REGENCIA CVA PATHO

8/2/2019 REGENCIA CVA PATHO

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CEREBRAL VASCULAR ACCIDENT

Predisposing factors:

1. Advancing age

2. Gender (males)3.Race (African Americans)

4. Family history of stroke

Precipitating factors:

1.Hypertension

2. Heart disease

(atrial fibrillation)

3. Diabetes mellitus4. Sleep apnea

5. Blood cholesterol

levels6. Smoking

7. Sickle cell disease

8. Substance abuse9. Living in the stroke

belt10. Prior stroke, carotid stenosis,

and a history of TIA11.Heavy alcohol consumption

12. Obesity

13. Specific to women: oralcontraceptive use, pregnancy,

childbirth,menopause, migraineheadaches with aura, autoimmune

d/os (diabetes and lupus), clotting

factor disorders

Atherosclerosis

Atherosclerotic plaques





RELEASE THE

CAN DEVELOP ANYWHERE

enzyme Adenosine

Diphosphate

initiates the clotting

sequence

THROMBUS

FORMS

small, deep penetrating

arteries( lenticulostriate arteries)from the middle cerebral artery

common site: internalcarotid artery, vertebral arteries

and the junction of the vertebral and basilar

arteries

OCCLUSION

LACUNAR

STROKE

thrombus may remain in place

and continue to enlarge



INITIATES

WITHIN FEW

MONTHS OF THE

INFARCTION

BEGINS

WHEN

INFARCTION

part of it may break off

EMBOLUS

carried through

the arterialsystem

Brain

lodged in a vessel too narrow to permit

further movement (most common

site: left middle cerebral artery)

completely occluding

the lumen of the

vessel

disruption of thecerebral blood

flow

ISCHEMICCASCADE

cerebral blood flow

falls to<25ml/100g/min

DIE

only minor deficits

are seen since theseareas are very small

cells DISTAL tothe occlusion

cells

CRITICALLY

more severemanifestations

may developincluding paralysis

and sensory loss

Necrotic brain cells areREABSORBED by macrophage activity

a very small cavity or

lake is formed



RENDERS

INCREASING

THE POTENTIAL

neurons can no longer maintain aerobic

respiration

Mitochondria

switch

Anaerobic respiration

large amounts of

lactic acid

change in the pH level

neuron incapable of producing

sufficient quantities of adenosine triphosphate

(ATP)

NA- K pump fails

breaks up into

smaller fragments

not absorbed

>drowsiness, stupor,

coma

>contralateral hemiplegiaof the arm and face

>contralateral sensorydeficits of the arm and face

>global aphasia (if dominanthemisphere is involved)

>homonymous hemianopia

absorbed by the

body

manifestations

will persist

manifestations will

disappear in a few hours

to a few days

weakenedvessel wall

CEREBRAL

HEMORRHA

GE

HPN



OCCURS WHEN

SUDDEN ENTRY

BLOOD ENTRY OF BLOOD IF CONTINUED

INTO

RESULT

increase in

intracellular calcium

release of glutamate

activate a number of

damaging

pathways

generation of free radicals,

vasoconstriction,

release of more calcium and glutamate,destruction of the cell membrane

Cerebral

vessel ruptures

BRAIN TISSUE

brain tissue affected

by pressure due tomass formation of

blood clot

displaces

brain tissue

decreases cerebral blood flow

rupture of acerebral

aneursym

sudden onsetof a severe

headache

SUBARACHNOID SPACE/VENTRICLES

Irritates the

meningesand brain tissue

Inflammatoryreaction impairing absorption

and circulation of CSF

MINI STROKE/

TRANSIENT ISCHEMICATTACK

sudden onset and

often disappears w/ minutes or hour s

If managed: tPA,

calcium channel blockers



IF NOT MANAGED

ischemia and

infarction

Blood vessel

spasm

infarction

edema

>weakness of one side(including the face, arm

and leg)>slurred speech

>deviation of theeyes

SEVERE

HEMORRHAGE

>hemiplegia

>fixed and dilated pupils>abnormal body posturing

>coma

Putaminal &Internal

capsule

Hemiplegia with more

sensory than motor lossthalamus

Problems w/ visionand eye movement

subthalamus

>contralateral numbnessor weakness of the leg,

hand, forearm

and corner of themouth( middle cerebral artery involvement)

>aphasia (ischemia

of the left hemisphere);>visual disturbances

such as blurring( posterior cerebral artery

involvement)

IRREVERSIBLECEREBRAL

DAMAGE

release of metalloprotease(zinc & calcium- dependent

enzymes)

breakdown of collagen, hyaluronic acid and other elements of connective tissue



severe headache, vomiting,

loss of ability to walk,

dysphagia, dysarthria,eye movement

disturbances

cerebellum

pons

>respiration affected>hemiplegia

>paralysis>coma

>abnormal body posturing>fixed pupils

>hyperthermia

>DEATH

structural integrity loss of brainand tissue and blood vessels

breakdown of the protective

blood brain barrier

CEREBRAL EDEMA

VASCULAR

CONGESTION

Compression

of tissue

increase intracranial

pressure



Impaired perfusion

and function

Contralateralhemiparesis

or hemiplegia,unilateral Neglect,

alteredconsciousness,

homonymous

anopsia,inability to turn

eyes toward

affected side,Vision changes,

dyslexia,Dysgraphia,

Aphasia, agnosia,Memory deficits,

vomiting

ContralateralHemiparesis,Foot and leg deficitsgreater than the arm,

foot drop,gait disturbances,

ContralateralHemisensoryAlterations,

Deviation of Eyes toward

Affected side,Expressive

Aphasia,Confusion,

Amnesia,Flat affect,

Apathy, shortenedAttention span,

Incontinence, acuityApraxia, acuity

Mild contralateralHemiparesis,

Intention tremor,Diffuse sensory

Loss,Pupillary dysfunction,

Loss of conjugateGaze, nystagmus,

Loss of depth

Perception,Cortical blindness,Homonymous

Hemianopsia,Perseveration,

dyslexia,Memory deficits,

Visual hallucinations

Contralateral

Hemiparesis w/

Facial asymmetry,Contralateral

SensoryAlterations,

HomonymousHemianopsia,

Ipisilateral periodsof blindness,aphasia

If dominantHemisphere

is involved,

Horner'ssyndrome

Carotid bruits

Alternating motor Weaknesses,Ataxic gait,dysmetria,

ContralateralHemisensoryImpairments,

Double vision,HomonymousHemianopia, Nystagmus,

Conjugate gaze,Paralysis,Dysarthria,

Memory loss,Disorientation,

Tinnitus,Hearing loss,dysphagia,

vertigo,coma

Ipsilateral

Ataxia, facialParalysis,

Ipsilateral lossof sensation

in face,Sensation changes

onTrunk

and limbs, Nystagmus,

Horner's syndrome,

Tinnitus, hearingloss

Ataxia, paralysis

Of the larynx

And soft palate,Ipsilateral

Loss of sensationIn face,

Contralateral on

Body, Nystagmus,

dysarthria,Horner's

Syndrome,Hiccups

And coughing,

Vertigo, Nausea

And vomting

Anterior cerebral

artery

Posterior cerebralartery

Middle

Cerebral

Artery

InternalCarotid

Vertebrobasilar System

Anteroinferior

cerebellar

Posteroinferior cerebellar

Lateral

hemisphere,

Frontal, parietal

And temporal

Lobes,

basal ganglia

Frontal lobe Occipital lobe;Anterior & medialPortion of temporal

lobe

Branches into

opthalmic,

PCA, anterior

Choroidal,ACA, MCA

Cerebellum,

brain stemCerebellum

Cerebellum



If managed:Palliative care- monitoring v/s

and neurovital signs, intubation,ICP monitoring, intubation,

Mechnical ventilation, vasodilators,Osmotic, diuretics, ventriculostomy

Poor cerebral perfusion

Poor improvement

If not managed

Continued insufficiency of

Blood flow

Further compressionOf tissues

coma

Cerebral death

Loss of neural

feedback mechanisms

Cessation of

physiologic functions



Cardiovascular

Loss of cardiac

musclefunction

Relaxationof venous

valves

Decreased

Cardiac output

Bradycardia Hypotension

Cardiopulmonary arrest

Pulmonary

system

Failure of

Accessory

MusclesFor breathing

Loss of lung

movement

GIT GUT Other systems

Relaxation of

intestinesand sphincters

Loss of bowel

control

Neurogenic bladder

Loss

of sphincter control Restlessness,

abnormal

Thermoregulation,

Mental

Confusion,

Increase

Secretions,

Decreased

urinary

output

Systemic failure

apnea

DEATH

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REGENCIA CVA PATHO