
- Control of breathing, chemoreceptors and lung reflexes
- High altitude and acclimatization
- Hypoxemic and hypercapnic respiratory failure
- CO₂ transport and the Haldane effect
- Renal handling of H⁺ and bicarbonate
- Cerebral blood flow, brain metabolism and intracranial pressure
Related conditions
- Respiratory acidosis
- Respiratory alkalosis
- Chronic obstructive pulmonary disease (COPD)
- Asthma
- Hypocalcaemia
In Biochemistry
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 26.5 Disorders of Acid-Base Balance (OpenStax (Rice University), 2022); Respiratory acidosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Respiratory alkalosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 31). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.