Influence of hypercapnia on cardiovascular responses to tracheal intubation

Laryngoscopy and tracheal intubation are often associated with tachycardia, hypertension, and arrhythmias. There is a risk of hypercapnia in the case of difficult mask ventilation. The circulatory response to hypercapnia is increases in arterial pressure and heart rate. We evaluated the difference of cardiovascular responses to tracheal intubation between normocapnia and hypercapnia during mask ventilation before tracheal intubation.

We studied 40 ASA physical status I to II patients under general anesthesia. Induction of anesthesia was achieved with midazolam 0.05 mg/kg, propofol 1.5 mg/kg, alfentanil 10 microg/kg, and rocuronium 0.6 mg/kg IV. The lungs were mechanically ventilated with a tidal volume of 10 mL/kg and 6 to 10 bpm in the hypercapnia group (n = 20) or 12 to 15 bpm in the normocapnia group (n = 20) during the induction period. Intubation was performed 3 minutes after the induction, and anesthesia was maintained using 1.5% sevoflurane (inspired) and 75% N(2)O in oxygen. Heart rate, systolic arterial pressure (SAP), and diastolic arterial pressure were recorded every minute throughout the study.

The proportion of the patients whose increase of SAP between just before intubation and 1 minute after intubation was more than 30 mm Hg in the hypercapnia group (40%) was greater than that in the normocapnia group (9.5%) (P = .0325). There were no differences in heart rate and diastolic arterial pressure between hypercapnia and normocapnia groups. For the SAP of the patients, the trend of changes was increased (P = .024).

Hypercapnia during mask ventilation before tracheal intubation may exaggerate the increase of SAP during intubation compared to normocapnia. Ventilation was important in minimizing hemodynamic responses during induction regardless of using drugs.