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PHAR2005 > Local Anaesthetics and Anti-Dysrhythmics > Flashcards

Local Anaesthetics and Anti-Dysrhythmics Flashcards

1
Q

What is the key action of LAs?

A

Reversible regional loss of sensation/pain - without loss of consciousness

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2
Q

What are the 3 components of the general structure of an LA?

A

Aromatic group
Intermediate chain - ester/amide bond
Tertiary/secondary amino group

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3
Q

Describe the pH of most LAs

A

Weak bases

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4
Q

What are LAs administered as?

A

Water-soluble hydrochlorides (B.HCl)

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5
Q

What happens to B.HCl upon entering the tissue fluid and what is the corresponding equation?

A

Alkaline pH of tissue fluid liberates tertiary amine base (B)
B.HCl + HCO3- B + H2CO3 + Cl-

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6
Q

Describe the hydrophilic pathway of LA action

A

B moves through nerve sheath, perineurium, and neuron membrane - into axoplasm
Becomes ionised - BH+
Moves into open Na+ channel - blocks
Use-dependent - faster and greater block with higher AP frequency - more frequent Na+ channel opening

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7
Q

Describe the hydrophobic pathway of LA action

A

B moves into neuron membrane
Moves through pore portal into Na+ channel
Ionised to BH+ - blocks

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8
Q

In which state does an Na+ channel have a higher affinity for an LA?

A

Inactivated

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9
Q

What determines LA potency?

A

Lipid solubility - ease of moving through neuronal membrane (positive correlation)

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10
Q

What determines block duration?

A

Capacity to bind to plasma and tissue proteins (positive correlation)

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11
Q

What is pKa?

A

pH where 50% of agent ionic - 50% non-ionic

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12
Q

Which fibre characteristics increase ease of block?

A

Small diameter

Myelination

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13
Q

Name an amino ester LA and describe its metabolism

A

Procaine

Rapidly hydrolysed in body - by plasma ChE

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14
Q

Name an amino amide LA and describe its metabolism

A

Lidocaine

Slowly metabolised - by hepatic amidases - in liver

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15
Q

What are the CNS side effects of LAs?

A

Low conc - tinnitus, blurred vision, drowsiness

High conc - Agitation, convulsions, CNS and respiratory depression

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16
Q

What are the cardiovascular side effects of LAs?

A

Vasodilation, myocardium depression, cardiac slowing (cardiac block) - hypotension

17
Q

Which LA can cause an allergic reaction and why?

A

Ester LAs - breakdown product is PABA - allergen

18
Q

Name and describe the methods of LA administration

A

Surface - topical application
Infiltration - inject into tissue to affect nerve endings
Nerve block - inject near nerve trunk to affect area innervated
Spinal - inject into subarachnoid space
Epidural - Inject into epidural space - diffuses across dura mater
Intravenous regional - intravenous injection distal to cuff on limb

19
Q

What are the phases of an electrocardiogram?

A

P - Atrial contraction
QRS - Ventricular contraction (and atrial relaxation)
T - Ventricular relaxation

20
Q

Describe the stages of a ventricular AP

A

Rest - large K+ permeability - leak K+ channels and some voltage-gated K+ channels open
Rising phase - voltage-gated Na+ channels open
Initial repolarisation - voltage-gated Na+ channels inactivate
Plateau - delayed voltage-gated K+ channels and voltage-gated Ca2+ channels open - cancel out
Repolarisation - voltage-gated Ca2+ channels inactivate - potential moves towards EK - some voltage-gated K+ channels close - voltage-gated Na+ channels close

21
Q

What is depolarisation in SA and AV nodes due to?

A

Ca2+ influx

22
Q

How does sympathetic stimulation of the SA and AV nodes affect pacemaker APs?

A

NA acts on B1-adrenoceptors - activates Na+ and Ca2+ currents - depolarisation - shorter time between APs

23
Q

How does parasympathetic stimulation of the SA and AV nodes affect pacemaker APs?

A

ACh acts on M2 receptors - increases K+ conductance - slows depolarisation - longer time between APs

24
Q

How does delayed hyperpolarisation cause a dysrhythmia?

A

Ca2+ increases above normal
Stimulates Na+/Ca2+ exchanger - 3Na+ in/Ca2+ out - net +2 charge entry - transient inward current
Depolarisation - ectopic (early) beat

25
Q

How does re-entry cause a dysrhythmia?

A

Damaged atrial muscle - unidirectional block
Activation wavefront of anterograde signal interacts with repolarisation of preceding wave
Re-excites tissue (if not refractory)
Circulates indefinitely

26
Q

How does abnormal pacemaker activity cause a dysrhythmia?

A

Damage makes ectopic foci - in atria/ventricles

Beats out of synchrony with normal rhythm

27
Q

How does heart block cause a dysrhythmia?

A

Failure of impulse generation in SA node/failure of propagation through AV node
Ventricular contraction maintained by abnormal pacemaker - slow

28
Q

What type of drugs are in class I of Vaughan-William’s classification, and what is their effect?

A

Na+ channel blockers
Slow depolarisation of SA node and slow conduction of propagating AP to extinguish before re-excitation in re-entry dysrhythmia
Class Ia also increase refractory period - cells not re-excited by re-entrant AP

29
Q

What type of drugs are in class II of Vaughan-William’s classification, and what is their effect?

A

B-adrenoceptor antagonists

Inhibit plateau phase

30
Q

What type of drugs are in class III of Vaughan-William’s classification, and what is their effect?

A

K+ channel blockers

Slow repolarisation

31
Q

What type of drugs are in class IV of Vaughan-William’s classification, and what is their effect?

A

Ca2+ channel blockers

Inhibit plateau phase and block conduction through AV node

32
Q

Name a class I anti-dysrhythmic drug

A

Quinine - quinidine isomer more effective

33
Q

Name a class II anti-dysrhythmic drug

A

Propranolol

34
Q

Name a class III anti-dysrhythmic drug

A

Amiodarone

35
Q

Name a class IV anti-dysrhythmic drug

A

Verapamil

36
Q

Name a cardiac glycoside and describe its action

A

Digoxin
Inhibit Na+/K+-ATPase - intracellular Na+ increases - inhibits Na+/Ca2+ exchanger - intracellular Ca2+ increases - increases contraction force
Lengthens refractory period of AV node - decreases contraction rate

37
Q

What is the action of adenosine?

A

Activates A1 receptors - opens linked K+ channels - AV node conduction block

38
Q

What is the QT interval, which drugs prolong it, and how?

A

Ventricular depolarisation
Class I and III antidysrhythmics, erythromycin, lithium, tricyclics, salbutamol
Occupy binding pocket in voltage-gated K+ channel - block - reduces IKr - prevents repolarisation - prolongs QT

PHAR2005 (24 decks)

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