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Anaesthesia > Pharmacology of Muscle Relaxant & Ancillary Drugs > Flashcards

Pharmacology of Muscle Relaxant & Ancillary Drugs Flashcards

1
Q

What are the main anticholinergics?

A

Atropine
Glycopyrrolate

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2
Q

Anticholinergics are used to

A

increase HR, & aim to increase BP

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3
Q

Anticholinergics produce competitive antagonism of

A

Acetylcholine at the post-ganlionic muscarinic receptrs of the parasympathetic system
Especially the vagus n. –> parasympathetic

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4
Q

What are the pharmacodynamics of anticholinergics

A
  • tachycardia
  • bronchodilation
  • decreased salivation
  • decreased bronchial secretions
  • mydriasis
  • GI stasis
  • decreased lower oesophageal sphincter tone
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5
Q

Atropine

Onset, Duration, Cautions, contraindications

A

Onset: 1-5 min
Duration: 20-40 mins
Cautions: atropinase in rabbits keeps from working, GI stasis so caution in horses, tachyarrhythomogenic, hypoxaemic, paradoxal transient bradycardia
Contraindications: pre-existing tachycardia, hyperthyroidism, phaeochromocytoma

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6
Q

Glycopyrrolate

Onset, duration, Cautions

A
  • Onset: about 5 mins
  • Duration: 1-2 hrs
  • Cautions: Do not use CPR, bradycardia & hypotensive
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7
Q

Mixed inotropes & vasopressor sympathomimetics

A

Dopamine, adrenaline, noradrenaline, ephedrine

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8
Q

Positive inotrope sympathomimetic

A

Dobutamine

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9
Q

Vasopressors

A

Phenylephrine
Vasopressin

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10
Q

alpha-1 receptors are on…

A

vascular smooth muscle

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11
Q

Vasopressors work on what receptors?

A

alpha-1

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12
Q

Beta-1 receptors are in the…

A

heart

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13
Q

inotropes act on…

A

beta-1 receptors in the heart

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14
Q

beta-2 receptors are in the

A

bronchi, vascular smooth muscle, uterus, heart

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15
Q

bronchodilators work on…

A

the beta-2 receptors

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16
Q

beta-3 receptors are present on

A

adipose tissue

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17
Q

Dopamine at low rates act on…

A

D1 receptors

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18
Q

Dopamine is a precursor to…

A

noradrenaline & adrenaline

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19
Q

Dopamine best given as a

A

CRI

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20
Q

Dopamine has what proprerties

A
  • dose-dependent effects
  • increases BP
  • low doses of D1 pulm receptors
  • beta/alpha receptors lead to vasoconstriction
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21
Q

What are the properties of Adrenaline/Epinephrine?

A
  • Endogenous
  • Stimulates both α & β receptors
  • Dose dependent (higher doses: α effect)
  • Bolus/CRI in Farm animals – to increase BP
  • Chronotrope (HR ↑), inotrope, & vasoconstrictor
  • Bronchodilation (β2 effect)
  • Reserved for life-threatening situations
  • Anaphylaxis
  • Severe hypotension (sepsis)
  • Risk of arrhythmias - Decreased threshold for V-fib depending on the dose
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22
Q

Noradrenaline/Norepinephrine

A
  • Endogenous
  • Agonist α1, α2, β1 agonist
  • Powerful vasoconstrictor
  • Use? Patients extremely vasodilated (septic, endotoxaemia) –> inability to vasoconstrict, used to gain normal tone of the vessels
  • BP monitoring – must use w/ arterial catheter & arterial BP monitoring
  • May cause tissue necrosis
  • Arrhythmogenic effect like adrenaline (monitor ECG & BP)
  • Reduces perfusion of kidney, liver
  • Concomitant use of dopamine to vasodilate on the dopernergic receptors (?)
23
Q

Ephedrine

A
  • not endogenous
  • stimulates release of endogenous noradrenaline (tachyphylaxis)
  • short-lived
  • tachycardia/bradycardia may occur
  • less profound effect than noradrenaline
  • decreases renal blood flow & GFR falls
  • vasoconstriction & positive inotropic effect
  • can be used as bolus, may be used as CRI
24
Q

Dobutamine

A
  • Acts on contractility
  • non-selecctive beta receptor agonist
  • predominantly B1 effects
  • synthetic analogue of dopamine
  • no change in vascular resistance, just changes contractility
  • short-acting (CRI req’d) - up to 5 mins
  • increases SV
  • Metabolised by COMT, urine excretion
  • common in horses
25
Q

Phenylephrine

A
  • A1 agonist
  • vasoconstriction
  • more potent than noradrenaline
  • reflex bradycardia
  • uses: hypotension, nasal oedema in horses, splenic contraction in horses
  • Special license req’d in IE for small animals so not really used
26
Q

Vasopressin (ADH)

A
  • not available in IE
  • stimulates release of catecholamines from adrenal medulla
  • increases contractility
  • used in CPR in humans & refractory hypotension
  • expensive
27
Q

Bronchodilators tend to work as

A

beta2 agonists

28
Q

Bronchodilators are primarily administered in

A

aerosol form due to faster onset of action

29
Q

Bronchodilators can cause

A

tachycardia at high doses due to B1 activation

30
Q

Bronchodilators are primarily used for…

A
  • asthmatic airways or things that require bronchodilation
  • hypoxaemic horses
31
Q

Salbutamol

A
  • relaxes bronchial smooth muscles
  • reverses hypoxic pulmonary vasoconstriction
  • causes tachycardia
  • relaxes gravid uterus
  • may cause tremor
  • decreases K+ at Na/K ATPase
32
Q

Terbutaline

A
  • injectable form used prior to bronchoscopy & BAL in small animal
  • inhaled form available
  • metabolism is the same as salbutamol
33
Q

Doxapram

A
  • CNS stimulant: drug-induced resp depression, direct stim of medullary resp centres, stims resp in neonates - controversial
  • fast onset –> emergency drug
  • increases minute-ventilation
  • not appropriate for assessment of laryngeal fxn
34
Q

Neuromuscular blocking agents include…

A

Succinylcholine/Suxamethonium

35
Q

Non-depolarizing agents

A

Aminosteroids: Vecuronium, Rocuronium, Pancuronium
Benzylisoquinolines: Atracurium, Cis-atracurium, Mivacurium

36
Q

Indications for NMB

A
  • ocular sx
  • deep abd/thx cavity sx
  • arrest ventilation
  • limb relaxation
  • when immobility is paramount
  • reduce reflexes
  • ease induction & intubation, avoid C, reduce laryngeal reflexes
  • ventilation in ICU
37
Q

Prior to NMB you must provide…

A
  • appropriate hypnosis
  • intubation & mechanical ventilation
  • means to monitor the effectiveness of the block
  • appropriate analgesia
38
Q

Succinylcholine

A
  • depolarizing agent (non-competitive)
  • agonist at the Ach receptor –> causes AP & muscle contraction prior to relaxation
  • Main use: faciltate intubation in cats (rare)
  • Duration of action: 3 min
  • recovery: 10-12 mins
39
Q

Side effects of Succinylcholine

A
  • Bradycardia (muscarinic stimulation in the sinoatrial node)
  • Increase in K+ concentration
  • If hyperkaliaemic, can be a concern
  • Increase IOP
  • Malignant hyperthermia (MH) – genetic condition, requires triggers
  • Increased intragastric pressure
  • Hypersensitivity (type I anaphylaxis)
  • Muscle pain?
40
Q

Succinylcholine contraindications

A
  • eye injuries
  • myopathies
  • GDV
  • Birds
  • burn patients
  • patients predisposed to MH
41
Q

What are non-depolarizing agents?

A
  • competitive mechanism w/ Ach, no AP
  • req’s at least 90% of receptors blocked
  • does not cross BBB
  • metabolised in liver or excreted unchangd in urine
42
Q

Atracurium undergoes what kind of elimination?

A

Hoffman elimination –> spontaneous degradation on pH & temp
req’s protection from light, keep in fridge

43
Q

Atracurium

A
  • Onset: 3-5 min
  • Duration: 40 mins
  • Possible histamine release (give slow, avoid in asthmatics)
  • Hoffman degradation & non-specific esterases (Laudanosine –> seizures)
  • suitable for renal/hepatic dz
  • store in fridge
44
Q

Cis-atracurium

A
  • isomer of atracurium, 4x more potent
  • Hoffman degradation
  • No direct CV effects: no histamine release, less laudanosine produced
45
Q

Mivacurium

A
  • Onset: 2 mins
  • Duration: 15 mins
  • Histamine release
  • Inactivated by plasma esterases –> long effects in dogs
  • can be reversed w/ neostigmine/edrophonium
  • offers no advantages over atracurium
46
Q

Vecuronium

A
  • Onset & duration similar to atracurium
  • No direct CVS efffects
  • Hepatic metabolism
  • renal & biliary excretion
  • Caution in liver/kidney patients
47
Q

Rocuronium

A
  • Fast onset, least potent
  • short/intermediate duration
  • high doses –> vagolytic
  • anaphylactoid rxns reported
48
Q

Reversal of NMB can be done by…

A
  • spontaneous recovery (depolarizing agents)
  • Achesterases can reverse non-depolarizing
49
Q

What is the use of anticholinesterases?

A
  • induce accumulation of Ach in post-ganglionic muscarinic receptors
  • leads to: Bradyarrhythmia/asystole, hypotension, bronchoconstriction, increases Resp tract mucus secretion, hyperperistalsis (defecation), urination
50
Q

Anticholinesterases should be given…

A
  • slow IV injection over several minutes
  • Should combine w/ atropine/glycopyrrolate
51
Q

Edrophonium

A
  • quarternary ammonium compound
  • anticholinesterase that binds to enzyme at anionic site
  • short-acting
  • fast onset –> combine w/ atropine
  • liver metabolism
  • less muscarinic effects than neostigmine in horses
    * used to Dx myasthenia gravis
52
Q

Neostigmine

A
  • quartenary ammonium compound
  • anticholinesterase that binds to enzyme
  • longer-acting than edrophonium
  • slower onset –> combine w/ glycopyrrolate
  • liver metabolism
53
Q

Sugammadex

A
  • initially for reversal of rocuronium
  • fast-acting
  • only for aminosteroids
  • ineffective against benzylisoquinoline NMBA’s
  • modified gamma-cyclodextrin
  • chelates NMBA molecule
  • no muscarinic effect

Anaesthesia (23 decks)

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