Neuromuscular Blockade

Question 1

Mechanism of action of non-depolarizing muscle relaxants.

Answer 1

Competitive antagonists of the nicotinic Ach receptor at the NMJ. Bind the receptor but don’t induce ion channel opening.

To completely block neuromuscular signal transmission, at least 95% of postsynaptic ACh receptors must be blocked.

Question 2

True or false: non-depolarizing muscle relaxants cant cross the placenta, BBB, or cell membranes because they are positively charged and have poor lipid solubility.

Answer 2

True.

Question 3

True or false: block recovery after a single bolus dose of NDMR is the result of redistribution rather than agent metabolism.

Answer 3

True

Question 4

What are advantages to using neuromuscular blockers?

Answer 4

1- improve conditions for tracheal intubation
2- provide immobility during surgery
3- facilitate mechanical ventilation

Question 5

True or false: volatile and local anesthetics potentiate neuromuscular blockade.

Answer 5

True

Question 6

True or false: glaucoma medications like echothiophate potentiate neuromuscular blockade?

Answer 6

true

Question 7

True or false: aminoglycoside antibiotics potentiate neuromuscular blockade

Answer 7

True

Question 8

T or F: erythromycin, penicillin, and cephalosporins do NOT potentiate neuromuscular blockade.

Answer 8

True

Question 9

True or false: cardiovascular drugs potentiate neuromuscular blockade

Answer 9

true- Beta-blocking drugs and calcium channel antagonists have been found to have neuromuscular effects in vitro, but in practice, the duration of action of neuromuscular blocking agents is not altered in patients taking these drugs chronically

Question 10

Which electrolyte conditions potentiate neuromuscular blockade?

Answer 10

hypermagnesemia, hypernatremia, hypocalcemia, hypokalemia

High Mg, Na
Low K, Ca

Question 11

Which physiologic states potentiate neuromuscular blockade?

Answer 11

Hepatic dysfunction
hypothermia
acidosis
alkalosis

Question 12

Name the two classes of non-depolarizing neuromuscular blockers. Which are histamine-releasing and which are vagolytic?

Answer 12

Benzylisoquinoliniums (the -curiums), tend to be histamine releasing, while aminosteroids (the -oniums), tend to be vagolytic

Question 13

How are non-depolarizing neuromuscular blockers metabolized?

Answer 13

reversal of blockade depends on redistribution, gradual metabolism, and excretion, and also administration of a cholinesterase inhibitor which increases the amount of Ach available at the NMJ

Question 14

How is pancuronium excreted?

Answer 14

Renally

Question 15

True or false: atracurium is associated with laudanosine toxicity and dose-dependent histamine release at high doses and rapid administration. Duration of action is MARKEDLY prolonged with hypothermia.

Answer 15

True- atracurium produces dose-dependent histamine release and can be associated with bronchoconstriction.

Question 16

Describe what happens to neuromuscular blocker sensitivity in the following disease states:
1- Muscle denervation injuries
2- Myasthenia gravis
3- Myasthenic syndrome
4- Huntington's chorea
5- Duchenne's muscular dystrophy

Answer 16

1- muscle denervation: chronic decrease in Ach stimulates a compensatory increase in AchR and extrajunctional AchR, leading to an exaggerated response to depolarizing drugs but resistance to non-depolarizing.

2- myasthenia gravis: antibodies to AchR cause their destruction. These pts are sensitive to non-depolarizing NMBD and are resistant to depolarizing NMBD.

3- myasthenic syndrome: a normal number of neuromuscular receptors but a decrease in the release of Ach. Sensitive to both depolarizing and non-depolarizing. Decreased levels of Ach in the junction will potentiate a neuromucular block.

4- Huntington’s chorea is associated with decreased plasma cholineseterase activity and prolonged response to Sch has been seen

5- Muscular dystrophy- Sch is contraindicated because of the risk of rhabdomyolysis, hyperkalemia, and cardiac arrest. Ok to use non-depolarizing.

Question 17

True or false regarding neuromuscular blocking agents and LIVER disease:

1- increased plasma volume may result in slower block onset and increased dose requirement
2- Recovery speed of single-dose NMBAs depends on redistribution, not elimination
3- liver failure has little influence on the effects of cis-atracurium
4- aminosteroid NMBA metabolism speed is increased in early liver failure and decreased in severe liver failure.

Answer 17

True

Question 18

T or F: rapacuronium was withdrawn from the market because of its histamine releasing effect on mucosal mast cells, which may cause bronchospasm.

Answer 18

True

Question 19

What are the four categories of succinylcholine adverse effects?

Answer 19

1- Anti-muscarinic effects- bradycardia, idioventricular arrhthmia, v-fib

2- Potassium-release related- Sch will increase plasma K levels by 0.5 mmol/L.

3- Allergic reactions- Sch is 3x more likely to cause allergic reactions than other muscle relaxants

4- Nonspecific effects- fasciculations causing myalgia, increased IOP, increased ICP, malignant hyperthermia

Question 20

Describe Phase I block after Sch administration.

Answer 20

• abscence of TOF fade and absence of posttetanic potentiation
• generalized reduction in all four TOF twitches

Question 21

Describe Phase II block after Sch administration.

Answer 21

• resembles nondepolarizing block
• TOF fade and posttetanic potentiation
• the period during which neostigmine or edrophonium may be administered.

Question 22

T or F: the 3-desacetylvecuronium metabolite has about 70-80% potency of vecuronium. It also has a slower clearance rate and longer duration of action. It is highly dependent on the kidney for elimination.

Answer 22

True

Question 23

T or F: atracurium causes histamine release, which may cause hypotension in hypovolemic patients or bronchoconstriction in patients prone to asthma.

Answer 23

True