SCHEMATIC PATHOPHYSIOLOGY

Occlusion by major vessel

Atherosclerosis

Thrombosis

Hypertension

Formation of Plaque deposits

Predisposing Factors:

1) Age ۞2) Heredity ۞3) Race

4) Sex ۞5) Prior Stroke, TIA or heart attack ۞6) Socioeconomic Factors ۞

Precipitating Factors:

1) Hypertension ۞2) Cigarette Smoking

3) Diabetes Meliitus ۞4) Carotid or other Artery Disease ۞5) Atrial Fibrillation

6) Other heart disease

7) Sickle cell disease

8) Undesirable levels of cholesterol

9) Poor diet ۞10) Physical inactivity

11) Obesity

12) Alcohol Abuse

13) Drug Abuse

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If not managed

Lysed or moved thrombus from the vessel

Vascular wall becomes weakened and fragile

Leaking of blood from the fragile vessel wall

Guarded Prognosis

Cerebral Hemorrhage

If managed:Dx: CT scan, MRI, cerebral angiography,

arteriography, lumbar puncture, skull x-ray

Tx: chronic hypertensives, surgical decompression, evacuation and

aspiration, administration of fresh frozen plasma with fibrinogen or cryoprecipitate

If not managed

Hematoma evacuation

Sx:, headache,unconsciousness, nausea/vomiting,

visual disturbances

If managed:

Actual:Dx: Cranial CT scan (6/16/08)Capsuloganglionic bleedLacunar infarct, Bilateral Internal Carotid AteriosclerosisDoppler (6/16/08)Mean flow velocities and pulsatility index of both anterior and posterior circulation within normal limits

EEG/ECG, skull x-ray, carotid ultrasonography

TX: aspirin within 24 hrs, thrombolytics within 3 hours, carotid stenting,

hypothermia, anticoagulants, surgical

decompression (hemicraniectomy), carotid

endartectomy

Possible:Dx: PET scan, MRI,

cerebral angiography, lumbar puncture,

EEG/ECG, skull x-ray, carotid ultrasonography

TX: aspirin within 24 hrs, thrombolytics

within 3 hours, carotid stenting, hypothermia,

anticoagulants, surgical decompression

(hemicraniectomy), carotid endartectomy

Formation of cavity surrounded by dense gliosis

Mass of blood forms and grows

Decreased ICP

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Formation of small and large clots

Vasospasm of tissue and arteries

CEREBRAL HYPOPERFUSION Sx: dizziness,

confusion, headache

Impaired distribution of oxygen and glucose

Tissue hypoxia and cellular starvation

Cerebral Ischemia

Initiation of ischemic cascade

Anaerobic metabolism by mitochondria

Production of oxygen free radicals and other reactive

oxygen speciesGenerates large amounts of lactic acid

Blood seeps into the ventricles

Obstruction of CSF passageway

Accumulation of CSF in the ventricles

Ventricles dilate behind the point of obstruction

If not managedIf managed:Ventriculostomy,

VP shunt, ICP Monitoring

Alternative route for return of CSF in the circulation

Unrelieved obstruction

Compression of brain tissues will

not occur

Guarded Prognosis

< 30 ml hemorrhage

30-60 ml hemorrhage

> 60 ml hemorrhage

Increased ICP

Lodges unto other cerebral

arteries

Poor prognosisIntermediate prognosis

Good prognosis

Metabolic Acidosis

Failure production of adenosine triphosphatase

Failure of energy dependent process

(ion pumping) 85

Release of excitatory neurotransmitter glutamate

Influx of calcium

Damage to the blood vessel endothelium

Activates enzymes that digest cell proteins, lipids

and nuclear material

Failure of mitochondria

Transient Ischemic Attack

If managed:-t-PA (urokinase,

streptokinase)-calcium channel

blockers

If not managed

Guarded Prognosis

Brain sustains an irreversible cerebral damage

Release of metalloprotrease(zinc and calcium-dependent enzymes)

Break down of collagen, hyaluronic acid and other elements of connective tissue

Structural integrity loss of brain tissue and blood vessels

Breakdown of the protective Blood Brain Barrier

Further energy depletion

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Cerebral edema

Vascular Congestion

Compression of tissue

Increased intracranial pressure

Impaired perfusion and function

Middle Cerebral Artery

Anterior cerebral artery

Posterior CerebraI Artery

Internal Carotid Artery

Vertebrobasilar System

Anteroinferior Cerebellar

Posteroinferior cerebellar

Lateral hemisphere,

frontal, parietal and temporal lobes, basal

ganglia

Frontal Lobe Occipital lobe; anterior and

medial portion of temporal lobe

Branches into ophthalmic, PCA, anterior choroidal, ACA, MCA

Cerebellum and brain stem

Cerebellum Cerebellum

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Sx:

Contralateral

hemiparesis or

hemiplegia,

unilateral

neglect, altered

consciousness

, homonymous

hemianopsia,

inability to turn

eyes toward

affected side,

vision changes,

dyslexia,

dysgraphia,

aphasia,

agnosia,

memory deficits,

vomiting

Sx:

Contralateral

hemiparesis,

foot and leg

deficits greater

than the arm,

foot drop, gait

disturbances,

contralateral

hemisensory

alterations,

deviation of

eyes toward

affected side,

expressive

aphasia,

confusion,

amnesia, flat

affect, apathy,

shortened

attention span,

loss of mental

acuity, apraxia,

incontinence

Sx:

Mild

contralateral

hemiparesis,

intention

tremor, diffuse

sensory loss,

pupillary

dysfunction,

loss of

conjugate

gaze,

nystagmus,

loss of depth

perception,

cortical

blindness,

homonymous

hemianopsia,

perseveration,

dyslexia,

memory

deficits, visual

hallucinations

Sx:

contralateral

hemiparesis

with facial

asymmetry,

contralateral

sensory

alterations,

homonymous

hemianopsia,

ipsilateral

periods of

blindness,

aphasia if

dominant

hemisphere is

involved, Mild

Horner’s

syndrome,

carotid bruits

Sx:

Alternating

motor

weaknesses,

ataxic gait,

dysmetria,

contralateral

hemisensory

impairments,

double vision,

homonymous

hemianopsia,

nystagmus,

conjugate

gaze,

paralysis,

dysarthria,

memory loss,

disorientation,

drop attacks,

tinnitus,

hearing loss,

vertigo,

dysphagia,

coma

Sx:

Ipsilateral

ataxia, facial

paralysis,

ipsilateral loss

of sensation in

face, sensation

changes on

trunk and

limbs,

nystagmus,

Horner’s

syndrome,

tinnitus,

hearing loss

Sx:

Ataxia,

paralysis of the

larynx and soft

palate,

ipsilateral loss

of sensation in

face,

contralateral on

body,

nystagmus,

dysarthria,

Horner’s

syndrome,

hiccups and

coughing,

vertigo, nausea

and vomiting

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If managed:Palliative care-

Frequent vital sign and neurovital signs,

intubation, mechanical ventilation,

vasodilators, osmotic diuretics,

ventriculostomy, ICP monitoring

If not managed:

Continued insufficiency of blood

flow

Further compression of tissues

Coma

Cerebral Death

Loss of neural feedback

mechanisms

Cessation of physiologic

functions

Poor cerebral perfusion

Poor improvement

Poor Prognosis

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Cardiovascular

System

Pulmonary

SystemGIT

GUT Other systems

Relaxation of

venous valves

Loss of cardiac

muscle function

Sx: bradycardi

a

Sx: hypotensio

n

Failure of accessory

muscles for breathing

Loss of lung

movement

Sx: apnea

Relaxation of

intestines and

sphincters

Neurogenic bladder Loss of sphincter

control

Cardiopulmonary arrest

Systemic Failure

DEATH

Decreased

cardiac output

Sx: restlessness, abnormal

thermoregulation, mental confusion,

increased secretions, decreased urinary

output.

Loss of bowel

control

90