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Slide 1: SCHEMATIC PATHOPHYSIOLOGY 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 Formation of Plaque deposits Thrombosis Hypertensio Occlusion by major vessel 83
Slide 2: If managed: Actual: Dx: Cranial CT scan (6/16/08) Capsuloganglionic bleed Lacunar infarct, Bilateral Internal Carotid Ateriosclerosis Doppler (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 If not managed 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 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 Decreased ICP Hematoma evacuation Formation of cavity surrounded by dense gliosis If not managed Sx:, headache, unconsciousness, nausea/vomiting, visual disturbances Mass of blood forms and grows 84
Slide 3: < 30 ml hemorrhage Good prognosis 30-60 ml hemorrhage Intermediate prognosis > 60 ml hemorrhage Poor prognosis Vasospasm of tissue and arteries Blood seeps into the ventricles Obstruction of CSF passageway Accumulation of CSF in the ventricles Ventricles dilate behind the point of obstruction Increased ICP Formation of small and large clots Sx: dizziness, confusion, headache CEREBRAL HYPOPERFUSION Impaired distribution of oxygen and glucose Tissue hypoxia and cellular starvation Lodges unto other cerebral arteries Cerebral Ischemia Initiation of ischemic cascade 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 85
Slide 4: 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 Further energy depletion Transient Ischemic Attack If managed: -t-PA (urokinase, streptokinase) -calcium channel blockers 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 86
Slide 5: Cerebral edema Vascular Congestion Compression of tissue Increased intracranial pressure Impaired perfusion and function Middle Cerebral Artery Lateral hemisphere, frontal, parietal and temporal lobes, basal ganglia Anterior cerebral artery Frontal Lobe Posterior CerebraI Artery Occipital lobe; anterior and medial portion of temporal lobe Internal Carotid Artery Branches into ophthalmic, PCA, anterior choroidal, ACA, MCA Vertebrobasilar System Cerebellum and brain stem Anteroinferior Cerebellar Cerebellum Posteroinferior cerebellar Cerebellum 87
Slide 6: 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
Slide 7: If managed: Palliative careFrequent 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 Poor cerebral perfusion Coma Poor improvement Cerebral Death Poor Prognosis Loss of neural feedback mechanisms Cessation of physiologic functions 89
Slide 8: 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 Sx: hypotensio Loss of bowel Failure of accessory Loss of lung movement Neurogenic bladder Sx: apnea control Decreased cardiac output muscles for breathing Loss of sphincter control Cardiopulmonary arrest Systemic Failure DEATH 90