What is the dibucaine #
Dibucaine inhibits normal psuedocholinesterase enzyme to far greater extent that variant.
Homozygous normal by 80%
heterzygous by 40-60% 1/500
homozygous abnormal 20% 1/3000 4-8 hrs (anticholinerstase not proven reliable, and FFP transfusion for endogenous pseudocholinesterase not recommended)
reasons for fade w TOF
3, abnormla metabolsim: 90% of dose is metabolismed before reaching NMJ, with atypical psuedo a larger dose makes it to NMJ resulting in phase 2 block
Causes of POVL
corneal abrasion: exacerbated by blinking, sensation foreign body, tearing, photophobia
Glycine toxicity: dilated nonreactive pupils, elevated glyceine levels
Acute glycoma: severe periorbital pain, dilated pupil
cortical blindess: inability to follow moving objects w head stationary, normal pupillary response, absent response to visual threat
hemorrhagic retinopathy:floaters, preretinal hemorrhages, retinal edema
retinal ischemia: edematous retina, painless visual loss;
ION:painless, ischemia of optic disk
petroleum based oitment, laser injury
CI to ECT
intracranial mass lesions
vascular malformations
increased ICP from any cause
recent stoke <1 month
recent MI (<3 months)
Pheo
physioloic effects of ECT
sym sympathetic activation associated with increased cerebral blood flow, increased ICP, and cerebral oxygen consumption
IOP and intragastric presssure may also increase
Drugs that change seizure duration
Increased Duration: Etomidate
No Effect: Methohexital, ketamine, remifentanil, alfentanil
Shortened Duration: Propofol, midazolam, lorazepam, thiopental, lidocaine
Pros and Cons of induction drugs for ECT
optimal seziure duration
30sec
Methohexital – gold standard for ECT, no change of seizure duration(vs prop), blunt sympathetic surg (vs etomidate)
Propofol: decrease seizure duration but blunt hemodynamic response.
Opioids are useful in the fact that they allow a lower dose of the anesthestic agent to be used, thus allowing faster wakeup and if using propofol or thiopental it will decrease the amount so the dose related decrease will help lengthen the seizure (
Hyperventilation (hypocarbia) will lengthen seizure duration and thus effectiveness of ECT.
How would you treat post ictal agitation?
post ECT myalgia
benzo, prop, precedex
NSAIDs-ketorlac
DDx for delayed emergence
rxn between intravitreal air and N20
increase intraocular pressure, central retinal artery occlusion, retinal/optic nerve ischemia
air-reabsorbed in 5 days
sulfur hexafluroride-10 days
perfluropropane- 30 days
emergence delerium
tx, prevention
RF
tx
sx PDPH
neuro: frontal-occipital H/A, positional, neck stiffness, seizures, CN stretch (6th nerve impaired eye abduction)
eyes: photophobia, blurred vision,
ears: tinnitis, hearing loss
GI: N/V
How to treat extrapyramidal symptoms
types EPS
imbalance between cholinergic and dopamine activity
benztropine, diphenhydramine
dyskinesias (repetitive movements-eye blinking), akathesia (internal/external restlessness
dystonia (very strong muscle contactions that result in twisting of body)
Prolonged non depolarizing muscle blockade.
When to reverse? Why not admin additional reversal
resistance
abx: aminoglycosides (gent), tetracylins, polymixins
Volatile (Des>sevo>iso) CCB, LA
hypernatremia, hypokalemia, hypoca/CCB, hyper mag, metabolic and resp acidosis,
lithium, phenytoin (acute use)
liver/ renal impairement/hypothermia
Use of EEG in neuro case uses (3)
waves
good for monitoring for (burst suppression, controlled hypotension, gauging anesthetic depth
beta (increased freq, decreased amplitude) >13hz
alpha (decreased freq) 8-13
delta (sleep)-4hz
why no nitrous in neuro case
increases CMRO2
VAE/pneumocephalus
Consideration HTN and neuro
R shift of cerebral autoregulation curve
What is burst suppression, what does it mean
Identified as periods of no activity punctuated by brief periods with high voltage bursts
What monitors are available for neurological monitoring during CEA
***None of these have been shown to improve outcome since postoperative emboli and not intraoperative hypoperfusion are most likely cause of periop stroke, but do aid in decision to shunt and BP maintenance.***
Why do surgeons care about SBP during CEA
collateral perfusion drived by SBP
Why it important to maintain normocarbia during CEA
EEG shows slowing durig CEA what should you do
What is cerebal hyperperfusion syndrome
H/A, AMS, seizure, focal neuro defict, intracranial hemorrhage
causes of hyponatremia and tx
why should delay case w sodium under 130
dilutional hyponatremia
SIADH: euvolemic, elevated urinary sodium, elevated ADH levels, raren urine sodium >100
tx water restriction, diuresis demeclocycline, NA Replacement
CSW: hypovolemic, urine sodium >100 (release of naturetic peptide from brain)
tx:both volume repletion and sodium administration
loopdiuretics
place pt at risk of cerebral edema