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119 Cards in this Set
- Front
- Back
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What is Sugammadex:
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Bridion, a reversal agent for Zemuron that will reverse 100% blockade immediately. Not on the market yet.
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What symptom is usually seen with anti-cholinesterase drugs after ambulatory surgery?
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N/V
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What are the typical combos of anticholinergic and anti-cholinesterase drugs?
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Atropine has a rapid onset ( 1 min) that more closely coincides with the onset of Edrophonium. Robinul has an onset of 2-3 mins which makes it more suitable with Neostigmine or Pyridostigmine.
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What are the effects of reversal agents?
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Blockade of the effects of acetylcholinesterase. This makes more Ach available to the receptors at the NMJ.
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What is the dose and supply of Neostigmine?
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0.04 mg/kg, supplied in 1mg/ml
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What is the pharmacologic principle involved with reversing ND NMB?
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The decrease of the effect of competitive blocking drugs by increasing the concentration of Ach at the NMJ (so Ach uses receptor sites and the muscles can move again).
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What population shows increased risk for hyperkalemia with NMB?
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neurologic diseases, DMD
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What patient population shows increase in K+in r/t Succ and is resistant to ND NMB?
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Hemiplegia, paraplegia and burn patients.
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Which condition is usually resistant to Succ and sensitive to ND NBB?
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Myasthenia Gravis
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Which drug is contraindicated with muscular dystrophy?
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Succ
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Do anticonvulsants increase or decrease resistance to ND NMB?
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Increase, so may need to give a higher dose.
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What antibiotics potentiate the effects of the NMB?
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Aminoglycosides and polymyxins
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Do local anesthetics potentiate the effects of the NMB?
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Yes, they do this in r/t the sodium channels
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T or F
Volatiles have dose dependent potentiation on NMB. |
True
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Mivacurium is eliminated by what?
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Plasma cholinesterase
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Cisatracurium is eliminated by?
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Hoffman elimination only
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What is Hoffman elimination dependent on?
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Temp and Ph
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How is Atricurium eliminated?
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Ester hydrolysis and Hoffman elimination
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Renal excretion is the primary route of elimination for which drugs?
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D-tubo and Metocurarine
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Biliary excretion is the primary route of elimination for which drugs?
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Vec and Roc
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Metabolism is the primary route of elimination for which drugs?
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Succ, atracurium, Cistracurium, and Mivacurium.
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Which drugs produce tachycardia? What can you do to balance this?
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Pancuronium and Gallamine, use Sufenta to balance
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Which drugs produce bradycardia? What can you do to balance this?
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Succ, use atropine to balance
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Which drugs signal histamine release?
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Succ, Mivacurium, Atracurium, D-tubo, and Metocurarine.
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Which drugs produce an autonomic ganglionic blockade?
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D-tubo and Metocurarine.
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Which drug can be substituted for Succ in a RSI?
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Roc 1 -1.5 mg/kg
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Which drug is secreted unchanged?
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Zemuron is not metabolized, but is 80 -90 % excreted in the bile and 10 % in the urine, so it is secreted unchanged.
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Which drug has teh most rapid onset and recovery of all ND NMB:
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Rapacuronium ( the duration of action is longer than Succ)
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What type of NMB is Mivacurium?
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Short acting benzylioquinoline
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What type of NMB IS Atracurium?
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Intermediate acting benzylisoquinoline
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What is the name of the metabolite from Atricurium that can cause convulsions?
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Laudanosine, a cerebral stimulant
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Do ND NMBs cross the BBB? Placental barrier?
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no, no
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What are some of the physiologic properties of ND NMB?
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Very high protein bound, no agonist activity, competitive antagonists at nicotinic receptors, and 100% ionized at physiologic Ph
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What are the 3 ways to classify ND NMB?
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Benzylisoquinoline or Aminosteriod: short , intermediate, or long acting: Organ or non organ metabolism
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What is the mechanism of action for ND NMB?
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It competitively blocks Ach from attaching to its receptor, so the sodium channel can not open. the channel stays closed and post synaptic membrane remains polarized. the muscles can not contract, so relaxation occurs.
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What are 2 major side effects of Succ?
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Transient increased in plasma K+( 0.5 - 1.0 mEq/L) and trigger for MH
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What is the principle indication for Succ?
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Facilitation of tracheal intubation
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Is the dose of Sicc increased or decreased if the patient was pre-medicated with a ND NMB? What is the new dose? why would you do this?
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Increased to 1.5 - 2.0 mg/kg. if not you will have a slower onset of action
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The onset of NMB effect of Succ is within ----------- following high dosing (1-2 mg/kg iv)?
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1 minute
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About how many patients have atypical plasma cholinesterase? What does this mean?
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1:1500 to 1:3000, they can not rapidly metabolize the Succ
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What are the other names for plasma cholinesterase? What does plasma cholinesterase do?
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Pseudocholinesterase and Butyrocholinesterase, it has an enormous capacity to hydrolyze Succ in the plasma to relatively inactive metabolites.
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What metabolites are seen with the hydrolysis of Succ?
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Succinylmonocholine and choline
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Succ produces features considered characteristic of what type of block in normal doses? High doses?
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Phase 1 depolarizing blockade, if @ high doses can be phase 2 non-depolarizing blockade
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What is the mechanism of action of depolarizing NMB?
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The resulting persistent depolarization due to sustained opening of the transmembrane sodium channels prevents propagation of action potentials and produces skeletal muscle relaxation.
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What is required for activation of the post synaptic nicotinic receptors?
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Simultaneous occupation of the receptor's 2 alpha subunits by ACH
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What 5 subunits compose the glcoprotein complex of the post junctional receptor?
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2 alpha proteins, 1 beta protein, 1 delta protein, 1 gamma protein
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Succ is the prototypical depolarizing NMB consisting of what?
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2 ACH molecules joined together
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Succ mimics the action of ACH by forming strong attachments to the ---------- ----------- cholinergic receptor's alpha subunits.
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post synaptic
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What terminates the action of ACH? What happens to the end products?
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Enzyme acetylcholinesterase ( AchE) which rapidly hydrolyzes Ach into acetic acid and choline. The choline is taken backup into the nerve terminal to be reused in the synthesis of new Ach and the acetic acid diffuses form the synaptic cleft.
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Where do neurotransmitters interact in the body? What does this interaction produce?
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Neurotransmitters act on receptors present on the membrane of post synaptic cells, it produces a functional change in the post synaptic cell.
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Name and explain the 2 classes of NMB?
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Depolarizing NMB are those that mimic the actions of ACH, they are non-competitive. ND NMB are those that interfere with the actions of ACH, they are competitive.
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T or F
Muscle relaxants are not anesthetics and should not be used to mask skeletal muscle movement in inadequately anesthetized patients. |
True
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Never paralyze a patient without first assuring -------------------------------------------------------.
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Sedation/hypnosis
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What should you always confirm before paralyzing a patient? Is there an exception?
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That the patient can be " bagged" prior to paralyzing. If not able to bag, try repositioning head, and oral airway, or wake the patient up. The exception is RSI.
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What is Enlon Plus?
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10 mg/ml concentration of edrophonium and atropine ( 0.14mg/ml)
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What is unique about Edorphonium?
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it is believed to have both pre and post synaptic effects ( others only have one, usually post)
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What should you do in between giving the induction agent and giving the muscle relaxant?
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Make sure you can ventilate the patient
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How long should you pre-oxygenate the patient and at what L/min?
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4-5 minutes, 8 - 10 L/min
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When should you give the muscle relaxant during induction?
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No eye reflexes
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When can you tell the patient is relaxed enough o attempt intubation?
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Ventilate until there are no twitches ( with volatile agent on)
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What should yo do after you tape the tube?
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listen again to make sure still in place
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What is the dose for Succ?
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1 -1.5 mg/kg
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What are the contraindications for Succ?
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Hyperkalemic patients b/c it raises serum k+ by 0.5 go 1.0 mEq, certain neuromuscular disorders, paralyzed patients,and burn patients
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What should be given to prevent fasciculations in patients receiving Succ?
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Non-depolarizing muscle relaxant ( 1/10 of normal dose)
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When is it ok to use Succ?
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Emergency cases, RSI to prevent aspiration, difficult airways, prolonged laryngospasms
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What is the dose for Roc?
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10 mg/ml ( comes in 5 or 10 ml vials, so prepare a 5 ml syringe)
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When do twitches start to come back with Roc?
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20 - 30 minutes, so can reverse at this time
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What is the dose for Vec?
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0.1 mg/ kg
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What form does Vec come in and what are the concentrations before and after mixing?
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comes in powder form ( 10 mg/vial), so dilute with 10 ml NS to 1 mg/ml, so prepare in a 10 ml syringe
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When do you get twitches back with Vec?
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30 -45 minutes, so can reverse at this time.
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What is the dose for cisatricurium?
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0.15 - 0.2 mg
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What is the concentration of Cisatricurium?
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2 mg/ ml or 5 mg/ml
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When do you get twitches back with Cisatricurium?
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30 - 60 minutes depending on the dose.
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How is cisatricurium metabolized?
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Hoffman elimination ( with the lungs) so can use in patients with liver or renal failure.
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What is the dose for Neostigmine?
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0.035 -0.075 mg/ kg
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What is the concentration of Neostigmine?
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1 mg/ ml in a 10 ml vial
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What is the typical dose for Neostigmine?
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3 mg ( never give more than 5 mg)
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What must always be given with Neostigmine and why?
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Robinul or atropine.
To prevent bradycardia |
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What reversal drug causes bradycardia and why? What drug do you give with it to help with the bradycardia?
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Neostigmine.
Neostigmine affects both nicotinic and muscarinic cholinergic receptors. Nicotinic receptors are found in the neuromuscular junction, but the stimulation of muscarinic receptors in the heart causes bradycardia. Robinul or atropine. |
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What must you always make sure is off before administering any type of reversal agent?
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Volatile gases
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Why is it important to have some twitches back before administering a reversal agent?
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When the reversal agent wears off you may still have some paralytic on board.
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What is the dose of Robinul?
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0.1 mg / kg
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What is the concentration of Robinul?
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0.2 mg/ l in 2 or 5 ml vials
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What is the rule of thumb when giving Robinul and neostigmine?
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Typical to give = amounts of both. For example, 3 ml ( 3 mg: 1 mg/ml) of Neostigmine and 3 ml ( 0.6 mg: 0.2 mg/ml) Robinul ( you can mix in the same syringe)
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What do the majority of the drugs used in anesthesia cause?
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cardiac depression and some agents cause vasodilation.
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What is the concentration of Ephedrine?
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50 mg/ ml in 1 ml ampoules, dilute with NS to 5 mg / ml, so prepare in a 10 ml syringe
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What kind of effect does Ephedrine have on the body?
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Vasoconstriction and increased Hr b/c it is beta and alpha agonist, so give when HR and BP are both down. it is useful in OB to treat hypotension after regional anesthesia.
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What is the concentration of phenylephrine?
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10 mg /ml ampules, so prepare in a 10 ml syringe
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What dose do you give for Neosynephrine bolus?
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Dilute to 100 mcg/ ml and give 0.5 - 1.0 ml
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How do you prepare a bag of Neosynephrine for infusion?
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10 - 30 mg / 250 ml IVF and titrate
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What kind of effect does Neosynephrine have on the body?
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Vasoconstriction, but no increase in HR b/c it is a pure alpha agonist ( may see reflex bradycardia)
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The Autonomic nervous system is voluntary or involuntary?
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Involuntary
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The ANS is divided into which two portions?
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The sympathetic and parasympathetic
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The receptors in the sympathetic ANS are?
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alpha and beta
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The nitrous oxide system does what int he vascular system?
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causes vasodilation
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Sodium Nitroprusside cause dilation of what?
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venous and arterial vascular smooth muscle
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When using Nipride one must be careful of what side effect?
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cyanide toxicity
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Nitro is used mainly for ?
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treatment of angina
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To prevent possible bad side effects when using Nipride on should maintain what dose for shot term? Long term?
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short term doses of 10 mck/kg/min an long term doses of 2 mcg/kg/min
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Nitroglycerin causes dilation of what?
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the venous smooth muscle, at high doses may cause arterial
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Nipride is used mainly for what problem?
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hypertensive crisis and controlled hypotension
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T or F
Nipride should be protected from light? |
True
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Large doses of Nitroglycerin can cause?
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methemogloinemia
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Nitro dosage is?
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2 mcg/kg/min
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neosynephrine is used for?
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treatment of systemic hypotension
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Neosynephrine stimulates which receptors?
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direct acting and stimulates the alpha 1 receptors
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Dosage for treatment of systemic hypotension with Neo is?
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50 - 200 mcg IV
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ephedrine stimulates which receptors?
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stimulates both alpha and beta receptors
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The usual adult dosage for Ephedrine is?
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5 - 25 mg for adults
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Dopamine is a ?
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neurotransmitter that is dose dependent on which receptors it acts on
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Dopamine should be mixed in?
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D5 W
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When dopamine is used for vasoconstriction it should be used at what dose?
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10 mcg/kg/min and at this dose stimulates the alpha receptors
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Dobutamine should be used at what dose?
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2 - 10 mcg/kg/min
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Levophed stimulates what receptors? Which does Levophed stimulate more?
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Levophed stimulates both beta 1 and alpha 1, intensely stimulates alpha 1 causing potent vasoconstriction in the venous and arterial beds
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What is the dosage of Levophed?
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4 - 16 mcg / min
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How does Fenoldopam work?
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Fenoldopam is a short acting DA-1 agonist and works to stimulate the kidneys
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When used for hypertension, Fenoldopam dose can be?
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as high as 1 mcg/kg/min as a diuretic fenoldopam should be used at a dose of 0.05 mcg/kg/min
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You have a pt in the OR that is hypotensive and also has a low heart rate should you give ephedrine or neosynepherine?
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Ephedrine should be used to help increase patients heart rate
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Does Dobutamine increase or decrease cardiac output?
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increases cardiac output
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