Structures Protecting the Brain/ ICP Flashcards

1
Q

Major bones

A
  • The brain is contained in the rigid skull, which protects it from injury.
  • The major bones of the skull are the frontal, temporal, parietal, occipital, and sphenoid bones.
    β€” These bones join at the suture lines (see Fig. 60-4) and form the base of the skull. Indentations in the skull base are known as fossae.
    β€” The anterior fossa contains the frontal lobe
    β€” the middle fossa contains the temporal lobe
    β€” the posterior fossa contains the cerebellum and brain stem.
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2
Q

meninges

A

The meninges (fibrous connective tissues that cover the brain and spinal cord) provide protection, support, and nourishment. The layers of the meninges are the dura mater, arachnoid, and pia mater (see Fig. 60-5):

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3
Q

Dura mater

A

the outermost layer;
- covers the brain and the spinal cord.
- It is tough, thick, inelastic, fibrous, and gray.
- There are three major extensions of the dura:
β€” the falx cerebri; which folds between the two hemispheres;
β€” the tentorium; which folds between the occipital lobe and cerebellum to form a tough, membranous shelf;
β€” the falx cerebelli, which is located between the right and left side of the cerebellum.
- When excess pressure occurs in the cranial cavity, brain tissue may be compressed against these dural folds or displaced around them, a process called herniation.
- A potential space exists between the dura and the skull, and between the periosteum and the dura in the vertebral column, known as the epidural space.
- Another potential space, the subdural space, also exists below the dura.
- Blood or an abscess can accumulate in these potential spaces.

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4
Q

Arachnoid

A
  • the middle membrane;
  • an extremely thin, delicate membrane that closely resembles a spider web (hence the name arachnoid).
  • The arachnoid membrane has cerebrospinal fluid (CSF) in the space below it, known as the subarachnoid space.
    β€” This membrane has arachnoid villi, which are unique finger-like projections that absorb CSF into the venous system.
    β€” When blood or bacteria enter the subarachnoid space, the villi become obstructed and communicating hydrocephalus (increased size of ventricles) may result.
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5
Q

Pia mater

A

the innermost, thin, transparent layer that hugs the brain closely and extends into every fold of the brain’s surface.

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6
Q

Cerebrospinal Fluid

A
  • CSF is a clear and colorless fluid that is produced in the choroid plexus of the ventricles and circulates around the surface of the brain and the spinal cord.
  • There are four ventricles:
    β€” the right and left lateral ventricles
    β€”- The two lateral ventricles open into the third ventricle at the interventricular foramen (also known as the foramen of Monro).
    β€” the third and fourth ventricles.
    β€”- The third and fourth ventricles connect via the aqueduct of Sylvius.
    β€”-The fourth ventricle drains CSF into the subarachnoid space on the surface of the brain and spinal cord, where it is absorbed by the arachnoid villi.
    β€”- Blockage of the flow of CSF anywhere in the ventricular system produces obstructive hydrocephalus.
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7
Q

CSF & immune and metabolic functions

A
  • CSF is important in immune and metabolic functions in the brain.
  • It is produced at a rate of about 500 mL/day; the ventricles and subarachnoid space contain approximately 125 to 150 mL of fluid.
  • The composition of CSF is similar to other extracellular fluids (such as blood plasma), but the concentrations of the various constituents differ.
  • A laboratory analysis of CSF indicates :
    β€” color (clear)
    β€” specific gravity (normal 1.007)
    β€” protein count, cell count
    β€” glucose, and other electrolyte levels
  • Normal CSF contains a minimal number of white blood cells and no red blood cells.
  • The CSF may also be tested for immunoglobulins or the presence of bacteria.
  • A CSF sample may be obtained through a lumbar puncture or intraventricular catheter
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8
Q

Cerebral Circulation

A
  • The brain does not store nutrients and requires a constant supply of oxygen.
    β€” These needs are met through cerebral circulation; the brain receives approximately 15% of the cardiac output, or 750 mL per minute of blood flow.
  • Brain circulation is unique in several aspects.
  • First, arterial and venous vessels are not parallel as in other organs in the body; this is due in part to the role the venous system plays in CSF absorption.
  • Second, the brain has collateral circulation through the circle of Willis (see later discussion), allowing blood flow to be redirected on demand.
  • Third, blood vessels in the brain have two rather than three layers, which may make them more prone to rupture when weakened or under pressure.
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9
Q

Cerebral Circulation
Arteries

A
  • Arterial blood supply to the anterior brain originates from the common carotid artery, which is the first bifurcation of the aorta.
  • The internal carotid arteries arise at the bifurcation of the common carotid.
  • Branches of the internal carotid arteries (the anterior and middle cerebral arteries) and their connections (the anterior and posterior communicating arteries) form the circle of Willis (see Fig. 60-6).
  • The vertebral arteries branch from the subclavian arteries to supply most of the posterior circulation of the brain.
  • At the level of the brain stem, the vertebral arteries join to form the basilar artery.
    β€” The basilar artery divides to form the two branches of the posterior cerebral arteries.
  • Functionally, the posterior and anterior portions of the circulation usually remain separate.
    β€” However, the circle of Willis can provide collateral circulation through communicating arteries if one of the vessels supplying it becomes occluded or is ligated.
  • The bifurcations along the circle of Willis are frequent sites of aneurysm formation.
    β€” Aneurysms are outpouchings of the blood vessel due to vessel wall weakness.
    β€” Aneurysms can rupture and cause a hemorrhagic stroke. See Chapter 62 for a more detailed discussion of aneurysms.
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10
Q

Cerebral Circulation
Veins

A
  • Venous drainage for the brain does not follow the arterial circulation as in other body structures.
  • The veins reach the brain’s surface, join larger veins, and then cross the subarachnoid space and empty into the dural sinuses, which are the vascular channels embedded in the dura (see Fig. 60-5).
  • The network of the sinuses carries venous outflow from the brain and empties into the internal jugular veins, returning the blood to the heart.
  • Cerebral veins are unique, because unlike other veins in the body, they do not have valves to prevent blood from flowing backward and depend on both gravity and blood pressure for flow.
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11
Q

Blood–Brain Barrier

A
  • The CNS is inaccessible to many substances that circulate in the blood plasma (e.g., dyes, medications, antibiotic agents) because of the blood–brain barrier. - This barrier is formed by the endothelial cells of the brain’s capillaries, which form continuous tight junctions, creating a barrier to macromolecules and many compounds.
  • All substances entering the CSF must filter through the capillary endothelial cells and astrocytes.
  • The blood–brain barrier has a protective function but can be altered by trauma, cerebral edema, and cerebral hypoxemia; this has implications for treatment and selection of medications for CNS disorders (Hickey & Strayer, 2020).
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12
Q

INCREASED INTRACRANIAL PRESSURE

A
  • The rigid cranial vault contains brain tissue (1400 g), blood (75 mL), and CSF (75 mL).
  • The volume and pressure of these three components are usually in a state of equilibrium and produce the ICP.
  • ICP is usually measured in the lateral ventricles, with the normal pressure being 0 to 10 mm Hg, and 15 mm Hg being the upper limit of normal (Hickey & Strayer, 2020).
  • The Monro–Kellie hypothesis, also known as the Monro–Kellie doctrine, explains the dynamic equilibrium of cranial contents.
    β€” The hypothesis states that because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others (Witherspoon & Ashby, 2017).
  • Because brain tissue has limited space to expand, compensation typically is accomplished by displacing or shifting CSF, increasing the absorption or diminishing the production of CSF, or decreasing cerebral blood volume.
  • Without such changes, ICP begins to rise.
  • Under normal circumstances, minor changes in blood volume and CSF volume occur constantly as a result of alterations in intrathoracic pressure (coughing, sneezing, straining), posture, blood pressure, and systemic oxygen and carbon dioxide levels.
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13
Q

ICP Pathophysiology

A
  • Increased ICP affects many patients with acute neurologic conditions because pathologic conditions alter the relationship between intracranial volume and ICP.
  • Although elevated ICP is most commonly associated with head injury, it also may be seen as a secondary effect in other conditions, such as brain tumors, subarachnoid hemorrhage, and toxic and viral encephalopathies.
  • Increased ICP from any cause decreases cerebral perfusion, stimulates further edema (swelling), and may shift brain tissue, resulting in herniationβ€”a dire and frequently fatal event.
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14
Q

Decreased Cerebral Blood Flow

A
  • Increased ICP may reduce cerebral blood flow, resulting in ischemia and cell death.
  • In the early stages of cerebral ischemia, the vasomotor centers are stimulated and the systemic pressure rises to maintain cerebral blood flow.
  • Usually, this is accompanied by a slow bounding pulse and respiratory irregularities.
  • These changes in blood pressure, pulse, and respiration are important clinically because they suggest increased ICP.
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15
Q

ICP & CO2

A
  • The concentration of carbon dioxide in the blood and in the brain tissue also plays a role in the regulation of cerebral blood flow.
  • An increase in the partial pressure of arterial carbon dioxide (PaCO2) causes cerebral vasodilation, leading to increased cerebral blood flow and increased ICP.
  • A decrease in PaCO2 has a vasoconstrictive effect, limiting blood flow to the brain.
  • Decreased venous outflow may also increase cerebral blood volume, thus raising ICP.
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16
Q

Cerebral Edema

A
  • Cerebral edema or swelling is defined as an abnormal accumulation of water or fluid in the intracellular space, extracellular space, or both, associated with an increase in the volume of brain tissue.
  • Edema can occur in the gray, white, or interstitial matter.
  • As brain tissue swells within the rigid skull, several mechanisms attempt to compensate for the increasing ICP.
  • These compensatory mechanisms include autoregulation as well as decreased production and flow of CSF.
    β€” Autoregulation refers to the brain’s ability to change the diameter of its blood vessels to maintain a constant cerebral blood flow during alterations in systemic blood pressure.
    β€” This mechanism can be impaired in patients who are experiencing a pathologic and sustained increase in ICP.
17
Q

Cerebral Response to Increased Intracranial Pressure

A
  • As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage.
  • The brain can maintain a steady perfusion pressure if the arterial systolic blood pressure is 50 to 150 mm Hg and the ICP is less than 40 mm Hg.
  • Changes in ICP are closely linked with cerebral perfusion pressure (CPP).
  • The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP).
    β€” For example, if the MAP is 100 mm Hg and the ICP is 15 mm Hg, then the CPP is 85 mm Hg.
  • The normal CPP is 70 to 100 mm Hg.
  • As ICP rises and the autoregulatory mechanism of the brain is overwhelmed, the CPP can increase to greater than 100 mm Hg or decrease to less than 50 mm Hg.
  • Patients with a CPP of less than 50 mm Hg experience irreversible neurologic damage.
    β€” Therefore, the CPP must be maintained at 70 to 80 mm Hg to ensure adequate blood flow to the brain.
    β€” If ICP is equal to MAP, cerebral circulation ceases.
18
Q

ICP & Cushing’s response

A
  • A clinical phenomenon known as the Cushing’s response (also called Cushing’s reflex) is seen when cerebral blood flow decreases significantly.
  • When ischemic, the vasomotor center triggers an increase in arterial pressure in an effort to overcome the increased ICP.
  • A sympathetically mediated response causes an increase in the systolic blood pressure with a widening of the pulse pressure and cardiac slowing.
  • This response is seen clinically as an increase in systolic blood pressure, widening of the pulse pressure, and reflex slowing of the heart rate.
  • It is a late sign requiring immediate intervention; however, perfusion may be recoverable if the Cushing’s response is treated rapidly.
  • At a certain point, the brain’s ability to autoregulate becomes ineffective and decompensation (ischemia and infarction) begins.
  • When this occurs, the patient exhibits significant changes in mental status and vital signs.
  • The bradycardia, hypertension, and bradypnea associated with this deterioration are known as Cushing’s triad, which is a grave sign.
19
Q

Herniation
ICP after Cushing triad

A
  • herniation of the brain stem and occlusion of the cerebral blood flow occur if therapeutic intervention is not initiated.
  • Herniation refers to the shifting of brain tissue from an area of high pressure to an area of lower pressure (see Fig. 61-2).
  • The herniated tissue exerts pressure on the brain area into which it has shifted, which interferes with the blood supply in that area.
  • Cessation of cerebral blood flow results in cerebral ischemia, infarction, and brain death.