Effects of profound hypotension on cerebral blood flow during surgery for intracranial aneurysms

1981 ◽  
Vol 55 (6) ◽  
pp. 857-864 ◽  
Author(s):  
J. Keith Farrar ◽  
Francis W. Gamache ◽  
Gary G. Ferguson ◽  
John Barker ◽  
George P. Varkey ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Arterial Spasm ◽  
Arterial Blood ◽  
Flow Disturbances ◽  
Group I ◽  
Increased Risk ◽  
Profound Hypotension

✓ The progression of changes in cerebral blood flow (CBF) and neurological status were measured in 12 patients in whom profound hypotension (mean arterial blood pressure (MABP): 30 to 40 mm Hg) was used during intracranial aneurysm surgery. Nine patients (Group I) showed autoregulation of CBF to an MABP of 40 to 50 mm Hg during surgery. None of these patients had arterial spasm preoperatively. Postoperatively, mild flow disturbances were noted at the site of retraction. Three Group I patients developed arterial spasm postoperatively, but there was no associated neurological deterioration. The remaining three patients (Group II) had impaired autoregulation during surgery, and CBF decreased by 35% to 65% at an MABP of 50 mm Hg. Two of these patients had angiography immediately before surgery, and both showed moderate to severe arterial spasm. Relatively severe flow disturbances were noted postoperatively at the site of retraction, and two patients developed ischemic deficits of late onset. Brain retractor pressure and the degree and duration of hypotension were equivalent in the two patient groups. There was no correlation between intraoperative reductions in CBF (to as low as 20 ml/100 gm/min in the unretracted hemisphere) and immediate postoperative neurological deficits. The use of halothane and mannitol and the relatively short duration of the flow reductions were suggested as factors contributing to the protection from ischemia that was observed. Arterial spasm was found to produce hemodynamic instability and reduced CBF, although neurological status was unaffected in the majority of patients. Patients with impaired autoregulation during surgery were at increased risk of delayed ischemic complications postoperatively, and showed characteristic flow disturbances at all three stages of their clinical course.

Cerebral blood flow following induced subarachnoid hemorrhage in the monkey

1972 ◽  
Vol 37 (3) ◽  
pp. 316-324 ◽  
Author(s):  
K. C. Petruk ◽  
G. R. West ◽  
M. R. Marriott ◽  
J. W. McIntyre ◽  
T. R. Overtone ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Neurological Status ◽  
Neurological Deficits ◽  
Content Type ◽  
Arterial Vasospasm ◽  
Experimental Subarachnoid Hemorrhage ◽  
Angiographic Demonstration

✓ The acute effects of experimental subarachnoid hemorrhage on cerebral blood flow were investigated in 14 adult rhesus monkeys injected with fresh autogenous blood through a needle positioned within the subfrontal subarachnoid space. Cerebral blood flow was measured by the xenon133 tissue clearance method before hemorrhage, and afterward at 30-minute intervals for a 3-hour period. Post-anesthetic neurological status was graded according to Botterell's classification. Twelve monkeys showed a significant decrease in cerebral perfusion, eight displayed focal neurological deficits, and four were moribund. There was a correlation between the degree of impaired circulation and the severity of neurological deficit. Four additional monkeys subjected to subarachnoid acidic saline injection showed no reduction in cerebral blood flow. In three animals cerebral perfusion was increased during the first hour after injection. It is suggested that measurement of cerebral blood flow may be a more valuable prognostic indication of cerebral function and survival than the angiographic demonstration of arterial vasospasm.

Pontosubicular Necrosis and Hyperoxemia

PEDIATRICS ◽  
1980 ◽  
Vol 66 (6) ◽  
pp. 840-847
Author(s):  
Mamdouha Ahdab-Barmada ◽  
John Moossy ◽  
Michael Painter
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Developmental Period ◽  
Blood Oxygen ◽  
Neuronal Necrosis ◽  
Arterial Blood ◽  
Group I ◽  
Critical Phase ◽  
Group Ii ◽  
Arterial Blood Oxygen

Pontosubicular necrosis (PSN) is confined to a short perinatal developmental period and is apparently related to asphyxia at birth. Neuronal necrosis with karyorrhexis and proliferative changes in astrocytes are most prominent in the pontine gray matter and subiculum of the hippocampus. We have observed a striking association of PSN in neonates with high arterial blood oxygen (Po2) levels during the first week of life. All autopsies performed on neonates in 1977 at Magee-Womens Hospital (University Health Center of Pittsburgh) were reviewed, and all 64 neonates who survived long enough to have multiple Po2 determinations were studied. All had severe hypoxia, respiratory distress, and/or apnea. Twenty-seven (group I) did not have Po2 levels higher than 150 torr whereas 37 (group II) had Po2 levels higher than 150 torr for a sustained period. PSN was not seen in group I; it was prominent in group II. PSN was most severe between the gestational ages of 26 to 36 weeks. Hyperoxemia may decrease cerebral blood flow selectively at this critical phase of development or there may be a greater sensitivity to the toxic action of high blood oxygen levels in the presence of acidosis and hypoxia. A combination of these factors seems most probable.

scholarly journals Examination of Potential Mechanisms in the Enhancement of Cerebral Blood Flow by Hypoglycemia and Pharmacological Doses of Deoxyglucose

1997 ◽  
Vol 17 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Naoaki Horinaka ◽  
Nicole Artz ◽  
Jane Jehle ◽  
Shinichi Takahashi ◽  
Charles Kennedy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Plasma Glucose ◽  
Plasma Lactate ◽  
Insulin Hypoglycemia ◽  
Glucose Levels ◽  
Arterial Blood ◽  
Arterial Plasma

Cerebral blood flow (CBF) rises when the glucose supply to the brain is limited by hypoglycemia or glucose metabolism is inhibited by pharmacological doses of 2-deoxyglucose (DG). The present studies in unanesthetized rats with insulin-induced hypoglycemia show that the increases in CBF, measured with the [14C]iodoantipyrine method, are relatively small until arterial plasma glucose levels fall to 2.5 to 3.0 m M, at which point CBF rises sharply. A direct effect of insulin on CBF was excluded; insulin administered under euglycemic conditions maintained by glucose injections had no effects on CBF. Insulin administration raised plasma lactate levels and decreased plasma K+ and HCO3– concentrations and arterial pH. These could not, however, be related to the increased CBF because insulin under euglycemic conditions had similar effects without affecting CBF; furthermore, the inhibition of brain glucose metabolism with pharmacological doses (200 mg/kg intravenously) of DG increased CBF, just like insulin hypoglycemia, without altering plasma lactate and K+ levels and arterial blood gas tensions and pH. Nitric oxide also does not appear to mediate the increases in CBF. Chronic blockade of nitric oxide synthase activity by twice daily i.p. injections of NG-nitro-L-arginine methyl ester for 4 days or acutely by a single i.v. injection raised arterial blood pressure and lowered CBF in normoglycemic, hypoglycemic, and DG-treated rats but did not significantly reduce the increases in CBF due to insulin-induced hypoglycemia (arterial plasma glucose levels, 2.5-3 m M) or pharmacological doses of deoxyglucose.

scholarly journals Cerebral blood flow autoregulation in ischemic heart failure

2017 ◽  
Vol 312 (1) ◽  
pp. R108-R113 ◽  
Author(s):  
J. R. Caldas ◽  
R. B. Panerai ◽  
V. J. Haunton ◽  
J. P. Almeida ◽  
G. S. R. Ferreira ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Healthy Volunteers ◽  
Neurological Complications ◽  
Ischemic Heart ◽  
Step Response ◽  
Ischemic Heart Failure ◽  
Arterial Blood ◽  
End Tidal

Patients with ischemic heart failure (iHF) have a high risk of neurological complications such as cognitive impairment and stroke. We hypothesized that iHF patients have a higher incidence of impaired dynamic cerebral autoregulation (dCA). Adult patients with iHF and healthy volunteers were included. Cerebral blood flow velocity (CBFV, transcranial Doppler, middle cerebral artery), end-tidal CO2 (capnography), and arterial blood pressure (Finometer) were continuously recorded supine for 5 min at rest. Autoregulation index (ARI) was estimated from the CBFV step response derived by transfer function analysis using standard template curves. Fifty-two iHF patients and 54 age-, gender-, and BP-matched healthy volunteers were studied. Echocardiogram ejection fraction was 40 (20–45) % in iHF group. iHF patients compared with control subjects had reduced end-tidal CO2 (34.1 ± 3.7 vs. 38.3 ± 4.0 mmHg, P < 0.001) and lower ARI values (5.1 ± 1.6 vs. 5.9 ± 1.0, P = 0.012). ARI <4, suggestive of impaired CA, was more common in iHF patients (28.8 vs. 7.4%, P = 0.004). These results confirm that iHF patients are more likely to have impaired dCA compared with age-matched controls. The relationship between impaired dCA and neurological complications in iHF patients deserves further investigation.

Diurnal variation in time to presyncope and associated circulatory changes during a controlled orthostatic challenge

2010 ◽  
Vol 299 (1) ◽  
pp. R55-R61 ◽  
Author(s):  
N. C. S. Lewis ◽  
G. Atkinson ◽  
S. J. E. Lucas ◽  
E. J. M. Grant ◽  
H. Jones ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diurnal Variation ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Cerebral Blood Flow Velocity ◽  
Orthostatic Challenge ◽  
Arterial Blood ◽  
Neurally Mediated Syncope

Epidemiological data indicate that the risk of neurally mediated syncope is substantially higher in the morning. Syncope is precipitated by cerebral hypoperfusion, yet no chronobiological experiment has been undertaken to examine whether the major circulatory factors, which influence perfusion, show diurnal variation during a controlled orthostatic challenge. Therefore, we examined the diurnal variation in orthostatic tolerance and circulatory function measured at baseline and at presyncope. In a repeated-measures experiment, conducted at 0600 and 1600, 17 normotensive volunteers, aged 26 ± 4 yr (mean ± SD), rested supine at baseline and then underwent a 60° head-up tilt with 5-min incremental stages of lower body negative pressure until standardized symptoms of presyncope were apparent. Pretest hydration status was similar at both times of day. Continuous beat-to-beat measurements of cerebral blood flow velocity, blood pressure, heart rate, stroke volume, cardiac output, and end-tidal Pco2 were obtained. At baseline, mean cerebral blood flow velocity was 9 ± 2 cm/s (15%) lower in the morning than the afternoon ( P < 0.0001). The mean time to presyncope was shorter in the morning than in the afternoon (27.2 ± 10.5 min vs. 33.1 ± 7.9 min; 95% CI: 0.4 to 11.4 min, P = 0.01). All measurements made at presyncope did not show diurnal variation ( P > 0.05), but the changes over time (from baseline to presyncope time) in arterial blood pressure, estimated peripheral vascular resistance, and α-index baroreflex sensitivity were greater during the morning tests ( P < 0.05). These data indicate that tolerance to an incremental orthostatic challenge is markedly reduced in the morning due to diurnal variations in the time-based decline in blood pressure and the initial cerebral blood flow velocity “reserve” rather than the circulatory status at eventual presyncope. Such information may be used to help identify individuals who are particularly prone to orthostatic intolerance in the morning.

Surfactant Therapy and Intracranial Hemorrhage: Review of the Literature and Results of New Analyses

PEDIATRICS ◽  
1993 ◽  
Vol 92 (6) ◽  
pp. 775-786
Author(s):  
J. Harry Gunkel ◽  
Phillip L.C. Banks
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Birth Weight ◽  
Intracranial Hemorrhage ◽  
Incidence Rates ◽  
Surfactant Therapy ◽  
Controlled Study ◽  
Hemodynamic Changes ◽  
Increased Risk ◽  
Risk Of Hemorrhage

Background and objective. Surfactant replacement is a powerful therapy for newborns with respiratory distress syndrome, but limited observations suggest that alterations of cerebral blood flow can accompany the use of several available surfactants. An early European multicenter controlled study with beractant demonstrated an increased rate of intracranial hemorrhage in treated patients. Nine additional controlled studies were subsequently performed and included follow-up evaluations through 2 years adjusted age. This clinical experience provided a database of approximately 1700 infants to examine retrospectively for any relationship between surfactant therapy and intracranial hemorrhage. Methods. Cumulative incidence rates, hazard ratios, and 95% confidence intervals for intracranial hemorrhage were computed for each study and for appropriately pooled studies of similar design. Where an association between surfactant and the risk of intracranial hemorrhage was found, additional analyses were performed to attempt to identify intermediate physiologic events that might link administration of surfactant to the occurrence of intracranial hemorrhage. These analyses were guided by literature reports of hemodynamic changes observed in association with surfactant therapy. Results. During the controlled studies with beractant, treated newborns of 600 to 750 g birth weight were at higher risk for grades I and II intracranial hemorrhage than control newborns. There was no increased risk for grades III and IV hemorrhage among these newborns, nor was there increased risk of hemorrhage among any other patient groups. This finding did not result in increased morbidity for the affected patients; at 2 years adjusted age, they were not different from the control infants of 600 to 750 g birth weight. Retrospective examination of the database could not pinpoint the mechanism behind the finding, but it might have been related to changes in cerebral blood flow after surfactant uncompensated by ventilator management of oxygenation and ventilation. Conclusion. Surfactant therapy may set in motion hemodynamic changes that could predispose to intracranial hemorrhage in certain circumstances, but this can probably be compensated by careful management of oxygenation and ventilation. A relationship between surfactant therapy and intracranial hemorrhage is probably not isolated to any particular surfactant preparation or method of delivery; studies comparing surfactants have shown no differences in rates of intracranial hemorrhage.

Carotid Arterial Blood Flow in the Ovine Fetus as a Continuous Measure of Cerebral Blood Flow

1996 ◽  
Vol 3 (2) ◽  
pp. 60-65 ◽  
Author(s):  
Robert Gratton ◽  
Lesley Carmichael ◽  
Jacobus Homan ◽  
Bryan Richardson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Flow ◽  
Continuous Measure ◽  
Arterial Blood ◽  
Ovine Fetus ◽  
Carotid Arterial

Effect of the Ace Inhibitor Ceronapril on Cerebral Blood flow in Hypertensive Patients

1996 ◽  
Vol 30 (6) ◽  
pp. 578-582 ◽  
Author(s):  
Neal R Cutler ◽  
John J Sramek ◽  
Azucena Luna ◽  
Ismael Mena ◽  
Eric P Brass ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diastolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Combined Therapy ◽  
Arterial Blood

Objective To assess the effect of the angiotensin-converting enzyme inhibitor ceronapril on cerebral blood flow (CBF) in patients with moderate hypertension. Design Patients received chlorthalidone 25 mg for 4 weeks, and if diastolic blood pressure remained in the range of 100–115 mm Hg, they were given titrated doses of ceronapril (10–40 mg/d based on blood pressure response) in addition to chlorthalidone for 9 weeks. Setting Outpatient research clinic. Subjects Eligible patients had moderate essential hypertension (diastolic blood pressure 100–115 mm Hg) assessed when the patients were receiving no medications. Thirteen patients were entered into the study; 1 withdrew for reasons unrelated to the study drug. Twelve patients (11 men, 1 woman; mean age 52 y) completed the study. Intervention Ceronapril, given with chlorthalidone. Main Outcome Measures CBF measurements were taken at the start and end of ceronapril therapy using intravenous 133Xe; blood pressures were determined weekly. Results Mean arterial blood pressure decreased from 130 ± 4 to 120 ±7 mm Hg after 4 weeks of chlorthalidone administration, and fell further to 108 ± 8 mm Hg after an additional 9 weeks of combined chlorthalidone-ceronapril therapy (p < 0.05). CBF fell from 44 ± 15 to 34 ± 5 mL/min/100 g during the 9 weeks of combined therapy (p = 0.05). No adverse effects consistent with decreased CBF were observed. The decrease in CBF was not linearly correlated with the change in systemic blood pressure, but was strongly correlated (r = –0.937; p < 0.001) with the initial CBF. Conclusions The decrease in mean arterial blood pressure was not associated with a decrease in CBF. Patients with high CBF may be predisposed to a decrease in CBF when treated with ceronapril and chlorthalidone.

Serial measurement of regional cerebral blood flow in patients with SAH using 133Xe inhalation and emission computerized tomography

1984 ◽  
Vol 60 (5) ◽  
pp. 916-922 ◽  
Author(s):  
Bruce Mickey ◽  
Sissel Vorstrup ◽  
Bo Voldby ◽  
Helle Lindewald ◽  
Aage Harmsen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Computerized Tomography ◽  
Cerebral Arteries ◽  
Three Dimensional ◽  
Neurological Deficits ◽  
Content Type ◽  
Serial Measurement ◽  
Regional Flow ◽  
Delayed Neurological Deterioration

✓ A noninvasive three-dimensional method for measuring cerebral blood flow (CBF), xenon-133 inhalation and emission computerized tomography, was used to investigate the CBF changes accompanying delayed neurological deterioration following subarachnoid hemorrhage (SAH). A total of 67 measurements were performed on 20 patients in Hunt and Hess' clinical Grades I to III in the first 21 days post SAH. Five patients with normal CBF tomograms on admission developed delayed neurological deficits in the 2nd week after hemorrhage, at which time repeat CBF tomograms in four patients revealed large areas of well defined regional flow decrease in the vascular territories of the anterior or middle cerebral arteries. Severe vasospasm was noted in three of these patients in whom arteriography was performed in the 2nd week post SAH. Diffuse bihemispheric CBF decreases were noted later in the course of delayed neurological deficits; however, measurements obtained soon after the onset of focal symptoms suggest that the only CBF decreases directly produced by vasospasm in Grade III patients are regional changes.

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