Effect of arterial puncture on ventilation

Background: Clinicians frequently assume that during arterial puncture for measuring arterial blood gases patients hyperventilate from pain and anxiety. This assumption leads clinicians to falsely interpret a PaCO₂ and pH near the upper limit of normal as a chronic respiratory acidosis corrected by an acute respiratory alkalosis.

Objective: Determine if participants hyperventilate during arterial puncture from pain and anxiety.

Methods: We recruited participants from a pulmonary function laboratory referred for arterial blood gas measurement. We excluded those with heart failure and included those with any respiratory condition (COPD, asthma, sleep apnea). We measured end tidal PCO₂ (P_ETCO₂), respiratory rate, and heart rate 15 min before topical anesthesia, during anesthesia, during arterial puncture, and 15 min later. We assessed generalized anxiety before and measured pain during and after arterial puncture.

Results: 24 participants were recruited (age: 54 ± 12 years; men: 54%). PaCO₂ was 41 ± 5 mmHg. One had acute respiratory alkalosis. Respiratory rate increased from (19 ± 6 breaths per minute (bpm)) before to a maximum (21 ± 6 bpm) during arterial puncture (p = 0.001). Heart rate was stable throughout. The lowest P_ETCO₂ during the procedure (35 ± 5) was similar to P_ETCO₂ before the procedure (p = 0.1). The change in P_ETCO₂ and respiratory rate did not correlate with pain, anxiety, or lung function.

Conclusion: Respiratory rate increased slightly during arterial puncture without any change in P_ETCO₂. Hence, acid-base status must be interpreted without the assumption of procedure induced hyperventilation.