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Neuromuscular blockg
Neuromuscular Blocking Agents
| Question | Answer |
|---|---|
| What are neuromuscular agents used for? | relax skeletal muscle, prevent fractures/dislocations with ECT, control muscle spasms of tetanus, sustained NM blockade in critically ill patients |
| Name 4 non-depolarizing competitive antagonists that are isoquinolone derived? | tubocurarine, atracurium, cistracurium, mivacurium |
| Name 2 non-depolarizing competitive antagonists that are steroid derived? | pancuronium, vecuronium |
| Is there a mneumonic to distinguish the isoquinoline vs steroid derived NM blockers? | isoquinoline = ends with "curium", steroid = ends with "curonium". |
| Name the only depolarizing NM agonist? | succincylcholine |
| Do non-depolarizing or depolarizing agents cause fasiculations? | depolarizing |
| Are NM blocking agents useful given orally? | No. They are highly polar and are inactive orally |
| Name 3 muscle relaxants? | baclofen, diazepam, dantrolene |
| Name 3 properties shared by all NMB agents? | all have a structural relationship to acetycholine, all have at least one quarternary N+, all are highly polar and inactive orally |
| Why do NM blockers have hypotensive effects? | cause histamine release & decreased circulating epi & norepi |
| Do NM blockers cross the BBB? | NO. highly polar |
| Which anesthesia inhalent augments the effects of NM blockers? | halothane |
| Which antibiotics interfere with release of acetylcholine at the NM junction? | aminoglycosides - vancomycin, gentamycin, tobramycin, amikacin |
| How does serum potassium interact with NM blockers? | Low K+ potentiates; high K+ opposes |
| Which populations are more sensitive to NM blockers? | newborns, aged, myasthenics |
| What is the duration of succinylcholine? | brief - 5 minutes |
| What is the duration of mivacurium? | short - 10-20 minutes |
| What is the duration of atracurium & cistracurium | intermediate - 30-60 minutes |
| What is the duration of vecuronium? | intermediate - 60-90 minutes |
| What is the duration of tubocurarine | Long - 80-120 minutes |
| What is the duration of pancuronium | Long - 120-180 minutes |
| Which NM blockers are eliminated by plasma cholinesterase? | succ's and mivacurium (atracrurium to some degree) |
| Which NM blockers are eliminated spontaneously? | cistracurium and atracurium (plasma cholinesterase also) |
| Which NM is eliminated via the liver? | vecuronium |
| Which NM blockers are eliminated by the kidneys, not metabolically? | tubocurarine and pancuronium |
| Is succinylcholine reversible by AcHe inhibitors? | No. it will increase the blockade. |
| What is the most significant danger with administration of succ's? | hyperkalemia |
| In what patient population should you avoid succ's administration? | CHF patients om digoxin or diuretics, burn patients for up to 6 months, patients with high serum potassium levels and patients with genetic variant that causes them to not be able to readily breakdown succ's. |
| What is the pathophysiology of malignant hyperthermia? | MH reaction involves an autosomal-dominant inherited sensitivity anesthetics which can cause rapid accumulation of Ca+ in striated muscle with resulting muscle contracture, rhabdomyolysis and an intense heat-producing reaction. |
| One of the main causes of death due to anesthesia? | malignant hyperthermia |
| What triggers malignant hyperthermia? | anesthetics or succ's |
| What are signs and symptoms of MH? | The clinical picture is often dramatic with intense tachycardia, increased CO2 production, muscle rigidity, rapid hyperthermia, respiratory and metabolic acidosis, hyperkalemia, and terminal hemodynamic collapse. |
| What is the drug of choice for MH? | dantrolene |
| What is the mechanism of action of Baclofen? | increased K+ conductance which causes hyperpolarization, decreased Ca+ influx, decreased excitatory NT release, decreased motor neuron activity |
| Is baclofen like diazepam or dantrolene in its effects? | effective as diazepam with less sedation and little effect on muscle strength, unlike dantrolene |
| Baclofen is agent of choice for...? | spinal spasticity and spasticity d/t MS |
| What patient poulation may need smaller doses? | elderly and MS patients |
| Can baclofen be stopped abruptly? | Abrupt discontinuation of oral baclofen may cause seizures and hallucinations. Abrupt discontinuation of intrathecal baclofen may result in high fever, rebound spasticity, muscle rigidity, and rhabdomyolysis that can progress to failure of several organs. |
| Generic name for Baclofen? | lioresal |
| Generic name and drug class of Valium? | diazepam; benzodiazepine(BDZ) |
| What is the generic name for Dantrium? | dantrolene sodium |
| What is diazepam used for? | to control extensor and flexor spasms, spinal spasticity, MS and anxiety |
| Is diazepam a GABA agonist | No but it enhances GABA effect and acts at all GABA-A synapses but reduces spasticity partly at spinal cord level. |
| What drug class is lioresal? | a GABA receptor agonist |
| How is diazepam metabolized? | liver |
| Are muscle relaxants better than NSAIDs for localized muscle spasm? | no, NSAIDs have proven to be better. |
| What is the most popularly prescribed muscle relaxant? | cyclobenzaprine (Flexeril) |
| chlorzoxazone | Parafon Forte |
| carisoprodol | Soma |
| Does flexeril cross BBB? | yes. #1 side effect is sedation. |
| methocarbamol | Robaxin |
| tizanidine | Zanaflex |
| What is dantrolene's drug classification? | peripheral acting skeletal muscle relaxant |
| What is activity of dantrolene ? | acts at level of muscles (not CNS), inhibits calcium release from Sarcoplasmic Reticulum and uncouples excitation-->contraction |
| Does dantolene alter membrane potential? | No |
| What is biggest problem associated with dantrolene administration? | dose dependent muscle weakness |
| What are other problems associated with dantrolene administration? | diarrhea, hepatotoxicity |
| Besides MH, what other disease processes is dantrolene used for? | MS, spasticity associated with spinal cord lesions, cerebral palsy |
| What is the general order of muscle sensitivity to NM blocking agents? | smaller rapid muscles first and progress to larger slow moving muscles--> eyes > face > limbs > abdominal > intercostals > diaphragm |
| What is the order of recovery after NM blocker administration? | diaphragm > ICs > abdominal > limbs > face > eyes |
| The administration of succinylocholine to a patient led to the appearance of dysarrhythmias, conduction abnormalities and finally cardiac arrest. The most likely cause is: | hyperkalemia |
| Which of the NDMRs have the shortest duration? | mivacurium |
| What is Pseudocholinesterase deficiency? | an uncommon genetic disorder that makes an affected person very sensitive to any of several anesthetic agents, especially those derived from the drug known as choline like succ's and mivacurium |
Created by:
psfisher50
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