Ba. Mckinley et Bd. Butler, Comparison of skeletal muscle P-O2, P-CO2, and pH with gastric tonometric P-CO2 and pH in hemorrhagic shock, CRIT CARE M, 27(9), 1999, pp. 1869-1877
Objectives: To monitor Po-2, Pco(2), and pH in the interstitium of skeletal
muscle (Pmo(2), Pmco(2), and pHm) during hemorrhage, shock, acid resuscita
tion using fiber-optic sensors and to compare Pco(2) and pH in the intersti
tium of gastric mucosa (Prco(2) and pHi) obtained using gastric CO, tonomet
ry.
Design: Prospective, controlled observational study in an acute experimenta
l preparation.
Setting: Physiology laboratory in a university medical school.
Subjects: Nine mongrel dogs (20 to 35 kg).
Interventions: Anesthesia was induced with pentobarbital (25 mg/kg iv) and
maintained (10 mg/hr) after hemorrhagic shock. Mechanical ventilation was e
stablished to maintain baseline Paco(2) approximate to 35 torr. Arterial, v
enous, and pulmonary artery catheters were placed. Blood flow probes were p
laced around the right femoral artery and vein. A probe (0.5 mm in diameter
) with fiber-optic Po-2, Pco(2), and pH sensors was placed percutaneously i
n the adductor muscle of the right thigh. A gastric tonometer catheter was
placed in the stomach lumen. After baseline data collection, controlled hem
orrhage to mean arterial pressure (MAP) of 45 to 50 mm Hg was maintained fo
r 1 hr. Shed blood was then reinfused. Blood gas, hemodynamic, and gastric
tonometric data were collected during shock and reinfusion at 30-min interv
als and hourly after reinfusion for 4 hrs. Normothermia was maintained.
Measurements and Main Results: Pmo(2) decreased rapidly from 42 +/- 13 torr
(mean +/- so) to 13 +/- 9 torr within 15 mins and to 6 +/- 4 torr within 3
0 mins of MAP reaching 45 mm Hg, and it recovered to baseline with reinfusi
on. pHm decreased gradually from 7.23 +/- 0.09 to 6.89 +/- 0.25 during the
1-hr shock period and increased slowly toward baseline after reinfusion. pH
i decreased from 7.43 +/- 0.14 to 6.91 +/- 0.23, and on average it returned
to baseline 2 hrs after reinfusion. Pmco(2) increased from 50 +/- 12 to 11
3 +/- 49 torr, increased further to 124 +/- 73 torr during reinfusion, and
returned slowly toward baseline after reinfusion. Prco(2) increased from 35
+/- 8 to 60 +/- 19 torr and returned to baseline within 15 mins after rein
fusion. During shock and reinfusion, oxygen delivery, mixed venous Po-2, mi
xed venous oxygen saturation, and Pmo(2) responded with similar time course
s. After reinfusion, on average, Pmo(2) exceeded baseline Pmo(2) and mixed
venous Po-2, and oxygen availability exceeded demand, suggesting an oxygen
consumption defect. On average, Pmco(2) and pHm did not return to baseline
values 4 hrs after reinfusion, suggesting the persistence of anaerobic meta
bolic effects in skeletal muscle beyond the relatively short time that is r
equired to reestablish baseline MAP, blood flow rates, oxygen delivery, Prc
o(2), and pHi.
Conclusions: Pmo(2), Pmco(2), and pHm, monitored simultaneously using fiber
-optic sensors in a single, small probe placed percutaneously, appear to in
dicate greater severity of shock and more prolonged resuscitation than conv
entional systemic or gastric tonometric variables.