Nagelhout Video 3 - Exam 1 Flashcards
-Succinylcholine (Anectine)
-ED95
-intubation
ED95: 0.5-0.63mg/kg
I: 1-1.5mg/kg
per Nag, give 100mg to everyone for rest of career to keep it simple
Succinylcholine (Anectine)
-onset
-DOA
O: 30-60s
DOA: 5-15min (ultrashort)
Mivacurium (Mivacron)
-ED95
-intubation
ED95: 0.08mg/kg
I: 0.2mg
Mivacurium (Mivacron)
-onset
-DOA
O: 3 min
DOA: 20-40 min (short)
Atracurium (Tracrium)
-ED95
-intubation
ED95: 0.15mg/kg
I: 0.5mg/kg
Atracurium (Tracrium)
-onset
-DOA
O: 2-4 min
DOA: 30-60 min
Cisatracurium (Nimbex)
-ED95
-Intubation
ED95: 0.05mg/kg
I: 0.1mg/kg
Cisatracurium (Nimbex)
-onset
-DOA
O: 2-4 min
DOA: 30-60 min
Rocuronium (Zemuron)
-ED95
-Intubation
ED95: 0.3mg/kg
I: 0.6-1mg/kg
The Rock stays relevant by starring in anything he can for 0.3 of the year
The Rock stars in 0.6-1 cringe movies every year
-Nag says for intubation just keep it easy at 1mg/kg unless case is <1.5 hr
Rocuronium (Zemuron)
-onset
-DOA
O: 1-1.5min
DOA: 30-60 min
It only takes The Rock 1-1.5 min to make contact in the ring
The Rock can last 30-60 min in the ring if you make fun of his fanny pack
Vecuronium (Norcuron)
-ED95
-intubation
ED95: 0.05mg/kg
I: 0.1mg/kg
I have a tiny hand VECuum that’s effective (0.05mg)
My regular VECuum is very small too (0.1)
Vecuronium (Norcuron)
-onset
-DOA
O: 2-4 min
DOA: 30-60min
I start to VECuum after seeing 2-4 dust bunnies in the house
It takes me 30-60 min to VECuum my whole house
Pancuronium (Pavulon)
-ED95
-intubation
ED95:0.05mg/kg
I: 0.08-1.8mg/kg
0.05% of Pandas don’t prefer bambu
Panda bears range in sizes between 0.08-1.8m
Pancuronium (Pavulon)
-onset
-DOA
O: 2-4 min
DOA: 60-90min (LONG)
It takes Pandas 2-4 minutes to start eating food sitting right in front of them
Pandas eat for 60-90 minutes at a time
What is the priming technique for administering NMBD?
giving ~10% of the calculated dose to the pt RIGHT before induction, then following with the remaining NMB agent
-thought to increase speed of onset
-give induction agent asap after the 10% dose to avoid paralyzing an aware pt
What is the timing technique for administering NMBD?
-giving the FULL dose of the NMBD before the induction agents
-requires absolute precision and everything ready to go once paralyzed
If unable to give succinylcholine, which NDMR could you give instead?
Roc
-fastest onset of its class
Nag: “Dose for intubation with a NMBD is (roughly) _ x its ED95
I = ED95 x 3
If giving gas with NMBD:
just know to ease up on it before trying to reverse
Qualitative signs of NMBD recovery:
-RR smooth, unlabored
-opens eyes on command, no diplopia, purposeful tongue movement
-+ swallow, sustained bite, cough, hand grip, arm lift, head lift >5s
Numerical signs of NMBD recovery(not quantitative):
-Vt and RR WNL
-VC >/= 15mL/kg
-NIF of -25 to -30cmH2O
-sustained tetanic response to 50Hz for 5 s
-TOFR > 0.9 w/o fade
-DBS w/o fade
Risks of residual NMBD:
-aspiration ( from poor pharyngeal force, - cough, swallow, etc~airway reflexes)
-postop hypoxemia
-upper airway obstruction occurring enroute to PACU (no thanks)
-profound muscle weakness
-delays in meeting PACU discharge criteria, longer intubation times
-postop pulmonary complications (atelectasis, pneumonia)
Main thing we want to see when ensuring NMBD is reversed
TOFR >0.9
Pt factors contributing to residual NMBD
-age extremes
-gender
-pmh (renal/liver or neuromusc dysfunctions)
-meds (antiseizure meds especially)
-acidosis, hypercarbia, hypoxia, and hypothermia
Method of NMBD monitoring associated with LOWEST risk of residual:
acceleromyography
Which TOF count is associated with higher risk of residual NMBD, 1-2 or 2-3?
1-2
indicates deeper block, higher risk
Which method of anesthesia is more likely to be associated with residual NMBD, IA or TIVA?
IA
2 common medication classes given intraoperatively that could extend the period of paralysis:
opioids and abx
Efficacy of reversing a NMBD depends on:
-amount of current spont recovery? (0 twitches, 4 small twitches?)
-time between giving last paralytic (~15-30 min; should give Neostigmine anyways if <4hr since NMBD given)
-intensity of effect from NMBD given (when in doubt, wait it out -vent)
Neostigmine
-dose
25-75mcg/kg
Ne Yo has broken 25-75 mics in his career from his voice alone
(Fun fact: Ne Yo is a huge Matrix fan, hence his stage name)
Neostigmine
-onset
-DOA
O: 5-10 min
DOA: 45-90min
Ne Yo starts work 5-10 minutes late
Ne Yo will antagonize you for 45-90 min if you listen to his album
Neostigmine can increase the incidence of _
PONV
Edrophonium
-dose
500-1000mcg/kg
Ed has 500-1000 contacts in his phone
Edrophonium
-onset
-DOA
O: 5-10 min
DOA: 30-60 min
Ed is on the phone within 5-10 mins of hearing juicy gossip
Ed spends 30-60 mins on the phone spilling the tea
Atropine
-dose
15mcg/kg
Atropine
-onset
-DOA
O: 1-2 min
DOA: 1-2hr
Edrophonium is not ideal for _ blocks
deep
Atropine goes best with _
Edrophonium
-similar onset
Glycopyrrolate
-dose
10-20mcg/kg
Glyco Gecko weighs 10-20mcg
Glycopyrrolate
-onset
-DOA
O: 2min
DOA: 2-4hr
Every 2 minutes, somebody STARTS saving money by switching to Glyco
Each Glyco ad lasts 2-4hrs
Glycopyrrolate has _ initial tachycardia than atropine, is a _ antisecretion drug, and has _ CNS effects
less
better
no
Sugammadex
-dose
2-8mg/kg
-up to 16mg/kg safely
Sugammadex
-onset
-DOA
O: 1-2min
DOA: 2-16hr
Neostigmine
-MAX dose
5mg
-ceiling effect; will have 100% inhibition of AChE
Edrophonium
-Max dose
1mg/kg
Which reversal agent is a faster onset and shorter duration
Edrophonium
-less effective; give if pt has 4/4 twitches
Which reversal agent is slower onset and longer duration?
Neostigmine
How do AChE Inhibitors (reversal drugs) work?
by increasing ACh release or inhibiting degradation of ACh by AChE
-Neostigmine and others bind to active site and form carbamyolated enzyme that AChE hydrolyzes instead of ACh, this continues until enough extra ACh is made
Why give an anticholinergic (antimuscarinics) along with AChE Inhibitors?
bc AChE Inhibitors often work systemically and activating the nicotinic and muscarinic cholinergic receptors will cause a large vagal/parasympathomimetic response
-bradycardia, secretions, bronchoconstriction, diarhea
Which anticholinergics go with each AChE inhibitor?
Edrophonium and Atropine
Neostigmine and Glycopyrrolate (Robinul)
What kind of drug is sugammadex?
gamma-cyclodextrin ; paralytic reversal drug
How does sugammadex work?
Encapsulates and inactivates STEROIDAL NMBD
-encapsulates them and makes them water soluble
Sugammadex pharmacokinetics shows a linear dose relationship in doses up to _mg/kg
8
What happens if I gave my pt sugammadex but they need to go back to the OR?
use a different NMBD in a different class - nonsteroidal
Which drugs does Sugammadex work on?
Vec and Roc; sugammadex is a selective relaxant binding agent (SRBA)
~3min
Elimination half life of Sugammadex?
2.3hr
Up to _% of Sugammadex is eliminated thru urine in 24hr
80
Which pts are at higher risk for complications if not properly reversed?
major renal disease (NAG enzyme)
BMI>35
major resp disease
poor resp reserve
OSA
major coronary disease
hx of arrhythmias
hx PONV
major abdom/thoracic surg
-give sugammadex
T/F Sugammadex binds to plasma proteins and erythrocytes
false
Sugammadex
-dosing
TOFR (0.5) = 0.22mg/kg
TOF (2/4) = 2mg/kg
PTC (1-2)= 4mg/kg
RSI, high dose Roc, or can’t intubate/ventilate = 16mg/kg
Sugammadex
A/E
-dry mouth, dysgeusia, N/V, cough, low BP, chills, large amt of N-acetylglucosaminidase in urine
-allergy (tachycardia, rash, at higher doses/faster admin)
-this happens within 5-10min of admin
-negates oral contraceptives (need other method for 1mo)
2 kinds of nACh receptors exist
Neuronal(pre-synaptic)
Muscular (post-synaptic)
-both have 2 alpha, beta, delta, subunits
How do NDMR and DMR differ?
NDMR cause blocks by blocking ACh from postsynaptic alpha subunits
DMR (sux) causes prolonged depolarization causing reduced sensitivity in post synaptic nAChr and inactivates Na+ channels to inhibit propagation
How is a twitch and fade different?
Fully blocking a twitch occurs from blocking postsynaptic nAChr
Fade is caused by blocking the presynaptic nAChr
What metabolizes Succinylcholine?
hydrolyzed by butyrylcholinesterase
NDMR are classified as either:
steroidal or benzyl isoquinol inium
The speed of onset is _ proportional to the potency of NDMR
inversely
-more potent = slower onset
-bc we’re only giving few mg at a time (hence 100mg sux vs 3-4mg Nimbex)
-molar potency is highly predictive of onset (Roc= 0.54 mcM/kg)
Which NM units get blocked and recover quicker, central or peripheral?
central (laryngeal adductors, diaphragm, masseter muscle)
-hence why we watch the face first when inducing and ulnar n when emerging
Testing facial n we’re looking for movement with the
orbicularis oculi and the corrugator supercilli
Testing ulnar n we’re looking for movement with the
adductor pollicis
Long acting NMBD undergo minimal metabolism and are primarily eliminated by
renal excretion
Intermediate duration NMBD clear quicker than longer acting ones bc
they are degraded, metabolized, and eliminated
If myalgia is a concern when giving sux, what can be done?
give small, rapid acting defasciculating dose of NDMR as well
OR just give Roc ~1min and ready
Which 2 drug classes most likely cause anaphylaxis?
ABX and NMBD
-more common long and intermediate acting NMBD
2 most common NMBD
Roc and Sux
In terms of reversal of paralytics, what should be common practice?
full dose of reversal given AFTER some spontaneous reversal is seen
Pt has increased IOP and needs surg, but sux increases IOP. What should be done?
-give sux anyways, propofol can decrease IOP so give it before sux
-use topical and regional anesthesia where possible
What do Alzheimer’s drugs do?
weak AChE Inhibitors
-increase ACh in brain
Examples of drugs for Alzheimers disease:
-Donepezil (Aricept)
-Rivastigmine (Exelon)
-Galantamine (Razadyne)
-Tacrine (Cognex)
Will sux interact with Alzheimer drugs?
yes, will make NMBD last longer, but not by much ~25% inhibition
Which NMBD will Alzheimer medications NOT interact with?
Neostigmine and NDMR
-these don’t cross BBB
What is Physostigmine?
AChE inhibitor, increases ACh in brain CROSSES BBB
-used sometimes in PACU to wake ppl tf up
What is Phospholine Iodide ?
eye gtts with AChE inhibitors used to treat glaucoma and lower IOP
-can increase duration of sux (boards question despite drug not being common now)
What are 2 main types of local anesthetics?
esters and amides
-esters have 1 “i” and amides have 2 (lidocaine = amide, procaine =ester)
3 parts of LA structure
Lipophilic Benzene Ring (aromatic group)
Hydrophilic Quaternary Amine (base)
Intermediate chain in between them (made of ester or amide)
-if chain has a N in it = amide
-if chain has 2 oxygen groups = ester
Which LA have higher allergy potential?
esters
T/F If pt has an allergy to an ester, they can just have a different ester
false
T/F If pt has an allergy to an amide, they can just have a different amide
true
-can also have an ester too
How are amide LAs metabolized?
in liver by CYP1A2 and CYP3A4
-if pt is ultrarapid metabolizer will have a significant blood level
How are ester LAs metabolized?
catalyzed by plasma and tissue cholinesterase via hydrolysis
-does this rapidly
Are esters synthetic or natural?
mostly synthetic
-except cocaine
Which LA are longer acting and why?
amides
-more lipophilic and protein-bound, require transport to liver to metabolize
Longest acting LA ester?
Tetracaine
Examples of ester LAs
Cocaine
Procaine (Novacaine)
Chloroprocaine (Nesacaine)
Tetracaine (Pontocaine)
Benzocaine (Anbesol, Cepacol)
Examples of amide LAs
Lidocaine (Xylocaine)
Prilocaine (Citanest)
Ropivacaine (Naropin)
Bupivicaine (Marcaine, Sensorcaine)
Mepivicaine (Cabocaine)
What is N-Acetylglucosamine (NAG)?
biomarker for renal tubule damage
-seen as an A/E to sugammadex admin
Common abx and paralytic drug interaction
Aminoglycoside abx - mycins
-can’t reverse them, just put on vent and leave in PACU
Which complications can occur if sugammadex is given too quickly?
Bronchospasm, severe bradycardia
-other A/E (HoTN, rash, anaphylaxis)
Tx for Sugammadex hypersensitivity reaction:
Epi 10-20mcg boluses PRN
Epi 25-50mcg for bronchospasm
LR bolus
Albuterol 4-10 puffs PRN
Hydrocortisone 100mg IV
Diphenhydramine (H1blocker) 50mg IV
Famotidine (H2 blocker) 20mg IV
Why give an H1 and H2 blocker for sugammadex hypersensitivity?
H1 blocker prevents bronchoconstriction
H2 blocker prevents cardiovascular collapse
Which NDMR are steroidal?
Roc
Vec
Pancuronium
Which AChE inhibitor is likely to cause PONV
neostigmine
What is best thing to document after reversal agent was given and extubated successfully before sending to PACU?
T1/T4 ratio >0.9
VS obviously along w Vt
“good exchange after extubation”
H2 receptor activation causes
-increased gastric acid,
-systemic vasodilation and tachycardia
-+ inotrope
-+chronotrope
H1 receptor activation causes
-bronchoconstriction
-increased capillary permeability (swelling)
-increases gastric contraction
-negative dromotropic effects
Diphenhydramine blocks
H1 receptors
Famotidine or zantac can block
H2 receptors
Succinylcholine
-laryngospasm dose
0.2-2.0 mg /kg
-low for mild, high for severe
