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Antiarrhythmics Flashcards

(52 cards)

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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?

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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?

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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

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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

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A
  • Reduce abnormal impulse generation
  • Slow conduction through tissue
25
What are the pharmacological goals that antiarrhythmics achieve?
* Restore normal sinus rhythm (cardiovert) * Prevent lethal arrhythmias * **Decrease conduction velocity** * **Change the duration of ERP** * **Suppress abnormal automaticity**
26
Give an overview of the Vaughan-Williams classification and give some examples of drugs within each class
27
Which class does lidocaine belong to?
## Footnote **Class 1b** **Given IV only**
28
Describe the effects of lidocaine on cardiac activity
* **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
Give some uses of Class 1b drugs eg lidocaine
* **(acute) Ventricular tachycardia (eg post MI/during ischaemia)** * **NOT** used in atrial arrhythmias/AV junctional arrhythmias
30
Give some side effects of Class 1b drugs eg lidocaine
* Less proarrhythmic than class 1a (less QT effect) * CNS effects; **dizziness, drowsiness** * **Abdominal upset**
31
Which class does flecainide belong to?
## Footnote **Class 1c (Na+ channel blocker)** **Oral or IV (absorption and elimination)**
32
Describe the effects of flecainide on cardiac activity
* 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
Give some uses of flecainide (Class 1c)
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
Give some side effects of flecainide (Class 1c)
* **Proarrhythmia + sudden death;** esp with chronic use + **STRUCTURAL HEART DISEASE** * **Increased ventricular response to supraventricular rhythms (flutter)** * CNS effects * Gastrointestinal effects
35
Give some examples of Class 2 agents
**B-blockers** ***Propanolol (oral/IV)*** ***Bisoprolol (oral)*** ***Metoprolol (oral/IV)***
36
Describe the cardiac effects of B-blockers
* 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
Give some uses of Class 2 agents (B-blockers)
* 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
Give some side effects of B-blockers
* **Bronchospasm** * **Hypotension** * **DON'T USE IN PARTIAL AV BLOCK OR ACUTE HEART FAILURE (are used in stable heart failure)**
39
Give 2 examples of Class 3 agents (K+ channel blockers)
**Amioderone** **Sotalol** **Oral or IV**
40
Describe the cardiac effects of Class 3 agents (K+ channel blockers)
* **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
Why must Class 3 agents (B-blockers) like amioderone and sotalol be given via a central line, and not peripherally?
Due to **thrombophlebitic effects** if given peripherally
42
Give some uses and side effects of amioderone (class 3)
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
Describe the cardiac effects of sotalol (Class 3)
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
Give some uses and side effects of sotalol (class 3)
USES: * Wide spectrum; **supraventricular and ventricular tachycardia** SIDE EFFECTS: * **Proarrhythmia** * **Fatigue** * **Insomnia (due to B-antagonist effects)**
45
Give 2 examples of Class 4 agents
**Ca2+ channel blockers** **Verapamil (oral/IV)** **Diltiazem (oral)**
46
Describe the cardiac effects of Class 4 agents (Ca2+ channel blockers)
* **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
Give some uses and side effects of Class 4 agents (Ca2+ channel blockers)
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
Describe the properties, mechanism, cardiac effects and uses of adenosine (class V agent)
**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
Descibe the mechanism, cardiac effects, side effects and uses of ivabradine (Class V agent)
**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
Describe the mechanism and uses of digoxin
**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
Describe the mechanism, cardiac effects and uses of atropine
***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
Which channels does amioderone block?
## Footnote **Na+, K+ and Ca2+ channels** **Thus, amioderone acts as a NON-SELECTIVE B-BLOCKER**

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