Neuromuscular Pharm Flashcards
0
Q
What kind of receptor type are muscarinic receptors?
A
- G-protein linked
* Regulate production of second messenger
1
Q
What are the 2 cholinergic receptors?
A
- Nicotinic
- Muscarinic
2
Q
Where are muscarinic receptors found?
A
- Subsets, located on heart, airway smooth muscle, salivary glands
- Also on tissues innervated by cholinergic postganglionic nerves
3
Q
What type of receptors are nicotinic receptors?
A
• Selective ligand gated ion channel receptors
4
Q
Where are nicotinic receptors found?
A
• Located PNS cells, postganglionic SNS cells and skeletal muscle endplates
5
Q
Where are Nicotinic 1 receptors located (N1)?
A
autonomic ganglia
6
Q
Where is nicotinic 2 receptors located?
A
At NMJ
7
Q
What does activation of muscarinic receptors on heart, lungs, and salivary glands result in?
A
Heart- Bradycardia
Lungs- Bronchoconstriction
Salivary glands- increased saliva
8
Q
What does non-selective cholinoceptor stimulation would result in?
A
varied and diffuse alteration in function since receptors are both inhibitory and excitatory (fortunately we have mostly selective drugs!)
9
Q
What can determine organ specificity (pharmacokinetic selectivity)?
A
Route - example Muscarinic stimulation to modify occular function via eye drops (dilation of eyes)
10
Q
What breaks down Ach?
A
Acetylcholinesterase
11
Q
What would cause direct activation of a cholinoceptors?
A
Medications that directly bind to muscarinic and nicotinic receptors
12
Q
What would cause indirect activation of cholinoceptors?
A
• Inhibitors of hydrolysis of Ach (indirect activation) [some inhibitors of Achesterase also have mild direct acting properties ie. neostigmine]
13
Q
What is methacholine commonly used for?
A
- Pulmonary function (challenge) tests to diagnose asthma
- Causes bronchoconstriction (increase in parasympathetic)
14
Q
What does Succinylcholine’s molecular structure consist of?
A
It is basically two Ach molecules stuck together
15
Q
What is the basis of neuromuscluar drug reversal?
A
Acetylcholinesterase inhibitors which causes build up of Ach to reverse non-depolarizing blockade
16
Q
What is Bethanecol used for?
A
- To treat urinary retention by relaxing the detrussor muscle (rest and digest)
- Stimulates muscarinic receptors without any effect on nicotinic receptors
17
Q
What are the 3 classes of Neuromuscular Blocking drugs?
A
- Depolarizing
- Aminosteroids
- Benzylisoquinolines
(O&J pg. 98)
18
Q
Is Succinylcholine broken down by Acetylcholinesterase?
A
- *No pseudocholinesterase
- pseudocholinesterase deficiency will prolong effects
19
Q
How well are esters absorbed and distributed?
A
Esters are poorly absorbed and distributed due to hydrophilic properties (not lipophilic)
20
Q
How is Ach metabolized?
A
- rapidly hydrolyzed by acetylcholinesterase.
- Methacholine 3x more resistant
- Other compounds have longer DOA because of greater resistance to acetylcholinesterase
21
Q
How are most direct acting cholinoreceptor stimulants metabolized and cleared?
A
Hepatic metabolism, urinary clearance
22
Q
How are tertiary alkaloids such as Nicotine absorbed?
A
fairly well absorbed (sufficiently lipid soluble to be absorbed transdermal)
23
Q
How are quaternary amines such as Muscarine absorbed compared to tertiary alkaloids?
A
less completely absorbed in GI but can be enough to be toxic ie. Certain mushrooms
24
What is the MOA of Muscarinic drugs?
- Ach can activate muscarinic receptors on effector organs directly or..
- At pre-synaptic autonomic junctions to inhibit release of neurotransmitter (negative feedback loop)
- Uses 2nd messenger mechanism
25
What is the MOA of Nicotinic drugs (Sucx)?
- Depolarization of nerve cell or neuromuscular endplate
- If agonist occupancy is prolonged the response is abolished (neuron stops firing), skeletal muscle relaxes (“depolarizing blockade”) (no repolarization)
26
What happens with cholinoceptor stimulation of the eye?
Smooth muscle contraction (miosis and accommodation, outflow of aqueous humor)
27
What happens with cholinoceptor stimulation of the cardiovascular system?
o Decrease rate, contraction, conduction velocity,
Muscarinic agonists release **EDRF (endothelium-derived relaxing factor) resulting in venous and arterial dilation in small doses. In large doses a direct vasoconstriction effect
28
What happens with cholinoceptor stimulation of the Respiratory system?
o Contraction of bronchial muscle (constriction)
| Stimulation of bronchial glands
29
What happens with cholinoceptor stimulation of the GI system?
- Increased motility,
- sphincter relaxation
- Increased secretions
30
What happens with cholinoceptor stimulation of the Urinary bladder?
- Contraction of detrussor muscle
- Relaxation of trigone and sphincter
- This class of drugs can be used for urinary retention
31
What happens with cholinoceptor stimulation of the Glands?
increased sweat, salivation, lacrimal and nasopharyngeal secretions
32
What happens with cholinoceptor stimulation of the central nervous system?
Nicotine-tremor, stimulation of respiratory center, high levels cause seizures
33
What is EDRF?
endothelium-derived relaxing factor (released from muscarinic agonists) resulting in venous and arterial dilation in small doses. In large doses a direct vasoconstriction effect
34
What happens at the motor endplate (neuromuscular junction) with cholinoceptor stimulation?
Depolarization of endplate caused by increased permeability to Na and K ions
35
How do indirect cholinoceptor stimulants work?
- Indirect acting cholinoceptor stimulants inhibit acetylcholinesterase thereby allowing increased concentration of ach
- (may also inhibit pseudocholinesterase but to a lesser extent)
36
What are Indirect Acting Cholinoceptor Stimulants most commonly manufactured as?
insecticides
37
What are the 3 commonly used Indirect Acting Cholinoceptor Stimulants groups?
1. Organic derivatives of phosphoric acid (organophosphates)
2. Simple alcohols with a quaternary ammonium group (edrophonium)
3. Carbamic acid esters of alcohol with quaternary ammonium (neostigmine) or
tertiary ammine group (physostigmine)
38
How are the Indirect Acting Cholinoceptor Stimulants Organophosphates absorbed (such as insecticides?
Highly lipid soluble, well absorbed by skin (Wear gloves)
39
What is/was the organophosphate Ecothiophate used for?
glaucoma
40
What is the Organophosphate soman?
a potent nerve gas (anticholinergics used to reverse= atropine)
41
What are the organophosphates Parathione and malathione
insecticides are converted to the phosphate derivatives in plant and animals and are better suited for insecticide use
42
Compare lipid solubility of Quaternary ammonium drugs to the lipid solubility of Tertiary amines?
* know* Quaternary ammonium drugs are poorly lipid soluble-Tertiary amines are more lipid soluble
- Quaternary carbamates (neostigmine) are poorly absorbed via skin, lungs, PO
- Tertiary amines (physostigmine) are well absorbed (Cross BBB) (Eserine eye drops) and more readily distributed to the CNS than quaternary structures
43
What accounts for differences in potencies of Indirect Acting Cholinoceptor Stimulants?
differences in affinity for ach-esterase
44
What are the 3 mechanisms which Indirect Acting Cholinoceptor Stimulants inhibit ach-esterase?
o Reversible inhibition
o Formation of carbamyl esters (Also reversible)
o Irreversible inactivation
46
What is Reversible inhibition and give an example of it?
* Example is edrophonium
* No carbamyl group
* Electrostatic and hydrogen (weak) bond attachment on enzyme (prevents Ach from approximating with the enzyme)
46
How does Edrophonium work?
- Acetylcholinesterase inhibitor that works presynaptic to prevent binding of Ach-esterase to Ach (may explain relatively shorter DOA than other agents)
- Muscarinic effects are relatively less than other agents
47
How does Edrophonium work?
- it is an acetylcholinesterase inhibitor that works presynaptic to prevent Ach from binding to Ach-esterase binding site by occupying the binding site (may explain relatively shorter DOA than other agents)
- Muscarinic effects are relatively less than other agents
48
What are examples of Carbamyl-Esters that are reversible acetylcholinesterase inhibitors?
neostigmine, pyridostigmine, physostigmine
49
How do Carbamyl-Esters prevent the breakdown of Ach?
- Form a carbamyl ester complex at esteratic site of acetylcholinesterase enzyme (carbamylated Ach-esterase can’t hydrolyze ACH therefore increasing endogenous Ach around receptor sites)
- Carbamylating Ach-esterase makes the enzyme in active rather than preventing binding like Edrophonium
50
How can Edrophonium's Ach-esterase inhibition be reversed?
-increases in Ach can compete with Edrophonium for binding site on Ach-esterase since no covalent bond exists (reversible)
51
How long will Carbamyl-Esters inactivate Ach-Esterase and prevent hydrolyisis of Ach?
until the Carbamate-ester covalent bond dissociates
52
How does irreversible inactivation work and give an example of this group of drugs?
* Organophosphates form irreversible bond with the enzyme to form an ineffective complex
* This complex can’t be hydrolyzed
* Reversal of effects requires new enzyme production
53
In the Neuromuscular Junction what is the prejuction?
Motor nerve ending (terminus)
54
In the Neuromuscular Junction what is the junction?
The fluid filled space in between the prejunction and postjunction
55
In the Neuromuscular Junction what is the post junction?
Folded membrane of the skeletal muscle fiber= Sarcolemma (motor end plate)
56
What can be found in the motor nerve ending (terminus)?
- Mitochondria
- synaptic vesicles (Ca+ dependent for release)
- endoplasmic reticulum to allow for synthesis and storage of neurotransmitter (Ach)
57
What is the resting potential maintained by at the postjuncitonal motor end plate?
the distribution of K and Na ions across the membrane (-90 mv)
58
What are the 3 types of neuromuscular junction nicotinic receptors?
1. Presynaptic on nerve ending. Influence release of transmitters. Some drugs have effects here.
2. Postsynaptic on skeletal muscle (junctional) directly opposite site of Ach release in the junction
3. Postsynaptic non-junctional. Typically only active in pathologic states, can alter action of NDMR
59
Some neuromuscular blocking drugs block Nicotinic prejunctional receptors Na channels but not Ca what does this result in?
- Result is interference with mobilization of Ach from **synthesis to release site** but not interference with Ca dependent release
- Blocking Na+ channels prevents choline from reuptake and repackaging to make more Ach in the prejunction (terminus)
60
What type of Nicotinic receptors are found in adults in comparison to a fetus?
- In adults large numbers of nicotinic postjuctional receptors directly opposite nerve terminal are needed to elicit action potential (lots of vesicle Ach release is needed)
- In the fetus before muscle innervation occurs, the muscle cells synthesize extrajunctional receptors which allows for single Ach quanta (vesicle) to elicit action potentials
61
By what age are extrajunctional nicotinic receptors replaced by densely packed postjunctional receptors
around 2 years of age (Nag & P pg. 821)
62
When can extrajunctional nicotinic receptors be found in an adult?
- Anything that suppresses neural activity so normally not present in large numbers
- During periods of decreased motor activity they proliferate (denervation injuries/diseases, skeletal muscle trauma)
63
How quickly can extrajunctional nicotinic receptors form after nerve injuries etc.?
Form and dissolve rapidly (within 48 hrs) so present in many clinical situations and highly responsive to Ach (explains unpredictable responses to NMBDs in these patients)
64
How do extrajunctional nerve receptors respond differently to non-depolarizing muscle relaxants in comparison to depolarizing?
- they are resistant to non-depolarizing muscle relaxants so will need larger doses
- they are more easily activated by depolarizing muscle relaxants such as succ's so will need less dose than normal
65
Why should you be careful when giving succ's to patients with denervation injuries/burns/skeletal muscle trauma?
Can cause dangerous levels of succinylcholine-induced hyperkalemia
66
What is Myasthenia Gravis?
- Autoimmune process produces antibodies, which decrease functional nicotinic receptors on endplates. Symptoms are weakness and fatigue which improves with rest and worsen with exercise. Often difficulty speaking, swallowing, breathing
- Prejuctional Ach pool is normal
67
What drug effects resemble myasthenia gravis?
Curare (Non-Depolarizer)
68
Patients with Myasthenia Gravis are VERY sensitive to what group of drugs?
non-depolarizing muscle relaxants
69
What is used in treatment of Myasthenia Gravis?
- Cholinesterase inhibitors (prevent hydrolysis of Ach and increase Ach available to limited recptors)
- most commonly pyridostigmine is used for treatment then neostigmine
70
What is Myasthenia Gravis crisis?
-Patients with weakness may have MG crisis requiring more drug (not enough Ach binding to post junctional receptors= respiratory distress, weakness)
71
What is cholinergic crisis and what symptoms can be seen with it?
- result of too much drug (too much Ach almost acting as succ's)
- symptoms: muscarinic side effects= bradycardia, resp distress, abdominal cramping, diarrhea, increased secretions
72
What will happen if Edrophonium (Tensilon challenge) is given in Myasthenia Gravis crisis compared to Cholinergic crisis?
1. MG- pt will improve due to increased Ach
| 2. Cholinergic crisis- pt will get worse due to excessive Ach
73
What drugs can cause closed channel blockade (diminished presynaptic Ach release) and potentiate neuromuscular blockade?
- Antibiotics
- cocaine
- quinidine
- TCA's
74
What drugs can cause open ion channel blockade?
- NDMR's
| - Succinylcholine
75
What happens in receptor desensitization?
- mechanism unknown
| - agonist-receptor binding, but no opening of ion channel
76
What drugs causes/promotes receptor desensitization (potentiate neuromuscular blockade)?
- Volatile Anesthetics
- Alcohols
- Barbiturates
- Agonists
- Ach-esterase Inhibitors
- Local Anesthetics
- Phenothiazines
- Phencyclidine
- Ca Channel Blockers
77
What are the general physic-chemical properties of muscle relaxants?
* Highly Water Soluble/ Relatively Hydrophilic
* Easily excreted in urine
* Do not cross lipid membranes (most cells, BBB, placenta)
* Small volume of distribution
* Relatively less actively metabolized by the liver than lipophilic compounds
78
What is a depolarizing blockade?
- Action is same as Ach, only longer due to slower hydrolysis by plasma (pseudo) cholinesterase
- Reacts with nicotinic receptor on sarcolemma to open channel and cause depolarization of end plate
79
What is the only depolarizing muscle relaxing agent available in USA?
Succinylcholine (Sux, SCh)
80
What is a phase I block from a depolarizing muscle relaxer?
- The desired/expected block
- Succinylcholine causes depolarization of the muscle and maintains the membrane potential above threshold, it does not allow the muscle cell to repolarize. When acetylcholine binds to an already depolarized receptor, it cannot cause further depolarization.
81
What accompanies a phase I depolarizing block?
- fasciculations= involuntary muscle contraction and relaxation which may be visible under the skin
- It is a normal side effect of the drug's administration, and can be prevented with a small dose of a nondepolarizing neuromuscular blocker prior to the administration of succinylcholine, often 10% of a nondepolarizing NMB's induction dose.
82
How is phase I depolarizing block reversed?
Hydrolysis of Ach by Ach-esterase
83
What will happen if you give a anticholinesterase agent during a phase I depolarizing block?
**know this** It will augment (increase) the block and not reverse it
84
What is a phase II depolarizing block?
-From continued exposure to succinylcholine (high dose or inadequate hydrolysis
i.e. pseudocholinesterase deficiency)
-MOA is unclear, possibly the result of blockade of channels as opposed to the
agonist effect of succinylcholine
-Characteristics nearly identical to NDMB
85
What will happen if you give an anticholinesterase agent during a phase II block?
It will reverse the blockade (MOA is unclear seems opposite of what you would think)
86
Why is the duration of succinylcholine so brief?
- Due to rapid hydrolysis by pseudocholinesterase
- Much of drug is hydrolyzed in plasma before reaching NMJ
- Termination of action occurs by diffusion of drug out of NMJ and into extracellular fluid
87
Where is Pseudocholinesterase is produced?
-in liver- (Only effected by advanced liver disease)
88
What can degree of pseudocholinesterase activity be affected by
- genetics-Some patients may have atypical pseudocholinesterase
- Neostigmine decreases pseudocholinesterase
89
What is succinylcholine broken down into?
-Broken down to succinylmonocholine (weakly active) which is broken down to succinic acid and choline
90
What is another name for Atypical Pseudocholinesterase?
Dibucaine-related variant because the local anesthetic dibucaine is used to diagnose it
91
What is seen in patients with Atypical Pseudocholinesterase?
-After giving standard dose of anesthetic drug broken down by pseudocholinesterase to a person with pseudocholinesterase deficiency, the patient can experience prolonged paralysis effects
92
What does the dibucaine number reflect?
the dibucaine number reflects quality of the enzyme (ability to hydrolyze Succinylcholine) not quantity of available enzyme
93
What is a normal Dibucaine number?
80, occurrence= (96%)
94
What is a slightly prolonged response dibucaine number?
60-75, occurrence= (1:200-480)
95
What is a greatly prolonged response dibucaine number?
20-45, occurrence= (1:20,000)
96
What are the cardiac side effects of succinylcholine?
- Bradycardia, sinus arrest, due to muscarinic stimulation
- Worse after subsequent doses
- Worse in pediatrics (more vagal tone)
- Can produce autonomic ganglion stimulation resulting in increased HR and BP (not really seen significantly clinically)
97
When can given succinylcholine cause severe hyperkalemia?
o May be the result of proliferation of extrajunctional cholinergic receptors in nerve damaged or denervated states providing sites for K+ to leak from cells during depolarization
o May occur in patients with muscular dystrophy, unhealed 3rd degree burns, denervation states, motor neuron lesions and severe skeletal muscle
trauma
o If K+ in normal range succ's is considered safe to use in renal patients
98
What should you always do prior to given a neuromuscular blocker?
Check TOF to get baseline
99
Why is myalgia a side effect of succinylcholine?
* Speculated to be related to fasciculations
* Worse in young adults, muscular people, minimal in pediatrics
* Can be the source of sore throat
* Precurarization may help
* Becomes a significant issue in ambulatory surgery
100
What is Precurarization?
- Giving small dose of NDMR (Roc, Vec, etc.) prior to succ's to prevent fasciculations
- Warn patient that they may experience weakness with this small dose
101
Why is myoglobinuria commonly seen after succ's administration?
- Likely due to micro muscle damage from fasciculations
| - May be seen, more often in pediatrics
102
Why could there be an increased aspiration risk after succ's administration?
-Intragastric pressure
| • Possibly related to fasciculations
103
What can succ's administration do to ocular pressure?
• Increase Intraocular pressure
• Transient, last 5-10 minutes after injection
• Mechanism may be contraction of extraocular muscles, may be due to inhibited
• outflow of aqueous humor
Theoretical concern with open eye injury may cause extrusion of global contents
104
Does succ's cause increased ICP?
• No consistent reports, controversial
105
What can the side effect of sustained muscle contraction of the masseter muscle be confused with after giving succ's?
Can be confused with MH-Strong triggering agent
106
What is Malignant Hyperthermia?
-an autosomal dominant inherited skeletal muscle
disorder triggered by volatile agents and succinylcholine
-During a crisis intracellular calcium is greatly increased and there is a problem with reuptake due to a defective channel receptor
-Result is sustained muscle contraction and severe cellular oxygen debt
-Constant demand for ATP leads to glycolysis and subsequent lactic acidosis, leads to membrane instability,cell rupture, rhabdomyolysis
107
How is malignant hyperthermia diagnosed?
by muscle biopsy
108
How is malignant hyperthermia crisis manifested?
```
• Tachycardia
• Increased end tidal etCO2
• Muscular rigidity
• Decreased oxygen saturation
• Increased body temperature
• Hyperkalemia, acidosis
(Symptom can be confused with other causes)
```
109
How would you treat malignant hyperthermia?
- Remove triggering agent
| - Dantrolene IV, 2.5 mg/kg, and repeat the dose until the signs are controlled. Can add up to 8-10 mg/kg
110
How does dantrolene work?
acts by impairing calcium release from sarcoplasmic reticulum causing relaxation
111
What types of meds and supplies would you find in a malignant hyperthermia cart?
- 36 vials of dantrolene
- sterile H2O
- lasix
- Ca
- antiarrhythmic drugs
- bicarb
- cold IVs
- ice
112
What things would you do post MH crisis?
- Monitor ABGs, renal function, temperature, EKG
- Report case to MH Hotline at 800-644-9737
- Dantrolene PO form given post crisis
113
How is IV Dantrolene supplied?
- 20mg dantrolene
- 3g mannitol
- prepared in 60ml water
114
How would you plan a case if a patient had a history of malignant hyperthermia?
Regional, N2O and TIVA anesthetics are safe
115
How do nondepolarizing muscle relaxants cause their effects at the receptors?
• Competitive antagonist at nicotinic receptors, no intrinsic activity
• Compete with Ach at postjunctional receptor and at high doses may block ion
receptor channels
• Minor effect on prejunctional receptors
116
Approximately what percentage of receptor occupancy must take place before evidence of a blockade shows on blockade monitor?
70% (Wide safety margin)
117
What are the cardiovascular effects of NDMR's
The result of the release of histamine and other vasoactive substances, decrease BP
118
What cardiac effects are seen by Pavulon?
- may block cardiac muscarinic receptors (atropine-like effect) increased HR
- (Succs= bradycardia)
119
NDMR's effects can be enhanced by what other drugs?
* Volatile anesthetics
* Aminoglycoside antibiotics
* Local anesthetics
* Antidysrythmics
* Diuretics
* ***Magnesium***., lithium, ganglionic blockers
* Additive when combining NDMR
120
NMDR's effects can be enhanced by what changes in physiology?
- Hypotension
- Hypokalemia
- Hypothermia
- Acidosis
121
What does hyperkalemia do to NDMR effects?
Causes resistance
122
What does burn injuries do to NDMR effects?
Causes resistance
123
Why might paresis (weakness of voluntary muslce movement) cause resistance to NDMR's?
possibly due to proliferation of extrajunctional
| receptors
124
Who is typically more resistant to NDMR's Men or Women?
Men (more muscle tissue)
125
Which NDMR's is/was an Isoquinolinium?
-D-Tubocurarine (curare)
126
Which NDMR's is/was a Benzylisoquinolinium
- Atracurium
- Cisatracurium
- Mivacurium
- Doxacurium
127
Which NDMR's is/was a Biisoquaternary aminosteroid?
- Pancuronium
| - Pipecuronium
128
Which NDMR's is/was an Monoquaternary aminosteroid?
- Vecuronium
| - Rocuronium
129
What was the prototypical NDMR that had lots of histamine release and is rarely used anymore?
D-Tubocurarine (curare)
130
How is D-Tubocurarine (curare) excreted?
45% renal excretion
131
When considering duration what was D-Tubocurarine (curare) classified as?
Intermediate acting
132
What is a self-taming dose?
- pretreated a patient with a small (10-mg) dose of succinylcholine ("self-taming") before administration of large dose 1-1.5mg/kg
- Helps manage fasciculations and prevent large increase in potassium
133
What is the duration classification, elimination/metabolism, and side effects of Pancuronium (Pavulon)?
- Long acting- (DOA 60-90 minutes)
- Elimination, 55-70% unchanged in urine, remainder undergoes hepatic metabolism
- Increased HR (selective vagal blockade) Slight increased BP due to HR
- Rare histamine release
134
What is the duration classification, elimination/metabolism, and side effects of Doxacurium (Nuromax)?
(Not used anymore historical purpose)
- Long acting- (DOA 30-60 minutes (Maybe longer))
- renal elimination
- No histamine release
- cardiac stable (only advantage over mivacurium)
135
What is the duration classification, elimination/metabolism, and side effects of Pipecuronium (Arduan)?
(Not used anymore historical purpose)
- Long acting- (DOA 60-120 minutes)
- renal elimination
136
What is the duration classification, elimination/metabolism, and side effects of Atracurium (Tracrium)?
- Intermediate acting- (DOA: 20-35 minutes)
- Undergoes Hoffman Elimination and plasma hydrolysis 1.Chemical mechanism dependant on normal temp and pH (if acidic may not metabolize) 2. Biologic mechanism of ester hydrolysis
- **Histamine release
- Can cause hypotension, vasodilation
137
What is the major metabolite of Atracurium (Tracrium) and does it cause accumulation?
- laudanosine which is CNS stimulant and excreted via kidney
| - No significant cumulative effects
138
What is the duration classification, elimination/metabolism, and side effects of Cisatracurium (Nimbex)?
Isomer of atracurium with similar profile except for histamine release and slower onset
• Intermediate acting-(DOA: 30-60 minutes)
• Mainly undergoes Hoffman elimination with some additional ester hydrolysis
• Cardiac stability,** little/no histamine release
139
What is the duration classification, elimination/metabolism, and side effects of Vecuronium (Norcuron)?
* Intermediate acting (DOA 20-40 minutes)
* Hepatic metabolism
* Renal excretion (30%) and biliary excretion as well (40-70%)
* Considered safe for patients with **renal or hepatic compromise**
* Active metabolite (half of parent drug activity)
* Cardiac stability, some incidence of Bradycardia
* No significant histamine release
* Does not significantly cross placenta
* No change in IOP
140
What is the duration classification, elimination/metabolism, and side effects of Rocuronium (Zemuron)?
• Intermediate acting (DOA: 20-40 minutes
DOA and Onset is dose dependent)
• Similar in structure to vecuronium but faster onset, less potent
• Metabolized to inactive metabolites in liver
• Largely excreted in bile
• Effects can be prolonged in liver failure
• Cardiac stability
• Rare if any histamine release
141
What is the duration classification, elimination/metabolism, and side effects of Mivacurium (Mivacron)?
* Short acting (DOA: 12-20 minutes)
* Questionable product availability/discontinuance
* Hydrolyzed by plasma cholinesterase
* Possible prolongation by atypical pseudocholinesterase
* Increasing dose has less impact on DOA as other NDMR due to rapid hydrolysis
* Histamine release but minimal cardiovascular effects
142
Does Mivacurium (Mivacron) need reversal drug?
-reversal is controversial (theoretical increase effect by Neostigmine. **If used Enlon is best choice)
143
What 2 muscle relaxants are most commonly used for RSI's?
1. Succinylcholine
| 2. Rocuronium (Zemuron)- when sux is contraindicated (use low end of dose)
144
When choosing a muscle relaxant what things should you consider?
1. Class of Muscle Relaxant
2. Onset Time
3. Duration of Action
4. Pharmacokinetic Profile
5. Cardiovascular Effects
6. Need for Reversal
7. Disease States • Hepatic • Renal • Cardiac
145
When should you give priming dose prior to intubating dose?
approx 4 min
146
Which muscle relaxer may cause tachycardia?
Pavulon
147
Which muscle relaxers may cause bradycardia?
- Sux
| - some cases of Vecuronium
148
Which muscle relaxers give histamine release/hypotension?
D-Tubocurarine
Atracurium (Tracrium)
Mivacurium (Mivacron)
149
What does phase II block of succinylcholine mimic?
Non-depolarizing muscle relaxants
150
What should you consider if you have a patient with low cardiac output prior to give muscle relaxers?
Will take longer than normal to circulate and cause its effects.
