cva Flashcards
stroke
neuro deficits lasting >24 hr
CVA
brain attack
ischemic = 87%, hemorrhagic = 13%
800,000/yr, 4th leading COD, leading cause of serious disability, increased r with oa
rf
htn: hemorrhagic, aneurysm, increased F in BV in brain
hld: increased chol, plaque buildup
tobacco, DM, obesity, OH, fam hx, race
oral contraceptives: increase fibrinogen and coag factor activity
age: but better recovery bc brain atrophy allows more room for expansion
M, sickle cell, phys inactivity, arterial disease, hx TIA, a fib, drug abuse (IV, cocaine), HF (ef <25%)
cm
numb (asymmetric weakness)/weak on 1 side of body, sudden confusion, trouble speaking, slurred speech (dysarthria), trouble seeing (1 or both eyes), ataxia (poor voluntary movements), severe HA (w/o cause, esp with hemorrhagic)
dx
CT w/o contrast - 1st to tell hemorrhagic v ischemic so we know if ok to admin antithrombolytic or anticoag
blood = white - hemorrhagic
dark = damaged tissue - ischemic
ischemic
occlusion of cerebral artery -> thrombus or embolus: presentation and tm similar bc part of brain occluded, etiology and prevention different)
may not know of presence if it is just a small vessel that is occluded
neuro deficit w/n 1 min, continued loss l/t irreversible damage
ischemic: hemorrhagic conversiton
can happen after
extravasation (hemorrhage) or blood from peripheral circ across disrupted BBB, blood return with reperfusion (natural or with therapy)
ischemic: thrombotic
atherosclerosis (damage, narrowed vessel), hypercoagulable state (cancer, birth control), covid
ischemic: embolic
cardiac source: mural thrombosis (in vent), a fib (LA thrombus? emboli?), venous clot if atrial septal defect or patent foramen ovale, thrombus of vegetation of valves (mitral) - from infection
carotid plaque rupture -> clot -> hear carotid bruit - from impaired BF
ischemic: penumbra
ischemic area that is still viable, just injured
ischemic: goal
salvage penumbra w/n 3 hr
hemorrhagic stroke
bleed w/n brain parenchyma
associated w/ long standing, severe, htn
38% mortality: min - hrs
aneurysm, usually htn
large area affected -> mortality depends on size: increased ICP w/ inflam (blood is irritating to brain tissue), herniation (no room), death
hemorrhagic: presentation
rapid LOC change , worst HA ever, photophobia, nuchal rigidity - meninges irritated, subarachnoid bleed
30-60, high morbidity or mortality, serious disability
hemorrhagic: prognosis
age: older = better recovery
location (poor if in brain stem) and size
how rapid the bleed causes brain distortion and shift on screen: push brain lobe to others side, no room, midline shift
types of intracranial hemorrhage
epidural
subdural
subarachnoid
epidural
btw skill and dura
skull fracture, arterial (bleed alot), usually less severe
subdural
below dura
bridging veins: injury, carry blood outer -> inner, venous blood so accumulate over time
brain moves w/n skull, vessels dont, rapid decline (severe injury), can be slow (2-10 days later)
treat by evacuating collected blood
subarachnoid
btw arachnoid membrane and pia, where CSF is
rupture of cerebral aneurysm, aterio venous malformaiton
can see blood in CSF w lumbar puncture (most sensitive 12 hrs after s onset)
subarachnoid: tm
bed rest with sedation,
BP tightrope: parameters to prevent further bleed
asap sx clipping (aneurysm), prophyl anticonvulsant
nimodipine: CCB - slow blood flow, narrow vessels
triple H: keep brain perfused, htn - pressor, hypervol - colloid, hemodilution - hct 33)
r/o re bleed esp 1st 24 hr
berry aneurysm
near brainstem, often death
arterio venous malformation
increased r/o intracranial hemorrhage
not normal cap system, clumping, too large, can rupture bc increased P: direct flow from artery -> vein w/o slowing down through cap
BEFAST
balance: HA, dizzy
eyes: vision, pupil change
face: uneven, smile
arm: weak, pronater drift
speech: difficult
time: 911, want to know last known normal, tm w/n 3 hr
tm: first steps
A: tilt head back and pull chin forward, GCS <8 - intubate
B: chest rise and fall?, listen, feel for breathing with ear
C: pulse
tm: CT
w/o contrast to exclude hemorrhage
better than MRI in acute stage - MRI better detail but too long
tm: hemorrhagic
reverse anticoag (antidote for meds), manage htn, manage increased ICP (raise HOB, antipyretic, neutral head position)
tm: ischemic - thrombolytics
fibrinolytics = remove formed thrombi
alteplase: convert plasminogen to plasmin
tPA
fibrinolytic
Dissolve clot by converting plasminogen into plasmin which dissolves the clot
STEMI (acute MI)
PE, ischemic stroke
Route: IV – monitor BP and HR (hypoT and dysR with reperfussion)
Bleed – CI with hx brain bleed
Increased r/o intracranial bleeding
Most effective
Best w/n 30 – 70 min of s/s onset
Always given with heparin and antiplt (prevent new clots, clopidogrel)
Antidote = aminocaproic acid (antithrombolytic, don’t give unless hemorrhage life threatening)
tm: ischemic - penumbra procedure
go in and remove clot
mechanical thrombectomy
tm: consequences
L v R brain damage
eval for asp before PO: barium swallow
motor and sensory deficits: neglect = no sensory input
flaccidity (weak muscle) on contralateral side, spasticity (w/n 6 wk), contractures
visual disturbances: contralateral field blindness, homonymous hemianopia (R side of both fields or L side of both fields)
depression: disability
memory: names, words, objects
aphasia: read, write, say
tm: consequences - behavior
increased emotional response, may underestimate own abilities, slow rxn times, hesitant and cautious, may be apathetic, confused, disoriented
tm: consequences - language
aphasia: speak, comprehend
dysphasia: speech
dysarthria: imperfect speech sounds
word finding
incorrect use of verbs or nouns
expressive aphasia: comprehension intact but cant express
receptive aphasia: can communicate but cant comprehend what is being said
