schematic pathophysiology cva
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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
83
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
84
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
86
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
87
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
88
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
89
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
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