The Effect of Positive end Expiratory pressure on the Pulmonary Capillary Pressure in Acute Lung Injury Patients.
10.4046/trd.2000.49.5.594
- Author:
Byung Chun CHUNG
;
Chang Gyoo BYUN
;
Chang Youl LEE
;
Hyung Jung KIM
;
Chul Min AN
;
Sung Kyu KIM
;
Cheung Soo SHIN
- Publication Type:Original Article
- Keywords:
Acute lung injury;
Positive and expiratory pressure;
Pulmonary capillary pressure
- MeSH:
Acute Lung Injury*;
Anoxia;
Arterial Pressure;
Capillaries*;
Catheters;
Central Venous Pressure;
Edema;
Humans;
Lung;
Positive-Pressure Respiration*;
Prospective Studies;
Pulmonary Circulation;
Pulmonary Edema;
Ventilation
- From:Tuberculosis and Respiratory Diseases
2000;49(5):594-600
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Positive end expiratory pressure (PEEP) ventilation is well established as an integral part of the management of patients with the acute lung injury. PEEP is a key element in the treatment of hypoxemia resulting from pulmonary edema. Pulmonary capillary pressure (Pcap) is the most important factor influencing lung edema formation, and an understanding of how Pcap is altered by variations of PEEP or pulmonary arterial occlusion pressure (PAOP) is important to improve the treatment of acute lung injury patients. This study was performed to evaluate the effects of PEEP on the pulmonary capillary pressure in acute lung injury patients. METHODS: This was a prospective study of 11 acute lung injury patients. The effect of PEEP on pulmonary circulation at four different levels (0,4,8, and 12cm H2O) was analyzed. Pcap was estimated visually at bed side with Swan Ganz catheters. The pulmonary vasculature was analyzed by calculating the pressure difference at the arterial and venous parts of the circulation. RESULTS: As PEEP increased from 0 to 12 cm H2O, the mean puhnonary arterial pressure (PAP) and Pcap increased respectively from 22.7 ± 7.4 to 25.3 ± 7.3 mmHg and 15.3 ± 3.3 to 17.8 ±3.2 mmHg (p<0.05). Similarly, PAOP increased from 9.8 ± 2.1 to 12.8 ± 2.1 mmHg and the central venous pressure increased from 6.1 ± 1.6 to 9.3 1: 2.3 mmHg(p<0.05). However, the pressure gradient at the arterial (PAP-Pcap) and venous (Pcap-Pcwp) part of pulmonary circulation remained unchanged at all evaluated PEEP levels. CONCLUSION: Although Pcap increasoo gradually with increased PEEP, the pressure gradient at the arterial and venous part of the pulmonary vasculature remained unchanged at all evaluated PEEP levels in acute lung injury patients.
