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CPT > Session 7 Cardiac Arrhythmia Drugs > Flashcards

Session 7 Cardiac Arrhythmia Drugs Flashcards

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1
Q

What are arrhythmias?

A

Heart condition where disturbances in:

  • pacemaker impulse formation
  • contraction impulse conduction
  • combination of the two
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2
Q

What do arrhythmias results in? (Refer to rate etc)

A

Results in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal cardiac output

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3
Q

What is meant by resting potential and what is it caused by?

A

= a transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell

Caused by unequal distribution of ions inside vs outside ell

  • Na+ higher outside than inside cell
  • Ca+ much higher outside than inside cell
  • K+ higher inside cell than outside

Maintenance by ion selective channels, active pumps and exchangers

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4
Q

What are the effects of class 1 drugs?

What do they block?

A

Block Na+ channels

= marked slowing conduction in tissue (phase 0 - the steep upward stroke)

Plus minor effects on action potential duration

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5
Q

What are the effects of class 2 beta-blockers?

A

They diminish phase 4 depolarisation and automaticity

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6
Q

Effect of class 3 drugs?

what do they block?

A

Block K+ channels

= increase action potential duration

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7
Q

What are the effects of class 4 drugs?

What do they block?

A

Calcium blockers

= calcium channel blockers DECREASE INWARD Ca2+ currents .. this results in a DECREASE of phase 4 spontaneous depolarisation

= they affect plateau phase of action potential

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8
Q

What drugs affect automaticity?

A

Beta agonists - increase the slope at phase 4 (i.e. make it steeper)

Muscarinic agonists, adenosine - decrease slope at phase 4

(Check this)

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9
Q

What are the two classes of rhythms associated with abnormal impulse generation?

NB: think about flow chart in slides

A
  1. Automatic rhythms

2. Triggered rhythms

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10
Q

What can automatic rhythms be broken down into (class wise)?

A

Enhanced normal automaticity —> increased AP from SA node

OR

Ectopic Focus —> AP arises from sites other than SA node

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11
Q

What can ‘triggered rhythms’ be broken down into?

A

delayed afterdepolarisation

OR

Early afterdepolarization

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12
Q

When referring to abnormal conduction, what two classes of problems come under this?

A 
Conduction block (1st, 2nd or 3rd degree) 
 =when the impulse is not conducted from the aria to the ventricles

Reentry (circus movement or reflection)

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13
Q

What is wolf-Parkinson-white syndrome?

A

An example of abnormal anatomic conduction that is present only in small populations

It leads to preexcitation

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14
Q

What are the actions of drugs either;

A) if there is abnormal generation

B) if there is abnormal conduction

A

Abnormal generation

  • decrease of phase 4 slope (in pacemaker cells)
  • raises the threshold

Abnormal conduction

  • decrease conduction velocity
  • increase EPR (so the cell wont be reexcited again)
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15
Q

Why do arrhythmias occur? 2

A

Automatic or triggered activity

Re-entry due to scar, anatomy of AV node slow and fast pathway/WPW

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16
Q

What is the goal for anti-arrhythmic drugs?

A

To restore normal sinus rhythm and conduction and to prevent more serious and possible lethal arrhythmias from occurring

These drugs are used to
A) decrease conduction velocity
B) change the duration of ERP
C) suppress abnormal automaticity

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17
Q

Class 1A drugs:

Action

Drug example

A

Action = moderate phase 0

Drugs = Quinidine, procainamide

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18
Q

Class 1B drugs

Action

Drug name

A

Action = no change in phase 0

drug name = lidocaine

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19
Q

Class IC drugs

Action

Drug name

A

Action = marked phase 0

Drugs = flecainide, propafenone

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20
Q

Class II drugs

Action

Drugs

A

Action = beta-adrenergic blockers

Drugs = bisoprolol, metoprolol, propranolol (esmolol)

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21
Q

Class III drugs

Action =

Drugs =

A

Action = prolong repolarisation

Drugs = amiodarone, sotalol

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22
Q

Class IV drugs

Action

Drugs

A

Action = calcium channel blockers

Drugs = verapamil, diltiazem

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23
Q

Class 1A agents

Absorption and elimination?

24
Q

Class 1A agents

Effects on cardiac activity?

Study These Flashcards
A

Decrease conduction (decrease phase 0 of the action potential (Na) )

Increase refractory period (increase APD (K+) and increase Na inactivation)

Decrease automaticity (decrease slope of phase 4, fast potentials)

Increase threshold (Na+)

25
Class 1A agents Effects on ECG?
Increase QRS +/- PR Increase QT
26
Uses of class 1A drugs?
Wide spectrum Quinidine = maintain sinus rhythms in atrial fibrillation and flutter and to prevent recurrence, Brugada syndrome Procainamide = acute IV treatment of supraventricular and ventricular arrhythmias
27
Side effects of class 1A drugs?
Hypotension Reduced CO Proarrhythmia (generation of a new arrhythmia) E.g. Torsades de Points (increased QT interval) Dizziness, confusion, insomnia, seizure (at high doses) GI effects (common) Lupus-like syndrome (particularly with procainamide)
28
Class 1B agents Absorption and elimination?
Lidocaine = IV only Mexiletine = oral phase
29
Class 1B agents. Effects on cardiac activity
Fast binding offset kinetics No change in phase 0 in normal tissue (no tonic block) APD slightly decreased (normal tissue) Increase threshold - Na+ Decrease phase 0 conduction in fast beating or ischaemic tissue
30
Class 1B agents Effects on ECG?
None in normal In fast beating or ischaemic Increase QRS
31
Class 1B agents Uses
Acute: ventricular tachycardia (esp during ischaemia) NB: Not used in atrial arrhythmias or AV junctional arrhythmias
32
Class 1B agents Side effects?
They’re less pro-arrhythmic than class 1A (less QT effect) CNS effects: dizziness and drowsiness Abdominal upset
33
Class 1C agents Absorption and elimination?
Oral or IV
34
Class 1C agents Effects on cardiac activity
Very slow binding offset kinetics (>10 s) Substantially decrease phase 0 (Na+) in normal Decrease automaticity so increase threshold Increase APD (K+) and increase refractory period
35
Class 1C agents Effects on ECG?
Increase PR Increase QRS Increase QT
36
Class 1C agents Uses?
Wide spectrum Supraventricular arrhythmias (fibrillation and flutter) Premature ventricular contractions WPW syndrome does
37
Class 1C drugs Side effects
Pro arrhythmias and sudden death especially in chronic disease structural heart disease - there is Increased ventricular response to supraventricular arrhythmias (flutter)
38
Class 2 agents Absorption and elimination = Cardiac effects = Effects on ECG = Uses = Side effect =
Absorption and elimination * propranolol = oral or IV * metoprolol 5mg IV (oral too) * bisoprolol = oral * esmolol = IV ONLY (very short acting - half life is 9 mins) Cardiac effects * increase APD and refraction period in AC node to slow AV conduction velocity * decrease phase 4 depolarisation (catecholamine dependent) Effects on ECG * increase PR * decrease HR Uses * treating sinus and catecholamine dependent tachycardia * converting reentrant arrhythmias at AV node * protecting the ventricles from high atria rates (slow AV conduction) in atrial flutter or atrial fibrillation Side effect * bronchospasm * hypotension
39
Class III agents - AMIODARONE Absorption and elimination = Cardiac effects = Effects on ECG = Uses = Side effect =
Absorption and elimination = oral or IV (half life is about 3 months) Cardiac effects * increase refractory period and increase APD * decrease phase 0 and conduction * increase threshold * decrease phase 4 (beta blocker and calcium block) * decrease speed of AV conduction Effects on ECG * increase PR * increase QRS * increase QT * decrease HR Uses * very wide spectrum! Effective for most arrhythmias Side effect * serious ones that increase with time! * pulmonary fibrosis * hepatic injury * increase LDL cholesterol * thyroid disease * photosensitivity * optic neuritis (transient blindness)
40
Class III = SOTALOL Absorption Cardiac effects ECG effects Uses Side effects
Absorption = oral Cardiac effects * increase APD and refractory period in atrial and ventricular tissue * slow phase 4 (beta blocker) * slows AV conduction ECG effects * increases QT interval * decreases HR Uses * wide spectrum! * supraventicular and ventricular tachycardia Side effects * proarrhythmia * fatigue * insomnia
41
Class IV agents : verapamil and diltiazem Absorption Cardiac effects ECG effects Uses Side effects
Absorption / administration * verapamil = oral or IV * diltiazem = oral Cardiac effects * slow conduction through AV (calcium) * increase refractory period in AV node * increases slope of phase 4 in SA to slow HR ECG effects * increases PR interval * can increase OR decrease HR depending on BP response and baroreflex Uses * control ventricles during supraventricular tachycardia * convert supraventricular tachycardia (re-entry around AV) Side effects * caution when partial AV block is present as can get asystole if beta blocker being used * caution when hypotensive, decrease CO or sick sinus * some GI problems e.g. constipation
42
Adenosine Administration Mechanism Cardiac Effects Uses
Administration * rapid IV bolus (very short half life - seconds!) Mechanism * natural nucleoside that Indus A1 receptors an activates K+ currents in AV and SA node * decrease APD and hyperpolarisation can lead to decreased HR Cardiac Effects * slows AV conduction Uses * convert re-entrant supraventricular arrhythmias * diagnosis of coronary artery disease (scans)
43
Vernakalant Admin Mechanism Cardiac effects Side effects Uses
Vernakalant Admin = IV bolus over 10 minutes Mechanism = blocs atrial specific K+ channels Cardiac effects = slows atrial conduction * increased potency with higher heart rates Side effects * hypotension * AV block * sneezing and taste disturbances Uses * convert recent onset atrial fibrillation to normal sinus rhythm
44
Ivabradine Administration Mechanism Cardiac effects Side effects Uses
Admin = orally in 2.5 mg bolus dose up to 10mg Mechanism = blocks If ion currently that is highly expressed in Sinus node Cardiac effects = slows the sinus node but does not affect BP Side effects = flashing lights / teratogenicity not known so avoid in pregnancy Uses = reduce inappropriate sinus tachycardia * reduce HR in heart failure and angina - as it avoids BP drops
45
Digoxin Mechanism Uses
Mechanism * enhances vagal activity - increased K+ currents, decreases Ca2+ currents and increases refractory period * slows AV conduction and slows HR Uses * treatment to reduce ventricular rates in atrial fibrillation and flutter
46
Atropine Mechanism Cardiac effects Uses
Mechanism = selective muscarinic antagonist Cardiac effects = block vagal activity to speed AV conduction and increase HR Uses = treats vagal bradycardia
47
Which anti-arrhythmic drug has the most efficacy?
Amiodarone
48
Which anti arrhythmic drug is the worst in terms of safety and tolerability? And the best?
Worst = amiodarone Best = beta blockers
49
Which drugs should be used in AF?
* rate control - slow conduction though AV node to reduce heart back to normal levels = bisoprolol = verapamil = diltiazem +/- digoxin * rhythm control = sotalol = flecainide with bisoprolol = amiodarone
50
Which drugs for VT?
Depends on what drugs already prescribed! - metoprolol/bisoprolol - lignocaine/mexiletine - amiodarone IV metoprolol/lignocaine or amiodarone
51
Should flecainide be used alone in atrial flutter?
No Give AV nodal blocking’s drugs to reduce ventricular rates in atrial flutter
52
Best drug for treatment of WPW?
Flecainide | Amiodarone
53
List drugs that could be used in re-entrant NCT
Acutely (IV) * adenosine * verapamil * flecainide Chronic (repeated episodes - orally) * bisoprolol, verapamil * sotalol * flecainide, procainamide * amiodarone
54
Which drugs for ectopic beats?
* bisoprolol = first line Then flecainide, sotalol or amiodarone
55
Which drugs to treat sinus tachycardia?
* Ivabradine (no drop in BP!) | * bisoprolol, verapamil

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