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Pharmacology > Anti Arrythmics > Flashcards

Anti Arrythmics Flashcards

1
Q

Where are APs rhythmically generated in the heart?

A

The SA node acts as a primary pacemaker, as it discharges at 70-80bpm.

The AV node & His bundles make secondary discharges at 40-60bpm but overridden by SAS.

(Remember nodal cells have only phase 0, 3 & 4.

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2
Q

Describe the general conduction pathway for an AP in the heart?

A

SA node -> Aria -> AV node -> Bundles of His -> Ventricles

Normal cardiac action is conducted in an orderly sequence.

This pattern can become disrupted by:

Heart disease (IHD), hormones, drugs or anatomical anomaly. This disruption can cause an arrhythmia, which decreases cardiac efficiency and increases O2 consumption.

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3
Q

What are arrhythmias?

A

They are abnormal rhythms that can cause sudden death. They may originate from either the atria or AV node (supraventricular), or from the ventricles.

They have multiple causes.

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4
Q

What are the two major causes of arrhythmias?

A
  1. Defects in impulse generation (SA node) - may result in tachy or brady
  2. Defects in impulse conduction - may result in dropped beats or heart block
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5
Q

Describe how defects in impulse generation at the SA node can cause arrthymias?

A
  • There can be an enhanced/altered automaticity
    • There is automatic tissue beside the SA node which paces the heart (lke AV node, His bundles, purkinje fibres)
    • The latent pacemaker cells (atria and ventricles) produce ectopic beats
  • Mechanisms of triggered activity: normal AP triggers extra abnormal depolaristions
    • Extra after-depolarisations
      • Associated with abnormally prolonged AP, ion channel mechanisms may be unknown
    • Delayed after-depolarisations
      • Typically the result of cellular Ca2+ overaload
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6
Q

What causes early after-depolarisations?

A

There is a channelopathy with the K+ channels, where they fail to open properly to repolarise the cell - so another action potential can be induced to cause Torsades de Pointes

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7
Q

How do defects in impulse conduction cause aryythmias?

A

By the following:

  • Conduction block: in conduction block there is a lock of SA control of cardiac contraction because of impaired conduction through ischaemic or refractory tissue.
    • Manifested as bradycardia
  • Re - entry: This is a major cause of ventricular tachycardia and fibrillation
    • It requires unidirectional block of an impulse and re-excited tissue beyond the block
    • Manifested as tachyarrhythmias
  • Accessory tract pathways
    • ​These are manifested as tachyarrythmias
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8
Q

How does re-entry cause tachyarrhythmias?

A

It can go back up due to there being excitable tissue after going around the loop

But it can’t go down because theres an area of non-excitable tissue.

If by the time it reaches the top junction and 1 has recoverd (channels no longer inactivated) it will go back down this path. If it has it will keep going around in a loop. Whether it goes around in a loop depends on the refractory period and conduction velocity.

Some drugs will prolong the refractory period to stop this from happening and stop the re-entry from occurring - e..g antiarrthymics

Conduction velocity: if its really slow branch 1 may have recoverd and it can go around again, if it is fast it may not have and it terminates.

Refractory: depend on how long it takes to recovered - if long refractory period it will terminate, if short it will go back around

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9
Q

What causes Atrial fibrillation?

A
  • IHD, hypertension, HF, hyperthyroidism, excess alcohol intake, pneumonia, pericarditis - there are many causes, and most causes are symtpmatic
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10
Q

What types of AF are there?

And what are the risks of AF?

A
  • Paroxysmal (short term)
  • Persistent (responsive to treatment
  • Permanent Long standing

In AF blood cannot be pushed into the ventricles (since atria become hypokinetic), and stasis of blood occurs and thrombi form. This can form embolisms (if on right side can cause cerebral infarction, left side = embolism)

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11
Q

What are the two aims of drug treatment for AF?

A
  1. We need to treat the rate/ rhythm
  2. Prevention of Embolic Complications
  • ​See attendant antiplatelet (aspirin), anticoagulant (wafarin) lecture
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12
Q

What does the success rate depend upon with treating AA with drugs?

A
  • type of arrhythmia
  • Drug or drug combination used
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13
Q

What are the four antiarrhythmic drugs, and where do they act?

A

Metoproplol: Supraventricular & ventricular

Amiodarone: Supraventricular & ventricular

Diltiazem: Supraventricular

Digoxin: Supraventricular

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14
Q

What two AA drugs act supraventricular and ventricular levels?

A

Metoprolol and amiodarone

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15
Q

What AA drugs act at just the supraventricular level?

A

Diltiazem and digoxin

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16
Q

What is the Vaughan Williams (VW) Classifications systems based upon?

A
  • Based upon the electrophysiology of normal His-purkinje cells
  • Classified on drugs ability to block specific ion currents (i.e. Na+, K+, Ca2+) and B-adrenergic receptor action

But many AADs don’t fit this classification e.g. digoxin, adenosine (or atropine)

17
Q

What does class I mean in the VW classification?

A

Drugs that interfere with the Na+ channel. They reduce phase 0 slope and peak of action potential

18
Q

What does class II mean in the VW system?

A

Drugs that act as beta blocks.

These block sympathetic activity on SA node so reduce rate and conduction (also reduce force of contraction) e.g. metoprolol

19
Q

What do class III drugs do in the VW system?

A

They reduce K+ efflux.

They delay repolarisation (phase 3), so increase AP duration and refractory period.

E.g. Amiodarone, Sotalol

20
Q

What do class IV drugs do under the VW system?

A

They are Ca2+ blockers.

They are most effective at SA and AV nodes, and reduce the rate and conduction e.g. diltiazem.

21
Q

What are the 3 drugs that don’t come under the VW classification?

A

Digoxin, atropine, adenosin

22
Q

Describe class I AADs, and which drugs it includes and their MOAs, and effects

A

Class I drugs are Na+ channel atagonists. It is divided into 3 subclasses: Ia, Ib & Ic

Class I includes: Lignocaine, Flecainide

MOA: Their mechanism is to block the fast Na+ channels in a use-dependant way. e.g. Lignocaine binds to Na+ channels most strongly in the open (fast upstroke) and inactivated states. This makes these drugs useful in stopping re-entrant circuits.

Effects: Decreases the rate/magnitude of depolarisation during phase 0. This results in

  • a decrease in conduction velocity in non-nodal tissue
  • Causes adjacent cells to depolarise more slowly.

Indications: Lignocaine may be used for polymorphic VT, whereas flecainide is used for chemical cardioversion.

Unwanted effects: Can induce arrhythmias by slowing conduction

23
Q

Describe Class II AADs, their MOA, effects and unwanted effects

A
  • Metoprolol, propranolol
  • MOA: Class II drugs block the effects of adrenaline/ NA on the heart
  • Effects: Abolish the increased firing at the SA node producted by B-receptor activation
    • Because sympathetic innervation increases SA node automaticity.
  • Slows conduction velocity, particulary at AV node
    • which lengthens refractory period (means it takes longer for another depolarisation, and thus contraction, to occur
    • May prevent re-entrant tachycardia at this site
  • Main uses: Class II drugs are used for rate control
    • they treat conditions which are precipitated by exercise, since Class II drugs blunts and inhibits the SNS affects onto the heart by blocking the beta1 receptors.
    • They prevent recurrent tachycardias
    • And decrease mortality post MI - since in MI you get a reduced ejection fraction, and this is detected by baroreceptors which try to increase heart rate via SNS. Beta blockers prevent this, and thus prevent the heart from working too hard.

Adverse effects:

  • Bronchospasm (asthmatics)
  • -ve inotropic effects (decreased contractility)
  • bradycardia, severe AV node block (can make His bundles become dominant)
  • Increased fatigue
  • Uncompensated heart failure
  • Metoprolol can traverse BB barrier to produce insomnia and depression
24
Q

What is the MOA, effects and uses of Class III AADs

A
  • Class III drugs pretty much just prolong the AP
  • MOA: Class III drugs can block K+ channels involved in membrane repolarisation.
    • They can modulate lipid membrane properties and affect Na+ fluxes (decreaes nodal cell rate of firing) & Ca2+ ion channels (Affects both SA and AV nodes)
    • Plateau and AP duration are prolonged
    • Substantially prolongs ERP, thereby decreasing chance of re-entry
  • Effects: Prolongs atrial and ventricular repolarisation
  • Contractility is unchaged or increased (may prolong QT interval
  • Uses: Rate control in AF
  • Effective against a wide range of arrhythmias (including supraventricular and ventricular)
25
Q

What are the ADRs with class III drugs?

A
  • photosensitiev skin rashes and discolouration
  • thyroid abnormalities
  • pulmonary fibrosis
  • corneal deposits
  • neurological and GI disturbances
26
Q

How do Class IV drugs work? (Diltiazem)

A

Class IV drugs, such as diltiazem, act on L-type Ca2+ channels (Slows down conduction at SA node by affecting Ca entry)

  • In pacemaker cells
    • ​Class IV drugs decrease the rate of discharge at SA node
    • They slow conduction and lengthen refractory period at AV node (since nodal cells require slow inward Ca2+ current (phase 4) in order to discharge spontaneously.
  • in ventricular cells
    • ​They depress myocardial contraction (verpamil mainly) by inhibiting L-type Ca2+ channels, and therefore have -ve inotropic and chronotropic actions

uses:

Rate control in AF (only suitable for SV arrhythmias) Avoid combined use with beta blockers (don’t use Ca blocker with Beta blokcer)

27
Q
A
28
Q

What does digoxin do, and what are it’s two MOAs

A

Its cardiac glycoside, and increases force of contraction and slows rate (it impacts upon Na/K+ pumps)

MOA1: Potent inhibitors of cellular Na+/K+ ATPase

  • Cardiac myocytes have a Na+/Ca2+ exchanger
  • Ca2+ and Na+ can move in either direciton
    • depends upon membrane potential and chemical gradient for ions
  • If intracellular Na+ conc is raised, intracellular Ca2+ coc. accumulates -> increases force of contraction

MOA2: Digoxin also increases vagal activity (ACh)

  • ACh impact reduces SA firing rate (HR drops)
  • This reduces AV conduction velocity
    • this decreases ventricular rate
  • ​​Mechanism of vagal increase not fully understood

indications for digoxin use: Heart faliure, rate control in AF

29
Q

What is the biggest risk of using digoxin?

A

Very narrow therapeutic index: 0.5 to 2.0 ng/ml, toxic level = 2.5 ng/ml

30
Q

describe the cardiotoxicity of digoxin, and why it causes arrthymias?

A
  • Decreases automaticity of AV node
  • Decreases conduction through AV node
  • Increases automaticity of purkinje fibres
  • Shortened refractory period in ventricular muscle

toxicity: may facilitate ectopic pacemaker activity in His bundles and completely block conduction between atria and ventricles

can produce AF at toxic levels

31
Q

What do you do if the patient develops a dysrrhythmia with digoxin overdose?

A
  • Withhold the digoxin and K+ sparing diuretics
  • Keep track of serum K+
  • Administer antidysrrhythmic drugs: lodcaine, atropine

neutralise digoxin

  • Fab antibodiy fragments
  • Cholestyramine
  • activated charcoal

Pharmacology (13 decks)

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