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Semester 4 - Clinical Pharmacology And Therapeutics > Cardiac Arrhythmia Drugs > Flashcards

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

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

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2
Q

What creates the resting potential?

A

Unequal distribution of ions (interior of the cell is negative with respect to the outside).

Na+ higher outside than inside the cell
Ca2+ much higher outside than inside
K+ higher inside than outside.

It is maintained by ion selective channels, active pumps ad exchangers

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3
Q

Explain the ventricular cardiac action potential

A

Phase 0 - Opening of voltage gated Na channels

Phase 1 - Transient outward K+ current

Phase 2 - Opening of voltage gated Ca2+ channels (some K+ channels also open).

Phase 3 - Ca2+ channels inactivate, voltage gated K+ channels open.

Phase 4 - resting.

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4
Q

What effect do class 1 drugs have?

A

Block Na channels which slow the conduction in tissue (phase 0). It has a minor effect on action potential duration.

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5
Q

What effects do class 2 drugs have?

A

Beta blockers which bloke sympathetic action (act on B1 adrenoreceptors in the heart) so, decrease the slope of the pacemaker potential in the SA node and slow conduction at AV node.

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6
Q

What effects do class 3 drugs have?

A

Block K+ channels so prolong plateau phase and increase AP duration.
This prolongs the refractory period.

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7
Q

What effects do class 4 drugs have?

A

Ca2+ channel blockers which decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarisation.

They decrease slope of AP at SA node, decrease AV nodal conduction, decrease force of contraction (negative isotropy)

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8
Q

Where is slow cardiac action potential?

A

SA and AV node

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9
Q

Explain the slow cardiac action potential

A

Pacemaker potential / Funny current (If)- Na+ in via HCN channels.

Opening of voltage gated Ca2+ channels.

Then opening of voltage gated K+ channels so K+out

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10
Q

How do Ca2+ channel blockers affect slow Cardiac AP?

A

Reduce conduction velocity

Decrease AV nodal conduction

Decrease slope of AP at SA node.

Decrease force of contraction

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11
Q

What drugs affect automaticity?

A

Catecholamines (B agonist)- increase phase 4

Muscarinic agonist and adenosine - slow down phase 4

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12
Q

What are some mechanisms of arrhythmias?

A

Abnormal impulse generation - Automatic rhythms (enhanced normal automaticity and exotic focus), triggered rhythms (delayed and early afterdepolarisations)

Abnormal conduction - conduction block (1st, 2nd, 3rd), reentry loops (circus movements, reflection)

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13
Q

Where can reentry occur?

A

WPW - ventricles to atrium and visa versa (AV node, bundles, pathway and renter atrium)

AV node - split into slow and fast pathway

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14
Q

If abnormal rhythm generation how could drugs work?

A

Decrease of phase 4 slope in pacemaker cells

Raise the threshold

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15
Q

In the case of abnormal conduction, how could drugs work?

A

Decrease conduction velocity

Increase (ERP) effective refractory period (so the cell won’t be reexcited again)

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16
Q

What are antiarrhythmic drugs used for?

A

They aim to restore normal sinus rhythm and conduction to prevent more serious and possibly lethal arrhythmias from occurring.

They are used to:
Decrease conduction velocity
Change duration of ERP
Suppress abnormal automaticity

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17
Q

Give examples of class 1A agents

A

Procainamide, quinidine, disopyramide.

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18
Q

What effects do class 1A agents have on cardiac activity?

A

Decrease conduction
Increase refractory period
Decrease automaticity
Increase threshold

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19
Q

What are class 1A drugs used for?

A

Wide spectrum

Quinidine: Maintain sinus rhythm in Atrial fibrillation and atrial flutter and to precent recurrence, brugada syndrome.

Procainamide: acute IV treatment of SV and Ventricular arrhythmias.

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20
Q

ADRs of 1A?

A

Hypotension, reduced CO, Proarrythmias, DIzziness, confusion, insomnia, seizures, GI effects, Lupus-like syndrome.

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21
Q

Give examples of class IB agents?

A

Lidocaine( IV), mexiletine (oral)

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22
Q

How do 1B agents affect cardiac activity?

A

Increase threshold

Decrease phase 0 conduction in fast beating or ischaemic tissue.

APD slightly decreased

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23
Q

When do you use 1B agents?

A

Ventricular tachycardia

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24
Q

Side effects of iB?

A

Less side effects than 1A
GI upset
Dizziness, drowsiness

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25
IC example?
Flecainide and propafenone
26
1C effect on cardiac activity?
Very slow binding offset kinetics Substantially decrease phase 0 in normal Decrease automaticity (increase threshold) Increase APD and refractory period especially in rapidly depolarising tissue.
27
What are 1C used for?
SV arrhythmias (fibrilation and flutter) Premature ventricular contractions WPW syndrome
28
What are the side effects of iC?
Proarrhythmias and sudden death (especially chronic use) Increase ventricular reasons to SV arrhythmias. CNS and GI effects
29
What is a CAST?
Cardiac Arrhythmia Suppression Trial
30
Class II examples?
Propranolol, Bisoprolol, Metoprolol, esmolol | B blockers
31
How does Class II work on cardiac tissue?
Increase APD and refractory period in AV node and to slow AV conduction velocity. Decrease phase 4 depolarisation (catecholamine dependant)
32
Effect of class II on ECG?
Increase PR and decrease HR
33
CLass II uses?
All arrhythmias (almost) Treating sinus and catecholamine dependant tachycardia Converting reentrant arrhythmias at AV node Protecting the ventricles from high atrial rates (slow AV conduction)
34
ADRS of class II?
Bronchospasm Hypotension Don't use in partial AV block or acute heart failure (used in stable HF)
35
Class III agent examples?
Amiodarone Sotalol
36
CLass III cardiac effects?
Increase refractory period and increase APD Decrease phase 0 and conduction Increase threshold Decrease phase 4 Decrease speed of AV conduction.
37
Effect of lLass III on ECG?
Increase PR, QRS, QT Decrease HR
38
What is amiodarone used for
Very wide spectrum. Effective for most arrhythmias.
39
Side effects of class III (amiodarone)?
Many serious side effects that may increase with time ``` Pulmonary fibrosis Hepatic injury Increase LDL cholesterol Thyroid disease Photosensitivity Optic neuritis (transient blindness) ```
40
Cardiac effects of sotalol?
Increase APD and refractory period in both atrial and ventricular tissue. Slow phase 4 (B bloker) Slow AV conduction
41
ECG effects of sotalol?
Increase QT and decrease HR
42
Uses of sotalol?
Wide spectrum: Supraventricular and ventricular tachycardia
43
Side effects of sotalol?
Proarrythmia, fatigue, insomnia
44
Class IV examples?
Verapamil and diltiazem
45
Cardiac effects of Class IV?
Slow conduction through AV node (Ca2+) Increase refractory period in AV node Increase slow of phase 4 in SA to slow HR.
46
CLass IV Effects on ECG?
Increase PR, alters heart rate (depending on BP response and baroreflex).
47
Uses of class IV?
Control ventricles during SVT Concert SVT (re-entry around AV)
48
Side effects of class IV agents?
Caution when partial AV block is present. Can get systole if B blocker is on board. Caution when hypotension, decrease CO or sick sinus Some GI problems (constipation).
49
Adenosine mechanism?
Natural nucleoside that binds A1 receptors and activates K+ currents in AV and S.A. nodes. Decrease APD, hyperpolarosation - decrease HR.
50
What are the cardiac effects of adenosine?
Slow AV coditction
51
Use of adenosine?
Convert re-entrant SV arrhythmias diagnosis of coronary artery disease (scans).
52
Mechanism of vernakalant?
Blocks atrial specific K+ channels (outwards channel class 3)
53
Cardiac effects of vernakalant?
Slows atrial conduction Increase potency with higher heart rates.
54
Side effects of vernakalant?
Hypotension, AV block, sneezing and taste disturbances.
55
Uses of vernakalant?
Convert recent onset AF to normal sinus rhythm
56
Ivabraine mechanism and cardiac effects?
Blocks If ion current highly expressed in sinus node. Slows the sinus node but does not affect BP.
57
Side effects of Ivabradine?
Flashing lights Teratogenicity not known (avoid in pregnancy)
58
Uses of ivabradine?
Reduce inappropriate sinus tachycardia Reduce heart rate in heart failure and angina (avoiding blood pressure drops)
59
Digoxin mehanism?
Enhances vagal activity Slows AV conduction and slows HR
60
Digoxin uses?
Treatment to reduce ventricular rates in atrial fibrillation and atrial flutter.
61
Atropine mechanism and cardiac effects and uses?
Selective muscarininc antagonist. Blocks vagal activity to speed AV conduction and increase HR. Used to treat vagal bradycardia
62
Which drugs could be used in AF?
Rate control: Bisoprolol, verapamil, diltiazem +/- digoxin. Rhythm control: Sotalol, flecainide with bisoprolol, amiodarone
63
Which IV drug first for VT?
Depends on what drugs are already prescribed. Metoprolol / bisoprolol (1st line if no meds) Lignocaine/ mexoletine Amiodarone
64
Should flecainide be used alone for atrial flutter?
No | Give AV nodal blocking drugs to reduce ventricular rates in atrial flutter.
65
Best drugs for WPW?
Flecainide | Amiodarone
66
List drugs used in re-entrant SVT?
Acutely (IV): Adenosine, Verapamil, Flecainide Chronic (repeated episodes, orally): Bisoprolol, verapamil, Sotalol, Flecainide, Procainamide, Amiodarone
67
Which drug for ectopic beats
Bisoprolol first line | Flecainide, sotalol or amiodarone
68
Which drugs for sinus tachycardia?
Ivabradine, Bosoprolol, verapamil
69
What is catheter ablation?
Catheter ablation is a minimally invasive procedure in which the doctor threads a flexible thin tube (catheter) through the blood vessels to your heart to terminate (ablate) abnormal electrical pathways in the heart tissue.

Semester 4 - Clinical Pharmacology And Therapeutics (26 decks)

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