BACKGROUND: Arterial vasospasm after subarachnoid hemorrhage may cause cerebral ischemia. Treatment with hemodilution, reducing blood viscosity, and hypervolemia, increasing cardiac performance and distending the vasospastic artery, are clinically established methods to improve blood flow through the vasospastic arterial bed. METHOD: Eight patients with transcranial Doppler verified vasospasm after subarachnoid hemorrhage were investigated with global (two-dimensional (133)Xenon) and regional (three-dimensional (99 m)Tc-HMPAO) cerebral blood flow (CBF) measurements, before and after 1/iso- and 2/hypervolemic hemodilution. Hematocrit was reduced to 0.28 from 0.36. Hypervolemia was achieved by increasing blood volume by 1100 ml. FINDINGS: Isovolemic hemodilution increased global cerebral blood flow from 52.25+/-10.12 to 58.56+/-11.73 ml * 100 g(-1) * min(-1) (p<0.05), but after hypervolemic hemodilution CBF returned to 51.38+/-11.34 ml * 100 g(-1) * min(-1). Global cerebral delivery rate of oxygen (CDRO(2)) decreased from 7.94+/-1.92 to 6.98+/-1.66 ml * 100 g(-1) * min(-1) (p<0.001) during isovolemic hemodilution and remained reduced, 6.77+/-1.60 ml * 100 g(-1) * min(-1) (p<0.001), after the hypervolemic hemodilution. As a test of the hemodilution effect on regional CDRO(2) an ischemic threshold was defined as the maximal amount of oxygen transported by a CBF of 10 ml * 100 g(-1) * min(-1) at a Hb 140 g/l which corresponds to a CDRO(2) of 1.83 ml * 100 g(-1) * min(-1). The brain volume with a CDRO(2) exceeding the ichemic threshold was 1300+/-236 ml before intervention. After isovolemic hemodilution the non-ischemic brain volume was reduced to 1206+/-341 (p<0,003). After hypervolemic hemodilution the non-ischemic brain volume remained reduced at 1228+/-347 ml (p<0.05). INTERPRETATION: The present study of controlled isovolemic hemodilution demonstrated increased global CBF, but there was a pronounced reduction in oxygen delivery capacity. Both CBF and CDRO(2) remained decreased during further hypervolemic hemodilution. We conclude that hemodilution to hematocrit 0.28 is not beneficial for patients with cerebral vasospasm after SAH.
BACKGROUND: Arterial vasospasm after subarachnoid hemorrhage may cause cerebral ischemia. Treatment with hemodilution, reducing blood viscosity, and hypervolemia, increasing cardiac performance and distending the vasospastic artery, are clinically established methods to improve blood flow through the vasospastic arterial bed. METHOD: Eight patients with transcranial Doppler verified vasospasm after subarachnoid hemorrhage were investigated with global (two-dimensional (133)Xenon) and regional (three-dimensional (99 m)Tc-HMPAO) cerebral blood flow (CBF) measurements, before and after 1/iso- and 2/hypervolemic hemodilution. Hematocrit was reduced to 0.28 from 0.36. Hypervolemia was achieved by increasing blood volume by 1100 ml. FINDINGS: Isovolemic hemodilution increased global cerebral blood flow from 52.25+/-10.12 to 58.56+/-11.73 ml * 100 g(-1) * min(-1) (p<0.05), but after hypervolemic hemodilution CBF returned to 51.38+/-11.34 ml * 100 g(-1) * min(-1). Global cerebral delivery rate of oxygen (CDRO(2)) decreased from 7.94+/-1.92 to 6.98+/-1.66 ml * 100 g(-1) * min(-1) (p<0.001) during isovolemic hemodilution and remained reduced, 6.77+/-1.60 ml * 100 g(-1) * min(-1) (p<0.001), after the hypervolemic hemodilution. As a test of the hemodilution effect on regional CDRO(2) an ischemic threshold was defined as the maximal amount of oxygen transported by a CBF of 10 ml * 100 g(-1) * min(-1) at a Hb 140 g/l which corresponds to a CDRO(2) of 1.83 ml * 100 g(-1) * min(-1). The brain volume with a CDRO(2) exceeding the ichemic threshold was 1300+/-236 ml before intervention. After isovolemic hemodilution the non-ischemic brain volume was reduced to 1206+/-341 (p<0,003). After hypervolemic hemodilution the non-ischemic brain volume remained reduced at 1228+/-347 ml (p<0.05). INTERPRETATION: The present study of controlled isovolemic hemodilution demonstrated increased global CBF, but there was a pronounced reduction in oxygen delivery capacity. Both CBF and CDRO(2) remained decreased during further hypervolemic hemodilution. We conclude that hemodilution to hematocrit 0.28 is not beneficial for patients with cerebral vasospasm after SAH.
Authors: Khalil M Yousef; Jeffrey R Balzer; Catherine M Bender; Leslie A Hoffman; Samuel M Poloyac; Feifei Ye; Paula R Sherwood Journal: J Neurosci Nurs Date: 2015-08 Impact factor: 1.230
Authors: Rajat Dhar; Allyson R Zazulia; Tom O Videen; Gregory J Zipfel; Colin P Derdeyn; Michael N Diringer Journal: Stroke Date: 2009-07-23 Impact factor: 7.914