Neuromuscular Blockade Flashcards Preview

Anesthesiology > Neuromuscular Blockade > Flashcards

Flashcards in Neuromuscular Blockade Deck (23):
1

Mechanism of action of non-depolarizing muscle relaxants.

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.

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.

True.

3

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

True

4

What are advantages to using neuromuscular blockers?

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

5

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

True

6

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

true

7

True or false: aminoglycoside antibiotics potentiate neuromuscular blockade

True

8

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

True

9

True or false: cardiovascular drugs potentiate neuromuscular blockade

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

10

Which electrolyte conditions potentiate neuromuscular blockade?

hypermagnesemia, hypernatremia, hypocalcemia, hypokalemia

High Mg, Na
Low K, Ca

11

Which physiologic states potentiate neuromuscular blockade?

Hepatic dysfunction
hypothermia
acidosis
alkalosis

12

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

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

13

How are non-depolarizing neuromuscular blockers metabolized?

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

14

How is pancuronium excreted?

Renally

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.

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

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

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.

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.

True

18

T or F: rapacuronium was withdrawn from the market because of its histamine releasing effect on mucosal mast cells, which may cause bronchospasm.

True

19

What are the four categories of succinylcholine adverse effects?

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

20

Describe Phase I block after Sch administration.

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

21

Describe Phase II block after Sch administration.

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

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.

True

23

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

True