NMBDs: Physiology/Succinylcholine (Exam III, Andy's Cards) Flashcards by Andrew Everett

Which of the following is the newest NMBD?
A. Atracurium
B. Vecuronium
C. Pancuronium
D. Cisatracurium

A. Atracurium (1980)
B. Vecuronium (1980)
C. Pancuronium (1960)
D. Cisatracurium (1995)

SPACR

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Why was Rapacurium (Raplon) discontinued in 2001?

Massive bronchospasm leading to death.

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The effect of NMBD is to interrupt the transmission of _____ _____ at the _____.

Nerve impulses

Neuromuscular Junction (NMJ)

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The MOA of NMBD is either depolarizing or non-depolarizing.

Depolarizing NMBD will _________ the action of ACh.
Non-depolarizing NMBD will ______ the action of ACh.

Depolarizing NMBD will mimic the action of ACh.

Non-depolarizing NMBD will interfere with the action of ACh.

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Purpose of NMBD for anesthesia.

Decrease airway trauma
Facilitate surgical exposure
Minimize injury from patient movement

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What classification of NMBD is Succinylcholine (Anectine)?

Depolarizing NMBD

Only depolarizing agent used in anesthesia.

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Name a long-acting non-depolarizing NMBD.

Pancuronium (Pavulon)

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Name a short-acting non-depolarizing NMBD.

Mivacurium (Mivacron)

Move a lot, short-acting

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What is the chemical classification of Pancuronium (pavulon)?

Aminosteroid

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What is the chemical classification of Mivacurium (mivacron)?

Benzylisoquinoline

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What is the chemical classification of Pancuronium (Pavulon)?

Aminosteroid

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Which intermediate-acting NMBDs are Benzylisoquinolines?

Atracurium (Tracrium)
Cisatracurium (Nimbex)

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Which intermediate-acting NMBD are Aminosteroids?

Vecuronium (Norcuron)
Rocuronium (Zemuron)

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What is ED₉₅ in regards to NMBDs?

The potency of NMBD. The dose that is necessary to produce a 95% suppression of a single twitch in the presence of nitrous/ barbiturate/ opioid anesthesia.

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What nerve is stimulated so that the adductor pollicis muscle will produce a single twitch at 1 Hz (thumb adduction)?

Ulnar nerve

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The order of block for NMBD is dependent on:

Number of presynaptic ACh-containing vesicles released.
Number of ACh receptors.
Blood Flow to the area.
Drug potency

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Small, rapidly moving muscles will be blocked ________ than large muscles.

Faster

Eyes will be paralyzed first before diaphragm.

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What does this graph show?

Both muscles experience a dramatic decrease in twitch percent height, but the adductor pollicis is more intensely blocked while the larynx got down to a twitch height of ≈20%.

The larynx recovers quicker.

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Checking a twitch in which muscle will assess the diaphragm and laryngeal muscle blockade.

Orbicularis Oculi

If there are no twitches to the facial nerve, the diaphragm and laryngeal muscles are assumed adequately blocked. Best indicator of intubating conditions.

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The orbicularis oculi underestimates _____________.

residual paralysis.

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Is checking a twitch in the adductor pollicis a good indicator for laryngeal relaxation?

No, it is not a good indicator of laryngeal relaxation.

Checking a twitch of the adductor pollicis is a good indicator or peripheral recovery.

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Which muscle is the gold standard to check a twitch on for recovery?

Adductor pollicis (Ulnar Nerve)

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What is the placement of electrodes on ulnar nerve?

What will the response be?

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What is a defasciculating dose of NMBD?

What symptoms will the patient experience with a defasciculating dose? (6)

Where small ND-NMB dose is given early to prevent fasciculation with SCh.

Blurred Vision
Mandibular weakness
Ptosis (droopy eyes)
Diplopia (double vision)
Dysphagia
Increased hearing acuity - people need to be quiet

Let patient know they might start to feel week and get blurry vision. Encourage them to close their eyes.

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A single twitch nerve stimulator starts at _____ Hz/second decreasing to ______ Hz/10 secs.

1 Hz/sec to 0.1 Hz/10 secs

With an onset of a block, a single twitch will ______.

fade with each stimulus

Double burst stimulator is _____ short bursts followed by ______ short bursts. The double burst stimulator setting uses ________ Hz

2-3, 2-3 50 Hz (supramaximal current)

Why was the double burst stimulator developed?

Developed to improve detection of residual block (fade). Fade in 2nd response vs 1st response. Qualitatively better than TOF.

Train of Four is ________ stimuli at _______ Hz with ______ seconds between each burst.

4 stimuli at 2 Hz with ½ seconds between each burst (4 stimuli over 2 seconds)

TOF reflects events at _________ membrane.

Presynaptic

Prior to NMBD what will be your twitches on the TOF? What will be the TOFR (Twitch 4 : Twitch 1)?

4/4 twitches Ratio 1

Experienced anesthetist are unable to qualitatively detect the fade of a TOFR < ______.

0.4

There will be significant residual block with a TOFR of ______ to _____.

0.7 to 0.9 *You will not feel a fade, but there will still be blockade at the NMJ. Patient will still need reversal agent.*

Tetanic stimulation is very rapid, it will be ________ Hz for _____ seconds.

50 Hz for 5 seconds

If a _____ NMBD is given, a tetanic stimulation will result in a sustained muscle response.

Depolarizing NMBD (Succinylcholine)

If a _____ NMBD is given, a tetanic stimulation will result in a non-sustained muscle response (fade).

Nondepolarizing NMBD (Roc/Vec) *The fade is a result of presynaptic depletion of ACh or inhibition of release*

What is post-tetanic stimulation?

Single twitch 3 seconds after tetanic stimulation. The post-tetanic stimulation will occur **d/t accumulation of calcium during tetany, the excess calcium will stimulate ACh release** ⇒ larger amplitude

No response in post-tetanic stimulation will mean ______.

intense blockade

What kind of blocks are in column A, B, and C? What kind of nerve stimulation is performed in row 1 through 4?

A study performed showed that _____ % of patients that were not given anticholinesterase drugs for NMBD reversal and no use of nerve stimulator had post-op blockade once extubated.

42% (with bedside criteria alone)

A study performed showed that less than ____ % of patients that were given anticholinesterase drugs for NMBD reversal and use of nerve stimulator had post-op blockade once extubated.

<4% (decreased with use of nerve stimulators and reversal)

The presynaptic motor neuron is large and _________ which helps with transmission of nerve impulses.

myelinated

The motor nerve ending is ________ and innervates single muscle fibers.

unmyelinated

The presynaptic motor neuron is responsible for what three things involving ACh?

- ACh synthesis - ACh uptake and storage in vesicles - ACh release and reuptake of choline

The synaptic cleft is _______ nm wide with fluid that contains ________ and _________.

20-50 nm Collagen and acetylcholinesterase

ACh release is dependent on what electrolyte?

Calcium

What does Acetylcholinesterase do to ACh?

Hydrolyze ACh to acetic acid and choline

Post-synaptically, the membrane has multiple _______. Post-synaptically, the resting membrane potential is _______. Membrane potential is largely maintained by what two electrolytes?

folds (invaginations) -90 mV Na+ and K+

How many subunits are on a transmembrane nicotinic acetylcholine receptor (nAChR)? Name them.

Five subunits. (Pentameric unit) 2⍺, β, 𝛿, 𝛾

If an ND-NMBD binds to nACh, there will be no ______ ______ and no ion flow.

conformational change

Succinylcholine only requires binding at one ________ subunit. It is postulated that this will cause ________ before total blockade.

one alpha subunit fasciculation

_________ is the only depolarizing NMBD in clinical practice. What are two unique characteristics of this drug? What is this NMBD most useful for? What is a large downside of this NMBD?

- Succinylcholine - Provides very intense and rapid paralysis - Offsets of effects prior to hypoxia - Rapid Sequence Induction - Histamine Release (tachycardia, rash, welps)

What is the dose of Succinylcholine? Onset: Duration:

Dose: 1 mg/kg IV Onset: 30-60 seconds Duration: 3-5 minutes

What is the MOA of succinylcholine (SCh)?

- Attaches to one or both alpha subunits of the nAChR. - Mimics the effect of ACh, but has a sustained opening of the receptor channel (hydrolysis is slower than ACh).

SCh will cause how much increase in serum K+?

0.5 mEq/L

What are characteristics of a phase I block?

Decrease contraction to single twitch stimulation. Decrease amplitude to continuous stimulation. TOF ratio > 0.7 (no fade) Absence of post-tetanic facilitation Skeletal muscle fasciculation

Phase II Blocks are typical of ___________ NMBD.

non-depolarizing

How can a Phase I block transition to a Phase II block?

Essentially an overdose - Large dose of SCh (2-4 mg/kg) - Lack of/ poorly functioning pseudocholinesterase

Succinylcholine is hydrolyzed by __________.

Butyrylcholinesterase (plasma cholinesterase)

What factors can decrease pseudocholinesterase activity? (5)

- Hepatic disease - Drugs (neostigmine, reglan, chemo) - Genetics - CKD - Estrogen (think pregnancy)

What factor can increase pseudocholinesterase activity? What does this mean clinically?

- Obesity Higher dosing of succinylcholine is necessary for obese patients.

What does dibucaine number mean? What does it mean in extremely simple terms?

Dibucaine number reflects the quality of the enzyme that inhibits the breakdown of butyrylcholinesterase. - ↑ Dibucaine number = Fast succinylcholine metabolism - ↓ Dibucaine number = Slow succinylcholine metabolism

What is normal dibucaine number?

80 *More butyrylcholinesterase will stick around and break down Sch*

What will a dibucaine number of 20 mean for SCh?

1 mg/kg of SCh will last 3 hours *Less butyrylcholinesterase will stick around ⇒ less hydrolysis of Sch*

What are the side effects of Succinylcholine? (8)

- Cardiac dysrhythmias - Hyperkalemia - Myalgia - Myoglobinuria - ↑ Gastric pressure - ↑ IOP - ↑ ICP - Masseter spasm

What is the pre-treatment to the side effects of SCh?

- Pre-treatment with non-depolarizing NMBD (5mg of Roc). *This defasciculating dose either decreases, prevents, or mask the side effects of SCh.*

What dysrhythmias can occur with succinylcholine administration?

- ↓HR - Junctional Rhythm - Sinus Arrest

Cardiac dysrhythmia's will usually present on the 1st dose of succinylcholine. T/F?

False. dysrhythmias most likely with the 2ⁿᵈ dose.

What are succinylcholine's actions at the ANS ganglia?

- ↑HR and BP - mimic ACh *This usually occurs with large doses.*

Patient's with _________ sites will have more hyperkalemia when given SCh.

Extrajunctional NMJ sites (more ion channels)

What patient populations are more susceptible to the hyperkalemic effects of succinylcholine? (4)

- Individuals with unrecognized muscular dystrophy (Duchenne's) - Unhealed 3rd degree burns - Denervation of Skeletal Muscles (bed-ridden patients) - Upper motor lesions

Who will experience myalgia with Sch? Where will the myalgia likely be located?

Young adults Neck, back, abdomen

Pediatric patients more frequently experience this with succinylcholine administration.

**Myoglobinuria** (damage to skeletal muscles), usually found later to have MH or muscular dystrophy. No succinylcholine for children

Sch will increase intragastric pressure and LES pressure, this will increase risk of _______.

Aspiration (may be offset by ↑LES pressure) *This is related to the intensity of the fasciculation and the direct increase in vagal tone.*

SCh will maximally increase intraocular pressure _______ minutes (range) after administration and last _________ minutes (range).

2-4 minutes after admin last 5-10 minutes

Sch will be contraindicated in ______________ chamber injury.

open anterior

Succinylcholine will increase ICP transiently, how can this effect be attenuated?

**By hyperventilating the patient**, the PaCO2 will decrease ⇒ cerebral vasoconstriction ⇒ decrease CBF and decrease ICP before Succinylcholine administration.

Sustained skeletal muscle contraction, incomplete jaw relaxation, and/or masseter muscle spasm d/t SCh could be an indication of what conditions?

Early indicator of Malignant Hyperthermia Inadequate dosage given in children

What is the hereditary rhabdomyolysis associated with all volatile anesthetics and SCh?

Malignant Hyperthermia (MH)

What main effects can MH have? (6)

Muscle destruction Hyperkalemia Acidosis Dysrhythmia Renal Failure DIC

MH is caused by mutations in what receptor that causes excessive calcium release from the SR?

Ryanodine Receptor (RyR1)

What ethnicity/nationality are susceptible to MH?

Native Americans

What are the symptoms of MH?

* Acute ↑ in Sk-M metabolism * ↑O2 consumption * Lactate formation * Rhabdomyolysis (*Spiked increase ETCO₂, ↑temp 1ºC/5mins, arrhythmias, rigidity.*)

What are the emergency ABCDs of malignant hyperthermia?

Dantrolene has decreased the mortality of MH from ____ to ____%.

80% →10%

What is the dose of dantrolene?

2mg/kg IV Repeat doses until symptoms subside or 10mg/kg IV

How does dantrolene work? How is dantrolene metabolized?

- Inhibits the Ca2+ release from the SR (RyR blocker). - Dantrolene is metabolized in the liver to 5-hydroxydantrolene

Patients on calcium channel blockers (verapamil, Cardizem) that receive dantrolene as a treatment can result in __________

Cardiovascular Collapse (*d/t excess Ca Channel blockade*)

What are the most common side effects of dantrolene? (4) What are less common side effects? (3)

Most Common: Weakness Respiratory Failure Phlebitis GI upset Less Common: Confusion Dizziness Drowsiness

What autoimmune disease develops Antibodies against the ACh receptor? Symptoms (Sx)? Treatment (Tx)?

Myasthenia Gravis (MG) Sx: * Increasing weakness and fatigue throughout the day * Diplopia * Ptosis * Extremity and Resp muscle weakness Tx: Cholinesterase Inhibitor

What part of the day would a Myasthenia Gravis patient be scheduled for surgery?

Should be the first of the day. When they have the most ACh and their ACh receptors are not worn out.

Myasthenia Gravis patients are _________ to Succinylcholine. Why? What is the dose of SCh for MG patients?

**Resistant to SCh.** More SCh is needed because the ACh receptors that are left do not function as well. 1.5-2.0 mg/kg

What is Lambert-Eton (LE) disease? LEMS has an increased sensitivity to which type of NMBD?

Autoimmune disease: LEMS can produce antibodies against calcium channels (P-type) and decrease the release of ACh presynaptically. LEMS has a sensitivity to both depolarizing and nondepolarizing NMBD.

Why does Lambert-Eton disease often develop?

Often results from small-cell lung cancers.