CVA primary care Flashcards
PE of pt with CVA
Neurological examination notable for expressive aphasia and mild weakness on Rt side of face and arm. CV examination: S4 gallop and dorsalis pedis pulses diminished bilaterally. ECG shows NSR. CBC and BMP show glucose normal. Spouse wants to know what else to do.
ABCD2 score
Score (Age, BP, uinlateral weakness, duration 10-59 min
two types of stroke
Ischemic (occlusive) vs hemorrhagic
ischemic is seen with occlusions 80% of stroke are ischemic 8/10 chance of ischemia seen with a fibb
(permanent brain infarction) –>accounts for 80% of all CVA.
o 3 main subtypes: thrombosis (49%), embolism (31%), systemic hypoperfusion
hemorrhagic strokes are caused by
usually derived from arterioles or small arteries –> causes bleeding directly into the brain, forming a localized hematoma which spreads along white matter pathways. Hematoma gradually enlarges
o Causes: HTN, trauma, bleeding diatheses: unusual susceptibility to bleed, amyloid angiopathy, illicit drug use (i.e. amphetamines, cocaine), vascular malformations
o Accounts for 20% of all CVA
why do we see thrombis
when ever an artery forks it is turbulent
susceptible to more damange
TIA
ischemia (transient ischemic attack TIA): transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, WITHOUT acute infarction
intrinsic pathophysiology of CVA
i.e. atherosclerosis, lipohyalinosis, inflammation, amyloid deposition, arterial dissection, developmental malformation, aneurysmal dilation, venous thrombosis
remote origin of cva
) The process may originate REMOTELY, as occurs when an embolus from the heart or extracranial circulation lodges in an intracranial vessel
describe inadequacy that leads to CVA
The process may result from INADEQUATE (CBF) cerebral blood flow 2˚ ↓ perfusion pressure or ↑ blood viscosity
statins don’t do anything about
that fats you ingest
they only effect the biosynthesis of cholesterol in the liver
you will get a better effect with lifestyle modfications
when does the liver biosynthesize cholesterol
at night
take statins at night
doesn’t have a great half life need to take at night when the liver is productive
what did the SPRACL trial find about the effects of CVA with statins
- ” Reduced CVA risk 3.4-2.7%
atorvastatin: reduces risk of recurrent stroke & major event over 5 years
Some concern about more hemorrhagic strokes in treatment group (55 vs 33)
but benefits outweight the risks
looking at lipid reductions with medications
what do you see with atorvastatin
35-39% reductions with 10 mg
40mg (53%)
10 mmHg reduction in SBP decreases risk by ___
regardless of whether or not you are HTN
10 mmHg reduction in SBP decreases risk by 1/3
but we are worried about people over 60 have perfusion of coronary arteries (occurs in diastole so make sure diastole is NOT TOO LOW)
volume tx for the management of HTN
: Diuretics/ACEI
tx that target the tone for the treatment of HTN
CCB
modifiable risk factors for the prevention of CVA
o HTN, atherosclerosis, dyslipidemia
AND
o Smoking, DM, sickle cell, carotid stenosis, atrial fibrillation: irregular heartbeat (arrhythmia) that can lead to blood clots, stroke, heart failure, or other heart-related complications
MCC of stroke
Elderly - thrombotic & embolic strokes 2˚ atherosclerosis MC
how do we manage HTN in post CVA pts
lower BP w/ 2 classes of agents
(↓ volume: ACE inhibitors & diuretics. ↓ Vascular tone: CCB)
how to we manage lipids in post CVA pts
o Lipids - treat dyslipidemia (LDL = ~ 130-159)
how do we promote anticoagulation
o Platelets - prevent blood clots w/ anticoagulants (ASA, ASA + ERDP, clopidogrel)
why do we use 81mg of ASA
Risk reduction equivalent at low & high doses = 50-100mg/day sufficient–> lower dose preferred, try to minimize the risk of GIB
daily ASA tx reduces
” ↓ CVA risk 22% (improves cardiac risk too)
how does ASA inhibit coagulation
Also Inhibits prostaglandin synthesis
Inhibits cyclooxygenase, prevents thromboxane A2 formation, platelet activation & aggregation
what should we do for our old pt who was on baby ASA and had a CVA
Aspirin + XR Dypyrimidole (ASA-ERDP)
save this for ASA failure
Possible vasodilator - inhibits platelet enzymes " Trials (ESPS-2 & ESPRIT) demonstrated improved risk over aspirin alone w/o bleeding risk " But: BID dosing & less well tolerated (BID reduces compliance)
o SE: HA –> causes 3x d/c rate than aspirin alone
o Expensive
“ Reserved for “ASA failures”
PLAVIX what is it
would you use this in a pt that had a CVA with
Inhibits ADP-dependent platelet aggregation
Improved stroke risk relative to ASA in pts with PVD
BUT No significant risk reduction in pts with previous ischemic stroke (MATCH Trial)
AND
Combination increases bleeding
surgery for CVA
if occlusion of carotid ?
endarterectomy can be effective
what is the decreased risk for pts with 70-99% stenosis of carotid endarterectomy
what about in pts with moderate stenosis (50-69%)
Fatal ipsilateral stroke or post-operative death decreased from 26% to 9% for those with severe symptomatic stenosis (70-99%occlusion)
with moderate stenosis (50-69%) had benefit to 5 years over medical therapy
what is the risk of post operative stroke
30d post-operative stroke risk = 6-7%
have to get to the point where the risk of the surgery is outweighed by the benefit
if you’re over 60% occlusion
26 –> 9
probably will take the risk
what are the different types of ischemic stroke causes
cardioembolic?
carotid occlusion?
coumidin?
if he has a fibb
would we treat out pt with a statin following a stroke?
With TIA or ischemic stroke and high lipid levels (independent of LDL), high intensity statin therapy recommended (SPARCL Trial)
we still want to see his lipid profile though
what are we managing after ischemic stroke?
ANTICOAGULATION
STATIN
BP
do we always treat pts with HTN medication following ischemic stroke?
really depends
even if they are not hypertensive it can be helpful
BUT we really want to make sure their heart is perfusing
looking a diastolic
MAP calculation
MAP = SBP + 2 (DBP)
3
if this pt is DM and hypertensive post stroke and your managing stroke risk?
if AA
ACE and metformin for blood sugar control
CCB
MCC of cardioembolic stroke
nonvalvular afib is the number one reason for a cardioembolic stroke
what diagnostic studies would you want for a pt post CVA
EKG and echo to evaluate for afibb
labs
