Raised intracranial pressure, cerebral oedema, and hydrocephalus

2011 ◽  
Author(s):  
Ian Whittle
Keyword(s):  
Intracranial Pressure ◽  
Dynamic Equilibrium ◽  
Venous Pressure ◽  
Venous Blood ◽  
Contributory Factor ◽  
Common Disease ◽  
Brain Vessels ◽  
Arterial Blood ◽  
Pressure Dynamics ◽  
The Brain

The brain is protected by the cranial skeleton. Within the intracranial compartment are also cerebrospinal fluid, CSF, and the blood contained within the brain vessels. These intracranial components are in dynamic equilibrium due to the pulsations of the heart and the respiratory regulated return of venous blood from the brain. Normally the mean arterial blood pressure, systemic venous pressure, and brain volume are regulated to maintain physiological values for intracranial pressure, ICP. There are a range of very common disorders such as stroke, and much less common, such as idiopathic intracranial hypertension, that are associated with major disturbances of intracranial pressure dynamics. In some of these the contribution to pathophysiology is relatively minor whereas in others it may be substantial and be a major contributory factor to morbidity or even death.Intracranial pressure can be disordered because of brain oedema, disturbances in CSF flow, mass lesions, and vascular engorgement of the brain. Each of these may have variable causes and there may be interactions between mechanisms. In this chapter the normal regulation of intracranial pressure is outlined and some common disease states in clinical neurological practice that are characterized by either primary or secondary problems in intracranial pressure dynamics described.

The Generation of Kinins in the Blood of Dogs during Hypotension Due to Haemorrhage

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane
Keyword(s):  
Blood Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Venous Blood ◽  
Systemic Circulation ◽  
Substantial Effect ◽  
Mixed Venous Blood ◽  
Shed Blood ◽  
Arterial Blood ◽  
Organ Technique

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.

Effect of positive end expiratory pressure ventilation on intracranial pressure in man

1977 ◽  
Vol 46 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Michael L. J. Apuzzo ◽  
Martin H. Weiss ◽  
Viesturs Petersons ◽  
R. Baldwin Small ◽  
Theodore Kurze ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Perfusion Pressure ◽  
Venous Pressure ◽  
Blood Gases ◽  
Pulmonary Injury ◽  
Positive End Expiratory Pressure ◽  
Central Venous ◽  
Content Type ◽  
Arterial Blood ◽  
Peep Ventilation

✓ This study was designed to define the effect of positive end expiratory pressure (PEEP) ventilation on intracranial pressure (ICP). In 25 patients with severe head trauma with and without associated pulmonary injury the following parameters were simultaneously monitored under mechanical ventilation with and without PEEP: ICP, arterial blood pressure, central venous pressure, arterial blood gases, and cardiac rate. In addition, the volume-pressure response (VPR) was evaluated in each patient to assess cerebral elastance. The results indicate a significant increase in ICP with the application of PEEP only in the 12 patients who manifested increased cerebral elastance by VPR. Half of this latter group manifested impairment of cerebral perfusion pressure to levels less than 60 mm Hg. Return to baseline ICP levels was observed with termination of PEEP. No significantly consistent changes in other parameters were noted.

Autoregulation of cerebral blood flow after experimental fluid percussion injury of the brain

1980 ◽  
Vol 53 (4) ◽  
pp. 500-511 ◽  
Author(s):  
W. Lewelt ◽  
L. W. Jenkins ◽  
J. Douglas Miller
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Injury ◽  
Content Type ◽  
Fluid Percussion ◽  
Arterial Blood ◽  
Fluid Percussion Injury ◽  
The Brain

✓ To test the hypothesis that concussive brain injury impairs autoregulation of cerebral blood flow (CBF), 24 cats were subjected to hemorrhagic hypotension in 10-mm Hg increments while measurements were made of arterial and intracranial pressure, CBF, and arterial blood gases. Eight cats served as controls, while eight were subjected to mild fluid percussion injury of the brain (1.5 to 2.2 atmospheres) and eight to severe injury (2.8 to 4.8 atmospheres). Injury produced only transient changes in arterial and intracranial pressure, and no change in resting CBF. Impairment of autoregulation was found in injured animals, more pronounced in the severe-injury group. This could not be explained on the basis of intracranial hypertension, hypoxemia, hypercarbia, or brain damage localized to the area of the blood flow electrodes. It is, therefore, concluded that concussive brain injury produces a generalized loss of autoregulation for at least several hours following injury.

scholarly journals Investigation of Hemodynamic Receptors of the Internal Carotid Artery Segments

2021 ◽  
Author(s):  
Mehmet Deniz Yener ◽  
Tuncay Colak ◽  
Belgin Bamac ◽  
Ahmet Ozturk ◽  
Selenay Humeyra Rencber ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Outer Surface ◽  
Laser Scanning ◽  
Internal Carotid ◽  
Venous Blood ◽  
Cervical Region ◽  
Tunica Media ◽  
Arterial Blood ◽  
The Brain

Abstract Objectives Internal carotid artery (ICA), the main artery of the brain, passes through the cavernous sinus (CS) which forms one of these venous pools. During this transition, while there is arterial blood in the lumen of ICA, its outer surface is in contact with venous blood from the brain. Herein, we aimed to detect the receptor differences of ICA in this highly specialized anatomical region of the skull base. Methods We performed the study on 10 human cadavers and searched CGRPR, TRP12, ASIC3 and ACTHR receptors via immunostaining using laser scanning confocal microscopy. Results We determined TRP12 receptor positive in the tunica media and tunica adventitia layers of the cavernous segment of ICA. We did not detect similar positivity in the cervical part of the ICA. In the receptor scan we made in terms of CGRPR, while we detected positivity in the tunica media layer of the cavernous segment, we found positivity in the tunica intima layer of the cervicalis segment of the ICA. We did not detect any positivity for ASIC3 and ACTHR receptors in both parts of the ICA. Conclusions As a result, we observed various differences in receptors between ICA segments. While the outer surface of the ICA in the cervical region did not show any receptor positivity, we detected TRP12 receptor positivity along the tissue contour of vessel in the CS. We assume that it may provide a new perspective on pathologies of the CS/ICA and preservation of brain hemodynamics for clinicians.

Oxygen tensions measured in cat cerebral cortex under hyperbaric conditions

1979 ◽  
Vol 46 (1) ◽  
pp. 53-60 ◽  
Author(s):  
F. G. Hempel
Keyword(s):  
Cerebral Cortex ◽  
Venous Blood ◽  
Sagittal Sinus ◽  
Venous Circulation ◽  
Arterial Blood ◽  
The Mean ◽  
Oxygen Tensions ◽  
The Brain ◽  
Cat Cerebral Cortex ◽  
Hyperbaric Conditions

Pyrenebutyric acid (PBA), the intracellular fluorescent indicator, was used to measure the partial pressure of oxygen (PO2) in the exposed cerebral cortex of anesthetized cats at hyperbaric pressures up to 4 ATA. The validity of the PBA method for determining cortical PO2 was confirmed by demonstrating a precise linear relationship between Pao2 and the reciprocal of the fluorescence of PBA in the brain as the cat was ventilated with sequentially greater oxygen pressures while holding the Paco2 nearly constant. Increments in the Paco2 while the Pao2 was maintained at a high (about 2,000 Torr) level resulted in stepwise greater oxygen tensions in the brain until an oxygenation end point was reached with a Paco2 averaging near 122 Torr. Greater amounts of CO2 did not bring the mean PO2 of the brain, 1,017 Torr, closer to 2,000 Torr. During normocapnia the cortical PO2 was greater than the PO2 of cerebral venous blood collected from the superior sagittal sinus; however, in hypercapnia (PaCO greater than 45 Torr), the PO2 of the sinus blood exceeded the value determined in the cortex. This latter observation is taken as evidence for convective shunting of cerebral arterial blood to venous circulation when hypercapnia is present.

Responses of cerebral arterioles to increased venous pressure

1982 ◽  
Vol 243 (3) ◽  
pp. H442-H447 ◽  
Author(s):  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Arterial Blood Pressure ◽  
Venous Pressure ◽  
Venous Hypertension ◽  
Arterial Hypotension ◽  
Arterial Blood ◽  
Pial Arterioles ◽  
Cerebral Arterioles ◽  
Arteriolar Vasodilation

The responses of pial arterioles to increased venous pressure were studied in anesthetized cats equipped with cranial windows for the observation of the pial microcirculation. Stable increases in venous pressure consistently induced arteriolar vasodilation, which averaged 6-12% of the control diameter. The vasodilation occurred when arterial blood pressure was normal and during arterial hypotension induced by bleeding; it also occurred irrespective of whether intracranial pressure was kept constant or was allowed to increase venous hypertension. The results are consistent with the view that autoregulatory adjustments in caliber of pial arterioles are mediated predominantly by metabolic rather than myogenic mechanisms.

Splenic baroreceptors control splenic afferent nerve activity

2006 ◽  
Vol 290 (2) ◽  
pp. R352-R356 ◽  
Author(s):  
Karli Moncrief ◽  
Susan Kaufman
Keyword(s):  
Blood Flow ◽  
Venous Pressure ◽  
Venous Blood ◽  
Splenic Vein ◽  
Afferent Nerve ◽  
Arterial Blood Flow ◽  
Venous Blood Flow ◽  
Nerve Activity ◽  
Vein Occlusion ◽  
Arterial Blood

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 ± 0.5 to 22.9 ± 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 ± 0.1 to 0.9 ± 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 ± 0.1 to 0.6 ± 0.1 ml/min, n = 6), and increased SANA (1.7 ± 0.4 to 2.2 ± 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 ± 0.1 to 0.7 ± 0.05, n = 6) or splenic venous blood flow (1.2 ± 0.1 to 0.5 ± 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (−0.4 ± 0.9 mmHg, n = 6 and +0.1 ± 0.3 mmHg, n = 5) or SANA (−0.11 ± 0.15 spikes/s, n = 6 and −0.05 ± 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure ( r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous ( r = 0.371, P = 0.236, n = 12) or arterial ( r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.

scholarly journals Mannitol versus hypertonic saline for intra-operative brain relaxation during aneurysm surgery

2015 ◽  
Vol 02 (01) ◽  
pp. 023-027
Author(s):  
Shalini Sharma ◽  
Vinod Grover ◽  
Preethy Mathew
Keyword(s):  
Hypertonic Saline ◽  
Serum Sodium ◽  
Venous Pressure ◽  
Double Blind Study ◽  
Aneurysm Surgery ◽  
Double Blind ◽  
Arterial Blood ◽  
Fisher Grade ◽  
Brain Relaxation ◽  
The Brain

Abstract Background: The study was designed to compare the effects of equiosmolar and equivolemic 3% hypertonic saline (HTS) and 20% mannitol (M) on brain relaxation during aneurysm surgery. Materials and Methods: A prospective, randomised, double-blind study was undertaken in patients scheduled for surgical clipping of intracranial aneurysms presenting with Fisher grade I, II or III. The patients received either 300 mL of 3% hypertonic saline (HTS group) or 300 mL of 20% mannitol infusion (M group) during a period of 15 minutes at the start of scalp incision. The PaCO2 was maintained at 3.4-4.7 kilo Pascal, arterial blood pressure was maintained within ± 20% of baseline and central venous pressure was maintained at 5-10 cm of water. The haemodynamics, arterial blood gases and serum sodium concentration were compared. Surgeons assessed the condition of the brain as bulging, firm, satisfactorily relaxed and perfectly relaxed. An anaesthesiologist also assessed intra-operative brain relaxation. Results: The brain relaxation achieved with hypertonic saline was as good as that with mannitol. Urine output with mannitol was higher than with hypertonic saline (P < 0.04). Hypertonic saline caused an increase in serum sodium over one hour (P < 0.001) but resolved in 24 hours. Conclusions: The brain relaxation was equal in both the groups as assessed by the anaesthesiologist as well as the surgeon while the transient rise in serum sodium in hypertonic saline group returned to normal within 24 hours.

Static filling pressure in patients during induced ventricular fibrillation

2003 ◽  
Vol 285 (6) ◽  
pp. H2510-H2515 ◽  
Author(s):  
J. D. Schipke ◽  
G. Heusch ◽  
A. P. Sanii ◽  
E. Gams ◽  
J. Winter
Keyword(s):  
Blood Pressure ◽  
Time Constant ◽  
Pressure Difference ◽  
Venous Pressure ◽  
Venous Blood ◽  
Central Venous ◽  
Equilibrium Pressure ◽  
Arterial Blood ◽  
Cardiac Pumping ◽  
Blood Pressure Difference

The static pressure resulting after the cessation of flow is thought to reflect the filling of the cardiovascular system. In the past, static filling pressures or mean circulatory filling pressures have only been reported in experimental animals and in human corpses, respectively. We investigated arterial and central venous pressures in supine, anesthetized humans with longer fibrillation/defibrillation sequences (FDSs) during cardioverter/defibrillator implantation. In 82 patients, the average number of FDSs was 4 ± 2 (mean ± SD), and their duration was 13 ± 2 s. In a total of 323 FDSs, arterial blood pressure decreased with a time constant of 2.9 ± 1.0 s from 77.5 ± 34.4 to 24.2 ± 5.3 mmHg. Central venous pressure increased with a time constant of 3.6 ± 1.3 s from 7.5 ± 5.2 to 11.0 ± 5.4 mmHg (36 points, 141 FDS). The average arteriocentral venous blood pressure difference remained at 13.2 ± 6.2 mmHg. Although it slowly decreased, the pressure difference persisted even with FDSs lasting 20 s. Lack of true equilibrium pressure could possibly be due to a waterfall mechanism. However, waterfalls were identified neither between the left ventricle and large arteries nor at the level of the diaphragm in supine patients. We therefore suggest that static filling pressures/mean circulatory pressures can only be directly assessed if the time after termination of cardiac pumping is adequate, i.e., >20 s. For humans, such times are beyond ethical options.

Effects of albumin infusion on renal function in the dog

1963 ◽  
Vol 205 (1) ◽  
pp. 153-161 ◽  
Author(s):  
Mary Jo Elpers ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Plasma Flow ◽  
Venous Pressure ◽  
Venous Blood ◽  
Urine Volume ◽  
Albumin Infusion ◽  
Arterial Blood ◽  
Vasa Recta ◽  
Anesthetized Dogs

Serum albumin (25%) was infused into anesthetized dogs undergoing a saline diuresis. No significant effect was seen on arterial pressure, but renal venous pressure was elevated slightly. GFR remained unchanged, while Cpah, renal plasma flow, total renal blood flow, and flow to medullary tissue increased significantly. Accompanying these changes were marked declines in PAH and creatinine extraction ratios. Urine volume, Cna, and Cosm declined appreciably during albumin infusion; TcHH2O tended to decrease. The ratio of Na and osmolar constituents in renal venous blood to that in arterial blood increased above unity, and calculations indicated that at this time Na was washed from the kidney. Tmpah remained unchanged during albumin infusion. It is concluded that during albumin infusion, there is an increase in plasma volume and renal blood flow accompanied by a diversion of part of this blood through aglomerular regions, possibly through A-V anastomoses, as evidenced by the accompanying decrease in Ecr and Epah. This could involve increased perfusion of the medullary papillary zone, including the vasa recta vessels, supported by the observations that during albumin infusion there is a washout of osmotic constituents, primarily Na, presumably from a zone of high Na concentration.

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