scholarly journals Personalizing the Definition of Hypotension to Protect the Brain

2020 ◽  
Vol 132 (1) ◽  
pp. 170-179 ◽  
Author(s):  
Kenneth M. Brady ◽  
Aaron Hudson ◽  
Ryan Hood ◽  
Bruno DeCaria ◽  
Choy Lewis ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intensive Care Unit ◽  
Blood Flow ◽  
Intensive Care ◽  
Cerebral Blood Flow ◽  
Population Data ◽  
Data Monitoring ◽  
Cerebral Blood Flow Autoregulation ◽  
Definition Of ◽  
The Brain

In this review, the authors argue that hypotension is an individual definition not accurately determined based on population data. Monitoring cerebral blood flow autoregulation provides a clinically feasible approach for judging the acceptable intraoperative and intensive care unit blood pressure.

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

Melatonin improves cerebral circulation security margin in rats

1998 ◽  
Vol 275 (1) ◽  
pp. H139-H144 ◽  
Author(s):  
Olivier Régrigny ◽  
Philippe Delagrange ◽  
Elizabeth Scalbert ◽  
Jeffrey Atkinson ◽  
Isabelle Lartaud-Idjouadiene
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Lower Limit ◽  
Mean Arterial Blood Pressure ◽  
Pressure Level ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation

Because melatonin is a cerebral vasoconstrictor agent, we tested whether it could shift the lower limit of cerebral blood flow autoregulation to a lower pressure level, by improving the cerebrovascular dilatory reserve, and thus widen the security margin. Cerebral blood flow and cerebrovascular resistance were measured by hydrogen clearance in the frontal cortex of adult male Wistar rats. The cerebrovasodilatory reserve was evaluated from the increase in the cerebral blood flow under hypercapnia. The lower limit of cerebral blood flow autoregulation was evaluated from the fall in cerebral blood flow following hypotensive hemorrhage. Rats received melatonin infusions of 60, 600, or 60,000 ng ⋅ kg−1 ⋅ h−1, a vehicle infusion, or no infusion ( n= 9 rats per group). Melatonin induced concentration-dependent cerebral vasoconstriction (up to 25% of the value for cerebrovascular resistance of the vehicle group). The increase in vasoconstrictor tone was accompanied by an improvement in the vasodilatory response to hypercapnia (+50 to +100% vs. vehicle) and by a shift in the lower limit of cerebral blood flow autoregulation to a lower mean arterial blood pressure level (from 90 to 50 mmHg). Because melatonin had no effect on baseline mean arterial blood pressure, the decrease in the lower limit of cerebral blood flow autoregulation led to an improvement in the cerebrovascular security margin (from 17% in vehicle to 30, 55, and 55% in the low-, medium-, and high-dose melatonin groups, respectively). This improvement in the security margin suggests that melatonin could play an important role in the regulation of cerebral blood flow and may diminish the risk of hypoperfusion-induced cerebral ischemia.

scholarly journals Dexmedetomidine in modern anesthesiology and intensive care

2020 ◽  
pp. 91-93
Author(s):  
S.O. Dubrov
Keyword(s):  
Intensive Care Unit ◽  
Mechanical Ventilation ◽  
Blood Flow ◽  
Intensive Care ◽  
Cardiac Death ◽  
Target Level ◽  
Sedation Scale ◽  
Treatment Procedures ◽  
The Brain ◽  
Excessive Sedation

Background. Sedation is a controlled medical depression of consciousness with the preservation of protective reflexes, independent effective breathing and response to physical stimulation and verbal commands. Sedation is indicated for patients in the intensive care unit in presence of agitation, delirium, withdrawal syndrome of alcohol, drugs or other potent medications and the need to protect the brain (blunt traumatic brain injury, posthypoxic encephalopathy). In addition, at the request of the patient, sedation can be used during invasive diagnostic and treatment procedures. Objective. To describe the role of dexmedetomidine in modern anesthesiology and intensive care. Materials and methods. Analysis of literature data on this issue. Results and discussion. When performing sedation, one should balance between the excessive sedation and its absence. Excessive sedation is accompanied by the lack of contact with the patient, inability to assess the neurological status of the patient, and respiratory depression. If the patient is optimally sedated, he is calm and able to cooperate; he is also adapted to mechanical lung ventilation and other procedures. The target level of sedation according to the Richmond excitation-sedation scale is from 0 to -1. Drugs such as benzodiazepines (diazepam, midazolam, lorazepam), barbiturates (sodium thiopental), propofol, ketamine, inhaled anesthetics (sevoflurane, dexflurane), dexmedetomidine, opioids (morphine, fentanyl, remifentanyl) are used for sedation. Dexmedetomidine is a highly selective α2-adrenoagonist, so it has anxiolytic, sedative, antinociceptive, sympatholytic, and hypothermic actions. In addition, this drug reduces heart rate, suppresses tremor and increases diuresis. The sedative effect of dexmedetomidine is due to the inhibition of neuronal activity in the locus coeruleus of the brain stem. The condition caused by dexmedetomidine is similar to the natural sleep. The use of dexmedetomidine allows to achieve the target level of sedation in a higher percentage of cases than the use of other drugs (propofol, midazolam) (Jacub S.M. et al., 2012). Cooperative sedation is a sedation with the possibility of interaction of the patient with the medical staff. Compared to other drugs, dexmedetomidine increases the patient’s ability to wake up and quickly orient, after which the patient can quickly return to a state of sedation. One of the major complications of critically serious diseases and their treatment is the deterioration of cognitive abilities. Dexmedetomidine has been shown to improve the patient’s cognitive performance by 6.8 points on the John Hopkins scale. In contrast, propofol reduces cognitive function by an average of 12.4 points (Mirski M.A. et al., 2010). Dexmedetomidine has no respiratory depressant effect. Patients on mechanical ventilation do not require discontinuation of dexmedetomidine prior to extubation. Importantly, dexmedetomidine increases coronary blood flow, reduces the incidence of perioperative myocardial ischemia and the risk of perioperative cardiac death. Dexmedetomidine reduces the intensity of pain in the postoperative period and the need for opioids, the incidence of delirium, and the duration of mechanical ventilation. The financial and economic reasonability of dexmedetomidine use has been proved. Conclusions. 1. Sedation is indicated for patients in the intensive care unit in presence of agitation, delirium, withdrawal syndrome and the need to protect the brain, as well as during invasive diagnostic and treatment procedures. 2. The target level of sedation is from 0 to -1 on the Richmond excitation-sedation scale. 3. Dexmedetomidine is a highly selective α2-adrenoagonist, which has anxiolytic, sedative, antinociceptive, sympatholytic, and hypothermic action. 4. Dexmedetomidine increases coronary blood flow and reduces the incidence of perioperative myocardial ischemia, the risk of perioperative cardiac death, pain, delirium incidence and the duration of mechanical ventilation.

Evaluation of Cerebral Blood Flow and Brain Metabolism in the Intensive Care Unit

2017 ◽  
pp. 327-338
Author(s):  
Pierre Bouzat ◽  
Emmanuel L. Barbier ◽  
Gilles Francony ◽  
Jean-François Payen
Keyword(s):  
Intensive Care Unit ◽  
Blood Flow ◽  
Intensive Care ◽  
Cerebral Blood Flow ◽  
Brain Metabolism

Alteration of pial vessel responses to blood pressure changes in rats after hypoxia

1987 ◽  
Vol 65 (11) ◽  
pp. 2265-2268 ◽  
Author(s):  
B. Y. Ong ◽  
J. J. Kettler ◽  
D. Bose
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Pial Arteries ◽  
Similar Time ◽  
Vascular Responses ◽  
Cranial Window ◽  
Arterial Blood ◽  
Cerebral Blood Flow Autoregulation ◽  
Pial Vessel

Previous studies in newborn lamb have shown impairment of cerebral blood flow autoregulation after hypoxia followed by reoxygenation. The present study was done to see if such a phenomenon existed in the adult rat and if it could be demonstrated at the level of the pial arterioles. Using an open cranial window preparation, we assessed the changes in pial vessel diameter during blood pressure alterations induced by hemorrhage and reinfusion of blood, before and after 30 s of hypoxia, in 15 male Sprague–Dawley rats. Mean diameters of pial arteries in the study group of rats were 128 ± 54 μm before hypoxia and 141 ± 61 μm after normoxia following hypoxia. The corresponding diameters in rats serving as time controls were 136 ± 52 and 138 ± 52 μm. Slopes of pial vessel diameters as a function of mean arterial blood pressures descreased significantly (p < 0.05) after hypoxia from −0.86 ± 0.45 to 0.03 ± 0.66 (mean ± SD). In the control rats not subjected to hypoxia, the slopes remained unchanged over a similar time period (−0.60 ± 0.16 and −0.42 ± 0.19). The negative slopes indicate that pial vessels dilate during hypotension and constrict during hypertension. Such vascular responses may play a role in autoregulation of cerebral blood flow. We found that a relatively brief period of hypoxia can cause a long-lasting impairment of vascular responses even after restoration of normoxia. These findings are consistent with a previous report of persistent impairment of cerebral blood flow autoregulation after a brief period of hypoxia.

Differential Effects of Migraine Drugs on Cerebral Blood Flow Autoregulation

Cephalalgia ◽  
1998 ◽  
Vol 18 (6) ◽  
pp. 306-312 ◽  
Author(s):  
T Vraamark ◽  
G Waldemar ◽  
OB Paulson
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Receptor Agonist ◽  
Lower Blood Pressure ◽  
Pressure Limit ◽  
Lower Blood ◽  
Blood Pressures ◽  
Cerebral Blood Flow Autoregulation ◽  
Wistar Kyoto

The effect of the migraine drugs ergotamine and sumatriptan on the cerebral blood flow (CBF) autoregulation was studied in halothane/nitrous oxide-anesthetized normotensive Wistar Kyoto rats. Ergotamine, an ergot alkaloid affecting 5HT, norepinephrine, and dopamine receptors, was administered intravenously as a single dose of 25 μg/kg. Sumatriptan, a selective 5HT1-like receptor agonist, was administered by intravenous infusion of 300 μg/kg/h. CBF was measured with the intracarotid 133Xe-injection method. The blood pressure limits of CBF autoregulation were determined by computerized least sum of square analysis. CBF autoregulation was preserved after both ergotamine and sumatriptan. Ergotamine shifted the lower blood pressure limit of CBF autoregulation towards higher blood pressures from 60 ± 3 mmHg to 82 ± 4 mmHg ( p<0.01), but did not significantly affect the upper blood pressure limit of CBF autoregulation. Sumatriptan had no significant effects on the blood pressure limits of CBF autoregulation.

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