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Pharm 2 > Test 2: Succinylcholine > Flashcards

Test 2: Succinylcholine Flashcards

1
Q

What type of molecule is Succinylcholine?

A

-Quaternary Ammonium Compound
-2 joined Acetylcholine molecules
-Hydrophilic (poorly lipid soluble)
-Does NOT cross BB Barrier or placenta
-Small volume of distribution
-Highly protein bound

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2
Q

What is the onset of action of Succinylcholine?

A

-30 to 90 seconds
-Intubating conditions within 1-1.5 minutes

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3
Q

What type of drug is Succinylcholine?

A

nAchR AGONIST
-high affinity for nAchR
-Depolarizing Muscle Relaxant

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4
Q

Is Succinylcholine competitive or non-competitive?

A

Non competitive: More ach won’t help. Has to be hydrolyzed.

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5
Q

T/F: The effects of Succ decrease before an adequately preoxygenated patient becomes hypoxic (Patient returns to spontaneous ventilation before hypoxia).

A

True

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6
Q

What is the MOA of Succinylcholine?

A

-Mimics Ach at the nAchR generating an AP
-Not metabolized by AchE. therefore producing a prolonged depolarization of the Motor End Plate
-The Motor End Plate cannot repolarize as long as Sux remains bound to the nAchR
-A depolarized postjunctional membrane cannot respond to a subsequent Ach stimulus
-Sodium channels are in the inactivated state = absolute refractory period
-Non-competitive block

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7
Q

What is the reversal for Succinylcholine?

A

Trick question; No specific agent exists to reverse a depolarizing block.

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8
Q

What is important to know regarding Succinylcholine and pediatrics?

A

-Typically C/I due to risk of MH due to possible undiagnosed MD
-Given in case of emergency (Laryngospasm)
-Children have increased water, so typically need a greater dose.

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9
Q

How do you calculate the dose of Succ for obese patients?

A

Use Total Body Weight (1 mg/kg)
-morbidly obese patients have increased fluid compartments and pseudocholinesterase levels and require higher doses to ensure adequate paralysis.

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10
Q

How is Succinylcholine metabolized?

A

-Rapidly metabolized by Pseudo-AchE

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11
Q

Does Succinylcholine have metabolites?

A

Yes; Succinylmonocholine (active metabolite)

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12
Q

What is the duration of action of Succ?

A

<10 minutes
-Full recovery in 12-15 minutes

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13
Q

What is the ED95 for Succ?

A

0.3 - 0.5 mg/kg

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14
Q

What is the Adult IV dose of Succ?

A

0.5 mg/kg - 1.5 mg/kg

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15
Q

What is the Peds dose of Succ?

A

-IV: 2.0 mg/kg - 2.5 mg/kg
-IM: 4 mg/kg - 5 mg/kg

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16
Q

What are the CNS effects of Succinylcholine?

A

-Fasciculations (not typically in children < 10 or the elderly)
-Myalgias
-Increased IOP
-Increased ICP

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17
Q

What are the Respiratory effects of Succinylcholine?

A

-Apnea
-Vocal cord paralysis
-Relaxation of airway musculature

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18
Q

What are the CV effects of Succinylcholine?

A

-Increase OR decrease in HR (profound bradycardia in children)
-Adults brady with 2nd dose
-Dysrhythmias
-Hyperkalemia

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19
Q

What are the misc effects of Succinylcholine?

A

-Increased intragastric pressure
-Increased LES tone
-Masseter Muscle rigidity

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20
Q

What is the ONLY muscle relaxant with an ultra rapid onset and ultra short duration of action?

A

Succinylcholine

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21
Q

How is neuromuscular blockade due to succ terminated?

A

By its diffusion away from the NMJ.

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22
Q

What is the effect of hypothermia on Succinylcholine?

A

Decreases its hydrolysis by P-AchE.
-Slows metabolism down

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23
Q

What conditions cause a decreased P-AchE level?

A

-Pregnancy
-Severe Liver disease
-Acute infections
-PE’s
-Muscular dystrophy
-Active MI
-Renal failure/Uremia
-Elderly males
-Malnutrition
-Burns
-Plasmapheresis
-Drugs (separate flash card).

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24
Q

What drugs decrease the amount of P-AchE?

A

-Echothiophate (Organophosphate)
-Neostigmine (Cholinesterase Inhibitors)
-Pyridostigmine
-Phenelzine (MAOI)
-Cyclophosphamide (Antineoplastic)
-Metoclopramide
-Esmolol
-Pancuronium
-Oral contraceptives

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25
Q

How does pregnancy affect Succinylcholine metabolism?

A

-40% decrease in P-AchE at term. Diluted in pregnancy due to increase in plasma volume without increased production of P-AchE. Perceived lower amount.
-May not clinically impact secondary to the increase in the pt’s volume of distribution

26
Q

What is the effect on succinylcholine if P-AchE levels are increased?

A

Decreased duration of blockade. Succ is hydrolyzed faster

27
Q

What conditions cause an INCREASE in the levels of P-AchE?

A

-Nephrotic syndrome
-Thyrotoxicosis
-Hemochromatosis
-Obese patients with diabetes
-Anxiety disorders

28
Q

What are the clinical effects of Atypical Pseudocholinesterase?

A

Don’t metabolize Succ normally. Prolonged block.

29
Q

What is heterozygous Atypical Pseudocholinesterase?

A

-one normal and one abnormal pseudocholinesterase gene
-Prolonged block of 20-30 minutes

30
Q

What is homozygous Atypical Pseudocholinesterase?

A

-two abnormal pseudocholinesterase genes
-Produce P-AchE that has little or no affinity for Sux
-Prolonged block of 3-8 hrs
-Pts require extended mechanical ventilation (and will also need some sedation)

31
Q

What does the Dibucaine # test tell you?

A

-Qualitative test
-A blood test that determines the presence of Normal P-AchE, NOT normal levels (u/L) of circulating P-AchE.

32
Q

What is Dibucaine?

A

A local anesthetic that inhibits NORMAL P-AchE
-Normal P-AchE = 80% inhibition by Dibucaine

33
Q

What are the results of the Dibucaine test with Heterozygous Atypical Pseudocholinesterase?

A

40-60% inhibition

34
Q

What are the results of the Dibucaine test with Homozygous Atypical Pseudocholinesterase?

A

20% inhibition

35
Q

What are the adverse effects associated with Succinylcholine?

A

-Dysrhythmias/ Bradycardia (linked to K+ flow)
-Fasciculations
-Hyperkalemia (avoid in hyperkalemic patients)
-Muscle Pain/Myalgia
-⬆ Intragastric Pressure & ⬆ Lower Esophageal Sphincter Tone
-⬆ Intraocular Pressure (concern with open globe injuries due to extrusion of intraocular contents)
-⬆ Intracranial Pressure
-Masseter Muscle Rigidity (Also called Trismus)
-Histamine Release
-Malignant Hyperthermia

36
Q

Which adverse effects of Succ can be diminished with a pre-treatment dose of a NDMR?

A

-Fasciculations
-Muscle pain/myalgia
-⬆ Intragastric Pressure & ⬆ Lower Esophageal Sphincter Tone
-⬆ Intracranial Pressure

37
Q

What do you need to know regarding Masseter Muscle rigidity and succ?

A

Could be a SE of the Succ, or could be an early sign of MH.
-Has to go away after 90 sec or risk of MH. If it releases within 90 sec or relaxes with anesthetic, it’s probably just a SE of succinylcholine administration.

38
Q

What are the CV effects of Succ at low vs high doses?

A

-Low Doses = low HR/BP
-High Doses = higher HR/BP & catecholamines

nAchR of the SNS and the PNS (esp Muscarinic receptors) in the SA Node can increase or decrease HR and BP.

39
Q

What are the CV effects of Succ in children and how do you prevent it?

A

-Profound bradycardia
-Pretreat with IV Atropine 0.02 mg/kg

40
Q

When do adults typically experience bradycardia with succ?

A

Typically do not brady unless a second dose of succ is given.
-Prevent with Atropine or pre-treat with small dose of Roc

41
Q

How does Succ cause Dysrhythmias?

A

-Associated with Succ Drips
-Succ goes to other Nicotinic receptors, like at the Autonomic ganglia.
-Blocks PNS, allowing for SNS override
-Can cause various dysrhythmias: Sinus Arrest, PVCs, AV nodal blockade with junctional rhythm, peaked T-waves associated with inc K+ (treat with CaCl).

42
Q

What are Fasciculations?

A

-Visible muscle contractions
-Disorganized muscle activity resulting from the depolarization of the nerve terminal
-Produced by the presynaptic receptors
-Typically not observed in young children < 10 or elderly
-Potential to cause pathologic fractures in patients with osteoporosis
-May worsen a pre-existing fracture
-Can lead to serious myalgias

43
Q

How can you prevent fasciculations with Succ?

A

Use a pre-treatment dose of NDMR given 3-5 minutes before Succ.
-Usually results in an increase dose of Sux (1.5 - 2.0mg/kg) for depolarizing block
-Ex. Rocuronium 0.06-0.1 mg/kg

44
Q

What is a “Self-Taming” Dose of Succ?

A

-The administration of small doses of Sux 1 min prior to the intubating dose to prevent fasciculations
-Ineffective and abandoned

45
Q

How much does Succ depolarization increase K+ levels?

A

0.5 - 1.0 mEq/L
-Within 3 min of admin lasting less than 10-15 minutes

46
Q

Why are patients who have upregulation of receptors at risk for hyperkalemia?

A

-Still have ion flow at these extrajunctional receptors even though they don’t affect paralysis of skeletal muscle.

47
Q

What conditions cause susceptibility to Succ induced Hyperkalemia? (Blue Box!)

A

-Burns
-Massive trauma/peripheral denervation
-Spinal Cord injury/transection
-Stroke
-Guillain-Barre Syndrome
-Prolonged total body immobility
-Closed head injury
-Myopathies
-Severe intra-abdominal infection
-Encephalitis
-Polyneuropathy
-Hemorrhagic shock with metabolic acidosis
-Tetanus
-Ruptured cerebral aneurysm

48
Q

Why is hyperkalemia r/t succ NOT altered by pre-treatment with a NDMR?

A

-Even with some ionic receptors being blocked by NDMR, the ones that are open can still lead to increased K+

49
Q

What is important to know regarding succ-induced hyperkalemia and renal patients?

A

-Not threatening in normokalemic renal patients
-Dialysis patients are relatively used to a high level of K+
-But, we have other choices, so don’t use it unless risk/benefit outweighs other options (ex: need for true RSI)
-Cisatracurium is better choice for renal dz patient.

50
Q

Myalgias/Muscle pain due to Succ administration is most common in what populations?

A

-Females and inactive patients
-Increased severity in young ambulating patients

51
Q

Where are myalgias/muscle pain due to succ located?

A

Subcostal region, trunk, neck, upper abs, shoulders

52
Q

What is important to know regarding succ administration and myalgias/muscle pain?

A

-May be prevented/decreased by NDMR pre-treatment & NSAIDs
-Onset 24-48 hours after admin but may last 2-7 days
-Decreased fasiculations = decreased myalgias
-Theory: the initial unsynchronized contractions increase myoglobin levels and creatinine kinase
-Indicates muscle damage/muscle injury
-Myoglobinemia is a rare complication after extensive fasciculation or in Malignant Hyperthermia (MH)

53
Q

What is important to know regarding the ⬆Intragrastic Pressure and ⬆LES Tone associated with Succ administration?

A

-Secondary to the abdominal wall muscle fasiculations
-⬆ Intragastric pressure increases the risk of aspiration
-Lower esophageal sphincter may open spontaneously at pressures of >28 cmH2O
-Risk of aspiration simultaneously ⬇ by the ⬆ in lower esophageal sphincter (LES) tone
-Both effects diminished/reduced by pre-treatment with NDMR

54
Q

How does succ administration affect Intraocular pressure (IOP)?

A

-Increases it by 5-15 mmHg for 10 min (less than the inc in IOP r/t coughing/bucking)
-Theory: Dilation of the choroidal vessels & the contraction of the extraoccular muscles
-Could compromise the already injured eye
-Theory: Extrusion of intraocular contents of an open eye injury
-NOT reduced by pre-treatment with NDMR

55
Q

What is the effect of Succ administration of increased Intracranial Pressure (ICP)?

A

-Increases ICP r/t increased cerebral activity and cerebral blood flow (CBF)
-Exact cause unknown, inconsistent observation
-Decreased or prevented with hyperventilation and/or pre-treatment with a NDMR and/or Lidocaine
-Have to counteract elevations in ICP with an at-risk patient

56
Q

What other things can cause increases in IOP & ICP? (Blue Box!)

A

Increases in IOP & ICP are also seen with inadequate anesthesia, inadequate relaxation, and the stimulation from intubation.

57
Q

What is important to know regarding Succ administration and Masseter Muscle rigidity?

A

-Transient increase in tone
-Potential for difficulty in opening the jaw for direct laryngoscopy (DL)
-Seen more often in children
-Marked increase in tone preventing DL
-May be a sign of MH
-If not MH, can do blind/fiberoptic nasal intubation, deepen anesthetic, or bag them for 10 minutes until it wears off (may need surgical airway if can’t ventilate)

58
Q

Does Succ cause Histamine release?

A

Yes, slightly.
-But causes anaphylaxis more than any other anesthetic drug (Barash).

59
Q

What is the relationship between Succ administration and Malignant Hyperthermia?

A

-Genetic predisposition
-Mechanism by which Sux triggers MH is unknown.

60
Q

What are Contraindications for the use of Succ?

A

-Malignant Hyperthermia
-Hyperkalemia
-Burn pts with burns over 35% TBSA 3rd degree burn
-Severe muscle trauma
-Severe sepsis
-Muscle wasting, prolonged immobilization,
-Extensive muscle denervation (Spinal cord injury)
-Duchenne Muscular Dystrophy
-Atypical P-AchE
-Allergy
-Children and adolescent patients

61
Q

Why is Succ avoided in children and adolescent patients?

A

-Especially those under 8 y.o.

Due to the risk of:
-Hyperkalemia
-Rhabdomyolysis
-Cardiac arrest in children with undiagnosed cardio-myopathies or dystrophies

Only used for emergency laryngospasm issues

62
Q

When and how does Succinylcholine cause bradycardia?

A

-Repeat dosing in adults
-Any dose in children
Due to:
-ANS ganglia and PNS muscarinic receptor stimulation
-Metabolite stimulates cholinergic receptors in the SA Node

Pharm 2 (40 decks)

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