Effects of Intravascular Volume Expansion on Cerebral Blood Flow in Patients with Ruptured Cerebral Aneurysms

Neurosurgery ◽  
1987 ◽  
Vol 21 (3) ◽  
pp. 303-309 ◽  
Author(s):  
Iwao Yamakami ◽  
Katsumi Isobe ◽  
Akira Yamaura

Abstract To clarify the effect of intravascular volume expansion on cerebral blood flow (CBF) in patients after subarachnoid hemorrhage (SAH), we performed 55 pairs of regional CBF measurements using the xenon-133 inhalation method before and after volume expansion in 35 patients with ruptured cerebral aneurysms. CBF was calculated as the hemispheric mean value of the initial slope index. To accomplish volume expansion, we transfused 500 ml of 5% human serum albumin in half an hour. After volume expansion with albumin, the hemoglobin value decreased significantly (P < 0.005). Volume expansion did not change the mean arterial blood pressure. During the first 2 weeks after SAH, CBF decreased significantly after volume expansion (P < 0.005). During the 3rd week after SAH and subsequently to the 4th week after SAH, volume expansion produced no change in CBF. In patients with symptomatic vasospasm, CBF decreased significantly after volume expansion (P < 0.005). In patients without symptomatic vasospasm, volume expansion produced no change in CBF. The results of this study suggest that increasing the intravascular volume above normal by volume expansion does not increase CBF or reverse symptomatic vasospasm.

1990 ◽  
Vol 73 (3) ◽  
pp. 368-374 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar

✓ Intravascular volume expansion has been successfully employed to promote blood flow in ischemic brain regions. This effect has been attributed to both decreased blood viscosity and increased cardiac output resulting from volume expansion. The physiological mechanism by which changes in cardiac output would affect cerebral blood flow (CBF), independent of blood pressure variations, is unclear, but impaired cerebral autoregulation is believed to play a role. In order to evaluate the relationship between cardiac output and CBF when autoregulation is either intact or defective, 135 simultaneous measurements of cardiac output (thermodilution method) and CBF (by the 133Xe inhalation or intravenous injection method) were performed in 35 severely head-injured patients. In 81 instances, these measurements were performed after manipulation of blood pressure with phenylephrine or Arfonad (trimethaphan camsylate), or manipulation of blood viscosity with mannitol. Autoregulation was found to be intact in 55 of these cases and defective in 26. A wide range of changes in cardiac output occurred after administration of each drug. No correlation existed between the changes in cardiac output and the changes in CBF, regardless of the status of blood pressure autoregulation. A significant (40%) increase in CBF was found after administration of mannitol when autoregulation was defective. These data support the hypothesis that, within broad limits, CBF is not related to cardiac output, even when autoregulation is impaired. Thus, the effect of intravascular volume expansion appears to be mediated by decreased blood viscosity rather than cardiac output augmentation.


Neurosurgery ◽  
1983 ◽  
Vol 13 (4) ◽  
pp. 394-401 ◽  
Author(s):  
Iwao Yamakami ◽  
Katsumi Isobe ◽  
Akira Yamaura ◽  
Takao Nakamura ◽  
Hiroyasu Makino

Abstract To clarify the relationship of vasospasm to the reduction of cerebral blood flow (CBF) and the delayed ischemic neurological deficit, serial rCBF studies with the use of the xenon-133 inhalation method were conducted in 35 postoperative patients with ruptured intracranial aneurysms. The CBF was calculated as an initial slope index (ISI) derived from the desaturation curve of each head probe, and the hemispheric mean value of the ISI (mean ISI) was calculated in both hemispheres. The mean ISI in the hemisphere ipsilateral to the operation was low compared to that of the contralateral hemisphere. In relation to the presence of vasospasm, angiographic findings were classified into the following five types: diffuse, peripheral, proximal-severe, proximal-mild, and no spasm. Patients with vasospasm of the diffuse, peripheral, and proximal-severe types showed a markedly decreased mean ISI, and vasospasm of the diffuse type caused the greatest degree of reduction. The mean ISI of the patients who developed delayed ischemic neurological deficit (DIND) due to vasospasm was significantly decreased (37.4± 4.6) compared to that of the patients who did not develop DIND (52.2± 5.6). None of 3 cases of no spasm and only 1 of 14 cases of proximal-mild spasm developed DIND. On the other hand, all of 4 cases of diffuse, 2 of 3 cases of peripheral, and 2 of 6 cases of proximal-severe spasm developed DIND. Thus, if these three types of vasospasm are joined together as severe vasospasm, 8 of 13 cases with severe vasospasm developed DIND. These results suggest that severe vasospasm causes a reduction of CBF and that the reduced CBF brings about DIND.


1976 ◽  
Vol 231 (3) ◽  
pp. 929-935 ◽  
Author(s):  
MJ Hernandez-Perez ◽  
DK Anderson

Internal carotid artery blood flow (IFBF) was determined in each of nine Macaca mulatta by means of a flow transducer implanted around an internal carotid artery. The monkeys were lightly anesthetized, intubated, and paralyzed. Normoxia and normocarbia were maintained stable throughout the experiment. ICBF was monitored while mean arterial blood pressure (MABP) was lowered by withdrawal of blood. MABP was kept within the known limits of autoregulation in order not to compromise CBF. Cerebrospinal fluid (CSF) from the cisterna magna was analyzed for pH PCO2, and PO2 before and after a 30-min hypotensive period in which MABP was lowered from 116 +/- 4 to 70 +/- 2 mmHg (mean +/- SE). Corresponding HCO3- concentrations were calculated. The decrease in MABP did not result in a significant reduction in ICBF but elicited a 37% reduction in calculated cerebrovascular resistance, indicating normal autoregulation. Mena CSF pH was not significantly decreased (P less than 0.05); it changed from 7.320 +/- 0.010 to 7.317 +/- 0.010 after the induced hypotensive period. Thus CSF pH does not appear to have a significant role in cerebral blood flow autoregulation.


1986 ◽  
Vol 64 (7) ◽  
pp. 1023-1026 ◽  
Author(s):  
B. Y. Ong ◽  
C. MacIntyre ◽  
D. Bose ◽  
R. J. Palahniuk

The cerebral blood flow of newborn lambs at reduced and elevated arterial blood pressures, induced by intravenous infusion of sodium nitroprusside and phenylephrine hydrochloride as well as blood withdrawal and reinfusion, were compared. Both blood withdrawal and sodium nitroprusside infusion reduced mean arterial pressure from 83 to 60 mmHg (1 mmHg = 133 Pa). Reinfusion of blood increased arterial pressure to 94 mmHg. Phenylephrine hydrochloride infusion increased arterial pressure to 102 mmHg. The cerebral blood flows at corresponding arterial pressures were similar (coefficient of correlation = 0.88, P < 0.01). Cerebral blood flow before and after infusion of phenylephrine hydrochloride and sodium nitroprusside into the brain via the carotid artery did not change. The results indicate that blood-borne phenylephrine hydrochloride and sodium nitroprusside, in concentrations that would alter arterial blood pressure significantly from its resting level, do not change cerebral blood flow directly.


1989 ◽  
Vol 9 (3) ◽  
pp. 422-425 ◽  
Author(s):  
Palle Petersen ◽  
Jens Kastrup ◽  
Regitze Videbæk ◽  
Gudrun Boysen

In nine patients with atrial fibrillation (AF) of <3 months' duration, CBF was measured the day before and after and again 30 days after electrical cardioversion therapy to sinus rhythm. The day before cardioversion therapy, median CBF (expressed as initial slope index 1, ml/100 g · min−1) was 35.8 and the day after it was 37.1. After 30 days in sinus rhythm, CBF was 39.4 (NS), although the end-tidal Pco2 values were lower than the pretreatment values. After correction for changes in end-tidal Pco2, the median CBF had increased significantly from 35.8 to 40.3 on day 1 and to 46.7 on day 30. The reduced CBF during AF could be a contributing factor in the development of cerebrovascular complications in patients with AF.


1990 ◽  
Vol 69 (2) ◽  
pp. 430-433 ◽  
Author(s):  
J. B. Jensen ◽  
A. D. Wright ◽  
N. A. Lassen ◽  
T. C. Harvey ◽  
M. H. Winterborn ◽  
...  

Changes in cerebral blood flow (CBF) were measured using the radioactive xenon technique and were related to the development of acute mountain sickness (AMS). In 12 subjects, ascending from 150 to 3,475 m, CBF was 24% increased at 24 h [45.1 to 55.9 initial slope index (ISI) units] and 4% increased at 6 days (47.1 ISI units). Four subjects had similar increases of CBF when ascending to 3,200 m 3 mo later, indicating the reproducibility of the measurements. In nine subjects, ascending from 3,200 to 4,785-5,430 m, CBF increased to 76.4 ISI units, 53% above estimated sea-level values. CBF and increases in CBF were similar in subjects with or without AMS. In six subjects, CBF was measured before and after therapeutic intervention. At 2 h CBF increased 22% (71.3 to 87.3 ISI units) above pretreatment values in three subjects given 1.5 g acetazolamide, while three subjects given placebo showed no change. Symptoms remained unaltered in all subjects during the 2 h of the study. Overall, the results indicated that increases in CBF were similar in subjects with or without AMS while acetazolamide-provoked increases of CBF in AMS subjects caused no acute change in symptoms. Alterations in CBF cannot be directly implicated in the pathogenesis of AMS.


1987 ◽  
Vol 26 (05) ◽  
pp. 192-197 ◽  
Author(s):  
T. Kreisig ◽  
P. Schmiedek ◽  
G. Leinsinger ◽  
K. Einhäupl ◽  
E. Moser

Using the 133Xe-DSPECT technique, quantitative measurements of regional cerebral blood flow (rCBF) were performed before and after provocation with acetazolamide (Diamox) i. v. in 32 patients without evidence of brain disease (normals). In 6 cases, additional studies were carried out to establish the time of maximal rCBF increase which was found to be approximately 15 min p. i. 1 g of Diamox increases the rCBF from 58 ±8 at rest to 73±5 ml/100 g/min. A Diamox dose of 2 g (9 cases) causes no further rCBF increase. After plotting the rCBF before provocation (rCBFR) and the Diamox-induced rCBF increase (reserve capacity, Δ rCBF) the regression line was Δ rCBF = −0,6 x rCBFR +50 (correlation coefficient: r = −0,77). In normals with relatively low rCBF values at rest, Diamox increases the reserve capacity much more than in normals with high rCBF values before provocation. It can be expected that this concept of measuring rCBF at rest and the reserve capacity will increase the sensitivity of distinguishing patients with reversible cerebrovascular disease (even bilateral) from normals.


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