scholarly journals Peranan Hiperventilasi terhadap Penurunan Tekanan Intrakranial dalam Kasus Bedah Saraf

2020 ◽  
Vol 9 (1) ◽  
pp. 60-70
Author(s):  
Irwan Wibowo ◽  
M Sofyan Harahap
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Perivascular Space ◽  
Main Concern ◽  
Short Term ◽  
Cerebral Vasoconstriction ◽  
The Brain

AbstrakHiperventilasi telah ditemukan sebagai salah satu cara untuk menurunkan aliran darah otak (cerebral blood flow) (CBF) sejak tahun 1920-an. Pada saat itu telah dilaporkan bahwa penggunaan hiperventilasi dapat mengurangi peningkatan tekanan intrakranial (intracranial pressure/ICP) dengan vasokonstriksi serebral sehingga mampu menurunkan volume darah di daerah serebral. Secara teoritis, manfaat hiperventilasi mungkin lebih khusus diharapkan pada pasien di mana peningkatan ICP terjadi terutama karena peningkatan volume darah otak akibat mekanisme vasodilatasi. Efek vasokonstriksi tersebut akan menghilang setelah pH pada ruang perivaskular kembali normal setelah 24 jam. Yang menjadi perhatian utama dalam metode ini adalah tindakan tersebut mampu menginduksi terjadinya iskemia serebral baik secara regional maupun global. Risiko kerusakan iskemik tersebut bergantung pada sejauh mana dan seberapa lama otak mengalami aliran darah yang rendah. Masih terdapat data yang kontroversial antara yang mendukung ataupun menentang penggunaan terapi hiperventilasi, namun menurut penelitian yang telah dilakukan, tindakan ini mampu menurunkan ICP jika dilakukan dalam jangka pendek. Pemantauan multimodalitas terhadap pasien tetap diperlukan untuk memantau keberhasilan dalam tindakan ini. Hyperventilation Management for Decrease Intracranial Pressure in Neurosurgery CasesAbstractHyperventilation has been found as a way to reduce cerebral blood flow (CBF) since 1920s. At that time it was reported that the use of hyperventilation can reduce the increase in intracranial pressure (ICP) by causing cerebral vasoconstriction and decreasing cerebral blood volume. Theoretically, the benefits of hyperventilation may be more specifically expected in patients which has increasing ICP because of an increasing in blood volume and vasodilation mechanism. The vasoconstriction effect disappears after the pH in the perivascular space returns to normal after 24 hours. The main concern in treating patients with increased ICP using hyperventilation is to induce cerebral ischemia both regionally and globally. As with a stroke, the risk of ischemic damage depends on the extent and how long the brain experiences low blood flow. Controversial data still exists between those that support or oppose the use of hyperventilation therapy, but if hypocapnia monitoring is done to control the increase in ICP in the short term, hyperventilation therapy remains beneficial. Multimodality monitoring is needed so that hyperventilation therapy can be used safely in certain patients who may need this therapy. 

scholarly journals Changes in Human Cerebral Blood Flow and Cerebral Blood Volume during Hypercapnia and Hypocapnia Measured by Positron Emission Tomography

2003 ◽  
Vol 23 (6) ◽  
pp. 665-670 ◽  
Author(s):  
Hiroshi Ito ◽  
Iwao Kanno ◽  
Masanobu Ibaraki ◽  
Jun Hatazawa ◽  
Shuichi Miura
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Blood Velocity ◽  
Emission Tomography ◽  
Neural Activation ◽  
Cerebral Vasoconstriction ◽  
Positron Emission

Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF. The relation between changes in CBF and cerebral blood volume (CBV) during hypercapnia and hypocapnia in humans, however, is not clear. Both CBF and CBV were measured at rest and during hypercapnia and hypocapnia in nine healthy subjects by positron emission tomography. The vascular responses to hypercapnia in terms of CBF and CBV were 6.0 ± 2.6%/mm Hg and 1.8 ± 1.3%/mm Hg, respectively, and those to hypocapnia were −3.5 ± 0.6%/mm Hg and −1.3 ± 1.0%/mm Hg, respectively. The relation between CBF and CBV was CBV = 1.09 CBF0.29. The increase in CBF was greater than that in CBV during hypercapnia, indicating an increase in vascular blood velocity. The degree of decrease in CBF during hypocapnia was greater than that in CBV, indicating a decrease in vascular blood velocity. The relation between changes in CBF and CBV during hypercapnia was similar to that during neural activation; however, the relation during hypocapnia was different from that during neural deactivation observed in crossed cerebellar diaschisis. This suggests that augmentation of CBF and CBV might be governed by a similar microcirculatory mechanism between neural activation and hypercapnia, but diminution of CBF and CBV might be governed by a different mechanism between neural deactivation and hypocapnia.

Cerebral Blood Volume (CBV) in Humans during Normo- and Hypocapnia

2001 ◽  
Vol 95 (5) ◽  
pp. 1079-1082 ◽  
Author(s):  
Peter Reinstrup ◽  
Erik Ryding ◽  
Tomas Ohlsson ◽  
Peter Lee Dahm ◽  
Tore Uski
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Nitrous Oxide ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Brain Volume ◽  
Regional Distribution ◽  
Significant Difference ◽  
The Brain

Background It is generally argued that variations in cerebral blood flow create concomitant changes in the cerebral blood volume (CBV). Because nitrous oxide (N(2)O) inhalation both increases cerebral blood flow and may increase intracranial pressure, it is reasonable to assume that N(2)O acts as a general vasodilatator in cerebral vessels both on the arterial and on the venous side. The aim of the current study was to evaluate the effect of N(2)O on three-dimensional regional and global CBV in humans during normocapnia and hypocapnia. Methods Nine volunteers were studied under each of four conditions: normocapnia, hypocapnia, normocapnia + 40-50% N(2)O, and hypocapnia + 40-50% N(2)O. CBV was measured after (99m)Tc-labeling of blood with radioactive quantitative registration via single photon emission computer-aided tomography scanning. Results Global CBV during normocapnia and inhalation of 50% O(2) was 4.25 +/- 0.57% of the brain volume (4.17 +/- 0.56 ml/100 g, mean +/- SD) with no change during inhalation of 40-50% N(2)O in O(2). Decreasing carbon dioxide (CO(2)) by 1.5 kPa (11 mmHg) without N(2)O inhalation and by 1.4 kPa (11 mmHg) with N(2)O inhalation reduced CBV significantly (F = 57, P < 0.0001), by 0.27 +/- 0.10% of the brain volume per kilopascal (0.26 +/- 0.10 ml x 100 g(-1) x kPa(-1)) without N(2)O inhalation and by 0.35 +/- 0.22% of the brain volume per kilopascal (0.34 +/- 0.22 ml x 100 g(-1) x kPa(-1)) during N(2)O inhalation (no significant difference). The amount of carbon dioxide significantly altered the regional distribution of CBV (F = 47, P < 0.0001), corresponding to a regional difference in Delta CBV when CO(2) is changed. N(2)O inhalation did not significantly change the distribution of regional CBV (F = 2.4, P = 0.051) or Delta CBV/Delta CO(2) in these nine subjects. Conclusions Nitrous oxide inhalation had no effect either on CBV or on the normal CBV-CO(2) response in humans.

Hyperacute Stroke: Simultaneous Measurement of Relative Cerebral Blood Volume, Relative Cerebral Blood Flow, and Mean Tissue Transit Time

Radiology ◽  
1999 ◽  
Vol 210 (2) ◽  
pp. 519-527 ◽  
Author(s):  
A. Gregory Sorensen ◽  
William A. Copen ◽  
Leif Østergaard ◽  
Ferdinando S. Buonanno ◽  
R. Gilberto Gonzalez ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Blood Volume ◽  
Transit Time ◽  
Simultaneous Measurement ◽  
Cerebral Blood Volume ◽  
Hyperacute Stroke ◽  
Relative Cerebral Blood Volume

scholarly journals Effects of Acetazolamide on Cerebral Blood Flow, Blood Volume, and Oxygen Metabolism: A Positron Emission Tomography Study with Healthy Volunteers

2001 ◽  
Vol 21 (12) ◽  
pp. 1472-1479 ◽  
Author(s):  
Hidehiko Okazawa ◽  
Hiroshi Yamauchi ◽  
Kanji Sugimoto ◽  
Hiroshi Toyoda ◽  
Yoshihiko Kishibe ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Capillary Blood ◽  
Emission Tomography ◽  
Positron Emission ◽  
Capillary Blood Volume

To evaluate changes in cerebral hemodynamics and metabolism induced by acetazolamide in healthy subjects, positron emission tomography studies for measurement of cerebral perfusion and oxygen consumption were performed. Sixteen healthy volunteers underwent positron emission tomography studies with15O-gas and water before and after intravenous administration of acetazolamide. Dynamic positron emission tomography data were acquired after bolus injection of H215O and bolus inhalation of15O2. Cerebral blood flow, metabolic rate of oxygen, and arterial-to-capillary blood volume images were calculated using the three-weighted integral method. The images of cerebral blood volume were calculated using the bolus inhalation technique of C15O. The scans for cerebral blood flow and volume and metabolic rate of oxygen after acetazolamide challenge were performed at 10, 20, and 30 minutes after drug injection. The parametric images obtained under the two conditions at baseline and after acetazolamide administration were compared. The global and regional values for cerebral blood flow and volume and arterial-to-capillary blood volume increased significantly after acetazolamide administration compared with the baseline condition, whereas no difference in metabolic rate of oxygen was observed. Acetazolamide-induced increases in both blood flow and volume in the normal brain occurred as a vasodilatory reaction of functioning vessels. The increase in arterial-to-capillary blood volume made the major contribution to the cerebral blood volume increase, indicating that the raise in cerebral blood flow during the acetazolamide challenge is closely related to arterial-to-capillary vasomotor responsiveness.

Early changes measured by magnetic resonance imaging in cerebral blood flow, blood volume, and blood-brain barrier permeability following dexamethasone treatment in patients with brain tumors

1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Tumors ◽  
Mr Imaging ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Clinical Effects ◽  
Content Type ◽  
Fine Print

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.

Interaction among autoregulation, CO2 reactivity, and intracranial pressure: a mathematical model

1998 ◽  
Vol 274 (5) ◽  
pp. H1715-H1728 ◽  
Author(s):  
Mauro Ursino ◽  
Carlo Alberto Lodi
Keyword(s):  
Mathematical Model ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Nonlinear Interaction ◽  
Cerebral Blood Volume ◽  
Cerebral Hemodynamics ◽  
Pial Arteries ◽  
Arterial Circulation ◽  
Neurosurgical Patients

The relationships among cerebral blood flow, cerebral blood volume, intracranial pressure (ICP), and the action of cerebrovascular regulatory mechanisms (autoregulation and CO2 reactivity) were investigated by means of a mathematical model. The model incorporates the cerebrospinal fluid (CSF) circulation, the intracranial pressure-volume relationship, and cerebral hemodynamics. The latter is based on the following main assumptions: the middle cerebral arteries behave passively following transmural pressure changes; the pial arterial circulation includes two segments (large and small pial arteries) subject to different autoregulation mechanisms; and the venous cerebrovascular bed behaves as a Starling resistor. A new aspect of the model exists in the description of CO2 reactivity in the pial arterial circulation and in the analysis of its nonlinear interaction with autoregulation. Simulation results, obtained at constant ICP using various combinations of mean arterial pressure and CO2 pressure, substantially support data on cerebral blood flow and velocity reported in the physiological literature concerning both the separate effects of CO2 and autoregulation and their nonlinear interaction. Simulations performed in dynamic conditions with varying ICP underline the existence of a significant correlation between ICP dynamics and cerebral hemodynamics in response to CO2 changes. This correlation may significantly increase in pathological subjects with poor intracranial compliance and reduced CSF outflow. In perspective, the model can be used to study ICP and blood velocity time patterns in neurosurgical patients in order to gain a deeper insight into the pathophysiological mechanisms leading to intracranial hypertension and secondary brain damage.

scholarly journals Can Cerebral Blood Volume Be Measured Reproducibly with an Improved near Infrared Spectroscopy System?

2001 ◽  
Vol 21 (2) ◽  
pp. 110-113 ◽  
Author(s):  
Marjo J. T. Van de Ven ◽  
Willy N. J. M. Colier ◽  
Marco C. van der Sluijs ◽  
Diederik Walraven ◽  
Berend Oeseburg ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Infrared Spectroscopy ◽  
Blood Volume ◽  
Near Infrared Spectroscopy ◽  
Healthy Subjects ◽  
Baseline Level ◽  
Near Infrared ◽  
Cerebral Blood Volume ◽  
Spectroscopy System

In some circumstances, cerebral blood volume (CBV) can be used as a measure for cerebral blood flow. A new near infrared spectroscope was used for determining the reproducibility of CBV measurements assessed by the O2-method. Twenty-seven healthy subjects were investigated. An intrasubject coefficient of variation (CV) was calculated, based on four identical episodes of desaturation–resaturation (O2-method) procedures for CBV measurements. Two trials were performed, with (trial 1) and without (trial 2) disconnecting the equipment. A mean CV of 12.6% and 10.0% was found in trial 1 and 2, respectively. Cerebral blood volume values yield 3.60 ± 0.82 mL 100 g−1. Cerebral blood volume could be measured reproducible in adults using near infrared spectroscopy, if the arterial desaturation is limited to approximately 5% from baseline level.

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