Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation

1990 ◽  
Vol 73 (3) ◽  
pp. 368-374 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Volume Expansion ◽  
Physiological Mechanism ◽  
Brain Regions ◽  
Intravascular Volume ◽  
Wide Range

✓ 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.

Cerebral Blood Flow during Dynamic Exercise Correlates with Blood Pressure in Autonomic Brain Regions

2017 ◽  
Vol 49 (5S) ◽  
pp. 824
Author(s):  
Mikio Hiura ◽  
Akitaka Muta ◽  
Muneyuki Sakata ◽  
Satoshi Wagatsuma ◽  
Tetsurou Tago ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Regions ◽  
Dynamic Exercise

Effect of hypoxia and hypercapnia on neurohypophyseal blood flow

1986 ◽  
Vol 250 (1) ◽  
pp. H7-H15
Author(s):  
D. F. Hanley ◽  
D. A. Wilson ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Brain Regions ◽  
Regulatory Mechanisms ◽  
Similar Increase ◽  
Regional Cerebral Blood ◽  
Pressure Controlled

Neurohypophyseal blood flow responses to hypoxia and hypercapnia were studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either decreasing O2 tension (hypoxic hypoxia, HH) or by increasing carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2 tension. In all animals HH and COH resulted in similar increases in total cerebral blood flow (239 and 300%, respectively). Regional cerebral blood flow showed a similar increase for all brain regions except the neurohypophysis (NH). The NH increased its blood flow with HH (approximately 320% of control) but was unchanged with COH (117% of control). The responsiveness of NH blood vessels was tested under conditions of hypercapnia (10% CO2) and HH with blood pressure controlled by concurrent hemorrhage. The response of NH vessels to altered arterial O2 tension occurs independently of blood pressure. Systemic [H+] or CO2 tension produce only small changes in NH blood flow. These data suggest that hypoxic and hypercapnic regulatory mechanisms for the NH are different from those of other brain regions. The precise mechanism by which the NH hypoxic response occurs remains unclear, but our data suggest an important role for systemic arterial O2 tension and chemoreceptors.

scholarly journals Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike.

Stroke ◽  
1986 ◽  
Vol 17 (1) ◽  
pp. 44-48 ◽  
Author(s):  
J P Muizelaar ◽  
E P Wei ◽  
H A Kontos ◽  
D P Becker
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Viscosity

Influence of blood pressure and cardiac output on cerebral blood flow and autoregulation in acute stroke measured by TCD

1996 ◽  
Vol 3 (6) ◽  
pp. 539-543 ◽  
Author(s):  
J. Treib ◽  
A. Haass ◽  
D. Koch ◽  
M.T. Grauer ◽  
M. Stoll ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Acute Stroke

scholarly journals Local Cerebral Blood Flow and the Electrocorticogram during Sodium Nitroprusside Hypotension

1978 ◽  
Vol 6 (4) ◽  
pp. 290-296 ◽  
Author(s):  
C. L. Miller ◽  
D. G. Lampard ◽  
R. I. Griffiths ◽  
W. A. Brown
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Sodium Nitroprusside ◽  
Large Range ◽  
Local Cerebral Blood Flow ◽  
Hydrogen Electrode ◽  
Electrode Technique

Changes in local cerebral blood flow during sodium nitroprusside hypotension were measured using the hydrogen electrode technique. At mean arterial pressures from 90% to 50% of control values, local cerebral blood flow showed a significant decrease by 20%. When blood pressure was reduced below 50%, the local cerebral blood flow increased significantly and approached control levels. It is suggested that the flow increase may be due to local hypoxia. Associated with this increase were electrocorticogram changes indicative of hypoxia. The significant decrease in mean local cerebral blood flow and the large range of flows seen during mild hypotension indicate that autoregulation is impaired. During hypotension, intracranial pressure increased by, at most, 3 mm Hg. Cardiac output was usually unaffected and was never decreased by more than 20%.

scholarly journals Relative contributions of systemic hemodynamic variables to cerebral autoregulation during orthostatic stress

2018 ◽  
Vol 124 (2) ◽  
pp. 321-329 ◽  
Author(s):  
Hisao Yoshida ◽  
Jason W. Hamner ◽  
Keita Ishibashi ◽  
Can Ozan Tan
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Pressure Fluctuations ◽  
Dynamic Changes ◽  
Systemic Hemodynamic ◽  
Hemodynamic Variables ◽  
Central Volume ◽  
The Impact

Postural changes impair the ability of the cerebrovasculature to buffer against dynamic pressure fluctuations, but the mechanisms underlying this impairment have not been elucidated. We hypothesized that autoregulatory impairment may reflect the impact of static central volume shifts on hemodynamic factors other than arterial pressure (AP). In 14 young volunteers, we assessed the relation of fluctuations in cerebral blood flow (CBF) to those in AP, cardiac output, and CO2, during oscillatory lower body pressure (LBP) (±20 mmHg at 0.01 and 0.06 Hz) at three static levels (−20, 0, and +20 mmHg). Static and dynamic changes in AP, cardiac output, and CO2 explained over 70% of the variation in CBF fluctuations. However, their contributions were different across frequencies and levels: dynamic AP changes explained a substantial proportion of the variation in faster CBF fluctuations (partial R2 = 0.75, standardized β = 0.83, P < 0.01), whereas those in CO2 explained the largest portion of the variation in slow fluctuations (partial R2 = 0.43, β = 0.51, P < 0.01). There was, however, a major contribution of slow dynamic AP changes during negative (β = 0.43) but not neutral (β = 0.05) or positive (β = −0.07) LBP. This highlights the differences in contributions of systemic variables to dynamic and static autoregulation and has important implications for understanding orthostatic intolerance. NEW & NOTEWORTHY While fluctuations in blood pressure drive faster fluctuations in cerebral blood flow, overall level of CO2 and the magnitude of its fluctuations, along with cardiac output, determine the magnitude of slow ones. The effect of slow blood pressure fluctuations on cerebrovascular responses becomes apparent only during pronounced central volume shifts (such as when standing). This underlines distinct but interacting contributions of static and dynamic changes in systemic hemodynamic variables to the cerebrovascular regulation.

Volume Expansion in Focal Cerebral Ischemia: The Effect of Cardiac Output on Local Cerebral Blood Flow

Neurosurgery ◽  
1982 ◽  
Vol 29 (CN_suppl_1) ◽  
pp. 40-50 ◽  
Author(s):  
Ted S. Keller ◽  
John E. McGillicuddy ◽  
Virginia A. Labond ◽  
Glenn W. Kindt
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Volume Expansion ◽  
Focal Cerebral Ischemia ◽  
Local Cerebral Blood Flow
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