Respiratory Alkalosis

Key Points

• Respiratory alkalosis is an elevated pH state caused by reduced CO2 from hyperventilation.
• It may occur as a primary hyperventilation disorder, as compensation for metabolic acidosis, or iatrogenically during mechanical ventilation.
• Ventilator settings with excessive respiratory rate or tidal volume can induce hypocapnia.
• Accurate trend monitoring is essential to prevent treatment-induced overcorrection.

Pathophysiology

Respiratory alkalosis occurs when ventilation removes CO2 faster than metabolic production. Decreased PaCO2 reduces carbonic acid concentration and raises blood pH above normal physiologic range. The process can be adaptive (compensation) or pathologic/iatrogenic.

Because compensation and primary disease can look similar at first glance, clinical context is essential. Distinguishing intended respiratory compensation from harmful overventilation guides safe correction.

Classification

• Primary hyperventilation respiratory alkalosis: Excessive spontaneous ventilation lowers CO2.
• Compensatory respiratory alkalosis: Hyperventilation occurs to offset underlying metabolic acidosis.
• Iatrogenic respiratory alkalosis: Ventilator over-support (high RR or high tidal volume) drives excessive CO2 elimination.

Nursing Assessment

NCLEX Focus

Determine whether low PaCO2 is primary or compensatory before recommending correction, especially in critically ill patients.

• Confirm alkalemia with low PaCO2 on ABG trend review.
• Assess breathing pattern and signs of hyperventilation trigger or distress.
• Evaluate for metabolic-acidosis context where low CO2 may be compensatory.
• For mechanically ventilated patients, review RR and tidal-volume settings against current gas values.
• Monitor serial ABGs to prevent persistent hypocapnia-related instability.

Nursing Interventions

• Escalate symptomatic or persistent alkalemia and communicate whether the pattern appears primary or compensatory.
• In ventilated patients, coordinate setting reassessment when CO2 is over-corrected.
• Support treatment of underlying cause rather than suppressing necessary compensation.
• Reassess neurologic and hemodynamic stability while correcting ventilation trajectory.
• Continue trend-based monitoring until pH and CO2 stabilize near target.

Iatrogenic Overventilation Risk

Excessive ventilator support can unintentionally induce respiratory alkalosis and worsen overall instability.

Pharmacology

This source section emphasizes ventilation physiology and cause identification; no specific pharmacologic protocol is detailed.

Clinical Judgment Application

Clinical Scenario

A mechanically ventilated patient develops rising pH and low PaCO2 after an increase in set respiratory rate.

Recognize Cues: ABG indicates alkalemia with hypocapnia after ventilator adjustment. Analyze Cues: Ventilator-induced respiratory alkalosis is likely. Prioritize Hypotheses: Main priority is preventing ongoing iatrogenic overventilation while maintaining oxygenation. Generate Solutions: Reevaluate RR/tidal-volume targets and compare with current acid-base status. Take Action: Escalate to respiratory team and support prompt setting optimization. Evaluate Outcomes: CO2 and pH return toward normal range without oxygenation compromise.

Related Concepts

• acid-base-balance-principles - Base framework for pH and PaCO2 interpretation.
• hyperventilation - Primary physiologic driver of respiratory alkalosis.
• metabolic-acidosis - Common disorder that can produce compensatory respiratory alkalosis.
• arterial-blood-gas - Required trend tool for identifying primary vs compensatory changes.
• mechanical-ventilation - Key iatrogenic context when settings exceed physiologic need.

Self-Check

1. How do you determine whether respiratory alkalosis is compensatory or primary?
2. Which ventilator setting patterns most commonly produce hypocapnia?
3. Why can immediate suppression of hyperventilation be harmful in metabolic acidosis?