CIRCULATORY EFFECTS OF HYPOXIA, ACUTE NORMOVOLEMIC HEMODILUTION, AND THEIR COMBINATION IN ANESTHETIZED PIGS

Citation
H. Schou et al., CIRCULATORY EFFECTS OF HYPOXIA, ACUTE NORMOVOLEMIC HEMODILUTION, AND THEIR COMBINATION IN ANESTHETIZED PIGS, Anesthesiology, 84(6), 1996, pp. 1443-1454
Citations number
38
Categorie Soggetti
Anesthesiology
Journal title
ISSN journal
00033022
Volume
84
Issue
6
Year of publication
1996
Pages
1443 - 1454
Database
ISI
SICI code
0003-3022(1996)84:6<1443:CEOHAN>2.0.ZU;2-W
Abstract
Background: Because hemodilution decreases the oxygen-carrying capacit y of blood, it was hypothesized that severe hemodilution would decreas e the tolerance to alveolar hypoxia. Methods: Hemodynamics, oxygen tra nsport, and blood lactate concentrations were compared in ten pigs wit h normal hematocrit (33 +/- 4%), and ten hemodiluted pigs (hematocrit 11 +/- 1%; mean +/- SD) anesthetized with ketamine-fentanyl-pancuroniu m during stepwise decreases in inspired oxygen fraction (FIO2; 1.0, 0. 35, 0.21, 0.15, 0.10, 0.05). Results: Median systemic oxygen delivery (DO2SY) became critical (the DO2SY value when arterial lactate exceede d 2.0 mmol . l(-1)) at 10.4 ml . kg(-1). min(-1) (range 6.9-16.1) in h emodiluted animals and at 11.8 ml . kg(-1). min(-1) (5.9-32.2) in anim als with normal hematocrits (NS). The relationship between mixed venou s oxygen saturation and arterial lactate values was less consistent an d median critical mixed venous oxygen saturation was higher (P < 0.05) in the hemodiluted group (35%, range 21-64), than in animals with nor mal hematocrits (21%, 7-68%). In animals with normal hematocrit, decre asing FIO2 from 1.0 to 0.10 resulted in a decrease in DO2SY from 26.3 +/- 9.1 to 9.3 +/- 3.9 ml . kg(-1). min(-1) (P < 0.01). Cardiac output did not change, systemic oxygen extraction ratio increased from 0.23 +/- 0.08 to 0.68 +/- 0.13 (P < 0.01), and arterial lactate from 0.9 +/ - 0.2 to 3.4 +/- 3.0 mmol . l(-1) (P < 0.05). Cardiac venous blood how , as measured by retrograde thermodilution, increased from 5.7 +/- 2.9 to 12.6 +/- 5.7 ml . kg(-1). min(-1) (P < 0.01). When FIO2 was reduce d to 0.05, three animals became hypotensive and died. In the second gr oup, hemodilution increased cardiac output and systemic oxygen extract ion ratio (P < 0.01). Cardiac venous blood flow increased from 4.1 +/- 1.7 to 9.8 +/- 5.1 ml . kg(-1). min(-1) (P < 0.01), and cardiac venou s oxygen saturation from 22 +/- 5 to 41 +/- 10% (P < 0.01). During the subsequent hypoxia, cardiac output and DO2SY were maintained until FI O2 = 0.15 (DO2SY = 10.1 +/- 3.3 ml . kg(-1). min(-1)). Cardiac venous blood now was then 18.5 +/- 10.7 ml . kg(-1). min(-1) (P < 0.01), but in spite of this, myocardial lactate production occurred. At FIO2 = 0. 10 (DO2SY = 7.7 +/- 3.0 ml . kg(-1). min(-1)), arterial lactate concen tration increased to 8.5 +/- 2.3 mmol . l(-1) (P < 0.01), and most ani mals became hypotensive. All hemodiluted animals died when FIO2 was de creased to 0.05 (P < 0.01 when compared to animals with normal hematoc rit). Conclusions: Systemic and myocardial lactate production occurred at similar systemic oxygen delivery rates in hemodiluted and nonhemod iluted animals. Mixed venous oxygen saturation may be a less reliable indicator of inadequate oxygen delivery during hemodilution.