We determined the arterial pressure-flow relationship experimentally b
y means of step changes of blood flow in 30 adult patients undergoing
cardiopulmonary bypass (CPB). Anesthesia technique was uniform. CPB wa
s nonpulsatile; hypothermia to 25-28 degrees C, and hemodilution to 18
%-25% hematocrit were used. During stable bypass, mean arterial pressu
re was recorded first with blood flow 2.2 L.min(-1).min(-2). Flow was
then increased to 2.9 L.min(-1).m(-2) for 10 s and reverted to baselin
e for 1 min. Then it was decreased to 1.45 L.min(-1).m(-2) for 10 s, a
nd reverted to baseline for 1 min. Subsequently, it was decreased to 0
.73 L.min(-1).m(-2) for 10 s and then reverted to baseline. line. Simi
lar sets of measurements were repeated after 0.25 mg of phenylephrine
and once the patient was rewarmed. The pressure-flow function was indi
vidually determined by regression, and the critical pressure estimated
by extrapolation to zero flow. All patients had zero-flow critical pr
essure during hypothermia, with a mean value of 21.8 +/- 6.4 mm Hg (ra
nge 8.8-38.9). It increased after 0.25 mg phenylephrine to 25.4 +/- 7.
2 mm Hg (range 12.2-43.9, P < 0.001). During normothermia, critical pr
essure was 21.2 +/- 5 mm Hg (range 13.4-30.9), not significantly diffe
rent from hypothermia. During hypothermia, the slope of the pressure-f
low function (i.e., resistance) was 14.9 +/- 3.5 mm Hg.L-1.min(-1).m(-
2) (range 7.6-22.1). It increased significantly (P < 0.001) after phen
ylephrine, to 19.7 +/- 6.2 mm Hg.L-1.min(-1).m(-2) (range 11.4-40.5),
and returned to 15.4 +/- 3.4 mm Hg.L-1.min(-1).m(-2) (range 10.1-24.2)
during normothermic bypass. Systemic vascular resistance appeared to
vary reciprocally with blood flow, although this finding may represent
a mathematical artifact, which can be avoided by using zero-flow crit
ical pressure in the vascular resistance equation.