NUR 326: stroke, cva, brain attack & parkinson disease 💯

what is cerebral vascular accident

loss of blood flow to an area of the brain, causing neurons to die; brain ischemia

what are two major classifications of cerebral vascular accident

1. ischemic stroke: caused by blockage of blood flow
2. hemorrhagic stroke: caused by bleeding in the brain

what is ischemic stroke caused by

- caused by a blockage of blood flow that often occurs with dysrhythmias, arteriosclerosis, atherosclerotic plaques (common at carotid artery bifurcation), thromboembolism (when plaque/clot breaks off and travels to cerebral vessels)

what is hemorrhagic stroke caused by

- caused by bleeding in the brain that often results from prolonged hypertension, hypertensive crisis

what is transient ischemic attack

- transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain
- patho: may be due to microemboli that temporarily block blood flow, representing a warning sign of progressive cerebrovascular disease

what are key characteristics of transient ischemic attack

- key characteristics: symptoms typically last less than 1 hr
- TIA is a medical emergency because it can lead to ischemic stroke, 1/3 of clients who experience TIA will progress to stroke, 1/3 have additional TIA, 1/3 do not have another event

what are modifiable risk factors for cerebral vascular accident that is the biggest risk factor

lifestyle modifications and medical treatment can reduce risk → modifiable risk factors cause 90% of strokes
- hypertension! (single most important modifiable risk factor): often undetected and inadequately treated, can reduce risk up to 50%, goal is SBP <140
- heart disease: A fib causes 25% of strokes and pt are 5x more likely to have stroke, includes MI, cardiomyopathy, valve abnormalities, congenital defects, oral anticoagulants like warfarin/dabigatran are key for prevention
- diabetes: stroke risk is 5x higher in pt with diabetes

what are modifiable risk factors for cerebral vascular accident additional factors

- smoking
- obesity and physical inactivity: recommend exercise 150 mins moderate-intensity or 75 mins vigorous-intensity per week
- other modifiable factors: alcohol, illicit drug use (esp cocaine), poor diet, sleep apnea and metabolic syndrome, high dose oral contraceptives, migraines with aura (women)

what are nonmodifiable risk factors for cerebral vascular accident

- age: risk doubles >55
- gender: more common in men but more women diet from stroke
- race/ethnicity: african americans
- family history/genetics

what mneumonic is associated with cerebral vascular accident awareness

- BE-FAST → time is brain!
- balance
- eyes
- facial drooping
- arm
- speech
- time

what diagnostics do you perform for cerebral vascular accident

- immediate imaging:
→ CT scan (non-contrast): first line to differentiate ischemic vs hemorrhagic stroke
→ CT angiography: identifies vessel occlusion and guides thrombectomy decisions
→ MRI: more sensitive for early ischemic changes

what additional diagnostics can you perform for cerebral vascular accident

- ECG monitoring: detects A fib and cardiac complications
- cardiac enzymes: rule out MI
- coagulation studies
- blood glucose
- lumbar puncture

what are assessment tools for cerebral vascular accident

NIH stroke scale (NIHSS): measures stroke severity, predictor of short and long-term outcomes, essential for documentation

what are the 2 types of ischemic stroke

thrombotic and embolic strokes

what is thrombotic stroke (part of ischemic stroke)

- blood clot develops within the cerebral artery lumen
- thrombosis narrows the lumen, blocking blood flow
- often associated with atherosclerotic plaques

what is embolic stroke (part of ischemic stroke)

- an embolus (clot or debris) circulates in the blood
- lodges in a cerebral artery, too narrow to pass through
- most emboli originate from the heart (a-fib, MI, endocarditis, value prostheses)
- occurs suddenly with severe manifestations
- warning signs less common than thrombotic stroke
- little time for collateral circulation to develop
- effects may be temporary if clot breaks up, but small emboli continue obstructing smaller vessels

what are clinical manifestations of ischemic strokes regarding motor

motor deficits are most obvious
- contralateral effects: lesions on one side of the brain affects the opposite side of the body (lesions on right brain will affect left body)
- loss of skilled voluntary movement (akinesia)
- impaired mobility and integration of movements
- changes in muscle tone and reflexes
- initial hyporeflexia progressing to hyperreflexia
- middle cerebral artery stroke: greater upper extremity weakness than lower extremity
- affected should rotates internally, hip rotate externally
- foot is plantar flexed and inverted
- impaired respiratory function, swallowing, speech, gag reflex, and self care abilities

what are clinical manifestations of ischemic strokes regarding communication deficits

- aphasia: occurs when stroke damages dominant hemisphere (usually left)
→ receptive aphasia: loss of comprehension
→ expressive aphasia: inability to produce language
→ global aphasia: total inability to communicate
- dysarthria: muscular control problem affecting pronunciation, articulation, phonation (doesnt affect comprehension)

what are clinical manifestations of ischemic strokes regarding other manifestations

- headache (esp embolic stroke)
- client is often conscious during embolic stroke
- severe neurologic deficits occurring suddenly

what are priority interventions for ischemic stroke

- airway and respiratory: aspiration risk (dysphagia common), suction prn, encourage deep breathing
- blood pressure management: without tPA only lower BP if SBP > 220 or DBP >120; with tPA must be <185/110 before treatment maintain <180/105 for 24hr post-treatment

what is tPA administration considerations for ischemic stroke blood pressure management

- closely monitor vital signs and neurologic status during infusion
- assess for improvement or deterioration (intracerebral hemorrhage risk)
- no anticoagulants in emergency phases due to hemorrhage risk
- aspirin may be started 24-48 hours post-CVA

what is pharmacotherapy-acute phase for ischemic stroke

fibrinolytic therapy: tPA (tissue plasminogen activator)
- gold standard for acute ischemic stroke
- must be given within 3 o 4.5 hours of symptom onset
- produces localized fibrinolysis by converting plasminogen to plasmin, which digests fibrin and breaks down clot
- other fibrinolytic agents cannot be substituted for tPA

what is pharmacotherapy-post acute phase for ischemic stroke

- antiplatelet therapy:
→ aspirin (higher dose) started 24-48 hrs after strke onset: be careful of GI bleeding risk, esp with peptic ulcer disease history
→ anticoagulants: not recommended in emergency phase due to intracranial hemorrhage risk (need to do assessment to see if bleeding is present), heparin avoided acutely, after stabilization may use to prevent clots
- prevention (long-term): anticoagulants for high-risk pts → warfarin for clients with A-fib to prevent thrombi formation

what are screening requirements before tPA and during tPA

- screening requirements before tPA: non-contrast CT or MRI to rule out hemorrhagic stroke, coagulation studies, rule out recent GI bleeding, stroke, or head trauma (past 3 months), major surgery (past 14 days), active internal bleeding (past 22 days)
- critical monitoring during tPA: BP must be <185 before treatment, closely monitor VS and neurological status, assess for improvement or deterioration (intracerebral hemorrhage risk)

what is the pathophysiology of hemorrhagic stroke - intracerebral hemorrhage (ICH)

intracerebral hemorrhage (ICH)
- bleeding within the brain tissue caused by rupture of a vessel (usually in basal ganglia)
- hypertension is most common cause
- other causes: vascular malformations, coagulation disorders, anticoagulant/thrombolytic drugs, trauma, brain tumors, ruptured aneurysms

when does hemorrhagic stroke: intracerebral hemorrhage often occur

- often occur during periods of activity
- blood clot within the closed skill creates a mass that causes pressure on brain tissue, displaces brain tissue, decreased cerebral blood flow, and leads to ischemia and infarction
- poor prognosis: 30-day mortality rate is 40-80%, half of deaths occur within first 48 hours

what are clinical manifestations of general hemorrhagic strokes

- sudden onset with progression over minutes to hours (due to ongoing bleeding)
- severe headache
- nausea, vomiting
- decreased level of consciousness
- hypertension
- neurological deficits

what are clinical manifestations of location-specific hemorrhagic strokes

- putaminal/internal capsule: weakness of one side (face, arm, leg), slurred speech, eye deviation, progression = hemiplegia, fixed/dilated pupils, abnormal posturing, coma
- thalamic: hemiplegia with more sensory than motor loss
- cerebellar: severe headache, vomiting, loss of ability to walk, dysphagia, dysarthria, eye movement changes
- pon: (most serious): hemiplegia leading to complete paralysis, coma, abnormal posturing, fixed pupils, hyperthermia, death

what is the pathophysiology of hemorrhagic stroke - subarachnoid hemorrhage (SAH)

- intracranial bleeding into CSF-filled space between arachnoid and pia mater membranes
- often caused by rupture of a cerebral aneurysm (congenital or acquired weakness and ballooning of vessels)
- other causes: trauma, illicit drug use (cocaine)
- viewed as silent killer cause usually no warning signs until rupture

what are clinical manifestations of subarachnoid hemorrhage-specific strokes

- LOC ranging from alert to comatose
- focal neurological deficits (including cranial nerve deficits)
- seizures
- stiff neck
- cerebral vasospam complication (peak 6-10 days post-bleed) can cause cerebral infarction

what are priority interventions for hemorrhagic stroke

- increased intracranial pressure (ICP) management: monitor LOC closely due to rapid deterioration, elevate HOB 30 degrees, avoid activities that increase ICP (valsalva, hip flexion >90)
- blood pressure control: more aggressive BP lowering than ischemic strokes, prevent rebleeding
- seizure precautions: higher seizure risk than ischemic stroke, keep suction and oxygen at bedside
- vasospasm monitoring: peak risk days 6-10, monitor new neurological deficits

what is hemorrhagic stroke pharmacotherapy

- blood pressure control: IV antihypertensive agents
→ vasodilators: sodium nitroprusside (most effective), fenoldopam, nicardipine
→ adrenergic inhibitors: phentolamine, lebetalol, esmolol
→ calcium channel blockers: clevidipine

what should you monitor during hemorrhagic stroke IV therapy

- BP and HR every 2-3 mins initially
- arterial line or automated noninvasive BP monitoring
- titrate to MAP or SBP as ordered
- ECG monitoring for dysrhythmias, ischemia, or MI
- hourly urine output (assess renal perfusion)
- extreme caution with CAD or cerebrovascular disease
- keep client on bed rest (getting up may cause severe cerebral ischemia/fainting)

what are motor deficits post CVA management for CVA

- passive ROM excersizes starting day 1
- position each joint higher than proximal joint to prevent edema
- prevent contractures and deformities
- never pull patient by affected arm (prevent should displacement)
- use assistive devices: trochanter rolls, hand cones, arm slings, posterior leg splints
- progress to active exercises and mobility training

what is parkinson’s disease

- chronic, progressive, neurodegenerative disorder
- characterized by bradykinesia slowness in inititation and execution), rigidity (increased muslce tone), tremor at rest, and gait changes

why does parkinson’s disease happen

decreased dopamine (unbalanced acetylcholine) → dopamine deficit in cerebral cortex
(normal function = balanced dopamine (inhibitory neurotransmitter) and acetylcholine (excitatory neurotransmitter))

what are risk factors for parkinson’s disease

- primary PD: unknown cause, possibly genetic and environmental factors
- secondary/atypical parkinsonism: symptoms present after exposure to trigger (chemical, licit drug use and illicit drugs), most symptoms stop after exposure to trigger stops

what are clinical manifestations of parkinson’s disease

- gradual, unilateral onset (may progress to both side eventually)
- ongoing progression
- TRAP → tremor, rigitdity, akinesia, postural instability

what are early and late stage manifestations of parkinson’s disease

- early: mild symptoms
- late-stage: shuffling gait, unable to walk (leans forward), flexed arms, no postural reflexes, hypokinetic dysarthria (speech problems)

what are characteristics of parkinson’s disease

- blank facial expression
- slow monotonous slurred speech
- tremor
- short shuffling gait
- forward tilt posture
- drooling lots of saliva

what are motor complications for parkinson’s disease

- dyskinesias (spontaneous involuntary movement)
- weakness: infection (pneumonia, UTI) and skin breakdown
- neurologic (dementia > increased mortality)
- neuropsychiatric (depression, hallucinations, psychosis)

what is considerations for diet in parkinson’s disease

- high-fiber diet to prevent constipation
- limit protein to evening meals (if on levodopa)
- allow extra time for eating to avoid frustruation
- monitor weight and nutritional status
- appetizing food, easy to chew/swallow: high fiber and fruits, limit protein and vitamin B6 due to impaired absorption of levodopa, 6-small meals/day, ample time, cut food into bite-size pieces