H. Schou et al., CIRCULATORY EFFECTS OF HYPOXIA, ACUTE NORMOVOLEMIC HEMODILUTION, AND THEIR COMBINATION IN ANESTHETIZED PIGS, Anesthesiology, 84(6), 1996, pp. 1443-1454
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.