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CMT-uno > Stroke/TIA/Syncope > Flashcards

Stroke/TIA/Syncope Flashcards

1
Q

Is it stroke or TIA?

A
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2
Q

stroke

How do patients present…

A

Usually abrupt in onset
What they experience varies by location of stroke in the brain
Hemiparesis
Speech disturbance
Sensory los
Visual field defect
Ataxia/coordination

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3
Q

Frontal lobe

A

Planning
Reasoning
Personality
Emotions
Motor Functions (motor cortex)
Motor speech area (Brocas area)

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4
Q

Parietal lobe

A

Think Somatosensory Cortex
Sensory info/processing
Taste, temperature, pain
Understanding language
Memory
Reading and writing
Spatial awareness

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5
Q

Temporal lobe

A

Memory functions –hippocampus
Speaking/understanding written and verbal material
Hearing
Facial recognition
Learning
Wernickes area- on the LEFT (think Left-Language)- comprehension, forming logical sentences
Seizures potentially

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6
Q

Occipital lobe

A

The primary visual cortex is at the rear of this lobe
This controls vision
Visual processing

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7
Q

Anterior vasculature branches from

A

INTERNAL CAROTID arteries

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8
Q

Posterior vasculature branches off

A

VERTEBRAL/BASILAR arteries

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9
Q

ACA Stroke Sx (anterior cerebral artery)

A

Usually occur with MCA stroke (middle cerebral artery)
Contralateral motor and sensory (think motor and sensory cortex to anterior portion!)
Leg more affected then arm > homunculus

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10
Q

MCA Stroke Sx

A

Contralateral weakness to face and arm more than leg
Contralateral sensory loss
Aphasia if dominant hemisphere

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11
Q

PCA Stroke Sx

A
  • Contralateral visual field deficit
  • May have MILD contralateral motor and sensory deficit
  • Dysarthria
  • Diplopia
  • Dizziness – vertigo
  • Dysphagia
  • Decreased level of consciousness
  • Ataxia
  • Disturbed hearing
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12
Q

Brainstem Stroke

A

Midbrain, pons, medulla
Breathing, heart rate, temperature, swallowing, weakness, paralysis consciousness
Relay system to the rest of the brain

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13
Q

Stroke

RF

A

Non-modifiable: age, male gender, race, family history

Modifiable: HTN, dyslipidemia, CAD, hypercoagulability, diabetes

Behavioral: smoking, alcohol, obesity, physical inactivity, illicit drug use, oral contraceptive + smoking

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14
Q

Stroke

Ischemic

A

Ischemic- much more common- 85-87%
Not always seen on CT without contrast !!
CT is always was you get first
CT may show subtle indicators of infarction within six hours of stroke onset
MRI brain without contrast more sensitive
Might not be able to get MRI due to hardware….

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15
Q

Ischemic stroke

Causes

A

Thrombotic- produces stroke by reduced blood flow or by fragment-carotid arteries, plaque build up and rupture. Usually unilateral pattern.

Large vessel- atherothrombosis is most common pathology

Embolic- cardiac source: Atrial fibrillation, valve disease, PFO, also could be carotid for artery to artery embolism.
To clue you in on embolic- bilateral in appearance. “Showering” of emboli. Always check echocardiogram with bubble study.

Lacunar- small vessel- HTN, DM, atherosclerosis. Atheroma formation due to hypertension. These have a better prognosis.

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16
Q

Hemorrhagic stroke

Imaging

A

15% of strokes

CT without contrast! Blood will “light up” on CT.

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17
Q

Intracerebral hemorrhage

causes

A

HTN
AVM
Ruptured aneurysm
Coagulopathy
Eclampsia
Trauma

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18
Q

Subarachnoid hemorrhage (SAH)

S/Sx

A

Thunder clap headache
“The WORST headache of my life!”
Nausea/vomiting
Decreased level of consciousness
Nuchal rigidity (stiff neck)
Seizures

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19
Q

Subarachnoid hemorrhage (SAH)

general

A

Major cause is rupture of arterial aneurysm
Other causes: AVM, bleeding disorders, trauma, illicit drug use.
With other causes- bleeding is less abrupt and may continue over a longer period of time

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20
Q

SAH

RF

A

Risk factors for aneurysm: smoking, HTN, ETOH, family history of SAH or connective tissue disorder (Marfan’s), or personal previous SAH

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21
Q

Stroke

Tx steps

A
  1. A patient presents with stroke like symptoms.
  2. Assess/ NIHSS
  3. CT brain stroke protocol ASAP- TIME IS BRAIN.
  4. if bleed- control BP (SBP <160), anticoagulant reversal if taking, possible seizure prophylaxis, get neurosurgery on the phone
  5. If no bleed- tPA? Thrombectomy? Aspirin, VTE prophylaxis, swallow assessment bedside, admit for further work up
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22
Q

Stroke

FAST

A

FACE-droop
ARM- pronator drift
SPEECH- slurred, abnormal, dysarthric, no speech
TIME of onset- last known well (3-4.5 hours tPA) Tricky if woke up with symptoms or lives alone

23
Q

stroke

PE - looking out for

A

Keep an eye on vitals. Especially blood pressure.
Mental status, speech change
If able to do ophthalmologic exam- signs of HTN, DM, emboli
Any cardiac murmurs? Arrhythmias? Carotid bruits?
Neurologic deficits?

24
Q

stroke

Who gets tPA

Tissue plasminogen activator

A

After CT brain without contrast to rule out bleed

25
Q

Stroke

Thrombectomy

A

A procedure toremove a blood clot from a blood vessel using a catheter and clot retriever.

26
Q

Stroke

Importance of time

A

Close to 2 million brain cells die every minute a stroke goes untreated.
For best possible outcome, ideally, a stroke patient needs to receive thrombectomy within 24 hours.
If able, transfer for thrombectomy for large vessel occlusion
Call to neurointerventionalist, or stroke team, as they can help determine if appropriate

27
Q

Stroke

surgical options

A

Carotid endarterectomy-
If stenosis on ultrasound- 70% -99% on affected side.
If stenosis 50-70%- +/- medical therapy
If less than 50% stenosis- medical therapy preferred

Carotid stents per vascular surgeon

28
Q

Stroke

Anticoag Tx

A

If embolic – atrial fibrillation, mitral stenosis, prosthetic cardiac valve, thrombus in left ventricle, atrial myxoma- warfarin, apixaban are used to prevent further strokes as secondary prevention. May be primary prevention if a fib caught first.

If warfarin-can bridge with heparin until INR therapeutic (2-3)

NOACs do not require bridging or monitoring

Cost / transportation are barriers

29
Q

Stroke

Tx for secondary prevention

A

If thrombotic/lacunar- on no antiplatelet medications at presentation = aspirin 81mg PO daily

If on aspirin and have a stroke= overlap 21 days with aspirin 81mg PO daily and Plavix 75mg PO daily, then just continue Plavix thereafter
Note: if received tPA, delay ASA for 24 hours until post tPA CT confirms no hemorrhagic transformation

If have a stroke while on Plavix, dual antiplatelet therapy with Plavix AND aspirin.

If someone has a fib and still has a stroke, they can be treated with anticoagulation AND antiplatelet, but with increased risk of bleeding.

30
Q

HTN Tx

A

All tPA candidates should be treated with BP >185/110
Everyone with BP > 220/120
Everyone “in between” with end organ damage (acute CHF, aortic dissection, hypertensive encephalopathy
Treat inpatient with either labetolol or nicardipine via IV.

31
Q

HTN with Stroke

Labetolol and Nicardipine

A

Labetolol causes vasodilation with onset of 5-10 minutes. Not a substantial reduction in heart rate or cardiac output- we need perfusion!
Nicardipine- reduces vasospasm, rapid onset, decreased systemic vascular resistance

32
Q

stroke

Hypertensive treatment

A

Ace/ARB/ARNI
CCB
Spironalactone
Thiazide

33
Q

Stroke

Recovery

A

Physical therapy
Occupational therapy
Speech therapy
Discipline depends on symptoms but therapy is highly indicated for stroke patients
The brain is not a muscle but you have to work it like one

34
Q

stroke

Secondary prevention, non Rx

A

Control risk factors
Comply with treatment
Lifestyle modification- exercise, Mediterranean diet, stop smoking, stop ETOH
Statin
DM control
HTN control

35
Q

Syncope

General

A

Transient loss of consciousness and postural tone
Vasodepressor or cardiogenic causes with prompt, spontaneous recovery without resuscitative measures
Inadequate nutrient flow to the brain
Usually leads to a fall
Presyncope events are possible
Prodromal symptoms

36
Q

Syncope

RF

A

History of structural heart disease
Abnormal EKG
Age older than 60 years

37
Q

Syncope

Epi

A

30% of adults will experience ≥ 1 syncopal episode
Incidence increases with age, esp older than 70
Results in ~3% of ED visits
Can cause serious injury, esp in elderly
Specific cause identified in ~50% of cases during initial evaluation
Vasovagal most common
History is key in order to identify the causation
Prognosis favorable except with accompanying cardiac disease

38
Q

classification of syncope

Reflex (neurally mediated syncope):

A

May be due to excessive vagal tone or impaired reflex control of peripheral circulation
Subtypes below:
Vasovagal
Carotid sinus
situational

39
Q

classification of syncope

Vasovagal syncope -

A

“common faint”
Caused by a stressful, painful, or claustrophobic experience

40
Q

classification of syncope

Carotid sinus hypersensitivity

A

Stimulation of abnormally sensitive carotid body, with subsequent abnormal vagal response
Results in bradycardia and arterial relaxation/dilation

41
Q

classification of syncope

Situational syncope

A

Enhanced vagal tone with resulting hypotension
Coughing, sneezing, micturition, exercise

42
Q

classification of syncope

Orthostatic/postural hypotension (OH) :

A

Patients bp drops upon standing
Normal vasoconstrictive response to assuming upright posture usually compensates for abrupt decrease in venous return
Commonly in elderly patients
Symptoms more likely to occur in early morning, after heavy meals, with prolonged standing, when core body temperature rises

43
Q

Classification of Syncope

Cardiogenic syncope:

A

Mechanical or arrhythmic basis arising from heart
Brady: Sinus brady, sinus pauses, AV block
Tachy: Ventricular tachycardia
Mechanical: Aortic stenosis, Pulmonary stenosis, hypertrophic cardiomyopathy, congenital lesions, massive PE
Commonly exertional or post-exertional
Usually no prodrome
Injury secondary to falling is common

44
Q

Common Presyncope Symptoms

A
  • Lightheadedness.
    ●Feeling unstable in the upright position.
    ●A feeling of being warm or cold/clammy.
    ●Sweating.
    ●Palpitations – The sudden onset of palpitations immediately followed by syncope suggests a cardiac arrhythmia, but palpitations due to sinus tachycardia may also precede reflex syncope.
    ●Nausea, vomiting, or nonspecific abdominal discomfort.
    ●Visual “blurring” occasionally proceeding to temporary darkening or “white-out” of vision.
    ●Diminution of hearing and/or occurrence of unusual sounds (particularly a “whooshing” noise).
    ●Pallor reported by onlookers
45
Q

Syncope

Rx that can cause

A

Anti-hypertensives (including diuretics)
Βeta blockers
Anti-dysrhythmics
Antipsychotics
Anti-parkinson drugs
Antidepressants
Phenothiazines
Nitrates
Alcohol
Cocaine
Etc.

46
Q

Syncope workup

A

Patients with normal initial evaluation:
Unremarkable H&P, absence of cardiac disease, absence of significant comorbidities, normal baseline EKG
Note – EKG should be obtained in all patients with suspected syncope

May not need further testing

Routine comprehensive lab testing is not useful
Routine cardiac imaging is not useful in evaluation of patients with syncope unless cardiac etiology is suspected based on history, physical examination, or ECG
Carotid artery imaging is not recommended in routine evaluation of patients with syncope in absence of focal neurologic findings

47
Q

syncope

Low-risk features - suggest benign condition:

A

Prodrome typical of reflex syncope (lightheadedness, feeling of warmth, sweating, nausea, vomiting)
After sudden unexpected sight, sound, smell, or pain
After prolonged standing or crowded, hot places
During a meal or postprandial
Triggered by cough, defecation, or micturition
With head rotation or pressure on carotid sinus
Standing up from supine/sitting position

48
Q

syncope

High-risk features:

A

New onset of chest discomfort, breathlessness, abdominal pain, or headache
Syncope during exertion or when supine
Sudden onset palpitation immediately followed by syncope
ECG changes consistent with ischemia, etc

49
Q

Reflex syncope

Tx TLCs

A

Trigger avoidance
Increase fluids and salt
Compression stockings

Counterpressure maneuvers –Reduce venous pooling and improve cardiac output to stop an episode or allow for patient to move to a supine position
Leg-crossing with simultaneous tensing of leg, abdominal, and buttock muscles (very effective).
Handgrip, which consists of maximum grip on a rubber ball or similar object
Arm tensing, which involves gripping one hand with the other while simultaneously abducting both arms

May move to pharm treatment or pacemaker therapy if recurrent and severe

50
Q
A
51
Q

Orthostatic Hypotension Syncope Management

A
  • Avoiding physical deconditioning in the elderly which helps maintain muscle tone in lower extremities
  • External compression devices such as waist-high compression stockings, abdominal binders
  • Physical maneuvers such as lunges, calf-raise, squatting, leg crossing
  • Review of home medications and discontinue diuretics and vasodilators if possible
  • Increase water and fluid intake to about 2-3 liters per day, avoid dehydration
  • Increase salt in diet 6-10g/day, eating small frequent low carbohydrate meals a day in case of postprandial orthostatic hypotension, avoid alcohol intake
  • Raising the head of the bed to 10 degrees at night reduces nocturnal diuresis
  • Avoiding activities such as saunas, spas, hot tubes, prolonged hot showers and excessive high intensity exercise
52
Q

Orthostatic Hypotension Syncope Goal and Tx (Rx)

A

Goal is to increase blood volume:

Midodrine 2.5 to 15mg orally once to thrice daily
Fludrocortisone 0.1 to 0.2mg daily in the morning titrated up to 1mg daily if needed
Pyridostigmine 30 to 60 mg orally trice daily
Yohimbine 5.4 to 10.8mg orally trice daily
Octreotide 12.5 to 50 ug subcutaneously twice daily
Cafergot such as caffeine 100mg and ergotamine 100mg

53
Q
A
54
Q

Cardiogenic Syncope Management

A

Depends on causation
Ablation or device implantation may be required

CMT-uno (54 decks)

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