brain part 2 Flashcards
within how many hours can IV recombinant tPA be given after a patient exhibits sx of an acute ischemic CVA
within 4.5 hours of sx onset
risk factors for CVA include (6)
HTN (most important)
smoking
DM
HLD
ETOH excessive
elevated homocysteine level
usual first therapy for patients who suffered an ischemic (not hemorrhagic) CVA
PO așa
eligible CVA patients with large vessel occlusion should receive embolectomy within how many hours of sx onset
6
target BP for ischemic CVA patient
under 185/110
fluid, temp, BG anesthetic considerations for CVA patient
fluid supports CO, BP, CPP, and improves BF by decreasing blood viscosity
monitor BG’s, tx high BG with insulin. glucose is converted to lactic acid in severe ischemia and is associated with bad outcomes
-controlled hypothermia can reduce CMRO2
management considerations for cerebral vasospasm following SAH include
reducing HCT to 30
niMOdipine
daily trans cranial doppler exams
triple H therapy (HTN, hemodilution, hypervolemia)
most common cause of subarachnoid bleeding
aneurysm rupture in circle of willis
what increases risk of aneurysm rupture
HTN(?) or an acute reduction in ICP. basically ICP creates a tamponade effect.
surgical options for hemorrhagic CVA
aneurysm clipping or endovascular coiling
-to minimize risk of re bleeding, surgical repair should take place within 24-48h following initial bleed
if you heparinize for the endovascular coil to be placed and the aneurysm ruptures during this time, you should
reverse the heparin, lower map to low/normal range, can give adenosine to help surgeon stop bleeding
intraop BP control for hemorrhagic CVA
also considerations for open repair where surgeon is clamping
SBP should be between 120-150mmHg
-if patient undergoes an open repair, clamp is placed on proximal feeder vessel. this reduces transmural pressure and decreases the risk of aneurysm rupture so you won’t need controlled HoTN but you will need a normal/high BP to perfuse collateral circulation.
too high and no clamp- rupture could occur
too low- auto regulation is impaired and could not be perfusing
when cerebral vasospasms most commonly occur
how to monitor for them
presentation
dx
tx
most commonly occur 4-9 days following SAH
frequent neuro checks and daily transcranial doppler exams
most common presentation is new neurologic deficit or altered LOC
dx: cerebral angiography is gold standard
tx: aimed at maintaining CPP (increase MAP 20-30mmHg above baseline), if vasospasm occurs, triple H therapy (hypervolemia, HTN, hemodilution to 27-32%), nimodipine, balloon angioplasty
a medically refractory vasospasm can be treated with what before balloon angioplasty?
intra arterial vasodilators, CCB’s like verapamil or nicardipine. can also try papaverine and milrinone
define cerebral salt wasting syndrome
patients who suffer SAH are at risk for this
most common cause of hyponatremia in this population. brain releases natriuretic peptide which causes contraction, hyponatremia, and sodium washing by the kidney.
CSW is tx with isotonic crystalloids
distinction between CSW and SIADH
CSW is tx with isotonic crystalloids while SIADH is tx with fluid restriction since its associated with slight hypervolemia
if you have a minor head injury and satisfy these requirements, you do not need a CT
no physical evidence of trauma above the clavicles
no HA
no n/v
no neurologic deficit
no impairment of short term memory
no intoxication
no seizures
age <60y
review GCS and which number is associated with TBI
<8, TBI
ways to reverse wafarin (3)
FFP, prothrombin complex concentrate, recombinant factor 7a
ways to reverse clopidogrel and/or ASA
platelet transfusion,
anesthetic management of TBI, keep CPP
> 70mmHg
two things to specifically avoid in a patent with TBI
prolonged hyperventilation can worsen cerebral ischemia in patents with TBI
steroids can worsen neurologic outcomes
albumin and TBI
linked to poor outcomes
nitrous oxide and TBI
PTX can be lurking, you dont know. just dont touch it with TBI victim
jacksonian march
a partial seizure that progresses to a generalized seizure
tonic phase versus clonic phase
tonic: whole body rigidity. TONE
clonic: repetitive jerking motions
grand mal seizure key points/distinctions
acute tx
surgical tx
generalized tonic/clonic activity
respiratory arrest due to hypoxia an increased O2 consumption due to increased brain activity
acute tx: propofol, diltiazem, thiopental
surgical tx: vagal nerve stimulator or resection of foci
focal cortical sz sx
localized to particular cortical region
can be motor or sensory
usually no LOC
absence (petit mal) sz sx
temporary loss of awareness (but remains awake)
more common in children
akinetic sz sx
temporary LOC and postural tone, which can result in fall and head injury
more common in children
status epilepticus sz sx
acute tx (6)
sz activity that lasts >30 min or
2 grand mal seizures without regaining consciousness in between
respiratory arrest due to hypoxia and increased O2 consumption due to increased brain activity
acute tx: phenobarbital, thiopental, phenytoin, benzos, prop, GA
anesthetic agents and seizures
EEG activity
sx of sz under GA
all have been implicated in inducing sz activity
reduce EEG in dose dependent fasion
sx of sz under GA: tachycardia, HTN, increased EtCO2 and O2 consumption
etomidate and EEG
while it is associated with myoclonus, it is not associated with increased EEG activity in patients who do not have epilepsy
in patients with sz DO’s, which drugs can induce sz activity and help ID location of seizure foci during cortical mapping
methohexital, etomidate, alfentanil
LA’s and seizure threshold
reduce seizure threshold but properly placed regional anesthetic has no effect on this
drugs that have metabolites capable of inducing sz activity
atracurium produces laudanosine which can induce seizures but you’d only see this with long term infusion use in ICU
cis makes less of this and therefore its not really a thing
normeperidine (metabolite of meperidine) is capable of producing seizure activity
drug used as anti convulsant that is excreted unchanged by the kidneys
gaba
Phenytoin MOA/comments
valproic acid MOA/comments
carbamazepine MOA/comments
gabapentinoids MOA/comments
DOA of which drug would be prolonged in an Alzheimer’s patient who takes donepezil
succ, mivacurium, ester type LA’s because cholinesterase inhibitors are the main stay for alzheimers tx
alzheimers s/sx (4)
memory loss
apraxia
aphasia
agnosia
alzheimers pathophysiology and dysfunctions related to it
diffuse beta amyloid rich plaques and neurofibrillatory tangles in the brain
dysfx r/t plaque formation:
dysfunctional synaptic transmission (most common in Ach neurons)
apoptosis (programmed cell death)
alzheimers tx
cholinesterase inhibitors to restore Ach including donepezil, tacrine, rivastigmine, galantamine
anesthetic management of/considerations for alzheimer’s patients
short acting drugs under GA is best because the idea is to allow them to return to baseline cognition faster.
avoid preop sedation as it can worsen confusion
probs won’t cooperate for a MAC
cholinesterase inhibitors can increase parasympathetic tone so bradycardia/syncope/n/v can develop
if an anticholinergic is required, glyco is best since it doesn’t cross BBB
pathophysiology of Parkinson’s disease
dopaminergic neurons in basal ganglia are destroyed which favors an increase in cholinergic activity.
increased Ach activity in basal ganglia increases GABA activity in thalamus. since GABA is inhibitory, increased GABA suppresses thalamus.
thalamic inhibition suppresses cortical motor system and motor areas in brain stem. final result is over reactivity of EPS.
dx of Parkinson’s disease
you have 2 of the 4 cardinal signs
1. resting “pill roll” tremor
2. skeletal muscle rigidity
3. postural instability, loss of balance with an altered gait
4. bradykinesia- very slow movement and reflexes
-secondary signs include psychosis, depression, dementia, lack of facial expression, diaphragmatic spasm, oculogyric crisis.
Parkinsons tx: levadopa and carbidopa
levodopa and carbidopa- levodopa is precursor to dopamine. carbidopa is a decarboxylase inhibitor. by preventing levodopa metabolism in blood, more levodopa can enter CNS.
SE: increased inotropy, tachycardia, orthostatic HoTN, dyskinesia, n/v
levodopa has half life of 6-12 hours so make sure they take it morning of surgery!
Parkinsons tx: selegeline
MAO-B inhibitors restore dopa concentration by reducing metabolism in CNS
(unlike non selective MAOI’s, selegeline does not increase the risk of tyramine induced hypertensive crisis)
other tx’s for parkinsons include
dopamine agonists
anticholinergics
COMT inhibitors
amantadine
hormone replacement
anesthetic considerations for a patient with parkinsons disease
at risk for autonomic instability, orthostatic HoTN, dysrhythmias, aspiration.
antidopaminergic drugs such as metoclopramide and butyrphenones (haldol and droperidol) and phenothiazines (promethazine) may exacerbate EPS. these drugs are contraindicated
HoTN should be tx with intravascular volume expansion and direct acting agents like neo
monitor for postop ventilatory failure
alfentanil and the parkinson patient
may cause dystonic reaction due to interruption of central dopaminergic transmission
drug useful for sedation and reduction of tremors in the parkinson patient
diphenhydramine
DBS and levadopa
holding levodopa causes sx to worsen which can help facilitate optimal electrode placement
how is DBS performed (parkinson patient)
-requires a burr hole to insert electrodes into sub thalamic nucleus, globus pallidus, ventralis intermedius. done under stereotactic guidance.
-patients head is placed in a rigid frame
-to determine optimal electrode placement, patient has to be awake but can be lightly sedated with opioids/precedex
-patient is in sitting position which increases risk of VAE. can monitor with precordial doppler. if it occurs, tell patient NOT to take deep breath, tell patient to flood field
-to minimize ICH risk, SBP <140
-sz’s can be tx with small dose of prop, barbs, benzos
GABA and DBS
because of the crucial role of gaba in the thalamus, drugs that inhibit GABA (prop or benzos) are avoided as they can interfere with electrophysiologic brain monitoring
corneal abrasion
s/sx
dx
prevention
tx
s/sx: pain, foreign body sensation, photophobia, excessive tearing, conjunctival erythema, diminished visual activity. blindness is rare
dx: fluorescein stain. when examined with cobalt blue slit light or pen lamb, abrasion will appear green
prevention: tape horizontal, goggles
tx: abx drops for 24h, topical or PO NSAIDS, self limiting and resolves in 1-3d
patching is not recommended because it does not improve pain and can delay healing
most common cause of postop visual loss
ION
most likely explanation of ION
inadequacy of blood supply to optic nerve (CN2) due to venous congestion in optic canal, reducing ocular perfusion pressure.
increased intra abdominal or intra thoracic pressure can also increase IOP
ocular perfusion pressure =
MAP-intraocular pressure
when does vision loss from ION commonly occur
24-48h post surgery
anesthesia and patient risk factors for ION
difference between how ION and central retinal artery occlusion start
ION starts as nerve problem where CRAO starts as vascular problem
pathophys and sx of CRAO
occlusion of retinal artery (ex reduced venous out flow due to improper head position)
sx: sudden painless vision loss in one eye upon waking up from anesthesia
risk factors for CRAO
using a horseshoe in the prone position (better options include foam face pillow)
-embolism (most common after CPB)
-administering N2O after retinal detachment surgery with intraocular gas bubble
which anticonvulsants create resistance to non depolarizers?
phenytoin, carbamazepine
which anticonvulsant follows zero order kinetics
phenytoin
the DOA of which NMB will be increased if used on an alzheimer’s patient who takes donepezil
succ since mainstay tx for alzheimers is cholinesterase inhibitors
drugs you should not give to parkinson patients include
antidopaminergic drugs such as metoclopramide and butyrphenones (haldol and droperidol)
phenothiazines (promethazine)
alfentanil (can cause acute dystonic reaction due to interruption of dopa)
what do you use to tx parkinson sx exacerbation
anticholinergics (since theres too much Ach and not enough dopa)
MOA of selegeline
MAO-B inhibitor that reduces dopa metabolism to help restore balance of dopa
