NMBAs Flashcards
Other names for succinylcholine
- annectine
- SCh
- Quelicin
- Suxamethonium
Doses for SCH
RSI:
Small children:
IM:
Laryngospasm:
RSI: 1-1.5 mg/kg
Small children: 2 mg/kg (peds often give 1 mg/kg with atropine in same syringe)
IM: 3-5 mg/kg
Laryngospasm: 20 mg (1 cc)
Indication for annectine (6)
- rapid muscle relaxation
- routine intubation
- very short cases
- OB
- RSI (full stomachs)
- laryngospasm
Contraindication for Quelicin
- MH
- kids have increased risk for hyperK and cardiac arrest from undiagnosed myopathies
- prolonged block with pseudo cholinesterase abnormality/deficiency (pregnancy/liver disease)
MOA of Annectine
Bind to 2 alpha subunits of nicotinic cholinergic receptors
Allow Na and Ca influx, K efflux—> depolarizes cell and remains depolarized until diffuses away from receptors
Mimics ACh
CV and Respiratory effects of suxamethonium
CV: Muscarinic stimulation —> can decrease HR
**esp in peds
Resp: apnea
Neuro effects of SCh
Questionable increase in IOP and intragastric pressure, increases ICP
SCh could interact with what drug groups
Drugs used to treat Myesthenia Gravis and chemo drugs can prolong effects
Clinical implications of SCh
- used frequently in OB
- avoid in pts whose K is already high— burns, trauma, renal failure — immobilization and stroke causes extra receptors which can cause a profound increase in K
Onset and duration of Quelicin
O: 30-60 seconds IV; 2-5 min IM
D: < 10 IV; 10-30 min IM
Metabolism of SCh
Plasma cholinesterase (PCE); diffuses from NMJ, hydrolyzed in the plasma and liver by PCE
T or F: the weak active metabolite of SCh is succynltricholine
F- weak active: succinylmonocholine
T or F: there is severe histamine release from succyinlcholine
F- minimal Release of histamines
What can large or repeated doses of SCh cause
Phase II block
If a patient has pseudocholinesterase deficiency, what test will tell you severity of deficiency
Dibucaine number
Why is there no reversal of SCh
Only 10% of the drug administered reaches the NMJ
What can cause postop muscle pain after SCh administration
Fasciculation
Rocuronium (___)
is ________ acting
Zemuron
intermediate
Dosing of Zemuron
Intubation/surgical relaxation
Maintenance/repeated dose
RSI
Defasiculations
Intubation/surgical relaxation: 0.6 mg/kg
Maintenance/repeated dose: 0.1-0.2 mg/kg prn
RSI: 1.2 mg/kg
Defasiculations: 5 mg (0.03 mg/kg)
Indications for Zemuron
- routine induction
- surgical relaxation
- RSI
- defasiculation
CV effects of Zemuron
Histamine release?
- none
- rare histamine release
Clinical implications to keep in mind with OB patients & SCh:
Don’t defacisulate them… you will see eyes flutter but they don’t need it
rocuronium
- onset
- duration
- elimination
O: 1-2 min (dose dependent, large dose can mimic SCh)
D: ~ 30 mins (variable) (up to 70 min with RSI)
E: hepatic 70% renal 30%
Sequence for Zemuron use for defasicuations
A. Give 5-10 mg Roc, wait a minute
B. follow with inductions agent
C. Administer SCh
Special considerations for Roc (3)
- lack hormonal activity
- volatile anesthetics can enhance NMB activity
- burns may require higher doses
Vecuronium (___)
Norcuron
Dosage of Norcuron
Induction/intubation:
Priming:
Maintenance:
Induction/intubation: 0.08-0.1 mg/kg
Priming: 10% given 3-5 min prior
Maintenance: 0.01 mg/kg
CV effects of Vecuronium and is there histamine release?
CV = stable
Histamine = no histamine release
T or F: Vecuronium is very fast acting so it would be better for short cases
F: intermediate acting, best for long cases
Which NMBA is typically used for open heart surgeries
Vecuronium
Norcuron
Onset:
Duration:
O = 2-3 min (good intubating conditions) & 3-5 min (max blockade)
D = 25- 40 min (25% recovery) & 45-60 min (95% recovery)
Metabolite of Vec and potency:
3-desacetyl
60% potency of vec
Vec can precipitate with ________
Thiopental
T or F: Norcuron lacks hormonal activity
T
T or F: volatile anesthetics can enhance NMB activity
T
Pancuronium (___)
Pavulon
Pancuronium intubation and maintenance dose
I: 0.08- 0.12 mg/kg
Maintenance: 0.01 mg/kg
Caution for pancuronium in:
Caution in renal patients
CV effects of Pancuronium and is there histamine release? (5)
- CV = atropine like effect in SA node (antimuscarinic effects)
- tachycardia & increased CO due to antimuscarinic stimulation (it is a vagolytic)
- causes norepinephrine release and decreased reuptake by adrenergic nerves
- can be used in cardiac surgery to counteract bradycardia from high-dose opioid usage
- increases BP
No histamine release
Cautiously use PAncuronium in what patients
- pt who will not tolerate HR & CO increase —> poor choice in unstable cardiac patients
- renal patients
Pancuronium-
Onset
DOA
Metabolism
Excretion
O: 2-3 min
DOA: 60-100 min
Metabolism: hepatic 20%
E: renal 40-70%
Active metabolite of pancuronium
3-OH- pancuronium
NMBAs:
A. Amino steroids
B. Benzylquinolone
A. Rocuronium, vecuronium, pancuronium
B. Atracurium, cisatricurium, mivacurium
Atracurium (___)
Tracrium
Atracurium
Dose
Onset
DOA
0.3-0.6 mg/kg
2-3 mins
20-35 mins (begin recovery) & 60-70 mins (95% recovery)
System effects of tracrium
CV= minimal decrease in BP
Histamine= small
Other = in hyper parathyroidism, hypercalcemia decreases sensitivity, thus shorter DOA
T or F: Atricurium is a good choice for renal patients
T
Metabolism of atricurium
60% nonspecific ester hydrolysis
30% Hofmann elimination
10% renal
Active metabolite of atricurium
Laudanosine = can produce rare seizure activity (tertiary amine crosses BBB)
Onset and DOA of atricurium
O: 2-3 min
DOA: 20-35 min; 95% recovery in 60-70 min
Cisatracurium (___)
Nimbex
Dose for nimbex
0.1-0.15 mg/kg IV
CV effects and histamine release of nimbex
CV= NO changes HR or BP
Histamine = none
T or F: Nimbex is a good choice for NMBA in a renal transplant patient
T
Nimbex:
Metabolism
Onset
Peak
Duration
Metabolism: Hoffman elimination, metabolite breakdown by nonspecific esterase metabolism
Onset: 2-3 min
Peak: 3-5 min
Duration: 40-70 min; 20-35 min to begin recovery; up to 93 min for 90% return
Cisatracurium is the potent ___ isomer of ___.
cis-cis; atracurium
Rate each of the following as Short acting (SA), Intermediate acting (IA), or long acting (LA)
- Roc
- Vec
- Pancuronium
- atracurium
- Nimbex
- mivacurium
- Roc = IA
- Vec = IA
- Pancuronium = very LA
- atracurium = IA
- Nimbex = IA/LA
- mivacurium = SA
Mivacurium (_______)
Mivacron
Doses for mivacurium
Intubation
Infusions
Intubation: 0.15-0.2 mg/kg
Infusions: 4-10 mcg/kg/min
Contraindication for mivacurium
Asthma and low BP due to large histamine release
T or F: there is a small histamine release with rapid administration of mivacurium
F- LARGE histamine release
Onset, DOA, and metabolism of mivacurium
O: 1 min
DOA: 10-20 min
M: hydrolysis by plasma cholinesterase
3 ways to cause muscle relaxation
- muscle relaxants
- IAs
- blocks
Succinylcholine C/I:
- Severe hyperkalemia (burns, severe abdominal infections, metabolic acidosis)
- MH history
- Upregulation (burns, hemiplegia, long ICU stays, CVA)
Anaphylaxis under GA presents as:
increased PIP on vent (have to look for different signs than awake patients)
Which three drugs are the most likely to cause anaphylaxis in the perioperative period?
32% Sugammadex
27% Rocuronium
23% Antibiotics
*we typically give all three together so it can be difficult to determine the cause of anaphylaxis
Cisatracurium metabolism:
nonspecific ester hydrolysis & Hofmann elimination
What side effects does histamine release cause?
Skin flushing, tachycardia, hypotesion
Which of the NMBs produces the active metabolite Laudanosine?
Atracurium and Cisatracurium (Hofmann elimination is what produces this)<br></br>However, Cisatracurium is a much more potent drug than Atracurium, so because we are able to give a much smaller dose of Cisatracurium, there is extremely minimal risk of Laudanosine.
Which of the benzylisoquinolinium NMBs has an active metabolite that we worry about?
Atracurium – Laudanosine (tertiary amine which can produce seizure activity)
Which of the benzylisoquinolinium NMBs has an active metabolite that we worry about?
Atracurium – Laudanosine (tertiary amine which can produce seizure activity)
Which of the benzylisoquinolinium NMBs has an active metabolite that we worry about?
Atracurium – Laudanosine (tertiary amine which can produce seizure activity)
Which of the nondepolarizing NMBs may cause changes to BP?
Mivacurium and Atracurium (due to histamine release)
Panc metabolism
70% renal
20% hepatic
vec metabolism
~ 50/50 hepatic/renal
How do we know when a patient is ready for intubation?
- TOF, but BEST mode is single twitch, so you can see when it starts to fade (meaning patient is ready)
- time (agent-dependent)
- patient becomes easier to ventilate
Aminosteroid NMBs:(small/large) volume of distribution (limited/high) lipid solubility
small
limited
Aminosteroid NMBs:
highly (unionized/ionized) at physiological pH
ionized
Aminosteroid NMBs:
_____ histamine release
minimal
Aminosteroid NMBs:
primarily ___ breakdown and ___ excretion
primarily liver breakdown,
kidney excretion
Nondepolarizing NMB MOA:
compete with/block ACh at the nicotinic receptor alpha subunits on motor endplate – inhibits depolarization
MH occurs more commonly in:
(peds/adults)
(males/females)
peds (1 in 15,000) … vs 1 in 10,000 to 50,000 in adults
males
How do you reconstitute Ryanodex?
Reconstitute 250 mg vial with 5 cc of STERILE WATER - (50 mg/cc)
Administer 2.5 mg/kg rapidly through large bore IV
How do you reconstitute Dantrolene?
Reconstitute the 20 mg vial with 60 cc of STERILE WATER
Dantrolene dose:
2.5 mg/kg
How do we administer GA to patients with a history of MH?
Propofol TIVA, O2, N2O, regional?
What are the first signs of MH?
rapidly increasing EtCO2
tachycardia
generalized muscle rigidity
Can we use N2O in patients with MH history?
YES! It is a gas, not a volatile agent
What are the top triggers for MH?
Volatile agents and SCh
What four drugs are most often involved in drug errors?
(17.1%) Succinylcholine
(13.2%) Inhalational Agents
(11.7%) Opioids
(9.3%) Local anesthetics
Succinylcholine dose:
(laryngospasm)
conc:
20 mg
(20 mg/cc)- give 1 cc
Succinylcholine
dose: (IM adults)
conc:
onset:
duration:
3-5 mg/kg IM
(20 mg/cc)
2-5 mins
10-30 mins
Succinylcholine
dose: (IV peds)
conc:
onset:
duration:
2 mg/kg (d/t larger volume of distribution and faster total clearance)
(20 mg/cc)
30-60 sec
10 mins
Succinylcholine metabolite:
Succinylmonocholine is a weak, active metabolite
Aside from a genetic deficiency of pseudocholinesterase, what else may cause a deficiency?
Pregnancy and liver disease (it is synthesized in the liver)
Succinylcholine metabolism:
Butyrylcholinesterase (pseudo/plasma cholinesterase) –> synthesized by the liver and found in the plasma —-> hydrolyzes SCh in the plasma after it diffuses away from the NMJ
Why do we only administer Succinylcholine in Peds for emergency situations?
Peds are at increased risk for fatal hyperkalemia and cardiac arrest (d/t undiagnosed myopathies)
What does a Dibucaine number measure?
Measures QUALITY pseudocholinesterase
Prolonged apnea after administration of Succinylcholine might be related to what?
Pseudocholinesterase abnormality;
check Dibucaine number
Succinylcholine (decreases/increases) intraocular pressure.
increases (peaks 2-4 mins; returns to normal by 6 mins)
Succinylcholine (decreases/increases) ICP.
increases (increased ICP more likely d/t lack of adequate anesthesia)
Succinylcholine (decreases/increases) intragastric and LES tone
increases (these two effects negate increased risk for aspiration)
Succinylcholine causes ___ histamine release.
minimal
Which of the NMBs normally causes a Phase I (no fade) TOF?
SCh, with large or repeated doses a Phase II (fade) TOF can result
For what reason is rapid sequence induction performed?
Aspiration risk!!
How do you determine which muscle relaxant to use?
Pre-existing conditions
Procedure length
Type of procedure
What are three ways to cause muscle relaxation?
Volatile anesthetics
NMBs
regional anesthesia
