Clinical Judgement Exam 2 Study Guide

Stroke: CVA (14 questions)

• Functional abnormality of the CNS that occurs when the blood

supply is disrupted. (ex: stroke, cerebral artery stenosis,
aneurysms, vascular malformations)

Cerebral Hemispheres & Brainstem:-

Frontal lobe: (MOST COMMON):- The frontal lobe influences

communication (talking and writing), emotions, intellect, reasoning
ability, judgement, and behavior. Contains Broca’s area, which is
responsible for speech.

• Expressive aphasia: Struggles to find the right words, and may put
incorrect strings of words together (“word salad”)

• Pt knows they have it and it is really frustrating for them since

they can’t express them.

• Ex of expressive aphasia: what’s your favorite color and they

respond by saying Truck.

Parietal lobe: (SENSORY PERCEPTION): tactile sensations including

touch, pain, temperature, shapes, and two-point discriminations.

• Stroke in the parietal lobe would cause “numbness and tingling”

Occipital lobe: (VISION): Influences the ability to read with

understanding and is the primary visual receptor center.

• Double vision
• Visual disturbances like blurry vision, hallucinations, or even
blindness

Temporal lobe: (AUDITORY STIMULI): receives and interprets impulses

from the ear. Contains Wernicke’s area which is responsible for
interpreting auditory stimuli.
 • Receptive aphasia or Wernicke’s aphasia:- affects your ability to
read and understand speech. You can hear what people say or see
words on a page, but you have trouble making sense of what they
mean.

• Don’t do the action because they can mimic you, but you want to
see if they understand what you are asking them.

Cerebellum: (MOTOR):- difficulty walking or controlling fine motor

movements. This loss of muscle control and coordination, known as
cerebellar ataxia.

• Those suffering from ataxia may have difficulty completing

movements smoothly or quickly. (UNBALANCED WALK)

• If LT sided cerebellum stroke occurs than the LT side is affected.

what are the bodily motor/sensory effects of a right vs left stroke in the
brain? Contralateral effects (except for cerebellum)

• Lt side stroke= RT sided weakness and vice versa

** Injury to the brain’s right hemisphere can cause left neglect. The
condition is also known as left side neglect. “Left neglect” is a term
describing a deficit in awareness that occurs following an injury to the
brain’s right side. Because of the injury, the brain has difficulty paying
attention to items falling into the left hemisphere.**

• Neglect causes: Heminanopsia, unilateral weakness/sensory/

cognition decline.
• Nursing intervention for neglect:
o Approach patient, and place needed objects(ex:call bell), on
side with intact vision.(Put objects on “good” side of patient.

o Educate pt. on Scanning: Visual scanning therapy (VST) aims

to improve visual scanning behavior by encouraging patients
with neglect to actively and consciously pay attention to
stimuli on the affected side)

o Encourage them to focus on neglected side (ex: tell them to

wash LT arm since they will forget)

Time is Brain, act F.A.S.T (know this)

During a stroke, every minute counts. You could save a life by

recognizing these signs of a stroke:

• FACE: Ask the person to smile, is one side of the face drooping?
• Arms: Ask the person to raise their arms. Is one arm weak?
• Speech: Ask the person to speck. Is their speech slurred?
(Dysarthria)
• Time: call 911 right away at the first sign of a stroke. (brain cells
need perfusion so that they don’t die) (can help decide what type
of stroke: sudden onset is always ischemic stroke)
STROKE PREVENTION:

Non-modifiable:
• Age (older than 55 years)
• African American
• Males (estrogen has protective factors)

Modifiable risk factors:-

• HYPERTENSION is the primary risk factor: Ask them “why they are
not compliant with meds”

• Previous stroke
• Cardiovascular disease (general) like A-fib and carotid stenosis
• Diabetes (unmanaged diabetes)
• Sleep apnea (fluctuation in 02)
• Smoking, drugs(cocaine, meth, injected heroin) and alcohol
• Periodontal disease
Preventive Treatment and Secondary Prevention:-
• Health promotion measures, healthy lifestyle, smoking cessation,
exercise, healthy diet and weight
• Antiplatelet therapy
• Stains: put on if you had a stroke regardless since they are high
risk
• Antihypertensive medication (*hypertension #1 risk factor so are
they complaint with their med)

Carotid artery stenosis treatments:-

• Carotid endarterectomy (CEA): (PREVENT STROKE NOT
TREATMENT) dangerous to do, invasive (can see atherosclerosis)
(ICU for 24 hr., want BP to be between 120-140 to ensure adequate
perfusion) (<120= not enough perfusion, >140= bleeding) (NEED
monitoring and frequent Neuro checks!)

• Carotid artery stenting (CAS): non-invasive: similar to stent

Transient Ischemic Attack (TIA): Mini stroke

 • Temporary neurologic deficit resulting from impairment of
cerebral blood flow.
• Symptoms last 1-2 hours

• Diagnostic workup is needed to investigate causes/risk factors and

try to prevent subsequent stroke: #1 priority: CT scan to rule out
other stuff like a brain bleed or clot because if they give them a
TBA and they have a brain bleed then they can die.

• Brain imaging shows NO evidence/damage of ischemia

• “WARNING OF AN IMPENDING STROKE”

Ischemic Stroke

Disorder etiology:
• Thrombotic: A clot
• Embolic: A clot that has moved

Main types of ischemic stroke:

• Transient ischemic attacks (warning sign, not a stroke)
• Cardiogenic embolic: clot comes from heart and then moved
• Small artery thrombotic
• Large artery thrombotic
• Cryptogenic : no known cause

Clinical Manifestations:-

• Motor weakness: face, arm or legs especially on 1 side (unilateral,

hemiparesis)
• Unilateral weakness (paresis) or paralysis
• F.A.S.T
• Speech changes: slurred dysarthria (difficulty forming words) or
troubling speaking (expressive aphasia) or understanding speech
(receptive aphasia)
• Balance/ coordination problems: ataxia
• Sensory changes: numbness/tinging (agnosia)
 • Vision changes: hemianopsia (diminished vision or full vision loss
in the left or right half of the visual field of one or both eyes) and
diplopia (double vision)
• Cognition changes: confusion, mental status changes

Stroke Diagnostics: what are key assessments& imaging

tests?

• Careful history: Time last seen well

• Glasgow scale: less than 8 intubate
• NIH stroke scale for suspected strokes: (HIGH SCORE=BAD)
• Non-contrast head CT scan: AHA practice standard is completion
within 25 mins of arrival to the ED, must be read within 45 mins
Ischemic Stroke: Acute Medical Management

Thrombolytic agent: t-PA (Tissue plasminogen activator)

• Extreme blood thinner: DISSOLVE CLOT!!

• Alteplase (Activase)
• Route: intravenous infusion 1 hour, weight based and given as a
bolus
• GOALS: ADMINISTER WITHIN 4.5 hours of symptom onset
• Administer within 60 mins of arrival to ED (if pt. had stroke at
home cant give them t-PA because you don’t know then stroke
started)
• Steps for treatment: 1) CT scan, 2)t-PA, 3) EKG
• #1 RISK= BLEEDING!! (24hrs put them on bleeding precautions)

Eligibility criteria for t-PA for ischemic stroke:-

• Patient history: Ischemic stroke or severe head trauma in the

previous 3 months
• Intracranial or intraspinal surgery within the prior 3 months (if
you already got t-PA)
• Persistent BP elevation (systolic >= 185 mmHg or diastolic >=110
mmHG (ex: 186/96 cant give them t-PA) (can cause brain
hemorrhage)
 • Active internal bleeding
• Current anticoagulant use with an INR >1.7
• Pregnancy: (cross blood brain and can cause baby to bleed)

t-PA Administration: BEFORE

• BLOOD PRESSURE CONTROL: BLOOD PRESSURE must be LESS THAN

185/110 prior to treatment
• BP needs to be LESS THAN 180/105 for first 24hrs post-TPA.

• Use BP meds if BP is HIGH: IV labetalol pushes or Nicardipine (BP

med) anti-hypertensive of choice.
• Bleeding risk: Try to initiate invasive procedures PRIOR to
administration (IV catheters, intra-arterial catheters, blood
draws, urinary catherization)
• Don’t delay TPA for anything it is #1 priority.

t-PA Administration: AFTER

• 24 hour “no touch” period: non-invasive procedures (NG tubes,

urinary catheters…)
• Bed rest: let them use a bed pan
• Frequent neuro assessment (every 15 min for the first 24 hrs.),
frequent vital signs (BP might change after bolus)
• If angioedema occurs:- stop med (airway risk)
• MAJOR COMPLICATIONS: intracranial ischemic to hemorrhagic
conversion

Acute surgical management: Endovascular therapy (thrombectomy)

(REMOVE THE CLOT)

• When pt doesn’t qualify for t-PA then they surgical remove the
clot.
 • They go through femoral to brain to remove clot (not available at
all hospitals)

Other therapies (supportive)

• Hemodynamic monitoring/management.

• ICP monitoring/management.: may require decompressive craniectomy

in very large ischemic strokes.

• Intubation (GCS<8), mechanical ventilation, and sedation (not best

option since you need frequently neuro assessments)

Post stroke work-up/Treatment

• Depending on size of stroke need to watch for secondary cerebral

edema (swelling of brain will show on CT scan): treatment with
hyperosmotic therapy and possibly decompressive
hemicraniectomy for full territory infarcts.

• Assess stroke risk factors-lipids, blood glucose control, smoking,

HTN (see modifiable risk and if it can be changed)

• Lifestyle modification: Educate (low sodium diet), stain therapy

(everyone goes on them)

• PT/OT/SLP(speech therapist/dysphagia (swallowing)): Rehab

needed=need to move (they can get a blood clot or bed sores if
they don’t move)

Stroke: Nursing process: Assessment

Acute Phase:

Neurological Assessment-focus is on neurological deficits/changes

• Frequent focal neuro checks (pupil size, LOC,GCS and reaction,

cranial nerves, extremity movements& strengths)

• Comprehensive neuro assessment (NIH stroke scale)

 • Any decline or change in neurological function or LOC must be
reported to provider immediately!

• Angioedema? (STOP MED)

Comprehensive head-to-toe assessments, including: (Respiratory,

cardiovascular (BLOOD PRESSURE), GU (risk of UTI), GI)

Cranial nerves:- (know this)

• 1 (smell) and 8(taste)=NOT ASSOCIATED WITH STROKE!! (not tested

on)
• 2,3,4 and 6= EYES
 • SOME SAY MARRY MONEY BUT MY BROTHER SAYS BIG BRAINS
MATTER MORE: (sensory/motor/both)

Mnemonic to remember:-

• Old Operators Occasionally Troubleshoot Tricky, Abducted Family

Veterans Galloping Valiantly Across History
Stroke Nursing process: interventions

Preventing immobility complications and joint deformities:

• Elevate extremities, DVT prophylaxis

• Range of motion (passive or active) and foot drop boots

• Ambulate and assist out of bed as soon as possible with PT/OT (get
BP before getting up because orthostatic hypotension is very
common with them)

Maintain skin integrity: regular position changes (q2hr in bed,q30 min

in chair)

Enhancing self-care: (need to normalize)

• Promote and include patient(and family) in care as early and often
as possible.
 • Set realistic goals
• Ensure the pt. does not neglect affected side

Assisting with nutrition:

• Dysphagia screening (RN and/ or speech therapist)
• Consult with speech therapy and nutrionsist (RD)
• Have pt. sit fully upright, preferably out of bed to eat
• Use of thickened liquids or special diet (per SLP recommendation)

Attaining bladder and bowel control:- (might forget that catheter is in

and will get up to go to the bathroom)

• Assess voiding and scheduled voiding

• Prevent constipation
Improving communication (aphasia):
• Eye contact, short phrases, clear speech
• Use gestures like pictures, objects, and writing.

Hemorrhagic Stroke:

Bleeding into brain tissue (intraparenchymal), the brain ventricles

(intraventricular), or subarachnoid space (SAH).

Causes:-
• #1 risk is hypertension: rupture of small vessels primarily related
to hypertension.

• Subarachnoid hemorrhage caused by a ruptured intracranial

aneurysm, trauma

• Cerebral amyloid angiopathy, arterial venous malformations

(AVMs) (THEY ARE BORN WITH!!)

Functional recovery plateaus at about 18 months (LONG RECOVERY)

Hemorrhagic stroke Clinical Manifestations:-

• Can have the same sx for ischemic stroke

 • SUDDEN AND SEVERE HEADACHE described as “WORST HEADACHE
OF LIFE” (WHOL).” “exploding or thunderclap headache” (specially
for subarachnoid hemorrhage (SAH)

• Vomiting, photophobia, nuchal rigidity(neck pain)

• Collapse, loss of consciousness

SUBARACHNOID HEMORRHAGE (SAH): Initial acute complications

• Cerebral ischemia (ineffective perfusion): want BP to be low (<150)

• Re-bleeding
• Increased ICP: (1st sign (WEAKNESS AND DROWSINESS) (late sign:
Pupil)(increased ICP= brain and brainstem herniation)

• Hypothalamus/Pituitary Dysregulation: (NEED TO CHECK SODIUM)

o Diabetes insipidus: increased Na (>145) (endocrine

abnormity: Decreased ADH) (Increased urine out: they pee a
lot but they hold on to sodium)

o SIADH: low Na (less common)

o Cerebral salt wasting (CSW): low Na( <135) (endocrine
abnormity: Increased BNP (Brain Naturetic peptide)
(increased urine output)

o CSW is seen first and then DI happens after

• Cardiac arrhythmias: broken heart syndrome

SUBARACHNOID HEMORRHAGE (SAH): other complications

Acute and sub-acute (first 21 days) (when your worried)

• Vasospasm: causes cerebral ischemia: (a week after you are
worried)(vein in brain constrict)

• Hydrocephalus: “water on the brain”

CEREBRAL VASOSPASM:-
**Secondary injury that subarachnoid hemorrhages are at risk for. Peak
is usually around days 7-10 post bleed. (monitor for 21. Days for
vasospasm)**

• PREVENTION: Nimodipine (calcium channel blocker)

Intermediate and long-term:

• Personality changes: can have significant effect on family/social
support

Increased Intracranial Pressure:

Increased ICP leads to:

• Decreased cerebral perfusion-> ischemia, cell death, and further
edema
• shifting of brain tissue-> herniation

CPP=MAP-ICP
• reference range for CPP is 70 to 100 mmHg (goal>60)
• A CPP less than 50 mmHg results in permanent neurologic damage

**DON’T LAY PT FLAT, IT WILL INCREASE ICP. KEEP HOB AT 30 degrees,

with head and neck midline.**

Clinical Manifestations of increased ICP:-

EARLY:-
• Decrease in LOC

LATE:
• Cushing triad: bradycardia, widening pulse pressure, irregular
respiration

• Loss of brainstem reflexes: pupil (dilated) ,gag, corneal

• Vital sign: decrease or erratic HR & RR, widening pulse pressure and
worsening respiratory pattern, including Cheyne breathing and
respiratory arrest.
Assessment of pt. with increased ICP:-

• Ongoing neurologic assessments (q 1 hr. need to be focused)

• Frequent vital signs (15 min to q hr.)

Preoperative and nursing management of increased ICP:-

• Reduce cerebral edema: use multiple IV meds: (IV MANNITOL, IV

HYPERTONIC SALINE)
• Prevent seizures

Brain Herniations:-

• Decerebrate (worse): pinch them and arm and legs go out (leads to
brain death)
• Decorticate: spinal reflex (abnormal posturing where the pt. is
stiff with bent arms in towards the body, clenched fists and legs
out straight.)
• Decorticate -> Decerebrate-> BRAIN DEATH