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PATHOPHYSIOLOGY OF CVA
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
Atherosclerosis
Actual: Dx: If Cranial CT scan (6/16/08) managed: Capsuloganglionic bleed Lacunar infarct, Bilateral Internal Carotid Possible: Ateriosclerosis Dx: PET scan, MRI, Doppler (6/16/08) cerebral angiography, Mean flow velocities and lumbar puncture, pulsatility index of both EEG/ECG, skull x-ray, anterior and posterior carotid ultrasonography circulation within normal limits TX: aspirin within 24 hrs, thrombolytics EEG/ECG, skull x-ray, within 3 hours, carotid carotid ultrasonography stenting, hypothermia, anticoagulants, surgical TX: aspirin within 24 hrs, decompression thrombolytics within 3 (hemicraniectomy), hours, carotid stenting, carotid endartectomy hypothermia, anticoagulants, surgical decompression (hemicraniectomy), carotid endartectomy Guarded Prognosis Cerebral Hemorrhage If not managed
If not managed
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 Decreased ICP Hematoma evacuation Formation of cavity surrounded by dense gliosis
Blood seeps into the ventricles Obstruction of CSF passageway Accumulation of CSF in the ventricles Ventricles dilate behind the point of obstruction Increased ICP
CEREBRAL HYPOPERFUSION Impaired distribution of oxygen and glucose Tissue hypoxia and cellular starvation
If managed: Ventriculostomy, VP shunt, ICP Monitoring Alternative route for return of CSF in the circulation Compression of brain tissues will not occur
If not managed Anaerobic metabolism by mitochondria Unrelieved obstruction Generates large amounts of lactic acid Guarded Prognosis Metabolic Acidosis Failure production of adenosine triphosphatase Failure of energy dependent process (ion pumping) Production of oxygen free radicals and other reactive oxygen species
Activates enzymes that digest cell proteins, lipids and nuclear material
If not managed
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
Guarded Prognosis
Cerebral edema
Vascular Congestion
Compression of tissue
Middle Cerebral Artery Lateral hemisphere, frontal, parietal and temporal lobes, basal ganglia
Posterior CerebraI Artery Occipital lobe; anterior and medial portion of temporal lobe
Internal Carotid Artery Branches into ophthalmic, PCA, anterior choroidal, ACA, MCA
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 Horners 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, Horners syndrome, tinnitus, hearing loss Sx: Ataxia, paralysis of the larynx and soft palate, ipsilateral loss of sensation in face, contralateral on body, nystagmus, dysarthria, Horners syndrome, hiccups and coughing, vertigo, nausea and vomiting
If managed: Palliative careFrequent vital sign and neurovital signs, intubation, mechanical ventilation, vasodilators, osmotic diuretics, ventriculostomy, ICP monitoring
If not managed:
Poor Prognosis
Loss of neural feedback mechanisms
Cardiovascular System
Pulmonary System
GIT
GUT
Other systems
Relaxation of Loss of cardiac muscle function Relaxation of venous valves intestines and sphincters Sx: restlessness, abnormal thermoregulation, mental confusion, increased secretions, decreased urinary output.
Sx: bradycardi a
Sx: hypotensio n Loss of bowel Failure of accessory Loss of lung movement Neurogenic bladder Sx: apnea control
DEATH