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test > Non Depolarizing Muscle Relaxers No Reversal > Flashcards

Non Depolarizing Muscle Relaxers No Reversal Flashcards

1
Q

What are the 4 main differences between all of the non-depolarizing muscle blockers?

A
  • Onset;
  • Duration of action;
  • Rate of recovery;
  • Metabolism
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2
Q

What is the MoA of non-depolarizing blockers?

A
  • Pre-junctional sites → block ACh release;
  • Post junctional → Compete with ACh at nACh-R for alpha subunits → no conformational change
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3
Q

What are the characteristics of a non-depolarizing block?

A
  • ↓ twitch response to a single stimulus;
  • Unsustained response (fade) to continuous stimulus;
  • TOF ratio < 0.7;
  • Post-tetanic potentiation;
  • Potentiation of other non-depolarizing drugs;
  • Antagonism by anticholinesterase drugs;
  • No fasciculations during onset
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4
Q

What is fade?

A
  • Fade suggestssomefibers are contracting while some are blocked (muscle contraction is all or nothing)
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5
Q

What causes the adverse CV effects of non-depolarizing blockers?

A
  • Release of histamine;
  • Effects at cardiac muscarinic receptors;
  • Effects on nACh-R at autonomic ganglia
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6
Q

Why do the adverse CV effects of non-depolarizing blockers vary between patients?

A
  • d/t underlying diseases, preop meds;
  • Adverse effects are rarely clinically significant
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7
Q

What is the “Autonomic Margin of Safety”?

A
  • Difference between dose thatproducesblockade (ED95) and dose thatcreatescirculatory effects
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8
Q

Which long term non-depolarizing blocker has the same dose that both causes blockade and adverse CV effects?

A
  • Pancuronium;
  • Vec, Roc, Cis all have very different ED95 doses and doses that produce CV effects
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9
Q

What adverse event have non-depolarizing blockers been shown to have in critically ill patients? What is another name for this condition?

A
  • Skeletal muscle weakness for weeks to months after the blocker is D/C;
  • Critical illness myopathy
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10
Q

For patient affected by critical illness myopathy, what three things did they have in common?

A
  • Had MSOF and vented for > 6 days;
  • Usually had an aminosteroid NMBD;
  • Administering Glucocorticoids prior to NMBD may ↑ risk
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11
Q

What is the MoA of critial illness myopathy?

A
  • Unknown;
  • Maybe ↓ clearance or Active metabolites?
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12
Q

What are some altered responses of non-depolarizing blockers when using volatile anesthetics? MoA of this?

A
  • Dose-dependent enhancement;
  • Desflurane>Sevoflurane>Isoflurane;
  • Onset as early as 30 minutes..;
  • MoA is unkown → maybe dose dependent inhibition of nACh-R
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13
Q

How do diuretics, corticosteroids, metoclopramide and LAs affect non-depolarizing blockers?

A
  • Enhances or prolong blockade;
  • ↑ acetylcholine release;
  • ↓ cholinesterase activity;
  • ↓ nerve conduction
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14
Q

How does Magnesium affect non-depolarizing blockers and SCh? MoA for this?

A
  • Enhances blockade;
  • MoA non-depol: ↓prejunctional release of Ach and ↓sensitivity to postjunctional membranes;
  • MoA SCh: unkown → maybe more rapid shift to PH2 block
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15
Q

How do SNS drugs affect non-depolarizing blockers? MoA for this?

A
  • Give Ephedrine p/t non-depolarizers = ↓ onset time d/t ↑ CO and skeletal muscle blood flow;
  • Give Esmolol p/t non-depolarizers = delayed onset of muscle block
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16
Q

How does Hypothermia affect non-depolarizing blockers? MoA for this?

A
  • Mild hypothermia = 2x the DoA for Vecuronium, Pancuronium;
  • MoA = Temp slowing of hepatic enzyme activity;
  • Mild hypothermia = ??? for Atracurium, Cisatracurium;
  • MoA = Temp dependent eliminatio process (ester hydrolysis and Hoffman elimination)
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17
Q

How doesacute hypokalemiaaffect non-depolarizing blockers?

A
  • Hyperpolarizes cell membrane;
  • Causes resistance todepolarizingNMBDs;
  • ↑ sensitivity tonon-depolarizingNMBD’s
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18
Q

How doesacute hyperkalemiaaffect non-depolarizing blockers?

A
  • ↓ resting membrane potential (partially depolarizes cell membrane);
  • ↑ effects ofdepolarizingNMBDs;
  • Resistance tonon-depolarizingNMBDs
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19
Q

How do burns affect non-depolarizing blockers? MoA?

A
  • Causes resistance to non-depolarizers;
  • Begins approx. 10 days post injury;
  • ↓ after 60 days;
  • MoA: Altered affinity of nACh-Rs (its not r/t altered # of receptors)
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20
Q

What percentage of the body needs to be affected by burns to cause altered response to non-depolarizing blockers?

A
  • 30% BSA or >
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21
Q

For a patient with burns, how can we offset the resistance to non-depolarizing blockers the burn causes?

A
  • using 1.2 mg/kg dose of Rocuronium
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22
Q

How does Paresis or Hemiplegiaaffect non-depolarizing blockers? MoA?

A
  • Paretic arm → will be resistant compared to unaffected side;
  • Unaffected arm → will be resistant compared to normal patients;
  • MoA:Proliferation of extrajunctional nACh-Rs
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23
Q

Which depolarzing/non-depolarizing blocker is the most likely to cause allergic reactions? Which is least likely to cause reaction?

A
  • SCh > Pancuronium, Vecuronium, Rocuronium;
  • Cisatracurium least likely
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24
Q

What makes a cross sensitivity reaction possible for depolarizing/non-depolarizing blockers?

A
  • Quaternary ammonium group
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25
Q

How can a patient get an allergic reaction from a depolarzing/non-depolarizing blocker on their 1st exposure?

A
  • Represents prior sensitization →Soaps/cosmetics (women > men)
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26
Q

How does Gender affect non-depolarizing blockers? MoA?

A
  • Women more sensitive (need 22% less Vec or 30% less Roc);
  • Duration of blocker greater in women;
  • MoA: unknown
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27
Q

What is the most common long acting NMBD?

A
  • Pancuronium (Pavulon)
28
Q

What is the chemical classification of Pancuronium? What properties does this drug have?

A
  • Bisquaternary aminosteroid;
  • Vagolytic properties
29
Q

What is the intubating dose, onset and duration of Pancuronium?

A
  • Dose: 0.1mg/kg;
  • Onset: 3-5 minutes;
  • Duration: 60-90 minutes
30
Q

How is the majority of Pancuronium metabolized?

A
  • 80% eliminated unchanged in urine
31
Q

What changes in metabolism of Pancuronium do we see with a renal failure patient?

A
  • 30-50% decreased plasma clearance;
  • 10-40% deasacetylpancuronium metabolite ½ as active (by liver)
32
Q

What changes in metabolism of Pancuronium do we see with a liver disease patient?

A
  • Increased VD;
  • Larger initial dose is needed;
  • Prolonged elimination ½ time
33
Q

What changes in metabolism of Pancuronium do we see with an elderly patient?

A
  • Decreased plasma clearance d/t renal function
34
Q

What CV effects do we see with Pancuronium?

A
  • ↑ HR;
  • ↑ MAP;
  • ↑ CO;
  • No changes in SVR or inotropy
35
Q

Does pancuronium cause histamine release?

A
  • no
36
Q

What are the two main causes for the CV effects of Pancuronium?

A
  • Vagal blockade → mostly at SA node and ↑ BP is d/t HR ↑;
  • SNS activation → presynaptic release of NE and block NE reuptake
37
Q

What are the 4 intermediate acting non-depolarizing blockers?

A
  • Vecuronium;
  • Rocuronium;
  • Cisatracurium;
  • Atracurium
38
Q

Compared to LA, NMBDS have…?

A
  • Similar onset of maximum blockade (except high dose roc);
  • Approximately 1/3 duration of action;
  • Minimal/absent cardiovascular effects;
  • Antagonized by anticholinesterase drugs approx 20 min.
39
Q

What chemical classification is Vecuronium?

A
  • Aminosteroid
40
Q

What is the intubating dose, onset and duration of Vecuronium?

A
  • Intubating Dose: 0.1 mg/kg;
  • Onset: 3-5 minutes;
  • Duration: 20-35 minutes
41
Q

What is the main way Vecuronium is metabolized?

A
  • Hepatic is principle method of elimination;
  • 3-desacetylvecuronium 50-80% as potent (but rapidly converted to metabolite with 1/10 the effects)
42
Q

With renal excretion, what percentage of Vecuronium appears unchanged in urine? How does renal dysfuction affect it?

A
  • Approx 30% appears unchanged (*70% metabolized in liver);
  • E 1/2 time ↑
43
Q

How does metabolism of Vecuronium change with the elderly?

A
  • ↓ volume of distribution (less muscle mass);
  • ↓ plasma clearance (less hepatic flow / delayed recovery with infusions)
44
Q

How does metabolism of Vecuronium change with an obstetric patient?

A
  • Insignificant effects to fetus;
  • ↑ clearance in 3rd trimester (progesterone);
  • ↑ duration early postpartum (give IBW)
45
Q

How do Acid-Base changespriorto NMBD affect Vecuronium?

A
  • No prolonged blockade
46
Q

How do Acid-Base changesafterNMBD affect Vecuronium?

A
  • Respiratory acidosis followin NMBD administration will prolong blockade
47
Q

How does respiratory acidosis that occurs after Vecuronium administration prolong the blockade?

A
  • Activity inversely proportional to bound drug…acidosis decreases bound amount;
  • Change in ionization at receptor increases attachment time;
  • Watch out for postop hypoventilation
48
Q

What CV effects does Vecuronium have? Does it release histamine?

A
  • No CV effects to worry about;
  • No histamine release
49
Q

What chemical class is Rocuronium?

A
  • Aminosteroid
50
Q

What is the intubating dose, onset and duration of Rocuronium?

A
  • Dose: 0.6 mg/kg or 1.2 mg/kg;
  • Onset: 3-5 minutes; 1-2 minutes;
  • Duration: 20-35 minutes
51
Q

How does a large dose of Rocuronium compare to SCh and Pancuronium?

A
  • Larger doses of Roc parallel onset of SCh but offset of pancuronium (quicker onset, longer duration)
52
Q

How is Rocuronium excreted?

A
  • Unchanged in bile
53
Q

Why will Rocuronium have a longer DoA in the elderly or with liver failure patients?

A
  • d/t ↓ clearance and ↑ Vd
54
Q

What percentage of Rocuronium is excreted renally?

A
  • 10-30% → only marginally affected by liver failure
55
Q

What are the CV effects of Rocuronium? Does it release histamine?

A
  • No CV effects (maybe slight vagolytic effect);
  • No histamine release
56
Q

What chemical class is Cisatracurium?

A
  • Benzylisoquinolone
57
Q

What is the intubating dose, onset and duration of Cisatracurium?

A
  • Intubating Dose: 0.1 mg/kg;
  • Onset: 3-5 minutes;
  • Duration of action: 20-35 minutes
58
Q

What is unique about the metabolism of Cisatracurium?

A
  • Cis- isomer of atracurium;
  • Recovery from infusion NOT affected by time;
  • Degraded by Hoffman elimination;
  • Degradation DOES NOT use non-specific plasma cholinesterase as much as Atracurium
59
Q

What changes occur in Cisatracurium when used in an elderly patient? What changes occur in an obese patient?

A
  • Elderly: Slight delay in onset d/t CO;
  • Obese:Duration of action prolonged IF dosed at actual body weight d/t ↑ Vd
60
Q

What CV effects does Cisatracurium have? Does it release histamine?

A
  • CV stabile;
  • No histamine release
61
Q

What is the only clinically useful short acting non-depolarizing blocker?

A
  • Mivacurium
62
Q

What chemical class is Mivacurium?

A
  • Benzvlisoquinolone
63
Q

What is the intubating dose, onset and duration of Micacurium?

A
  • Intubating Dose: 0.15 mg/kg;
  • Onset: 2-3 minutes (Conditions less desireable);
  • Duration: 12-20 minutes
64
Q

What 3 isomers occur in the metabolism of Mivacurium? Which isomers have NM blocking ability?

A
  • Cis-cis;
  • Cis-trans → NM blocking;
  • Trans-trans → NM blocking
65
Q

How is mivacurium cleared from plasma?

A
  • by plasma cholinesterase
66
Q

What are the CV effects of Mivacurium?

A
  • Minimal
67
Q

What negative side effects does Mivacurium have?

A
  • Release histamine;
  • Giving> 3 xED95 = transient MAP drop (More common with rapid, large doses);
  • MAP drops more in HTN pts than non-HTN pts

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