Influence of apneic oxygenation on cardiorespiratory system homeostasis

Purpose

The aim of this study was to elucidate the magnitude of variations in oxygenation indices and the pattern of hemodynamic changes in response to the net effect of tracheal apneic oxygenation (AO) with a view to define the safe time limit of its application.

Methods

After obtaining Animal Research Ethics Committee approval, AO was applied in 12 piglets for 40 min. Arterial (a) and mixed venous (v) blood samples for oxygen (O₂) and carbon dioxide (CO₂) tension (PaO₂/PvO₂, PaCO₂/PvCO₂), O₂ saturation (SaO₂/SvO₂), pHa, base excess (BEa), and bicarbonate (HCO₃a) determination and for alveolar O₂ tension (PAO₂), PaO₂/FiO₂ and PaO₂/PAO₂ ratio, arterial–mixed venous O₂ content (AVDO₂), and O₂ extraction ratio (O₂ER) estimation were collected on anesthesia induction, 10, 20, 30, and 40 min during AO and 10 and 20 min after reconnection to the ventilator. Concomitant hemodynamic data were obtained.

Results

Besides PvO₂ and PAO₂, AO adversely influenced PaO₂ (248–113 mmHg), PaCO₂ (35–145 mmHg), PvCO₂, PaO₂/FiO₂, and PaO₂/PAO₂ in a time-depended fashion, whereas SvO₂, AVDO₂, and O₂ER were minimally affected. P(a ? v)CO₂ was reversed throughout AO. Acid–base status derangement, consisting of HCO₃a elevation, BEa widening, and acidemia (pH 6.9) maximized 40 min after AO. During AO, heart rate, systemic and pulmonary circulation pressures, and cardiac output were progressively elevated, whereas systemic vascular resistance was reduced. All the studied parameters reverted almost to baseline within the 20-min period of ventilator reconnection.

Conclusion

Tracheal AO for 40 min ensures acceptable blood oxygenation, promotes notable hypercapnic acidosis, and consequent transient hemodynamic alterations, which are almost completely reversible after reconnection to the ventilator.