Stroke/TIA/Syncope Flashcards
Is it stroke or TIA?
stroke
How do patients present…
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
Frontal lobe
Planning
Reasoning
Personality
Emotions
Motor Functions (motor cortex)
Motor speech area (Brocas area)
Parietal lobe
Think Somatosensory Cortex
Sensory info/processing
Taste, temperature, pain
Understanding language
Memory
Reading and writing
Spatial awareness
Temporal lobe
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
Occipital lobe
The primary visual cortex is at the rear of this lobe
This controls vision
Visual processing
Anterior vasculature branches from
INTERNAL CAROTID arteries
Posterior vasculature branches off
VERTEBRAL/BASILAR arteries
ACA Stroke Sx (anterior cerebral artery)
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
MCA Stroke Sx
Contralateral weakness to face and arm more than leg
Contralateral sensory loss
Aphasia if dominant hemisphere
PCA Stroke Sx
- Contralateral visual field deficit
- May have MILD contralateral motor and sensory deficit
- Dysarthria
- Diplopia
- Dizziness – vertigo
- Dysphagia
- Decreased level of consciousness
- Ataxia
- Disturbed hearing
Brainstem Stroke
Midbrain, pons, medulla
Breathing, heart rate, temperature, swallowing, weakness, paralysis consciousness
Relay system to the rest of the brain
Stroke
RF
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
Stroke
Ischemic
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….
Ischemic stroke
Causes
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.
Hemorrhagic stroke
Imaging
15% of strokes
CT without contrast! Blood will “light up” on CT.
Intracerebral hemorrhage
causes
HTN
AVM
Ruptured aneurysm
Coagulopathy
Eclampsia
Trauma
Subarachnoid hemorrhage (SAH)
S/Sx
Thunder clap headache
“The WORST headache of my life!”
Nausea/vomiting
Decreased level of consciousness
Nuchal rigidity (stiff neck)
Seizures
Subarachnoid hemorrhage (SAH)
general
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
SAH
RF
Risk factors for aneurysm: smoking, HTN, ETOH, family history of SAH or connective tissue disorder (Marfan’s), or personal previous SAH
Stroke
Tx steps
- A patient presents with stroke like symptoms.
- Assess/ NIHSS
- CT brain stroke protocol ASAP- TIME IS BRAIN.
- if bleed- control BP (SBP <160), anticoagulant reversal if taking, possible seizure prophylaxis, get neurosurgery on the phone
- If no bleed- tPA? Thrombectomy? Aspirin, VTE prophylaxis, swallow assessment bedside, admit for further work up
Stroke
FAST
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
stroke
PE - looking out for
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?
stroke
Who gets tPA
Tissue plasminogen activator
After CT brain without contrast to rule out bleed
Stroke
Thrombectomy
A procedure toremove a blood clot from a blood vessel using a catheter and clot retriever.
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
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
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
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.
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.
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
stroke
Hypertensive treatment
Ace/ARB/ARNI
CCB
Spironalactone
Thiazide
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
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
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
Syncope
RF
History of structural heart disease
Abnormal EKG
Age older than 60 years
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
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
classification of syncope
Vasovagal syncope -
“common faint”
Caused by a stressful, painful, or claustrophobic experience
classification of syncope
Carotid sinus hypersensitivity
Stimulation of abnormally sensitive carotid body, with subsequent abnormal vagal response
Results in bradycardia and arterial relaxation/dilation
classification of syncope
Situational syncope
Enhanced vagal tone with resulting hypotension
Coughing, sneezing, micturition, exercise
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
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
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
Syncope
Rx that can cause
Anti-hypertensives (including diuretics)
Βeta blockers
Anti-dysrhythmics
Antipsychotics
Anti-parkinson drugs
Antidepressants
Phenothiazines
Nitrates
Alcohol
Cocaine
Etc.
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
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
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
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
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
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
Cardiogenic Syncope Management
Depends on causation
Ablation or device implantation may be required
