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Diploma in Anaesthesia > Suxamethonium apnoea > Flashcards

Suxamethonium apnoea Flashcards

1
Q

In what % of the population does sux have a prolonged duration of action

A

4%

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2
Q

Describe the structure of suxamethonium

A

Quaternary amine ester consisting of two molecules of acetylcholine joined at their non-quaternary ends.

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3
Q

Name the enzyme that metabolizes succinylcholine

A

Plasma cholinesterase

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4
Q

How much sux is excreted unchanged in urine

A

10%

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5
Q

What is the normal half life of sux

A

2- 4 minutes

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6
Q

Where is plasma cholinesterase synthesized

A

In the liver

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7
Q

Describe the structure of plasma cholinesterase

A

Four identical subunits with four catalytic sites

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8
Q

What causes sux apnoea

A

Alterations in level or efficacy of plasma cholinesterase

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9
Q

What can influence the activity of plasma cholinesterase?

A 
Inherited factors (genetic polymorphism)
Acquired factors - decreased availability or inhibition
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10
Q

What causes decreased availability of plasma cholinesterase?

A

DECREASED HEPATIC PRODUCTION
Severe hepatic dysfunction (Cirrhosis)
Hypothyroidism: reduces enzyme production

INCREASED DESTRUCTION
Extracorporeal circulation --> increased breakdown
- haemofiltration
- Plasmaphoresis
- Cardiac bypass

PREGNANCY
- Dilution
- Oestrogen impairs enzyme synthesis
(reduced by 20% but usually clinically insignificant)

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11
Q

What inhibits plasma cholinesterase and hence prolongs the effects of sux

A

Drugs that are either substrates or inhibitors of plasma cholinesterase will prolong the effects of sux:

  • Edrophonium (Achase inhibitor)
  • Neostigmine (Achase inhibitor)
  • Organophosphorus compounds (insecticides) (Achase inhibitor)
  • Local anaesthetic esters
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12
Q

Give four clinical examples of when the effects of sux may be prolonged and explain why

A

Pregnancy (Diluted and increase estrogen reduces synthesis of plasma cholinesterase)

Cocaine use (Cocaine is an ester local anaesthetic broken down by plasma cholinesterase - it is a substrate and therefore reduces efficacy of plasma cholinesterase from breaking down sux)

Renal dialysis (Plasma cholinesterase is destroyed by any extracorporeal circulatory procedure)

Malnutrition (Reduced production of plasma cholinesterase)

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13
Q

Describe the recognised gene mutations that affect the action of plasma cholinesterase. How do the different combinations affect the performance of plasma cholinesterase and hence the duration of action of SUX

A

Usual (u)
Atypical (a)
Fluoride (f)
Silent (s)

Normal - EuEu
3-5 min

Heterozygous - EuEa, EuEf, EuEs
5-30 min

Homozygous - EaEa, EsEs, EfEf
2-8 h

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14
Q

How is atypical cholinesterase activity tested for in vitro?

A

The Dibucaine number

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15
Q

What is the Dibucaine number?

A

Plasma cholinesterase is combined with substrate benzylcholine to produce a light emitting reaction.

Dibucaine is added. Dibucaine inhibits this reaction normally reducing light production. With an abnormal enzyme –> light production will not be significantly reduced

Dibucaine number 80 (EuEu) - normal - duration of sux 3 - 5 mins

Dibucaine number 20 (EaEa) - very abnormal duration sux 2 - 8 hours

Fluoride is used to detect the abnormal fluoride gene –> Fluoride number

No inhibition occurs with either dibucaine or fluoride if the patient is homozygous for the ‘silent’ gene .

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16
Q

How is SUX apnoea recognized

A

Suspicion: if patient does not require non-depolarizing muscle relaxant

Awareness

  • Sweating, lacrimation, dilated pupils
  • Minimal / irregular / jerking respiratory effort

SNS

  • HPT
  • Tachycardia
  • Intermittent desaturation
17
Q

How can the diagnosis of sux apnoea be confirmed?

A

Peripheral nerve stimulator
- Train of four twitch response: No response or equal reduction in strength for all four twitches
( Four normally strong twitches would indicate the patient has fully recovered from the neuromuscular block.)

18
Q

What is the differential diagnosis for postoperative apnoea

A

PHARMACOLOGICAL
Residual anaesthetic agent
Excess opioid effect
Inadequately reversed non-depolarizing neuromuscular block

PHYSIOLOGICAL
Hypo or hypercapnoea
Severe electrolyte abnormality
Severe metabolic acidosis
Intracranial pathology
Severe hypothermia
19
Q

Describe the management of suxamethonium apnoea

A
  1. IPPV –> Oxygenation and ventilation (normocapnoea)
  2. Sedation –> prevent awareness - use volatile or intravenous anaesthetic agents
  3. Maintenance fluids, temperature

Continue until the nerve stimulator demonstrates return of normal muscle strength or the patient make adequate respiratory effort.

Council patient and family
Take clotted blood for plasma cholinesterase activity, dibucaine and fluoride numbers
Communicate: GP, referral letter, test relatives and provide Medic alert

20
Q

Discuss treatment of patients with SUX apnoea with FFPs

A

The principle is that FFPs should contain plasma cholinesterase and might speed up the recovery in SUX apnoea.

However, the amount of plasma cholinesterase in each FFP is significantly variable and the effect unpredictable –> also there are potential infection and immunological risks when transfusing blood products

21
Q

What is the difference between a patient recovering from a depolarizing neuromuscular block versus a non-depolarizing neuromuscular block using the peripheral nerve stimulator

A

Depolarizing block - No fade. Equal amplitude twitches –> all twitches lower amplitude than normal

Non-depolarizing block - Fade is demonstrated.

22
Q

What are the side effects of succinylcholine

A

Related to the agonist effects on nicotinic and muscarinic AChRs

  1. Myalgia
  2. Cardiac dysrhythmias
  3. Hyperkalaemia (burns/rhabdo/denervation/UMND)
  4. Transient increase IOP
  5. Increased intragastric pressure with increased LES tone
  6. Increased intracranial pressure
  7. Hx malignant hyperthermia is absoulte CI
23
Q

How does succinylcholine cause cardiac dysrhythmias

A

GANGLIONIC stimulation
- Tachycardia and increased BP may be caused by ganglionic stimulation with an overall increase SNS to the heart

CARDIAC MUSCARINIC stimulation

  • Stimulation of cardiac M receptors may lead to sinus bradycardia, junctional rhythm or even asystole
  • Particularly in children (PreRx with atropine) or adults with repeated sux exposure within 5 minutes.
24
Q

How does succinylcholine cause hyperkalaemia, how significant is this rise in potassium and when is this clinically significant

A

Mechanism of hyperkalaemia
- SCh exaggerates transmembrane ion flux leading to a rise in serum K+ of 0.5 to 1.0 mEq/L

However, life threatening rise in serum potassium can occur in the following conditions due to either/or proliferation of extrajunctional AChRs and/or damaged muscle membranes and a massive potassium release upon stimulation

  1. Major burns (avoid SUX for 2 years)
  2. Massive tissue injury
  3. Extensive denervation of skeletal muscle
  4. UMN disease

Patients with mild elevations in K+ related to renal failure may safely receive sux

25
Q

How can side effects to sux be reduced

A

PreRx with NDNMB – Cisatracurium 1mg IV or Rocuronium 3mg IV 2 to 4 minutes before SCh –> may blunt visible fasciculations but is not uniformly effective at attenuating all other side effects

Awake patients receiving NDNMB –> diplopia/weakness/dyspnoea.

If pretreating in RSI –> give increased dose of SUX 1.5mg/kg

26
Q

What are the two different phases of neuromuscular blockade caused by succinylcholine

A

PHASE 1 BLOCKADE - Because SCh is not degraded by AChE as rapidly as ACh, it persistently depolarizes the motor endplate, leading to inactivation of the voltage-gated sodium channels in the perijunctional zone that are necessary for propagation of the depolarization.

  1. Transient muscle fasciculations followed by relaxation
  2. Absence of ‘fade’ to tetanic or TOF stimulation
  3. Presence of post-tetanic potentiation (PTP)
  4. AChE inhibitors potentiate rather than reverse the block.

PHASE 2 BLOCKADE is most likely to occur after repeated or continuous administration of SCh when the total dose exceeds 3 to 5 mg/kg. Phase II blockade is thought to be secondary to repeated channel opening, causing distortion of the normal electrolyte balance and desensitizing the junctional membrane to further depolarization. It has some of the characteristics of a nondepolarizing blockade:

  1. Fade after tetanic of TOF stimulation
  2. Presence of PTP
  3. Tachyphylaxis (increasing dose requirement)
  4. Prolonged recovery
  5. Partial or complete reversal by AChE inhibitors

Diploma in Anaesthesia (73 decks)

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