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CPT + Prescribing > Antiarrhythmics > Flashcards

Antiarrhythmics Flashcards

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1
Q

Outline the Vaughan Williams classification of antiarrhythmic drugs

A

CLASS 1: Na+ channel blockers

  • Lidocaine (1B)*
  • Flecainide (1C)*

CLASS 2: Beta blockers

  • Bisoprolol*
  • Metoprolol*

CLASS 3: K+ channel blockers

  • Amiodarone*
  • Sotolol*

CLASS 4: Ca2+ channel blockers

  • Diltiazem*
  • Verapamil*

CLASS 5: others

  • Adenosine*
  • Digoxin*
  • Atropine*
  • Ivabradine*
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2
Q

What is torsades de pointes?

A

Torsades de pointes is a specific form of polymorphic ventricular tachycardia in patients with a long QT interval. It is characterized by rapid, irregular QRS complexes

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3
Q

How is the coordination of a heart beat achieved?

A

Coordinated sequence of changes in membrane potentials; initiated in the SA node

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4
Q

Briefly describe how arrhythmias arise

A

Heart condition due to disturbances in:

  • Pacemaker impulse generation (SA or AV node)
  • Contraction impulse conduction (abnormal conduction through tissue)
  • Combination of the two

Results in rate/timing of contraction of the heart muscle being _insufficient to maintain the normal CO_

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5
Q

Describe the generation of the resting membrane potential

A
  • Transmembrane potential maintained; interior of cell -ve with respect to outside the cell
  • Caused by unequal distribution of ions inside vs outside a cell
  • Maintenance by ion selective channels, active pumps, exchangers

Via passive diffusion, ligand-gated ion channels, voltage-gated eg Ca2+ channels

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6
Q

Where does the fast cardiac action potential exist?

A

Cardiac tissue

Role of Na+/K+ ATP ase in restarting the action potential once reverted back to resting state

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7
Q

Describe the effects of Class 1 drugs (blocking Na+ channels)

A

C1: Na+ channel blockers

(Flecainide; used in AF, narrow complex tachycardias)

​

  • Slowing conduction in cardiac tissue (phase 0)
  • Minor effects on action potential duration (APD)
  • Phase 0 (upright phase) shifted to right
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8
Q

Describe the effects of Class 2 drugs (B-blockers)

A
  • Diminish phase 4 depolarisation and automaticity (any automatic or focal arrhythmias)
  • Inhibit Ca2+ inflow into the heart, thus affect the plateau
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9
Q

Give some other ways by which B-blockers have antiarrhythmic effects

A
  • Reducing HR
  • Reducing AV conduction velocity
  • Reducing delayed/early afterdepolarisations
  • Reducing conduction velocity
  • Reduce action potential duration (APD)
  • Reduce effective refractory period (ERP)
  • Reduce re-entry
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10
Q

Describe the effects of Class 3 drugs (K+ channel blockers)

A
  • Increase action potential duration (APD)
  • Increase refractory period

Increased refractory period leads to an extended QT interval- can lead to proarrhythmias/dangerous arrhythmias

Potassium Channel Blockers. A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS

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11
Q

Mechanism of Class 3 drugs

A
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12
Q

K+ channel blockers (Class 3)

A
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13
Q

Describe the effects of Class 4 drugs (Ca2+ channel blockers)

A
  • Decrease inward Ca2+ currents
  • Resulting in decreased phase 4 spontaneous depolarisation
  • Affect the plateau phase of action potential
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14
Q

Where does the slow cardiac action potential occur?

A

SA and AV node (pacemaker potential)

Upstroke due to Ca2+ NOT Na+!

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15
Q

Describe the effect of Ca2+ channel blockers on the slow cardiac action potential

A
  • Reduce conduction velocity (slope of phase 0 = CV)
  • Slowing SA and AV node conduction velocity
  • Increase refractory period
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16
Q

Mechanism of Ca2+ channel blockers on slow cardiac AP

A
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17
Q

Give some examples of drugs affecting the automaticity of the SLOW cardiac AP

A

B-agonist (eg salbutamol) - leads to sinus tachycardia (affecting SA node thus in sinus rhythm)

B-agonists increase the slope of the pacemaker potential (stimulation of sympathetic activity)

Muscarinic agonists (eg ADENOSINE) - affects slope of AP

Muscarinic agonists decrease the slope of the pacemaker potential (stimulation of parasympathetic activity)

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18
Q

REMEMBER

A

Fast AP in CARDIAC TISSUE

Slow AP in SA or AV node

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19
Q

Give the 2 main mechanisms of arrhythmogenesis

A
  1. Abnormal impulse generation (automatic rhythms)
  2. Abnormal conduction - re-entry
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20
Q

Explain the pathophysiology of Wolf-Parkinson-White syndrome

A
  • Presence of an accessory pathway (Bundle of Kent); connects the atrium + ventricle
  • Impluses are allowed to travel back up to the atrium, generating a re-entry loop
  • WOLK-PARKINSON-WHITE SYNDROME: in small population, congenital abnormality
  • Leads to pre-excitation

Treatment: catheter ablation to destroy accessory pathway (in high risk pt’s)

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21
Q

What is the conduction ratio?

A

Proportion of atrial contractions to ventricular contractions

Eg 2:1 ratio implies that 2 atrial contractions lead to 1 ventricular contraction

22
Q

Why can patients get a ventricular arrhythmia post MI?

A

Due to scar tissue formation in the heart post MI

Scar tissue can spontaneously depolarise and generate localised entry

This can lead to ventricular arrhythmias eg ventricular tachycardia

23
Q

Give an overview of the main actions of antiarrhythmic drugs

A

In case of ABNORMAL GENERATION:

  • Raises threshold
  • Decreases phase 4 slope (in pacemaker cells)- ie decreases slope of pacemaker potential (slow cardiac AP); mainly B-blockers, Ca2+ channel blockers

In case of ABNORMAL CONDUCTION:

  • Decreases conduction velocity (phase 0); mainly Na+ channel blockers
  • Increases effective refractory period (ERP) so cell won’t be re-excited again; mainly class 3 drugs
24
Q

Give the main mechanisms by which antiarrhythmics work

A
  • Reduce abnormal impulse generation
  • Slow conduction through tissue
25
Q

What are the pharmacological goals that antiarrhythmics achieve?

A
  • Restore normal sinus rhythm (cardiovert)
  • Prevent lethal arrhythmias
  • Decrease conduction velocity
  • Change the duration of ERP
  • Suppress abnormal automaticity
26
Q

Give an overview of the Vaughan-Williams classification and give some examples of drugs within each class

A
27
Q

Which class does lidocaine belong to?

A

Class 1b

Given IV only

28
Q

Describe the effects of lidocaine on cardiac activity

A
  • No change in phase 0 in normal tissue
  • APD slightly decreased (normal tissue)
  • Increased threshold (Na+)
  • Decreased phase 0 conduction in fast beating or ischaemic tissue

No effects on ECG in normal, increased QRS in fast beating/ischaemic

Fast binding offset kinetics; rapidly dissociates in time for next action potential

29
Q

Give some uses of Class 1b drugs eg lidocaine

A
  • (acute) Ventricular tachycardia (eg post MI/during ischaemia)
  • NOT used in atrial arrhythmias/AV junctional arrhythmias
30
Q

Give some side effects of Class 1b drugs eg lidocaine

A
  • Less proarrhythmic than class 1a (less QT effect)
  • CNS effects; dizziness, drowsiness
  • Abdominal upset
31
Q

Which class does flecainide belong to?

A

Class 1c (Na+ channel blocker)

Oral or IV (absorption and elimination)

32
Q

Describe the effects of flecainide on cardiac activity

A
  • Slow binding offset kinetics
  • Substantially decreases phase 0 (Na+) in normal
  • Reduced automaticity (increased threshold)
  • Increased action potential duration (K+) and increased refractory period
  • Works esp in RAPIDLY DEPOLARISING ATRIAL TISSUE

Increases PR, QRS AND QT interval (Torsades, lethal arrhythmia)

33
Q

Give some uses of flecainide (Class 1c)

A

Wide spectrum;

  • Supraventricular arrhythmias; atrial fibrillation, flutter (slowed conduction through atrial tissue) – give medication to slow AV conduction alongside
  • Premature ventricular contractions
  • Wolf-Parkinson-White syndrome - binds to Bundle of Kent + slows down conduction through atrial tissue

DO NOT USE IN ASCHAEMIA/POST MI (ie structural/ischaemic heart disease– sudden death)

34
Q

Give some side effects of flecainide (Class 1c)

A
  • Proarrhythmia + sudden death; esp with chronic use + STRUCTURAL HEART DISEASE
  • Increased ventricular response to supraventricular rhythms (flutter)
  • CNS effects
  • Gastrointestinal effects
35
Q

Give some examples of Class 2 agents

A

B-blockers

Propanolol (oral/IV)

Bisoprolol (oral)

Metoprolol (oral/IV)

36
Q

Describe the cardiac effects of B-blockers

A
  • Increased action potential duration in AV node to slow AV conduction velocity
  • Decreased phase 4 depolarisation (catecholamine eg adrenaline dependent) in slow cardiac AP

Effects of ECG:

  • Increased PR
  • Decreased HR
37
Q

Give some uses of Class 2 agents (B-blockers)

A
  • Sinus and catecholamine dependent tachycardia
  • Converting re-entrant arrhythmias at AV node
  • Protecting ventricle from high atrial rates (slow AV conduction) in atrial flutter/fibrillation
38
Q

Give some side effects of B-blockers

A
  • Bronchospasm
  • Hypotension
  • DON’T USE IN PARTIAL AV BLOCK OR ACUTE HEART FAILURE (are used in stable heart failure)
39
Q

Give 2 examples of Class 3 agents (K+ channel blockers)

A

Amioderone

Sotalol

Oral or IV

40
Q

Describe the cardiac effects of Class 3 agents (K+ channel blockers)

A
  • Increase refractory period and increase APD (K+)
  • Decreased phase 0 and conduction (Na+)– Na+ channels inactivated due to prolonged repolarisation
  • Increased threshold (for AP’s)
  • Decreased phase 4 (B block and Ca2+ block)
  • Decreased speed of AV conduction

Effects on ECG:

Increased PR

Increased QRS

Increased QT

Decreased HR

41
Q

Why must Class 3 agents (B-blockers) like amioderone and sotalol be given via a central line, and not peripherally?

A

Due to thrombophlebitic effects if given peripherally

42
Q

Give some uses and side effects of amioderone (class 3)

A

USES:

  • Wide spectrum; efective for most arrhythmias (esp life threatening eg ventricular tachycardias)

SIDE EFFECTS:

  • Pulmonary fibrosis; SOB
  • Hepatic injury (scarring); thus monitor liver function
  • Increased LDL cholestrol
  • Thyroid disease (AS CONTAINS IODINE)
  • OPTIC NEURITIS (TRANSIENT BLINDNESS)
43
Q

Describe the cardiac effects of sotalol (Class 3)

A

Oral absorption

  • Increases APD and refractory period in atrial and ventricular tissue
  • Slow phase 4 (as B-blocker at lower doses)
  • Slow AV conduction

ECG effects:

Increased QR (risk Torsades)

Decreased HR

44
Q

Give some uses and side effects of sotalol (class 3)

A

USES:

  • Wide spectrum; supraventricular and ventricular tachycardia

SIDE EFFECTS:

  • Proarrhythmia
  • Fatigue
  • Insomnia (due to B-antagonist effects)
45
Q

Give 2 examples of Class 4 agents

A

Ca2+ channel blockers

Verapamil (oral/IV)

Diltiazem (oral)

46
Q

Describe the cardiac effects of Class 4 agents (Ca2+ channel blockers)

A
  • Slow conduction through AV (Ca+)
  • Increase refractory period in AV node
  • Increase slope of phase 4 in SA to slow HR

Effects on ECG:

  • Increased PR
  • Increased/decreased HR (depdending on BP response; baroreflex)
47
Q

Give some uses and side effects of Class 4 agents (Ca2+ channel blockers)

A

USES:

  • Control ventricles in supraventricular tachycardia (as slow conduction through AV node)
  • Convert supraventricular tachycardia (re-entry around AC)

SIDE EFFECTS:

  • Caution; partial AV block
  • ASYSTOLE IF B-BLOCKER PRESENT; THUS DO NOT GIVE VERAPAMIL + B-BLOCKER (as excessive bradycardic effects on heart, thus heart may stop!)
  • Hypotension, decreased CO, sick sinus
  • GI problems (constipation)
48
Q

Describe the properties, mechanism, cardiac effects and uses of adenosine (class V agent)

A

Rapid, IV bolus, v short T 1/2

  • Natural nucleoside that binds A1 receptors and activates K+ currents in AV + SA node
  • Decreases action potential duration
  • Causes hyperpolarisation
  • Thus, decreased HR
  • Descreases Ca2+ currents- increased refractory period in AV node

Cardiac effects:

Slows AV conduction; terminates rhythms eg re-entry in WPW dependent on AV node

USES:

  • Convert re-entrant supraventricular arrhythmias
  • Diagnosis of coronary artery disease (SCANS); as heart normally speeds up after administration of adenosine
49
Q

Descibe the mechanism, cardiac effects, side effects and uses of ivabradine (Class V agent)

A

Oral administration

Blocks If ONLY IN SA NODE; thus no hypotensive effects

Blocks If current highly expressed in sinus node

Slows sinus node BUT DOES NOT AFFECT BLOOD PRESSURE

SIDE EFFECTS:

  • Flashing lights
  • Teratogenicity (avoid in pregnancy)

USES:

  • Reduce inappropriate sinus tachycrdia
  • Reduce heart rate in angina + heart failure

**AVOIDING BP DROPS

50
Q

Describe the mechanism and uses of digoxin

A

Cardiac glycoside; used as last resort

Enhances vagal activity - increased K+ currents, decreased Ca2+ currents, increased refractory period

Slows AV conduction + slows HR

USES:

  • Tx to reduce ventricular rates in atrial fibrillation + flutter
51
Q

Describe the mechanism, cardiac effects and uses of atropine

A

IV administration only

SELECTIVE MUSCARINIC ANTAGONIST

**RENALLY EXCRETED; CAUTION IN RENAL FAILURE

Blocks vagal activity to speed AV conduction and increase HR

USES:

To treat VAGAL BRADYCARDIA

52
Q

Which channels does amioderone block?

A

Na+, K+ and Ca2+ channels

Thus, amioderone acts as a NON-SELECTIVE B-BLOCKER

CPT + Prescribing (7 decks)

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