PREDISPOSING FACTORS:

Over weight / obesity Stress Smoking Cocaine use / abuse Sedentary lifestyle Diet ↑ in fats, Na, cholesterol

↑Serum ↑Fat on the Eat more Smoke Stimulation ↑LDL ↓O2 carry Vasoconstriction ↑CO in ↑RBC Induce Enhance of ↑BP Poor Accumulation of fatty ↑ Attraction of H2O Deposits of fatty materials in
Cholesterol abdomen more on of capacity of blood vasospasm tablet circulation streaks in the arterial wall in the blood the arterial walls of arteries
and hips ↑Serum catecholamine blood ↑Vascular resistance ↑Blood activity
↑LDL ↓HDL cholesterol High risk thickness ↑Cardiovascular disorder ↑Blood volume vascular changes
↑Workload ↑Blood sugar ↓Tissue Perfusion ↑BP of injury
Accumulate to intimal ↑Dot ↑Blood cholesterol level and BP
Of LDL ↑Blood viscosity arterial wall formation
PHARMACOLOGIC:
ANTI-PLATELET DRUG

PRDISPOSING FACTORS:
Hypertension Age Gender Previous heart disease Diabetes Familial disease

↑ Vascular ↑ Workload Degenerative changes in Male hormones Altered arterial wall integrity ↑Blood sugar ↑Risk for DM, heart
resistance of the heart the function of the heart diseases, hypercoagualable
←UNCONTROLLED ↓HDL ↑Lipid/platelet adherence to ↑Blood vscocity state, hypercholesterolemia
↑Pressure in Cardiomegaly ↓Elastin vessel walls
Cerebral Blood ↓Vessel Accumulation of ↑BP
Vessel Heart weakens ↓Elasticity of the blood vessel flexibility LDL in the arterial Atheroma/clot formation
over time wall PHARMACOLOGIC: ↑Workload of the heart
Recombant Tissue
Loss of Impaired Atherosclerosis Hardening Plasminogen
Activator
elasticity cerebral of arterial wall **monitor for ↑Size of heart
autoregulation ↑Risk for vessel injury
Weaker heart
Ruptured central ↑Lipid/platelet ↑risk for
blood vessel adherence to rupture ↓Cardiac output >> Maintain Cardiac Output @ 4-8 L/min.

vessel walls
↓Tissue perfusion
PHARMACOLOGIC:
Recombant Tissue
Plasminogen
Activator Microvascular changes
**monitor for

Chronic blood glucose

Atered macrovascular integrity

 Cerebral
Thrombotic Stroke Angiogram

Development of atherosclerosis of the blood vessel wall

Plaques develop on the inner wall of the affected blood vessel

Accumulates LDL within the arterial wall

Stimulate methodical cells to adhere to monocytes

Maturation of monocyte in the macrophages

Ingest LDL particles

Macrophage ingest a critical mass of LDL

Becomes foam cells

Constitutes fatty streaks on the inner arterial wall (earliest manifestation of arterial plaques)

Additional growth of the lesion through influence of inflammatory molecules

Form a fibrous cover over the liquid core

Separates it from blood flow through the vessel

Plaque rupture

Exposes foam cells to clot promoting elements in the blood

Clot formation

Dislodgement → Embolic Stroke Echocardiogram

If at sufficient size

Electrocardiogram
May interrupt blood flow to the brain tissue implies

CT scan
ISCHEMIA
PHARMACOLOGIC:
t-Pa Therapy
ANTI-PLATELET DRUG

Neutroxins (oxygen free radical nitric oxide glutamate) released

Local acidosis developed

Membrane depolarization occur

Influx of calcium sodium

Cytoxic edema and cell death → Stroke area or core

Zone of hyperperfusion (penumbra) becomes prone to death if circulation is not restored → neurologic damage

Embolus dislodgement

Travels to the cerebral arteries via carotid artery or vestibular system

Lodge in smaller cerebral arteries blood vessel at point of bifurcation or where the lumen narrow

Emboli occlude the vessel

t-Pa Therapy
Ischemia develop

If embolus break cell into fragments If damage to vessel wall is significant

PHARMACOLOGIC: Cerebral
Recombant Tissue
Enters the blood vessels Vessel integrity interrupted Plasminogen Angiogra
Lumbar puncture Activator m
**monitor for

Enters the small blood vessels Vasospasm ↔ Cerebral hemorrhage → HEMORRHAGIC STROKE CT scan
 Embolus is absorbed

Remission of S/Sx Nuchal Regidity Headache ↑ BP

>> Supplemental oxygen

>> Maintain hemoglobin and ↓ Cerebral perfusion Inflammatory process Entry of blood to menigeal space
hematocrit @ acceptable levels

CEREBRAL HYPOXIA Release leukocytes in ↑ Intracranial pressure

Interstitial space and
Neurologic altered neutrophils for CEREBRAL COMPRESSION
damage level of phagocytosis AND INJURY
consciousness
Coma
BRAIN TISSUE INFARCT MRI

+ DEATH +

Magnetic Resonance Angiography

NEROLOGICAL DEFICITS
OSMOTIC DIURETICS
Middle Cerebral Artery (MCA) – most commonly affected
>> Maintain PaCO2 @ 30-45mmHg.
Internal Carotid Artery – 2nd most frequently affected >> Elevate the head of the bed.
>> Supplemental oxygen
>> Obtain vital signs

Massive infarction of most lateral hemisphere and deeper structure of the frontal, parietal and temporal lobes

Hemiplegia Hemipharesis Apraxia Aphasia/Dysarthia Sensory Deficit Dysphagia

>> Have P atient sit in upright, preferably
in chair while eating or drinking.