Local Anaesthetics and Cardiac Dysrhythmias Flashcards

1
Q

Why are neurons that fire at a higher frequency more susceptible to Local Anaesthetics?

A
  • the neurons are depolarized more frequently so the inside of the cell is more positive. This drives the entry of uncharged LA
  • the inactivated Na channel has a higher affinity for LA’s than the resting channel
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2
Q

What are the main effects of Local Anaesthetics on the CNS?

A

Stimulatory effects. They result in hyperactivity and manic behaviour, convulsions followed by coma and respiratory depression

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3
Q

What are the main effects of Local Anaesthetics on the CVS?

A

Vasodilatory effects, depression on the myocardium and decrease of heart rate. These lead to hypotension (apart from cocaine)

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4
Q

State the 6 methods for the administration of Local Anaesthetics

A

1) Surface
2) Subarachnoid - between 2nd and 5th lumbar vertebrae
3) Epidural
4) Infiltration - directly into tissue to get nerve endings
5) Nerve Block - close to nerve trunk
6) Intravenous Regional

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5
Q

In terms of the movement and permeability of ions, what happens in the myocardium during Phases 0, 1, and 2 of the action potential?

A

Phase 0: fast inward Na+ current
Phase 1: inactivation of Na+ channels, entry of Cl- and efflux of K+
Phase 2: L-type Ca channels activate. Efflux of K+ and influx of Ca+ balances

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6
Q

In terms of the movement and permeability of ions, what happens in the myocardium during Phases 3 and 4 of the action potential?

A

Phase 3: L-type Ca channels deactivate while K+ efflux is sustained
Phase 4: K+ channels close and membrane returns to resting

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7
Q

What is the cause of Delayed After-depolarization?

A

Larger than usual Calcium influx

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8
Q

State the two ways in which damaged myocardium can be the cause of a dysrhythmia

A

1) Disordered Conduction Pattern (Re-entry) - damaged myocardiam can develop unidirectional block
2) Abnormal Pacemaker activity

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9
Q

What is the mechanism of action of Class I anti-dysrhythmia drugs

A

They block the voltage sensitive Na channels thus reduce the excitability and slow conduction velocity
= Lidocaine

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10
Q

What is the mechanism of action of Class II anti-dysrhythmia drugs

A

They are Beta Blockers. They block the excitatory effects of SNS stimulation by blocking Beta 1 receptors.
= Alprenolol

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11
Q

What is the mechanism of action of Class III anti-dysrhythmia drugs

A

They block K channels, prolong the length of the action potential and increase the refractory period
= Amiodarone

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12
Q

What is the mechanism of action of Class IV anti-dysrhythmia drugs

A

They block Ca channels, this results in slow AV conduction.

= Verapamil

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