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58 Cards in this Set
- Front
- Back
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Warning signs of stroke
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Sudden numbness/weakness of face, arms, or legs, esp. unilaterally
Sudden confusion, trouble speaking, or understanding Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance or coordination Sudden severe HA w/ no known cause (worst HA ever) |
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Timeline of tx for ischemic stroke
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t-PA: first 3 hrs, IV. Admin. 10% in 1 min, then rest over 1 hr
Anticoagulants: Need INR b/w 2 and 3.5, prevent more clot formation or further advanc. of clot Antiplatelets: inhibit plt aggregation. Clopidogrel and ASA Ca channel blockers: penumbra protection DON'T manage BP unless systolic >180 |
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Timeline of tx for hemorrhagic stroke
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Ca channel blockers, anxiolytics, analgesics, anticonvulsants, corticosteroids (reduce swelling), diuretics, anti-htn
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Citicoline
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Neuroprotective and neuroreparative, given w/in 24 hr of onset, improvement w/in 3 mos.
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Ancrod
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Phase 3 Testing, thrombolytic can be given w/in 6 hrs, directly degrades plasminogen
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Location of thrombotic strokes
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Large vessels: most common, substantial neurological defecits
Small vessels: "small strokes" or "silent strokes" or "mini strokes". Closely linked to htn |
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Etiology of thrombotic stroke
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Accelerated atherosclerotic process->fatty plaque in artery->turbulent blood flow-> damage to plaque-> immune response-> blood clot formation-> stroke
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Risk factors for thrombotic stroke
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2/3 r/t htn and DM (both accelerate atherosclerosis), oral contraceptives, polycythemia vera, polycythemia from chronic hypoxia, dehydration, renal hypoxia-> incr. RBC
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Etiology of embolic stroke
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Clot originates elsewhere and travels to brain, may be 2 to thrombotic. Most common cause is heart d/o...afib, MI, endocarditis
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Intracerebral hemorrhage
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Hemorrhage into brain tissue, usually caused by an aneurysm in a lg or sm artery, htn is primary cause
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Subarachnoid hemorrhage
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into subarachnoid space, pressure on brain tissue from collection of blood in subarachnoid space, most often caused by and aneurysm, htn inc risk of rupture
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S/S of R hemisphere stroke
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Left hemiplegia, L-sided neglect, spatial perceptual deficits, denies problems, performs activities rapidly, short attention span, impulsive, impaired judgment, impaired memory and time concepts, indifference to disability
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S/S of L hemisphere stroke
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Right hemiplegia, impaired speech, language aphasias, slow behavioral style, cautious, aware of deficits, depression, anxiety, impaired comprehension r/t lang. and math. Slower rehab, some not successful
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S/S of cerebellum stroke
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Problems w/ balance and coordination, dizziness, n/v
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S/S of brain stem stroke
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Especially devastating, impaired breathin, HR and rhythm, hearing swallowing difficulties, eye mov't, may have paralysis on both sides
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TIA
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Cerebral ischemic event lasting less than 24 hrs, typically lasting only minutes w/o apparent permanent neurologic deficits, few min. of symptoms of CVA, may have better collateral circulation
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Stroke in evolution
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Worsening of neurologic deficits over minutes or hours suggesting a widening of ischemic area
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Modifiable risk factors for stroke
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Cigarettes, excessive alcohol intake, obesity, high fat diet, drug abuse, cardiac dz, htn, dm, migrain ha, hypercoagulation states, obesity
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Non-modifiable risk factors for stroke
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Age, gender (slightly higher in males), race (slightly higher in AA), heredity (certain char. lead to decr. atherosclerosis)
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Patho of stroke
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Reduced cerebral bloodflow, cells lose ablility to prod. ATP, Intracellular Ca elevated, cells release excessive amts of glutamate, w/o neuroprotectors, nerve cells damaged w/in 5 min. Ca activates proteases (digest protein) and lipase (digest cell membrane). Free radicals form as a result of ischemic cascade
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Initial response to stroke
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Evaluate ABCs, perform neuro exam, obtain targeted hx (can get t-PA), O2 and IV saline. Don't tx elevated BP, will go down eventually
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Diagnostic tests for stroke
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CT, carotid ultrasound, MRI, EKG, CXR, blood and plt count, PT, lytes, BG, ABGs, ETOH and drug screen
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Ischemic stroke first 6 hrs
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Monitor and correct any compromise in ABC., do not tx BP w/o specific indications (S>180, D>120). Drugs: tPA, streptokinase, anticoagulation, Ca channel blockers (nimodipine, Cerestat), anxiolytic, seizure control, comfort family, monitor for cerebral perfusion changes (incr ICP >15 for 15-30 sec, decr. in GCS, decr. LOC, MAP <80 or s <100), monitor for bradycardia, altered pattern of breathing, loss of response to painful stimuli, chage in pupil reactivity, HA, vomiting
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Exclusion criteria for tPA
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Use of hep w/in 48 hrs, plt <100,000, current use of coumadin, PT >15, stroke or head injury w/in 3 mos, major surgery w/in 2 wks, pretx s>185, d>110, prior intracranial hemorrhage, GI or GU bleeding w/in 3 wks, seizure at onset of stroke, BG <50 or >400, recent MI, rapidly improving neruological signs
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Hemorrhagic stroke first 6 hrs
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Monitor and correct any compromise in ABC, tx elevated BP, assess w/ NIH scale, monitor for changes in cerebral perfusion, prepare pt for neurosurgical consult, Ca channel blockers, anxiolytics, analgesics, seizure control.
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Aphasia
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Damage to language centers of the brain, characterized by either partial or total loss of the ability to speak, listen, read, or write. May be temporary or permanent. Usually ischemic stroke in L hemisphere
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Expressive aphasia
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Broca's area, occurs w/ infactions in the frontal lobes of the brain, affects ability to write or speak words. Difficulty combining speech sounds into words. Best chance of recovery w/ extensive PT, aware of deficit
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Receptive aphasia
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Wernicke's area, occurs w/ infarctions in the termporal lobe, affects comprehension of written, printed, or spoken works. Can't understand. Output devoid of meaning, unaware of defecit, prognosis poor
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Postop care of endarterectomy
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Neruo assessments q1-2h, Assess facial, vagus, spinal accessory, and hypoglossal nerve function. Dysfunction is temporary but may last a few mos. Head alignment straight for airway and min. trauma to surgical site, antiplt agents, supine or side-no neck flexion, elevate HOB when VS stable, cold pack to site, assess breathing pattern, pulse, and BP (maintain w/in 20 mm of preoperative BP), Labile BP common b/c baroreceptors in carotid, monitor for swelling or hematoma, bleeding precautions
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Preventing aspiration in dysphagia
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Feeding: sit upright and tuck chin, 90 degrees, take b/w 1-1.5 hrs, , foods that require no chewing, pharyngeal reflexes, gradually progress foods, alternate liquids w/ solids, never give un-thickened liquids, check for food on affected side, NG in duodenum, place hand on forehead, approach from midline, plates w/ high arch
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Homonymous hemianopia
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visual loss in the same half of the visual field of each eye, may be either side, top, or bottom
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Elimination p stroke
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Uninhibited bladder (freq, urgency, and incontinence). Neurogenic bowel-pt. may seem fixated on having a bowel mov't. Other causes: memory lapses, inattention, emotional factors, inability, to communicate, impaired physical mobility, and infection.
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Unilateral neglect
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Most common in r-stroke, rehab considered complete p 6 mos (won't progress p this time), caregivers experience anxiety, depression, and alteration in lifestyle. A percieved lack of support by the pt can decr success of rehab. Want to incr. muscle strength, ROM, and mobility, prevention, ADLs, Safety, sustained attention training, video feedback, rx glasses w/ mirror, meds (ritalin), educational support for family, functional support, and emotional support
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General patho of shock
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Inadequate perfusion-cell hypoxia-energy deficit-lactic acid prod.-decr in pH-metab. acidosis:
1. cell membrane dysfunction and failure of Na pump-hysosomes release digestive enzymes (influx of Na and H2O, efflux of K)-toxic subst. enter circ-capillary endothelium damaged-further destruction and cell death 2. Metab. acidosis-vasoconstriction(CO2 and H)-failure of pre-capillary sphincters-peripheral pooling of blood-clotting-DIC |
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Hypovolemic shock
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Loss of fluid (through blood or fluid loss), approx 15-25% deficit. Can be internal or external loss.
Decr volume-decr venous return-decr filling pressure- decr. stroke volume- decr. CO- decr. tissue perfusion |
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Cardiogenic Shock
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Inability of heart to pump (MI, myocarditis, valvular dysfunction, dysrhythmias, obstruction to blood flow). Decr. pumping ability-decr emptying of ventr.-increased filling pressure-decr. SV-decr. CO-decr. tissue perfusion (continuous cycle)
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Vasogenic shock
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(Distributive shock) Massive vasodilation from interferences w/ sympathetic nervous system or effects of histamine or other toxins. Volume is adequate but not being distributed correctly.
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Types of vasogenic shock
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Neurogenic-injury/dz of spinal cord. May happen immediately p SCI b/c massive loss of spinal tone
Anaphylactic Septic |
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Patho of neurogenic shock
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D/O that interrupt the normal vasomotor center in medulla resulting in inhibition of symp. activity->massive vasodilation
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Patho of anaphylactic shock
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Histamine->vasodilation-decr BP
Serotonin->incr. capillary perm. (3rd spacing)-decr. volume-decr perfusion |
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Etiology of septic shock
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Gram negative though positive gaining. Most that die began as nosocomial infect. Usually in a pt. that is critically ill/already in ICU.
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Patho of septic shock
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Endotoxin released from cell wall-vasodilitation:
1. decr. venous return-decr filling pressure-decr. SV 2. decr peripheral resistance-decr afterload-skin warm and dry (warm shock). |
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Compensatory stage of shock
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Complex neurological, hormonal, and chemical responses to overcome ineffective circulation. Body activating every compensatory process trying to incr. perfusion, conserve Na and H2O, vasoconstrict, incr. CO
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Neuro changes in compensatory stage
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Incr. sympathetic nervous system involvement-stim. alpha and beta receptors, increases CO-incr. blood flow to heart and brain at expense of viscera and kidneys
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Hormonal changes in compensatory stage
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Hypothalamus releases ACTH to increase volume and BP. Slower is RAA response->retention of Na and H2O (ADH and aldosterone)
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Chemical changes in compensatory stage
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Chemoreceptors stimulate incr. resp. (initially), may see initial resp. alkalosis
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Clinical findings in compensatory stage
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BP normal but slightly elevated
HR-sinus tach. (around 120) Skin-cool, pale, clammy r/t vasoconstriction if vessels respond) Urine-decr. output <30 cc/hr LOC-restless, anxious or confused Resp-tachypnea Bowel sounds-decreased Pupil-dilated but reactive Labs-hyperglycemia, hypernatremia, hypoxemia, hypocapnia (r/t tachypnea), resp. alkalosis |
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Progressive stage of shock
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Compensatory mechanisms lose efficacy. MODS a result of symptoms. Anaerobic metabolism resulting in incr. in lactic acid and severe acidosis
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Clinical findings in Progressive stage
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BP-decr. w/ narrow pulse pressure
HR->150, dysrhytmias Fall in uring output Sx of ARF (BUN, creatinine) Altered LOC Incr. resp-shallow now-resp. acidosis. Crackles in lungs (fluid from leaky capillaries) Metabolic and respiratory acidosis w/ hypoxemia Pt complains of angina, palpitations, weakness, muscle aches, SOB, n/v, anorexia |
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Irreversible/Refractory Stage
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Shock state so profound that death is inevitable. Profound hypotn despite admin. of potent vasoactive drugs. BP of 50/?. Remains hypoxemic w/ O2, circulatory failure, DIC
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ABG changes
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Compensating: low PaCO2 w/ low pH and bicarb
Incr. PaCOx w/ low pH-need resp assist. |
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Assessment of fluid volume in shock
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ABC, pulse, BP, skin color, temp, heart sounds, peripheral pulses, state of hydration, skin perfusion, mucous membranes, sclera, conjuctivae, presence of pallor or cyanosis, JVD
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Shock positioning
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Modified Trendelenburg. Feet elevated, back flat, head and shoulders slightly elevated
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Fluid replacement for hypovolemic shock
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1: LR or NS, 3:1 rule (crystalloids)
2. Non blood plasma expanders (colloids) 3. Blood only in extreme emergencies |
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Fluid replacement for cardiogenic shock
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1. Perform fluid challenge-no change? Admin. NS or LR
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Fluid replacement for anaphylactic shock
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NS
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Fluid replacement for septic shock
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NS, if BP unresponsive, then Colloids. Blood if DIC develops
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Fluid replacement for neurogenic shock
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NS to restore volume
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