scholarly journals Intracranial pressure influences the level of sympathetic tone

2018 ◽  
Vol 315 (5) ◽  
pp. R1049-R1053 ◽  
Author(s):  
Sarah-Jane Guild ◽  
Utkarsh A. Saxena ◽  
Fiona D. McBryde ◽  
Simon C. Malpas ◽  
Rohit Ramchandra
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Nervous System ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Sympathetic Nervous ◽  
Renal Sympathetic

Sympathetic overdrive is associated with many diseases, but its origin remains an enigma. An emerging hypothesis in the development of cardiovascular disease is that the brain puts the utmost priority on maintaining its own blood supply; even if this comes at the “cost” of high blood pressure to the rest of the body. A critical step in making a causative link between reduced brain blood flow and cardiovascular disease is how changes in cerebral perfusion affect the sympathetic nervous system. A direct link between decreases in cerebral perfusion pressure and sympathetic tone generation in a conscious large animal has not been shown. We hypothesized that there is a novel control pathway between physiological levels of intracranial pressure (ICP) and blood pressure via the sympathetic nervous system. Intracerebroventricular infusion of saline produced a ramped increase in ICP of up to 20 mmHg over a 30-min infusion period (baseline 4.0 ± 1.1 mmHg). The ICP increase was matched by an increase in mean arterial pressure such that cerebral perfusion pressure remained constant. Direct recordings of renal sympathetic nerve activity indicated that sympathetic drive increased with increasing ICP. Ganglionic blockade, by hexamethonium, preventing sympathetic transmission, abolished the increase in arterial pressure in response to increased ICP and was associated with a significant decrease in cerebral perfusion pressure. This is the first study to show that physiological elevations in ICP regulate renal sympathetic activity in conscious animals. We have demonstrated a novel physiological mechanism linking ICP levels with sympathetic discharge via a possible novel intracranial baroreflex.

Attenuation of Haemodynamic Response to Placement of Mayfield Skull Pin Head Holder - Comparison of Dexmedetomidine Versus Propofol Infusion - A Randomized Interventional Trial Done in a Tertiary Centre in Central Kerala

2021 ◽  
Vol 8 (29) ◽  
pp. 2639-2643
Author(s):  
Sruthy Unni ◽  
Ranju Sebastian ◽  
Elizabeth Joseph ◽  
Remani Kelan Kamalakshi ◽  
Jamsheena Muthira Parambath
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Stress Response ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurosurgical Procedures ◽  
Sympathetic Nervous ◽  
The Brain ◽  
Group 1

BACKGROUND Anaesthesia for neurosurgery requires special considerations. The brain is enclosed in a rigid cranium, so the rise in intracranial pressure (ICP) which impairs cerebral perfusion pressure (CPP), results in irrepairable damage to various vital areas in the brain. Stable head position is required in long neurosurgical procedures. This is obtained with the use of clamps which fix the head rigidly. This is done usually under general anaesthesia because it produces intense painful stimuli leading to stimulation of sympathetic nervous system which in turn causes release of vasoconstrictive agents. This can impair perfusion in all organ systems. The increase in blood pressure due to sympathetic nervous system causes increase in blood flow. This causes increases in intracranial pressure which result in reduction in cerebral perfusion pressure once the auto regulatory limits are exceeded. We compared the effects of dexmedetomidine 1 µgm/kg and propofol 100 µgm/kg given as infusion over a period of 10 minutes before the induction of anaesthesia and continued till 5 minutes after pinning to attenuate the stress response while cranial pinning. In this study, we wanted to compare the effects of dexmedetomidine and propofol as infusion to attenuate the stress response while cranial pinning in patients undergoing neurosurgical procedures. METHODS This is a randomized interventional trial. Patients were divided into 2 groups of 20 each. Group 1 receiving dexmedetomidine and group 2 receiving propofol, both drugs given as infusion. Haemodynamic variables were monitored before and after cranial pinning. Data was analysed using IBM statistical package for social sciences (SPSS) statistics. The parameters recorded were analysed with the help of a statistician. RESULTS The two groups were comparable in demographic data. Incidence of tachycardia between group 1 and 2 showed that tachycardia to pinning was better controlled with propofol than dexmedetomidine (P < 0.05) which is statistically significant. There is no statistically significant difference in blood pressure values between group 1 and 2 after pinning. CONCLUSIONS From our study, we came to a conclusion that propofol was superior to dexmedetomidine in attenuating the heart rate response to cranial pinning. The effect of propofol and dexmedetomidine was comparable in attenuating the blood pressure response to cranial pinning. KEYWORDS Cranial Pinning, Dexmedetomidine, Propofol

Sevoflurane Increases Lumbar Cerebrospinal Fluid Pressure in Normocapnic Patients Undergoing Transsphenoidal Hypophysectomy 

1999 ◽  
Vol 91 (1) ◽  
pp. 127-130 ◽  
Author(s):  
Pekka Talke ◽  
James E. Caldwell ◽  
Charles A. Richardson
Keyword(s):  
Blood Pressure ◽  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Systolic Blood Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Csf Pressure ◽  
Sevoflurane Group ◽  
Lumbar Cerebrospinal Fluid

Background The data on the effect of sevoflurane on intracranial pressure in humans are still limited and inconclusive. The authors hypothesized that sevoflurane would increase intracranial pressure as compared to propofoL METHODS: In 20 patients with no evidence of mass effect undergoing transsphenoidal hypophysectomy, anesthesia was induced with intravenous fentanyl and propofol and maintained with 70% nitrous oxide in oxygen and a continuous propofol infusion, 100 microg x kg(-1) x min(-1). The authors assigned patients to two groups randomized to receive only continued propofol infusion (n = 10) or sevoflurane (n = 10) for 20 min. During the 20-min study period, each patient in the sevoflurane group received, in random order, two concentrations (0.5 times the minimum alveolar concentration [MAC] and 1.0 MAC end-tidal) of sevoflurane for 10 min each. The authors continuously monitored lumbar cerebrospinal fluid (CSF) pressure, blood pressure, heart rate, and anesthetic concentrations. Results Lumbar CSF pressure increased by 2+/-2 mmHg (mean+/-SD) with both 0.5 MAC and 1 MAC of sevoflurane. Cerebral perfusion pressure decreased by 11+/-5 mmHg with 0.5 MAC and by 15+/-4 mmHg with 1.0 MAC of sevoflurane. Systolic blood pressure decreased with both concentrations of sevoflurane. To maintain blood pressure within predetermined limits (within+/-20% of baseline value), phenylephrine was administered to 5 of 10 patients in the sevoflurane group (range = 50-300 microg) and no patients in the propofol group. Lumbar CSF pressure, cerebral perfusion pressure, and systolic blood pressure did not change in the propofol group. Conclusions Sevoflurane, at 0.5 and 1.0 MAC, increases lumbar CSF pressure. The changes produced by 1.0 MAC sevoflurane did not differ from those observed in a previous study with 1.0 MAC isoflurane or desflurane.

scholarly journals Comparison of static and dynamic cerebral autoregulation under anesthesia influence in a controlled animal model

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245291
Author(s):  
Alexander Ruesch ◽  
Deepshikha Acharya ◽  
Samantha Schmitt ◽  
Jason Yang ◽  
Matthew A. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Phase Lag ◽  
Arterial Blood

The brain’s ability to maintain cerebral blood flow approximately constant despite cerebral perfusion pressure changes is known as cerebral autoregulation (CA) and is governed by vasoconstriction and vasodilation. Cerebral perfusion pressure is defined as the pressure gradient between arterial blood pressure and intracranial pressure. Measuring CA is a challenging task and has created a variety of evaluation methods, which are often categorized as static and dynamic CA assessments. Because CA is quantified as the performance of a regulatory system and no physical ground truth can be measured, conflicting results are reported. The conflict further arises from a lack of healthy volunteer data with respect to cerebral perfusion pressure measurements and the variety of diseases in which CA ability is impaired, including stroke, traumatic brain injury and hydrocephalus. To overcome these differences, we present a healthy non-human primate model in which we can control the ability to autoregulate blood flow through the type of anesthesia (isoflurane vs fentanyl). We show how three different assessment methods can be used to measure CA impairment, and how static and dynamic autoregulation compare under challenges in intracranial pressure and blood pressure. We reconstructed Lassen’s curve for two groups of anesthesia, where only the fentanyl anesthetized group yielded the canonical shape. Cerebral perfusion pressure allowed for the best distinction between the fentanyl and isoflurane anesthetized groups. The autoregulatory response time to induced oscillations in intracranial pressure and blood pressure, measured as the phase lag between intracranial pressure and blood pressure, was able to determine autoregulatory impairment in agreement with static autoregulation. Static and dynamic CA both show impairment in high dose isoflurane anesthesia, while low isoflurane in combination with fentanyl anesthesia maintains CA, offering a repeatable animal model for CA studies.

Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs

1993 ◽  
Vol 265 (5) ◽  
pp. H1557-H1563 ◽  
Author(s):  
M. L. Kearney ◽  
J. E. Backofen ◽  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cardiovascular Response ◽  
Fetal Sheep ◽  
Peripheral Vasoconstriction ◽  
Significant Difference

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.

Cerebral Perfusion Pressure

2018 ◽  
pp. 91-94
Keyword(s):  
Blood Pressure ◽  
Traumatic Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Controlled Study ◽  
Improved Outcomes ◽  
Cerebral Monitoring ◽  
Current Guidelines

This case focuses on monitoring patients with traumatic brain injury (TBI) by asking the question: Does management of cerebral perfusion pressure (CPP) as the primary goal of therapy yield lower mortality and higher Glasgow Outcome Scale (GOS) scores than that achieved with traditional, intracranial pressure (ICP)-based techniques? This study analyzing patients with TBI who underwent monitoring using CPP, rather than the standard ICP-based monitoring, demonstrated lower rates of mortality and improved outcomes compared with other analyses of patients receiving standard ICP-based monitoring. However, because this was not a controlled study, it is not possible to draw firm conclusions. Current guidelines do not recommend one type of monitoring over another but do provide thresholds for blood pressure, ICP, CPP, and advanced cerebral monitoring.

Sign in / Sign up

Export Citation Format

Share Document