The pulmonary circulation is a high capacitance system that can adapt to a five fold variation in blood volume with little change in pressure. Maintaining a constant filtration pressure at the pulmonary capillaries is important in avoiding pulmonary edema which would impede air exchange. Until recently, it was assumed that pulmonary capillary pressure Ppc) could be approximated by the Gaar equation as Ppc=Pla + .4 (Ppa-Pla). Clinically Ppc is often assumed to be equal to the pulmonary arterial occlusion or wedge pressure Ppw). However, these approximations are not an accurate prediction of Ppc in a number of clinical conditions. The goal of these studies is to evaluate the accuracy, reproducibility and limitations of three techniques to estimate pulmonary capillary pressure (Ppc): the visual determination method, computer definition of the break point time in the pulmonary arterial pressure profile, and theoretical Ppc derived from computer simulation. These methods will be compared to one another in patients and in dogs and to the double occlusion PpC in open-chested dog lungs. The division of pulmonary vascular resistance (PVR) into pre (ra) and post (rv) capillary components and the Ppc as compared to the wedge pressure will be evaluated under altered physiological conditions. These include: acute changes in blood volume induced by aortic cross clamping during aortic reconstruction, chronic heart failure with extravascular volumeretention, viscosity changes after polycythemia, and alteration in airway pressure such as seen during mechanical ventilation and positive end expiratory pressure, oleic acid injury, increasing capillary permeability, and increasing vascular resistance (hypoxia) and capacitance and resistance can be arbitrarily changed and the resultant Ppc determined. The measured Ppc can then be compared to predicted theoretical values. In dog lungs standard experimental protocols will be used. In patients, analysis of the pulmonary artery pressure tracing requires no additional physiological trespass.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Clinical Investigator Award (CIA) (K08)
Project #
5K08HL002589-03
Application #
2210225
Study Section
Special Emphasis Panel (SRC (OG))
Project Start
1992-09-10
Project End
1997-08-31
Budget Start
1994-09-01
Budget End
1995-08-31
Support Year
3
Fiscal Year
1994
Total Cost
Indirect Cost
Name
University of South Alabama
Department
Anesthesiology
Type
Schools of Medicine
DUNS #
City
Mobile
State
AL
Country
United States
Zip Code
36688
Cope, D K; Impastato, W K; Cohen, M V et al. (1997) Volatile anesthetics protect the ischemic rabbit myocardium from infarction. Anesthesiology 86:699-709