scholarly journals Cerebral Blood Flow, Metabolism and Mean Arterial Pressure Changes Following Unilateral Internal Carotid Endarterectomy: Cerebral Ischemia and Elevated Systemic Arterial Pressure

Stroke ◽  
1972 ◽  
Vol 3 (4) ◽  
pp. 441-445 ◽  
Author(s):  
F. HAVEN JONES ◽  
MARK L. DYKEN ◽  
ROBERT KING
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Cerebral Ischemia ◽  
Arterial Pressure ◽  
Carotid Endarterectomy ◽  
Internal Carotid ◽  
Systemic Arterial Pressure ◽  
Pressure Changes

scholarly journals Impact of blood pressure changes in cerebral blood perfusion of patients with ischemic Moyamoya disease evaluated by SPECT

2020 ◽  
pp. 0271678X2096745
Author(s):  
Zhao Liming ◽  
Sun Weiliang ◽  
Jia Jia ◽  
Liang Hao ◽  
Liu Yang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Moyamoya Disease ◽  
Emission Computed Tomography ◽  
Study Cohort ◽  
Pressure Changes ◽  
The Impact

Our aim was to determine the impact of targeted blood pressure modifications on cerebral blood flow in ischemic moyamoya disease patients assessed by single-photon emission computed tomography (SPECT). From March to September 2018, we prospectively collected data of 154 moyamoya disease patients and selected 40 patients with ischemic moyamoya disease. All patients underwent in-hospital blood pressure monitoring to determine the mean arterial pressure baseline values. The study cohort was subdivided into two subgroups: (1) Group A or relative high blood pressure (RHBP) with an induced mean arterial pressure 10–20% higher than baseline and (2) Group B or relative low blood pressure (RLBP) including patients with mean arterial pressure 10–20% lower than baseline. All patients underwent initial SPECT study on admission-day, and on the following day, every subgroup underwent a second SPECT study under their respective targeted blood pressure values. In general, RHBP patients showed an increment in perfusion of 10.13% (SD 2.94%), whereas RLBP patients showed a reduction of perfusion of 12.19% (SD 2.68%). Cerebral blood flow of moyamoya disease patients is susceptible to small blood pressure changes, and cerebral autoregulation might be affected due to short dynamic blood pressure modifications.

scholarly journals Impact of Systemic Arterial Pressure, Collateral Vascular Resistance and Degree of Carotid Stenosis on Cerebral Blood Flow, Reserve Blood Flow, Critical Carotid Stenosis, Cerebral Ischemia and Carotid Hemodynamics

2021 ◽  
Author(s):  
Joseph P Archie
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Carotid Artery ◽  
Arterial Pressure ◽  
Carotid Stenosis ◽  
Vascular Resistance ◽  
Systemic Arterial Pressure ◽  
Patient Specific ◽  
Carotid Blood Flow

AbstractIntroductionCarotid artery stenosis related stroke is a major health care concern. Current risk management strategies for patients with asymptomatic carotid stenosis include ultrasound surveillance and occasionally an estimate of cerebral blood flow reserve. Other patient specific hemodynamic variables may be predictive of ischemic stroke risk. This study, based on a cerebral blood flow hemodynamic model, aims to investigate the impact of systemic arterial pressure, collateral vascular resistance and degree of carotid stenosis on cerebral ischemic risk, cerebrovascular blood flow reserve, critical carotid artery stenosis, carotid artery blood flow and carotid stenosis hemodynamics.MethodsThis study uses a three-component (carotid, collateral, brain) energy conservation cerebrovascular fluid mechanics model in combination with the Lassen cerebral blood flow autoregulation model that predicts cerebral blood flow in patients with carotid stenosis. It is a two-phase model, zone A when regional cerebral blood flow is autoregulated at normal values and zone B when cerebral blood flow is below normal and dependent on collateral perfusion pressure. The model solution with carotid artery occlusion defines collateral vascular resistance, with patient specific values calculated from clinical pressure measurements. In addition to cerebral blood flow the model predicts critical stenosis values and carotid and collateral blood flows as a function of systemic arterial pressure and percent diameter stenosis. Carotid stenosis blood flow velocities and energy dissipation are predicted from carotid blood flow solutions.ResultsThe model defines patient specific collateral vascular resistance, cerebral vascular resistance and critical carotid stenosis. It predicts carotid vascular resistance to be non-linearly proportional to area carotid stenosis. Solutions include reserve cerebral blood flow, the carotid and collateral components of cerebral blood flow, criteria for cerebral ischemia and carotid stenosis hemodynamics. Critical carotid stenosis is determined by mean systemic arterial pressure and the Lassen autoregulation threshold cerebral perfusion pressure. Critical stenosis values range from 61% to 76% diameter stenosis when mean systemic arterial pressures are 80mmHg to 120mmHg and the cerebral autoregulation pressure threshold is 50mmHg. When carotid stenosis is less than critical, cerebral blood flow is maintained normal and the ratios of carotid blood flow to collateral blood flow are inversely proportional to the carotid to collateral vascular resistance ratios. At stenosis greater than the critical, carotid blood flow is not adequate to maintain normal cerebral blood flow, cerebral blood flow is primarily collateral flow, all reserve blood flow is collateral and prevention of cerebral ischemia requires adequate collateral flow. Patient specific collateral vascular resistance values less than 1.0 predict normal cerebral blood flow at moderate to severe stenosis. Values greater than 1.0 predicts cerebral ischemia to be dependent on the magnitude of collateral vascular resistance. Systemic arterial pressure is a major determinant of carotid stenosis hemodynamics. Carotid blood flow velocities increase with carotid stenosis and have progressively higher variance depending on collateral blood flow as predicted by collateral vascular resistance. Turbulent flow energy dissipation intensity is similarly inversely proportional to collateral vascular resistance at severe carotid stenosis.ConclusionsCerebral, collateral and carotid blood flow solutions are determined by systemic arterial pressure, collateral vascular resistance and degree of stenosis. Critical carotid stenosis, systemic arterial pressure and collateral vascular resistance are primary determinants of cerebral ischemic risk in patients with significant carotid stenosis.

The Effects of Paco2 on Regional Cerebral Blood Flow and Internal Carotid Arterial Pressure during Carotid Clamping

1971 ◽  
Vol 35 (3) ◽  
pp. 286-300 ◽  
Author(s):  
Gudru n ◽  
H. J. Ladegaard-Pedersen ◽  
H. Henriksen ◽  
L. Olesen ◽  
O. B. Paulson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
Regional Cerebral Blood Flow ◽  
Internal Carotid ◽  
Regional Cerebral Blood ◽  
Carotid Arterial

Direct Cerebral Vasodilatory Effects of Sevoflurane and Isoflurane 

1999 ◽  
Vol 91 (3) ◽  
pp. 677-677 ◽  
Author(s):  
Basil F. Matta ◽  
Karen J. Heath ◽  
Kate Tipping ◽  
Andrew C. Summors
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
End Tidal

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

Effects of hypoxia, hyperoxia and hypercapnia on graded cerebral ischemic responses in rabbits

1992 ◽  
Vol 263 (6) ◽  
pp. H1839-H1846
Author(s):  
T. Takeuchi ◽  
J. Horiuchi ◽  
N. Terada ◽  
M. Nagao ◽  
H. Terajima
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Arterial Pressure ◽  
Internal Carotid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Left Internal Carotid Artery ◽  
Renal Nerve ◽  
Tissue Po2 ◽  
Cerebral Ischemic

This study was designed to determine how several factors interact to modify the cerebral ischemic pressor response (CIR) in anesthetized rabbits. After the carotid sinus and aortic nerves were bilaterally sectioned, blood flow through the left internal carotid artery (ICF), which was surgically restricted as the sole route of blood supply to the brain, was reduced by a servo-controller during ventilation with room air, and 8% and 90% O2 and 2 and 5% CO2 gas mixtures. Blood flow (MBF), tissue PO2, PCO2, and interstitial pH were measured in the rostral ventrolateral medulla. Internal carotid arterial pressure, tissue PO2, and MBF decreased proportionately as ICF decreased in the range from 4 to 0 ml/min. Hypoxia significantly increased the rise in renal nerve activity (RNA) and CIR caused by cerebral ischemia, while hyperoxia significantly decreased them. Hypercapnia had almost no influence on the increases in RNA and mean arterial pressure produced by cerebral ischemia. CIR showed a much higher correlation with changes in tissue PO2 than with the other factors. We examined how these factors interact to modify CIR and found that central hypoxia is the main factor in producing CIR.

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

1985 ◽  
Vol 63 (6) ◽  
pp. 937-943 ◽  
Author(s):  
David J. Boarini ◽  
Neal F. Kassell ◽  
James A. Sprowell ◽  
Julie J. Olin ◽  
Hans C. Coester
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Hypotension ◽  
Content Type ◽  
Blood Flows ◽  
Before And After ◽  
Regional Blood Flows ◽  
Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

POSTCAROTID ENDARTERECTOMY CEREBRAL HYPERPERFUSION CAN BE PREVENTED BY MINIMIZING INTRAOPERATIVE CEREBRAL ISCHEMIA AND STRICT POSTOPERATIVE BLOOD PRESSURE CONTROL UNDER CONTINUOUS SEDATION

Neurosurgery ◽  
2009 ◽  
Vol 64 (3) ◽  
pp. 447-454 ◽  
Author(s):  
Takakazu Kawamata ◽  
Yoshikazu Okada ◽  
Akitsugu Kawashima ◽  
Taku Yoneyama ◽  
Kohji Yamaguchi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Blood Pressure Control ◽  
Internal Carotid ◽  
Pressure Control ◽  
Cerebral Hyperperfusion Syndrome ◽  
Cerebral Hyperperfusion ◽  
Continuous Sedation

Abstract OBJECTIVE Cerebral hyperperfusion syndrome is a major complication after carotid endarterectomy (CEA). We investigated whether our strategy of minimizing intraoperative cerebral ischemia and strict postoperative blood pressure control under continuous sedation prevented postoperative hyperperfusion. METHODS Eighty consecutive patients undergoing CEA were studied. A shunt was used in all patients during CEA. All patients were managed postoperatively under continuous sedation for as long as 48 hours on the basis of the regional cerebral blood flow (rCBF) measured immediately after CEA. Postoperative hyperperfusion was assessed, on the basis of the cerebral blood flow study under sedation (propofol) after CEA, either as a greater than 30% increase in rCBF compared with the contralateral side, or a greater than 100% increase in the corrected rCBF (calculated from percentage reduction of the contralateral rCBF induced by propofol) compared with preoperative values. RESULTS No patient developed cerebral hyperperfusion syndrome. Postoperative hyperperfusion was found at very low rates (2.5% in the middle cerebral artery territory and 1.3% in the anterior cerebral artery territory by definition 1, and 0% in both territories by definition 2). Ratios of regional oxygen saturation after internal carotid artery clamping to preclamp baseline values were greater than 0.9 in 78 of 80 patients, indicating very mild intraoperative cerebral ischemia. Parameters related to cerebral ischemia during CEA, such as regional oxygen saturation, internal carotid artery cross-clamping duration, and stump pressure (index), did not affect the incidence of postoperative hyperperfusion. CONCLUSION The present study suggests that minimizing intraoperative cerebral ischemia using a shunt, followed by strict postoperative blood pressure control under continuous sedation, can prevent post-CEA hyperperfusion.

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