The Effect of Intratracheal Pulmonary Ventilation on Dead Space and Airway Pressures in Rabbits with Acute Respiratory Failure Induced by Oleic Acid Injection.
10.4097/kjae.1997.32.3.360
- Author:
Kook Hyun LEE
1
;
Ka Young RHEE
;
Yang Ja KANG
;
Kwang Woo KIM
;
Sung Lyang CHUNG
Author Information
1. Department of Anesthesiology, Seoul National University College of Medicine and Ul San University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Ventilation;
mechanical;
intratracheal pulmonary;
hybrid;
dead space;
peak inspiratory pressure;
Failure;
respiratory;
oleic acid
- MeSH:
Catheters;
Oleic Acid*;
Pulmonary Ventilation*;
Rabbits*;
Respiration, Artificial;
Respiratory Insufficiency*;
Respiratory Rate;
Tidal Volume;
Ventilation
- From:Korean Journal of Anesthesiology
1997;32(3):360-365
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Intratracheal pulmonary ventilation (ITPV) was developed to allow a decrease in physiological dead space during mechanical ventilation. To reduce anatomic dead space, a reverse thrust catheter (RTC) is introduced into an endotracheal tube (ETT) through an adapter and positioned just above the carina inside the ETT. ITPV can be combined with pressure control mode of mechanical ventilation to make hybrid ventilation(HV). The effect of HV on the reduction of dead space was compared with that of conventional mechanical ventilation(CMV) in rabbits with acute respiratory failure. METHODS: Oleic acid of 0.06 ml/kg was injected to induce acute respiratory failure in 7 rabbits. PaO2 and PaCO2 were measured 30 minutes after the injection. Oleic acid was injected in another 7 rabbits to compare CMV with HV while increasing the respiratory rate(RR). Tidal volume, dead space(VD) and peak inspiratory pressure(PIP) were measured at the same RR. RESULTS: PaO2 decreased significantly from 467+/- 68 mmHg to 156 +/-26 mmHg at FIO2 1.0 after the injection of oleic acid. In another 7 rabbits, the VD's of CMV were 34+/- 10 ml, 27 +/-10 ml, 20+/- 6 ml, and 18+/- 3 ml at respiratory rate of 20/min, 40/min, 80/min and 120/min, respectively. The VD's of HV were 28 +/-11 ml, 16+/- 8 ml, 9+/- 4 ml, and 7+/- 3 ml at the same respiratory rates as in CMV. The VD's of HV were lower than those of CMV. The PIP's were lower in HV than in CMV. CONCLUSION: We conclude that HV, as the modification of ITPV, can be applied to acute respiratory failure to minimize the airway pressures and dead space of CMV.
