Effect of hematocrit on regional oxygen delivery and extraction in an adult respiratory distress syndrome animal model.
BACKGROUND
The purpose of this prospective, randomized, controlled study was to investigate the effects of hematocrit (Hct) on regional oxygen delivery and extraction following induction of adult respiratory distress syndrome (ARDS) in an animal model.


METHODS
Animals were instrumented to monitor central venous pressure (CVP), systemic mean arterial pressure (MAP), pulmonary artery occlusion pressure (PAOP), and cardiac output (CO) and to measure blood flow in the renal, hepatic, and superior mesenteric arteries and portal vein. ARDS was induced, positive end expiratory pressure (PEEP) applied and CO was maximized with volume loading and epinephrine infusion. Data were acquired at baseline (BL) and at Hct levels ranging from 25% to 50%.


RESULTS
Systemic DO(2) increased steadily and significantly with increased Hct. Systemic O(2) extraction ratio (O(2)ER) decreased significantly with increasing Hct until a threshold value of 40%, after which further increases in Hct did not cause a statistically significant decrease in O(2)ER. Similarly, renal and hepatic DO(2) increased and O(2)ER decreased in a statistical significant manner with transfusions up to a Hct of 35%. In the splanchnic circulation blood transfusions did not cause any statistically significant increase in DO(2), and O(2)ER showed no decrease after an Hct of 35%. Systemic, renal, hepatic, and splanchnic VO(2) were not affected by changes in Hct. Blood viscosity decreased from a baseline value of 2.9+/-0.2 centipoise at a Hct of 38% to 2.3+/-0.1 centipoise at a Hct of 25% (P<0.05). Viscosity increased progressively with increasing hematocrits and reached the value of 4.2+/-0.2 centipoise at an Hct of 50% (P<0.05 versus Hct 30%, 35%, 40%, 45%).


CONCLUSIONS
Based on the results of this non-supply-dependent animal model we conclude that a progressive increase in Hct up to 40% causes a corresponding increase in systemic DO(2) associated with a decrease in O(2)ER. However, there is no improvement in renal, hepatic, and splanchnic DO(2) and O(2)ER after a threshold Hct of 35%. All other factors being the same, an Hct greater than 35% may in fact cause a decrease in blood flow rate and change in blood flow characteristics as a consequence of increased blood kinematic viscosity, which may alter and compromise cellular oxygen transfer.
Marini
C P
CP
Long Island Jewish Medical Center, Department of Surgery, Section of Critical Care, New Hyde Park, New York, USA.
Russo
G C
GC
Nathan
I M
IM
Jurkiewicz
A
A
McNelis
J
J
D000818:Animals; D001692:Biological Transport; D001794:Blood Pressure; D001809:Blood Viscosity; D002302:Cardiac Output / Q000502:physiology; D002496:Central Venous Pressure; D004195:Disease Models, Animal; D006400:Hematocrit; D007668:Kidney / Q000098:blood supply; D008102:Liver Circulation / Q000502:physiology; D008638:Mesenteric Arteries / Q000503:physiopathology; D010100:Oxygen / Q000008:administration & dosage / Q000378:metabolism*; D011175:Positive-Pressure Respiration; D011446:Prospective Studies; D011651:Pulmonary Artery / Q000503:physiopathology; D011897:Random Allocation; D012039:Regional Blood Flow; D012128:Respiratory Distress Syndrome / Q000503:physiopathology*; D013552:Swine; D013556:Swine, Miniature
D010100:Oxygen