Guide — Acid-Base
Respiratory Acidosis vs Alkalosis
Respiratory acid-base disorders are driven by changes in carbon dioxide (CO₂) — the respiratory acid. CO₂ is controlled entirely by ventilation, making respiratory disorders directly linked to breathing rate and depth.
9 min read · Acid-Base
Educational use only. Respiratory acid-base disorders require immediate clinical assessment and provider notification. Airway management and ventilator adjustments require provider and respiratory therapy involvement. Always follow institutional protocols. This material supports nursing education and exam review. It is not medical advice and is not a substitute for clinical judgment, institutional policy, or medical direction. Always follow facility protocols and current provider orders.
Overview
Carbon dioxide (CO₂) is the primary respiratory acid. It is produced by cellular metabolism and eliminated by the lungs. When CO₂ accumulates or is depleted, the pH shifts accordingly:
- Respiratory acidosis: CO₂ retention from hypoventilation → pH falls below 7.35
- Respiratory alkalosis: CO₂ depletion from hyperventilation → pH rises above 7.45
The kidneys compensate for respiratory disorders by retaining or excreting bicarbonate — but this process takes 2 to 5 days, making renal compensation slower than the rapid respiratory compensation for metabolic disorders.
Hypoventilation vs Hyperventilation
| Hypoventilation | Hyperventilation | |
|---|---|---|
| Definition | Decreased alveolar ventilation; CO₂ retained | Increased alveolar ventilation; CO₂ blown off |
| CO₂ effect | PaCO₂ rises (> 45 mmHg) | PaCO₂ falls (< 35 mmHg) |
| pH effect | pH falls — acidosis | pH rises — alkalosis |
| Disorder | Respiratory Acidosis | Respiratory Alkalosis |
ABG Findings at a Glance
| Parameter | Respiratory Acidosis | Respiratory Alkalosis |
|---|---|---|
| pH | < 7.35 (Low) | > 7.45 (High) |
| PaCO₂ | > 45 mmHg (High) | < 35 mmHg (Low) |
| HCO₃¹ (compensatory) | > 26 mEq/L (kidneys retain HCO₃¹) | < 22 mEq/L (kidneys excrete HCO₃¹) |
HCO₃¹ values reflect compensated states. In acute or uncompensated disorders, HCO₃¹ remains within normal range. Compensation takes 2–5 days for full renal response.
Respiratory Acidosis
Causes — Hypoventilation
- CNS depression: Opioid overdose, benzodiazepine overdose, anesthesia, head injury, stroke — suppress respiratory drive
- Neuromuscular disorders: Guillain-Barré syndrome, myasthenia gravis, ALS — impair respiratory muscle function
- Obstructive lung disease: COPD exacerbation, severe asthma — air trapping and CO₂ retention
- Airway obstruction: Foreign body, laryngospasm
- Chest wall restriction: Flail chest, morbid obesity (obesity hypoventilation syndrome)
- Mechanical ventilation: Inadequate ventilator rate or tidal volume settings
Clinical Manifestations
- Slow, shallow, or labored respirations
- Hypoxemia (PaO₂ often falls alongside rising PaCO₂)
- Confusion, restlessness progressing to somnolence and coma (CO₂ narcosis)
- Headache (cerebral vasodilation from elevated CO₂)
- Flushed skin, diaphoresis
- Asterixis (metabolic flap) in severe chronic hypercapnia
- Cyanosis in severe cases
Treatment Priorities
- Restore ventilation — the primary intervention in all cases of respiratory acidosis
- Opioid overdose: administer naloxone per order; prepare for repeat dosing
- Airway obstruction: position, suction, or assist with airway management
- COPD exacerbation: bronchodilators, corticosteroids, controlled oxygen delivery; avoid high-flow O₂ in known CO₂ retainers
- Severe cases: non-invasive positive pressure ventilation (NIPPV/BiPAP) or intubation and mechanical ventilation
- Supplemental O₂ with caution in COPD — use controlled FiO₂; target SpO₂ 88–92% in known hypercapnic patients
Respiratory Alkalosis
Causes — Hyperventilation
- Anxiety and pain: Most common cause; tachypnea drives CO₂ depletion
- Hypoxemia: Any cause of low O₂ stimulates the respiratory center to increase ventilation (hypoxic drive)
- Early sepsis: Fever and sepsis-induced tachypnea precede metabolic acidosis
- Mechanical ventilation: Excessive rate or tidal volume causing over-ventilation
- Pregnancy: Progesterone stimulates ventilation; mild respiratory alkalosis is normal in pregnancy
- CNS stimulation: Fever, salicylate toxicity, CNS disorders, altitude
- Liver failure: Central hyperventilation from ammonia accumulation
Clinical Manifestations
- Rapid, deep respirations (tachypnea)
- Light-headedness, dizziness, perioral numbness
- Tingling of extremities (paresthesias) — reduced ionized calcium from alkalosis
- Muscle cramps, carpopedal spasm
- Positive Chvostek's and Trousseau's signs in severe cases
- Anxiety, panic attacks (can both cause and be caused by respiratory alkalosis)
Treatment Priorities
- Treat the underlying cause — anxiety: calm reassurance, breathing techniques; pain: analgesia; fever: antipyretics
- Hypoxemia-driven hyperventilation: correct the hypoxemia with supplemental O₂
- Anxiety-driven: guided slow breathing, rebreathing into a paper bag (no longer routinely recommended — assess for hypoxemia first)
- Ventilated patients: notify provider, reduce RR or tidal volume per ventilator management protocol
- Sepsis: initiate sepsis workup and treatment; alkalosis will correct as underlying infection is managed
- Assess for hypocalcemia symptoms; reassure patient about paresthesias when anxiety is the cause
NCLEX Pearls
- Respiratory acidosis = hypoventilation = CO₂ retention = pH drops (ROME: Respiratory Opposite)
- Respiratory alkalosis = hyperventilation = CO₂ blown off = pH rises
- Opioid overdose is the highest-yield cause of respiratory acidosis on NCLEX — treatment is naloxone + ventilatory support
- Anxiety is the most common non-pathologic cause of respiratory alkalosis
- Early sepsis classically presents with respiratory alkalosis — tachypnea precedes the subsequent lactic metabolic acidosis
- In COPD patients, a “normal” PaCO₂ (35–45) may actually represent respiratory alkalosis relative to their elevated baseline
- Oxygen-induced hypercapnia in COPD is driven mainly by reversal of hypoxic pulmonary vasoconstriction (worsening V/Q mismatch) and the Haldane effect — NOT by suppression of a “hypoxic drive” (a disproven theory) — so still use controlled O₂ titrated to SpO₂ 88–92%, never withhold needed O₂
- Respiratory compensation is fast (minutes); metabolic compensation is slow (2–5 days)
Related Resources
Standards & sources
Fact-checked Jun 21, 2026This page is written to align with American Association for Respiratory Care (AARC) · Standard clinical chemistry / ABG references. It is an educational summary, not a citation of any single document — always verify specific doses, values, and protocols against current guidelines and your facility policy. How we source content →