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
# Stroke Thrombectomy
A procedure to remove a blood clot from a blood vessel using a catheter and clot retriever.
26
# Stroke Importance of time
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
# Stroke surgical options
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
# Stroke Anticoag Tx
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
# Stroke Tx for secondary prevention
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
HTN Tx
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
# HTN with Stroke Labetolol and Nicardipine
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
# stroke Hypertensive treatment
Ace/ARB/ARNI CCB Spironalactone Thiazide
33
# Stroke Recovery
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
# stroke Secondary prevention, non Rx
Control risk factors Comply with treatment Lifestyle modification- exercise, Mediterranean diet, stop smoking, stop ETOH Statin DM control HTN control
35
# Syncope General
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
# Syncope RF
History of structural heart disease Abnormal EKG Age older than 60 years
37
# Syncope Epi
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
# classification of syncope Reflex (neurally mediated syncope):
May be due to excessive vagal tone or impaired reflex control of peripheral circulation Subtypes below: Vasovagal Carotid sinus situational
39
# classification of syncope Vasovagal syncope -
“common faint” Caused by a stressful, painful, or claustrophobic experience
40
# classification of syncope Carotid sinus hypersensitivity
Stimulation of abnormally sensitive carotid body, with subsequent abnormal vagal response Results in bradycardia and arterial relaxation/dilation
41
# classification of syncope Situational syncope
Enhanced vagal tone with resulting hypotension Coughing, sneezing, micturition, exercise
42
# classification of syncope Orthostatic/postural hypotension (OH) :
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
# Classification of Syncope Cardiogenic syncope:
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
Common Presyncope Symptoms
* 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
# Syncope Rx that can cause
Anti-hypertensives (including diuretics) Βeta blockers Anti-dysrhythmics Antipsychotics Anti-parkinson drugs Antidepressants Phenothiazines Nitrates Alcohol Cocaine Etc.
46
Syncope workup
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
# syncope Low-risk features - suggest benign condition:
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
# syncope High-risk features:
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
# Reflex syncope Tx TLCs
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
51
Orthostatic Hypotension Syncope Management
* 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
Orthostatic Hypotension Syncope Goal and Tx (Rx)
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
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54
Cardiogenic Syncope Management
Depends on causation Ablation or device implantation may be required