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58 Cards in this Set

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  • Back
Warning signs of stroke
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)
Timeline of tx for ischemic stroke
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
Timeline of tx for hemorrhagic stroke
Ca channel blockers, anxiolytics, analgesics, anticonvulsants, corticosteroids (reduce swelling), diuretics, anti-htn
Neuroprotective and neuroreparative, given w/in 24 hr of onset, improvement w/in 3 mos.
Phase 3 Testing, thrombolytic can be given w/in 6 hrs, directly degrades plasminogen
Location of thrombotic strokes
Large vessels: most common, substantial neurological defecits
Small vessels: "small strokes" or "silent strokes" or "mini strokes". Closely linked to htn
Etiology of thrombotic stroke
Accelerated atherosclerotic process->fatty plaque in artery->turbulent blood flow-> damage to plaque-> immune response-> blood clot formation-> stroke
Risk factors for thrombotic stroke
2/3 r/t htn and DM (both accelerate atherosclerosis), oral contraceptives, polycythemia vera, polycythemia from chronic hypoxia, dehydration, renal hypoxia-> incr. RBC
Etiology of embolic stroke
Clot originates elsewhere and travels to brain, may be 2 to thrombotic. Most common cause is heart d/o...afib, MI, endocarditis
Intracerebral hemorrhage
Hemorrhage into brain tissue, usually caused by an aneurysm in a lg or sm artery, htn is primary cause
Subarachnoid hemorrhage
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
S/S of R hemisphere stroke
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
S/S of L hemisphere stroke
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
S/S of cerebellum stroke
Problems w/ balance and coordination, dizziness, n/v
S/S of brain stem stroke
Especially devastating, impaired breathin, HR and rhythm, hearing swallowing difficulties, eye mov't, may have paralysis on both sides
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
Stroke in evolution
Worsening of neurologic deficits over minutes or hours suggesting a widening of ischemic area
Modifiable risk factors for stroke
Cigarettes, excessive alcohol intake, obesity, high fat diet, drug abuse, cardiac dz, htn, dm, migrain ha, hypercoagulation states, obesity
Non-modifiable risk factors for stroke
Age, gender (slightly higher in males), race (slightly higher in AA), heredity (certain char. lead to decr. atherosclerosis)
Patho of stroke
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
Initial response to stroke
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
Diagnostic tests for stroke
CT, carotid ultrasound, MRI, EKG, CXR, blood and plt count, PT, lytes, BG, ABGs, ETOH and drug screen
Ischemic stroke first 6 hrs
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
Exclusion criteria for tPA
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
Hemorrhagic stroke first 6 hrs
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.
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
Expressive aphasia
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
Receptive aphasia
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
Postop care of endarterectomy
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
Preventing aspiration in dysphagia
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
Homonymous hemianopia
visual loss in the same half of the visual field of each eye, may be either side, top, or bottom
Elimination p stroke
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.
Unilateral neglect
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
General patho of shock
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
Hypovolemic shock
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
Cardiogenic Shock
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)
Vasogenic shock
(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.
Types of vasogenic shock
Neurogenic-injury/dz of spinal cord. May happen immediately p SCI b/c massive loss of spinal tone
Patho of neurogenic shock
D/O that interrupt the normal vasomotor center in medulla resulting in inhibition of symp. activity->massive vasodilation
Patho of anaphylactic shock
Histamine->vasodilation-decr BP
Serotonin->incr. capillary perm. (3rd spacing)-decr. volume-decr perfusion
Etiology of septic shock
Gram negative though positive gaining. Most that die began as nosocomial infect. Usually in a pt. that is critically ill/already in ICU.
Patho of septic shock
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).
Compensatory stage of shock
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
Neuro changes in compensatory stage
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
Hormonal changes in compensatory stage
Hypothalamus releases ACTH to increase volume and BP. Slower is RAA response->retention of Na and H2O (ADH and aldosterone)
Chemical changes in compensatory stage
Chemoreceptors stimulate incr. resp. (initially), may see initial resp. alkalosis
Clinical findings in compensatory stage
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
Bowel sounds-decreased
Pupil-dilated but reactive
Labs-hyperglycemia, hypernatremia, hypoxemia, hypocapnia (r/t tachypnea), resp. alkalosis
Progressive stage of shock
Compensatory mechanisms lose efficacy. MODS a result of symptoms. Anaerobic metabolism resulting in incr. in lactic acid and severe acidosis
Clinical findings in Progressive stage
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
Irreversible/Refractory Stage
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
ABG changes
Compensating: low PaCO2 w/ low pH and bicarb

Incr. PaCOx w/ low pH-need resp assist.
Assessment of fluid volume in shock
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
Shock positioning
Modified Trendelenburg. Feet elevated, back flat, head and shoulders slightly elevated
Fluid replacement for hypovolemic shock
1: LR or NS, 3:1 rule (crystalloids)
2. Non blood plasma expanders (colloids)
3. Blood only in extreme emergencies
Fluid replacement for cardiogenic shock
1. Perform fluid challenge-no change? Admin. NS or LR
Fluid replacement for anaphylactic shock
Fluid replacement for septic shock
NS, if BP unresponsive, then Colloids. Blood if DIC develops
Fluid replacement for neurogenic shock
NS to restore volume