Unit 5 Pharmacology: Neuromuscular Blockers Flashcards
(139 cards)
1
Q
Which subunits must be occupied to open the nicotinic receptor at the motor end plate?
A
Alpha and alpha
2
Q
What are the 2 types of nicotinic acetylcholine receptors (nAChRs) at the neuromuscular junction?
A
- The presynaptic Nn receptor is present on the presynaptic nerve
- The postsynaptic Nm receptor is present at the motor end plate on the muscle cell
3
Q
Describe the postsynaptic Nm receptor including type of channel and subunits.
A
Pentameric ligand-gated ion channel
5 subunits: 2 alpha, 1 beta, 1 delta, and 1 epsilon (a2B1D1E1 subtype)
4
Q
When 2 Ach molecules simultaneously bind to the 2 alpha receptor on an Nm receptor, what happens?
A
The channel opens, Na+ and Ca+ enter the cell and K+ exits the cell
5
Q
Why do anions such as chloride not pass through the nicotinic receptor?
A
They are repelled by the strong negative charges situated inside the channel
6
Q
At rest, the side of the muscle cell is negative relative to the outside, when Nm is activated by Ach what happens?
A
Na+ flows down its concentration gradient and enters the cell, this makes the cell interior more positive, activates voltage-gated sodium channels, depolarizes the muscle cell, and initiates an action potential. Depolarization of the myocyte instructs the endoplasmic reticulum to release Ca+ into the cytoplasm, where it engages the myofilament and initiates muscle contraction.
7
Q
How is Nm “switched-off”?
A
Acetylcholinesterase is positioned around the pre- and postsynaptic nicotinic receptors, it hydrolyzes Ace almost immediately after it activates these receptors
8
Q
What are the 2 pathologic variants of the nicotinic receptor?
A
The alpha2, beta1, delta1, gamma1 has a gamma subunit in lieu of an epsilon.
The a7 subtype consists of 5 alpha subunits
9
Q
What is the term for these pathologic variants of the nicotinic receptor?
A
Extrajunctional Receptors
10
Q
When are extrajunctional receptors present?
A
Early in fetal development
Denervation
Prolonged immobility
11
Q
What is the significance of these extrajunctional receptors to Anes?
A
Their presence predisposes a patient to hyperkalemia following succinylcholine administration
12
Q
What conditions represent contraindications to the use of succinylcholine due to their presence of extrajunctional receptors?
A
Upper or lower motor neuron injury Spinal cord injury Burns Skeletal muscle trauma CVA Prolonged chemical denervation (Mg, long-term NMB infusion, clostridial toxin) Tetanus Severe sepsis Muscular dystrophy (muscle atrophy from any cause)
13
Q
In the absence of extrajunctional receptors, how much can succinylcholine transients increase serum potassium? For how long?
A
0.5 - 1.0 mEq/L
For up to 10 - 15 minutes
14
Q
How are extrajunctional receptors affected by succinylcholine?
A
They are more sensitive and remain open for a longer period of time
15
Q
Does succinylcholine have a metabolite?
A
Choline
16
Q
Does the metabolite of succinylcholine, -choline, cause depolarization?
A
Yes, to the a7 receptor
17
Q
As a general rule, in the event of denervation injury, succinylcholine is best avoided for how long? Exception?
A
24 - 48 hours following the injury and for at least 1 year after.
Burns may be an exception, the risk of hyperkalmia may persist for several years after the burn (especially with contractures)
18
Q
What is the treatment for succinylcholine induced hyperkalemia?
A
IV calcium chloride
Hyperventilation
Glucose + insulin
19
Q
What happens with nondepolarizers in the presence of extrajunctional receptors?
A
Patients with upregulation of extrajunctional receptors are resistant to nondepolarizers - their potency is reduced
20
Q
Fade during train-of-four stimulation is caused by:
A
Antagonism of presynaptic nicotinic receptors (Nn)
21
Q
Why does succinylcholine not produce fade?
A
It agonizes the presynaptic nicotinic receptors (Nn)
22
Q
Acetylcholine is synthesized from what 2 things, in the presence of what?
A
Choline and CoA
Choline acetylcholinesterase
23
Q
After Ach is synthesized, where is it?
A
It is packaged in vesicles which are anchored by specialized proteins inside the presynaptic nerve terminal
24
Q
What are the 2 supplies of Ach vesicles?
A
- Ach that is available for immediate release
2. Ach that must be mobilized before it can be made available for immediate release (like a stockpile)
25
What channel opens with an action potential arrives at a nerve terminal in order to release Ach vesicles? Process that occurs?
Voltage-gated calcium channels open and calcium enters the nerve terminal, increased intracellular calcium destabilizes the proteins that hold Ach vesicles. The vesicles ext the nerve via exocytosis and each vesicles releases 5,000 - 10,000 Ach molecules into the synaptic cleft. Ach diffuses toward the postsynaptic Nn receptor on the motor endplate, where it depolarizes the motor endplate and initiates skeletal muscle contraction.
26
When an action potential arrives at a nerve terminal to initiate Ach release not all of the Ach released diffuses toward the motor endplate, where does some of it go and why?
A fraction of the Ach molecules bind to prejunctional receptors on the nerve terminal (Nn receptor) and cause mobilization of Ach vesicles inside the presynaptic nerve. This moves part of the “stockpile” to the front line where it is available to immediate release next time the nerve is stimulated.
27
Nondepolarizers competitively antagonize the presynaptic Nn receptors, what implication does this have?
This impairs the mobilization process of Ach, so now only the vesicles that are available for immediate release are able to be used. Since this is a limited quantity, nerve stimulation can quickly exhaust this supply with each successive stimulation less Ach is released, manifesting as a fade with train-of-four, double burst, and tetanus
28
In contrast to ND-NMB, succinylcholine stimulates the prejuctional receptors, what effect does this have?
Succinylcholine has the same effect as Ach, when succinylcholine binds to the presynaptic Nn receptor, it facilitates the mobilization process, so there is always Ach available for immediate release, so no fade is present.
29
Presence or absence of a fade distinguishes between what 2 types of block?
Phase I and Phase II
30
What type of block does succinylcholine produce? ND-NMB?
Sux: Phase I block.
ND: Phase II
31
How can succinylcholine cause a phase II block?
1. Dose > 7 - 10 mg/kg
2. 30 - 60 minutes of continuous exposure (IV infusion)f
It likely inhibits the presynaptic nicotinic receptor, impairs Ach mobilization and release from the presynaptic nerve terminal, and/or creates a conformational change in the postsynaptic receptor.
32
When is post-titanic potential present? When is it not?
Present: Normally and with a phase II block
| Not present: with a phase I block
33
What is the most sensitive indicator of recovery from neuromuscular blockade?
Inspiratory force better than -40 cm H2O
34
As a general rule, which group of muscles are paralyzed faster and recover sooner, more central muscles or peripheral muscles?
More central muscles are paralyzed faster and recover sooner
35
What is the best place to measure onset of blockade (intubation conditions)?
```
Muscle = orbicularis oculi (closes eye) or corrugator supercilii (eyebrow twitch)
Nerve = facial nerve
```
36
Best place to measure recovery of blockade (return of upper airway muscle function)?
```
Muscle = adductor pollicis (thumb adduction) or flexor hallucis (big toe flexion)
Nerve = ulnar nerve or posterior tibial nerve
```
37
Relaying on flexion of what digit overestimates recovery?
The fifth finger
38
What TOF ratio does full recovery occur?
> 0.9 at the adductor pollicis
39
Residual neuromuscular blockade is defined as a TOF ratio of?
< 0.9
40
Recovery from NM blockade Tidal volume:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
5 mL/kg or greater
| 80%
41
Recovery from NM blockade TOF:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
No fade
| 70%
42
Recovery from NM blockade Vital Capacity:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
20 mL/kg or greater
| 70%
43
Recovery from NM blockade Sustained Tetanus (50Hz):
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
No fade
| 60%
44
Recovery from NM blockade Double burst stimulation:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
No fade
| 60%
45
Recovery from NM blockade Inspiratory force:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
Better than -40 cmH2O (more negative is better)
| 50%
46
Recovery from NM blockade Head lift >5 sec:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
Sustained for 5 sec
| 50%
47
Recovery from NM blockade Hand grip same as preinduction:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
Sustained for 5 sec
| 50%
48
Recovery from NM blockade Holding tongue blade in mouth against force:
Acceptable Clinical Endpoint?
Max % of receptors occupied when acceptable clinical endpoint is achieved?
Can’t remove tongue blade against force
| 50%
49
What quantitative methods of measuring NMB recovery could solve the insensitivity problem with the bedside assessments?
Electromyography or acceleromyography
| These are not commonly available
50
What is the structure of succinylcholine?
2 acetylcholine molecules joined together
51
Succinylcholine side effects (7):
```
Bradycardia
Tachycardia
K+ release
Increased IOP
Increased ICP
Increased intragastric pressure
Malignant hyperthermia
```
52
How can succinylcholine cause bradycardia? What increases this risk? What is probably most responsible for this effect? What may prevent it?
By stimulating the M2 receptor on the SA node is can a use bradycardia or asystole.
A second dose increases this risk.
Its primary metabolite succinylmonocholine.
Antimuscarinics may prevent or reverse these bradyarrhythmias
53
What patient population is more susceptible to bradycardia with succinylcholine? Why? What should be done?
Children.
They have a higher vagal tone.
Atropine should always precede a second dose of Sux.
54
How can succinylcholine cause tachycardia?
By mimicking the action of Ach at the sympathetic ganglia it can cause tachycardia and HTN
55
In adults what is more common with the use of sux, tachycardia or bradycardia?
Tachycardia
56
How does succinylcholine cause potassium release?
The Ach causes opening of the nAchR at the neuromuscular junction and increases serum K+ by 0.5 - 1.0 mEq/L for up to 10 - 15 minutes.
57
Hyperkalemia increase the resting membrane potential of excitable tissue, this increases the risk of what?
Dysrhythmias
58
Is succinylcholine safe to use in patients with renal failure?
Yes as long as K+ level is normal
59
How much does succinylcholine affect IOP?
It transiently increases IOP by 5 - 15 mmHg for up to 10 minutes
60
Does pretreatment with a ND-NMB attenuate the risk in IOP from succinylcholine?
The text says it’s controversial and/or provides no little benefit
61
What is the debate with succinylcholine in a patient with an open globe injury that needs a TRUE RSI?
There is little evidence to support the risk of Sux increased IOP causing extrusion of intraocular contents and permanent blindness. Securing the airway is #1 priority, eye is a close second. Light anesthesia, laryngoscopy, intubation, coughing and/or straining cause a greater rise in IOP than succinylcholine
62
Succinylcholine temporarily increase ICP, what can prevent or minimize this?
Defasciculating dose
63
Contraction of the abdominal muscles increases intragastric pressure, what does succinylcholine do that cancels out this increase in risk of aspiration?
Raises lower esophageal sphincter tone
64
Does masseter spasm and the absence of other s/sx of MH warrant cancellation of a planned surgical procedure?
No
65
What enzyme metabolizes acetylcholine? What are the 5 different names for it?
```
Type 1 cholinesterase
Acetylcholinesterase
True cholinesterase
Specific cholinesterase
Genuine cholinesterase
```
66
What enzyme metabolizes succinylcholine? What are it’s 5 different names?
```
Type 2 cholinesterase
Butyrylchoilinesterase
False cholinesterase
Plasma cholinesterase
Pseudocholinesterase
```
67
Where is pseudocholinesterase produced?
In the liver and serves as an indicator of hepatic synthetic function
68
What is the plasma reference concentration of pseudocholinesterase?
2900 - 7100 units/L
69
At what level of pseudocholinesterase do neuromuscular symptoms begin? Become serious?
60% of normal
| Become serious at 20% of normal
70
What other 5 tissues is pseudocholinesterase found?
```
Smooth muscle
Intestines
White matter of the brain
Heart
Pancreas
```
71
What 8 drugs reduce pseudocholinesterase activity?
```
Metoclopramide
Esmolol
Neostigmine
Echothiophate
Oral contraceptives/estrogen
Cyclophosphamide
Monoamine oxidase inhibitiors
Nitrogen mustard
```
72
What 9 co-existing conditions reduce pseudocholinesterase activity?
```
Atypical PChE
Severe liver disease
Chronic renal disease
Organophosphate poisoning
Burns
Neoplasm
Advanced age
Malnutrition
Pregnancy - late stage
```
73
What test is used to make the definitive diagnosis of atypical PChE?
Dibucaine test
74
What type of drug is Dibucaine and what does it do? What does the result mean?
Amide local anesthetic.
It inhibits normal plasma cholinesterase, and has no effect on atypical PChE.
The number reflects the percentage of normal enzyme that is inhibited by dibucaine.
75
What is a normal result for the Dibucaine test? What does it mean?
80%. This means that dibucaine has inhibited 80% of the pseudocholinesterase in the sample and suggests that the normal enzyme is present.
76
What is an abnormal Dibucaine test result? What does it mean?
20%.
| This means that dibucaine did not inhibit the patient’s pseudocholinesterase and that an atypical variant is present.
77
```
Typical Homozygous PChE:
Genotype
Incidence
Dibucaine #
Duration of succinylcholine
```
Genotype: UU
Incidence: -
Dibucaine #: 70 - 80%
Duration of succinylcholine: 5 - 10 min
78
```
Heterozygous PChE:
Genotype
Incidence
Dibucaine #
Duration of succinylcholine
```
Genotype: UA
Incidence: 1 / 480
Dibucaine #: 50 - 60%
Duration of succinylcholine: 20 - 30 min
79
```
Atypical homozygous PChE:
Genotype
Incidence
Dibucaine #
Duration of succinylcholine
```
Genotype: AA
Incidence: 1 / 3200
Dibucaine #: 20 - 30%
Duration of succinylcholine: 4 - 8 hours
80
What is the treatment of choice for atypical variant PChE? What other treatments are there?
Postoperative mechanical ventilation and sedation are the treatment of choice because they are the safest and least expensive.
Whole blood, FFP, and purified human cholinesterase will all restore plasma pseudocholinesterase levels.
81
The routine administration of succinylcholine is contraindicated in young children because of the possibility of?
Hyperkalemic rhabdomyolosis
82
What is the black box warning on succinylcholine?
Risk of cardiac arrest and death secondary to hyperkalemia in children with undiagnosed skeletal muscle myopathy.
83
What is the most common skeletal muscle myopathy in children?
Duchenne muscular dystrophy
84
What is Duchenne muscular dystrophy?
X-link, recessive disease that results from the absence of dystrophin protein
85
List 4 skeletal muscle myopathies other than Duchenne’s:
Becker
Emery-Dreifuss
Facioscapulohumeral
Limb-girdle muscular dystrophy
86
What EKG changes occur with mild hyperkalemia?
Peaked T waves
| PR prolongation
87
What EKG changes occur with severe hyperkalemia?
Ventricular fibrillation
| Asystole
88
If a healthy inflation/child develops cardiac arrest following succinylcholine, particularly a boy < 8 years old, immediate treatment of hyperkalemia should begin. What are the 3 goals and what treatment do they include?
```
1. Stabilize the myocardium:
calcium chloride 20 mg/kg
Calcium gluconate 60 mg/kg
2. Shift potassium into cells
Glucose 0.3 - 0.5 g/kg as 10% solution
Insulin 1 unit per 4 - 5 g of IV glucose
Sodium bicarb 1 - 2 mmol/kg
Hyperventilation
Albuterol nebulizer
3. Enhance potassium elimination
Furosemide 1 mg/kg
Volume resuscitation
Hemodialysis
Hemofiltration
```
89
How much elemental calcium does each contain?
10% Calcium chloride
10% Calcium gluconate
10% Calcium chloride: 27.2 mg/mL of elemental Ca
| 10% Calcium gluconate: 9 mg/mL of elemental Ca
90
In children what situations should succinylcholine be reserved for?
Difficult intubation
Laryngospasm
RSI
IM use when IV access is unattainable
91
How long can postoperative myalgia persist for due to succinylcholine? How does it manifest? What is the believed cause of this myalgia?
24 - 48 hours
Muscle soreness in the neck, shoulders, subcostal region, upper abdominal muscles, and trunk muscles.
Sux causes uncoordinated muscle contractions before causing flaccid paralysis, these contractions are believed to be the cause of myalgia.
92
List 4 factors that increase the risk of myalgia from succinylcholine:
Young adults
Ambulatory surgery
Woman > men
Those that do not routinely engage in strenuous exercise
93
What 3 patient populations seem to have the lowest risk of myalgia from succinylcholine?
Children
Elderly
Pregnancy
94
Can pretreatment with ND-NMB decrease or eliminate the myalgia associated with succinylcholine?
It might be minimized, but not entirely eliminated
95
What other methods besides ND-NMB may reduce the risk of myalgia with Succinylcholine? (3)
NSAIDs
Lidocaine 1.5 mg/kg
A higher dose rather than a lower dose of succinylcholine
96
Do opioids decrease the incidence of myalgia with succinylcholine?
No
97
When using a defasciculating dose of a ND-NMB how should the dose of Succinylcholine change? Why?
Increase sux dose to 1.5 - 2.0 mg/kg
| The ND will competitively antagonize the nicotinic receptor, more sux must be given to overwhelm the ND
98
When should a defasciculating dose NOT be used? Why?
Those with pre-existing skeletal muscle weakness, such as myasthenia gravis.
Patient may experience muscle weakness, dyspnea, dysphasia, and diplopia
99
```
Diseases with altered responses to NMB: Sux vs ND
Amyotrophic lateral sclerosis
Charcot-Marie-Tooth
Duchenne’s muscular dystrophy
Guillain-Barre
Huntington chorea
Hyperkalemic periodic paralysis
Hypokalemic periodic paralysis
Malignant hyperthermia
Multiple sclerosis
Myasthenia gravis
Myotonic dystrophy
Up-regulation of AChRs
```
Amyotrophic lateral sclerosis: Sux hyperkalemia, ND sensitive
Charcot-Marie-Tooth: Sux hyperkalemia, ND normal
Duchenne’s muscular dystrophy: Sux hyperkalemia, rhabdomyolysis; ND sensitive
Guillain-Barre: Sux hyperkalemia; ND sensitive
Huntington chorea: Sux sensitive; ND sensitive
Hyperkalemic periodic paralysis: Sux hyperkalemia; ND normal
Hypokalemic periodic paralysis: Sux normal; ND normal
Malignant hyperthermia: Sux MH; ND normal
Multiple sclerosis: Sux hyperkalemia; ND sensitive
Myasthenia gravis: Sux resistant; ND sesitive
Myotonic dystrophy: Sux muscle contractures; ND normal or sensitive
Up-regulation of AChRs: Sux hyperkalemia; ND resistant or normal depending on timing of injury
100
ED95 is a measure of?
Potency
| They are inversely related
101
What is ED95 of NMB?
The dose at which there is a 95% decrease in twitch height
102
The higher the ED95 the _____ the potency, and the _____ the onset
Lower the potency
| Faster the onset - because there are more molecules to diffuse from the plasma to the biophase at the NMJ
103
The dose of NMB required to provide optimal conditions for tracheal intubation is ~ _____ times the ED95
2 - 3 x ED95
104
```
Mivacurium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
```
ED95: 0.067 mg/kg
Intubation dose: 0.15 mg/kg
Time to max block (onset): 3.3 min
Time to return to 25% control (~duration): 16.8 min
105
```
Cisatracurium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
```
ED95: 0.04 mg/kg
Intubation dose: 0.1 mg/kg
Time to max block (onset): 5.2 min
Time to return to 25% control (~duration): 45 min
106
```
Vecuronium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
```
ED95: 0.043 mg/kg
Intubation dose: 0.1 mg/kg
Time to max block (onset): 2.4 min
Time to return to 25% control (~duration): 45 min
107
```
Atracurium :
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
```
ED95: 0.21 mg/kg
Intubation dose: 0.5 mg/kg
Time to max block (onset): 3.2 min
Time to return to 25% control (~duration): 45 min
108
```
Rocuronium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
```
ED95: 0.305 mg/kg
Intubation dose: 0.6 mg/kg
Time to max block (onset): 1.7 min
Time to return to 25% control (~duration): 35 min
109
```
Pancuronium:
ED95
Intubation dose
Time to max block (onset)
Time to return to 25% control (~duration)
```
ED95: 0.067 mg/kg
Intubation dose: 0.08 mg/kg
Time to max block (onset): 2.9 min
Time to return to 25% control (~duration): 85 min
110
What are the 2 classes of ND-NMB?
Benzylisoquinolinium
| Aminosteroid
111
List the benzylisoquinolinium compounds:
Atracurium
Cisatracurium
Mivacurium
112
List the Aminosteroid compounds
Rocuronium
Vecuronium
Pancuronium
113
Why can renal insufficiency prolong the duration of any of the ND-NMB? Which class is this negligible with?
All the ND-NMB are inonized, each other undergoes some degree of renal elimination as unchanged drug.
Benzylisoquinolinium
114
Which ND compounds undergo spontaneous degradation in the plasma and are not dependent on hepatic or renal function for metabolism and elimination?
Benzylisoquinolinium compounds (cisatracurium, atracurium, and mivacurium)
115
How is atracurium metabolized?
| What other drugs are metabolized by this same method?
Hofmann elimination - 33%
Non-specific plasma esterases - 66% : esmolol and remifentanil
Renal elimination 10 - 40%
116
How is cisatracurium metabolized?
Hofmann elimination 77%
| Renal elimination 16%
117
How is mivacurium metabolized?
Pseudocholinesterase
118
What is Hofmann elimination? What does it depend on and how do these 2 things affect it?
Base-catalyze reaction
Dependent on normal blood pH and temperature
The reaction is faster with alkalosis and hyperthermia
The reaction is slower with acidosis and hypothermia
119
Which Benzylisoquinolinium compounds have a metabolite? Which produces more of the metabolite?
Laudanosine is a metabolite of atracurium and cisatracurium.
| Atracurium produces more.
120
What effect does the metabolite laudanosine have?
It is a CNS stimulant that is capable of producing seizures. More of a concern with prolonged infusion.
121
How is rocuronium metabolized and eliminated? Does it have a metabolite?
Metabolism: none
Liver elimination: > 70%
Renal elimination: 10 - 25%
No metabolite
122
How is vecuronium metabolized and eliminated? Does it have a metabolite?
Metabolism: hepatic deacetylation 30 - 40%
Liver elimination: 40 - 50%
Renal elimination: 50 - 60%
Metabolite 3-OH vecuronium - half a potent as its parent, rapidly metabolized into inactive metabolites
123
How is pancuronium metabolized and eliminated? Does it have a metabolite?
Metabolism: hepatic deacetylation 10 - 20%
Liver elimination: 15%
Renal elimination: 85%
3-OH pancuronium is half as potent as parent
124
What classes (and drugs) potentiate neuromuscular blockade?
VAs: DES > SEVO > ISO > N2O > propofol
ABX: aminoglycosides, polymyxins, clindamycin, lincomycin, tetracycline
Antidysrhythmics: verapamil, amlodipine, lidocaine, quinidine
LAs: probably all of them
Diuretics: furosemide
Other: dantrolene, cyclosporine, tamoxifen
125
What electrolyte disturbances potentiate neuromuscular blockade?
Increased lithium activates K+ channels
Increased Mg decreases Ach release from presynaptic nerve
Decreased Ca decreases Ach release from presynaptic nerve
Decrease K decreases RMP
126
What patient factors potentiate neuromuscular blockade?
Hypothermia decreases metabolism and clearance
| Gender - compared to men, women are more sensitive to the effects of NMBs
127
What NMB cause histamine release? (3)
Succinylcholine
Atracurium
Mivacurium
128
What NMB affect autonomic ganglia and how?
Succinylcholine stimulates -> tachycardia
129
What NMB affect M2 receptors on the heart? (3)
Succinylcholine stimulation -> bradycardia
Pancuronium - moderate blockade
Rocuronium - none to slight blockade
130
How long does the histamine release last from NMB? How can it be minimized? Who should not receive histamine releasing drugs?
Generally short lived 1 - 5 min
Can be minimized by slow administration
Those who are sensitive to a higher HR or reduced afterload, unless clinical benefit outweighs the risk
131
What is Pancuronium’s unique effect on the heart?
It has a vagolytic effect, it inhibits M2 receptors at the SA node -> stimulates the release of catecholamines, and inhibits catecholamine reuptake in adrenergic nerves -> increase in HR and CO with no or minimal effects on SVR
132
In what specific situation is Pancuronium used in cardiac surgery?
To mitigate opioid induced bradycardia in cardiac surgery
133
Patients with what disease should no receive pancuronium? Why?
```
Hypertrophic cardiomyopathy (idiopathic hypertrophic subaortic stenosis).
Hypertrophied ventricular septum and systolic anterior motion of the anterior leaflet of the mitral valve, when the ventricle contracts forcefully or quickly there is a greater tendency for the anterior leaflet to occlude the LVOT, which reduces flow through the aortic valve -> reduces CO and BP. Pancuronium’s vagolytic effect can be detrimental in this patient
```
134
In rare instances vecuronium and atracurium have cause what EKG rhythm? Why/how?
Asystole
| In all cases an opioid was also administered, it’s likely that the vagal effects of the opioid were left unchecked
135
What is the most common cause of perioperative allergic reactions?
Neuromuscular blockers
136
Why do NMBs cause anaphylaxis?
Their structures contain one of more antigenic quaternary ammonium groups that interact with Ig-E, causing mast cell and basophils degranulation
137
Cross sensitivity may occur in up to ____% of those who have experienced a previous allergic response related to NMBs.
70%
138
It is possible that sensitivity to any NMB may develop following exposure to what compounds? Why?
Soap or cosmetics
| They often contain antigenic quaternary ammonium group
139
Which NMB is most likely to cause anaphylaxis?
Succinylcholine
Rocuronium
-multiple choice: choose Sux, if not a choice then pick Roc
-multiple response: sux and roc
