Increased artificial deadspace ventilation is a safe and reliable method for deliberate hypercapnia

Objectives: To develop a simple method in an animal model to achieve deliberate hypercapnia, which can be used easily and safely to regulate the pulmonary vascular resistance without changing mean airway pressure and compromising oxygenation. Design: Prospective study, with each animal used as its own control. Subjects: Minipigs, weighing 11 to 14 kg (n = 7). Interventions: A quadrilumen thermodilution pulmonary artery catheter was placed in minipigs via the internal jugular vein. Systemic blood pressure was measured with use of a femoral arterial catheter. The animals' lungs were ventilated with an FIO 2 of 1.0, and a stable state of eucapnia was achieved and maintained for 30 mins. The artificial deadspace was increased every 30 mins, by connecting 45-mL (3- to 4-mUkg) corrugated tube segments until a total deadspace volume of 180 mL was added. Measurements and Main Results: Hemodynamic performance was evaluated at baseline and after 45 mL (3 to 4 mL/kg), 90 mL (6 to 8 mUkg), 135 mL (9 to 11 mL/kg), and 180 mL (12 to 15 mUkg) of added deadspace. Data were indexed to the animal's weight (in kg). Increased artificial deadspace produced a significant (p <.05) increase in Paco 2 . These increases in Paco 2 were associated with significant (p <.05) increases of 23%, 32%, 45%, and 46% in the mean pulmonary vascular resistance values, and 6%, 16%, 23%, and 23% in the mean pulmonary arterial pressure, respectively. The systemic pH was decreased from a mean baseline value of 7.45 to 7.39, 7.28, 7.20, and 7.11, respectively. There were no significant changes in Pao 2 , oxygen consumption, systemic vascular resistance, and cardiac output throughout the experiments. Conclusions: A gradual increase in artificial deadspace ventilation produces a state of deliberate hypercapnia. In our animal model, a moderate increase in artificial deadspace significantly increased the pulmonary vascular resistance but was not associated with detrimental respiratory acidemia. Larger volumes of added artificial deadspace had no detrimental effect on cardiac output, oxygen content, oxygen consumption, and systemic vascular resistance, but were associated with significant respiratory acidemia and therefore should be avoided.