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Pharmacology & Therapeutics > Anti-arrhythmics > Flashcards

Anti-arrhythmics Flashcards

1
Q

What are the general causes of arrhythmias?

A

Problem in pacemaker impulse formation

Problem in contraction impulse conduction

Combination if the above

= rate/timing of contraction of heart muscle that is insufficient to maintain cardiac output

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2
Q

Outline the stages of the cardiac muscle action potential.

A

4 = open K+ rectifier channels keep membrane potential stable at -90mV
(K+ moves out)

0 = rapid Na+ influx through open fast Na+ channels
(Na+ moves in)

1 = transient K+ channels open and K+ efflux returns membrane potential to 0mV
(K+ moves out)

2 = influx of Ca2+ through L-type Ca2+ channels balanced by K+ efflux through delayed rectifier K+ channels
(Ca2+ moves in and K+ moves out)

3 = Ca2+ channels close; K+ delayed rectifier channels return membrane potential to -90mV
(K+ moves out)

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3
Q

Outline the stages of the SAN action potential.

A

4 = Na+ influx (funny current) activated via HCN channels at -50mV
(Na+ moves in)

0 = Ca2+ influx; HCN channels closed
(Ca2+ moves in)

2 = Ca2+ influx
(Ca2+ moves in)

3 = K+ efflux and inactivation of Ca2+ channels —> unstable resting potential
(K+ moves out)

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4
Q

Outline the different mechanisms of arrhythmias.

A

ABNORMAL IMPULSE GENERATION

  • –> AUTOMATIC RHYTHMS
  • –> TRIGGERED RHYTMS

AUTOMATIC RHYTHMS:
—> Enhanced normal automaticity —> increased APs from SAN —–> tachycardia

—> Ectopic focus —> APs arise from sites other than the SAN ——-> abnormal conduction pathways (impulse uses these pathways instead of the slower SAN conduction pathway)

TRIGGERED RHYTHMS (abnormal ion channels)
---> delayed afterdepolarisation

—> early afterdepolarisation

ABNORMAL CONDUCTION
—> conduction block (impulse not conducted from atria to ventricles; 1st-3rd degree)

—> re-entry (alternate movement of conduction e.g. along fast and slow pathways) —> circus movement or reflection

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5
Q

What is the abnormality in Wolff-Parkinson-White syndrome?

A

Accessory pathway (Bundle of Kent)

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6
Q

How can MI lead to arrhythmias?

A

Area of infarct creates alternate conduction pathway

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7
Q

What is the general purpose of anti-arrhythmic drugs in different arrhythmias?

A

Overall goals:

  • restore normal sinus rhythm and conduction
  • prevent more serious and lethal arrhythmias from occurring

ABNORMAL GENERATION:

  • decrease phase 4 slope in pacemaker cells —> reduce automaticity —> bradycardia
  • raise threshold

ABNORMAL CONDUCTION:

  • reduce conduction velocity (e.g. prevent VT following MI)
  • increase effective refractory period (e.g. prevent ectopic beats)
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8
Q

Describe the mechanism of action and pharmacokinetics associated with class 1a anti-arrhythmics. Give some examples of drugs in this class. When are they indicated? Give some examples of ADRs associated with these drugs.

A

e.g. quinidine, procainamide

MECHANISM OF ACTION:

  • marked slow conduction in phase 0 (blocks Na+ influx)
  • minor effects on AP duration
  • increases threshold
  • reduces automaticity (reduced phase 4 slope)

note: quinidine also has anti-cholinergic action (increases AV conduction) and is an alpha-receptor antagonist

PHARMACOKINETICS:

  • PO or IV
  • ECG: lengthen QRS interval, lengthen QT interval

INDICATIONS:

  • quinidine used to maintain sinus rhythm in AF and atrial flutter
  • quinidine used to prevent recurrent tachycardia and fibrillation
  • procainamide used as acute treatment of supraventricular and ventricular arrhythmias

ADRs:

  • hypotension
  • proarrhythmic e.g. lengthened QT interval —> torsades de pointes
  • high dose = dizziness, confusion, insomnia, seizure
  • GI disturbances
  • SLE-like syndrome
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9
Q

Describe the mechanism of action and pharmacokinetics associated with class 1b anti-arrhythmics. Give some examples of drugs in this class. When are they indicated? Give some examples of ADRs associated with these drugs.

A

e.g. lidocaine, phenytoin, tocainide, mexiletine

MECHANISM OF ACTION:

  • increases Na+ threshold in phase 0 in fast-beating/ischaemic tissue —> reduced conduction
  • AP duration slightly decreased

PHARMACOKINETICS:

  • lidocaine is IV only, tocainide and mexiletine are PO
  • ECG = lengthened QRS interval in fast-beating/ischaemic tissue

INDICATIONS: acute treatment of VT and VF (especially during ischaemia)

ADRs:

  • proarrhythmic (but less so than class 1a; less effect on QT interval)
  • CNS = dizziness, drowsiness
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10
Q

Describe the mechanism of action and pharmacokinetics associated with class 1c anti-arrhythmics. Give some examples of drugs in this class. When are they indicated? Give some examples of ADRs associated with these drugs.

A

e.g. flecainide, propafenone

MECHANISM OF ACTION:

  • increases Na+ threshold —> reduced automaticity
  • substantially reduces phase 0 conduction
  • increases refractory period (esp. in rapidly depolarising atrial tissue) —> increases AP duration

PHARMACOKINETICS:

  • PO or IV
  • ECG = lengthened PR interval, QRS interval, QT interval

INDICATIONS:

  • supraventricular arrhythmias (AF and atrial flutter)
  • premature ventricular contractions not associated with abnormal structure, ischaemia, or infarct
  • Wolff-Parkinson-White syndrome

ADRs:

  • proarrhythmic —> sudden death
  • increases ventricular response to supraventricular arrhythmias e.g. atrial flutter (slowing of flutter circuits means AVN conducts all flutters, instead of the occasional one)
  • CNS = dizziness, drowsiness
  • GI disturbances
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11
Q

Describe the mechanism of action and pharmacokinetics associated with class 2 anti-arrhythmics. Give some examples of drugs in this class. When are they indicated? Give some examples of ADRs associated with these drugs.

A

Beta-blockers e.g. propanolol (B1 and B2 receptors), esmolol (B1 specific), bisoprolol

MECHANISM OF ACTION:

  • block K+ efflux and Ca2+ influx in phase 2
  • reduces phase 4 depolarisation (catecholamine dependent)
  • increases refractory period in AVN —> increases AP duration ——–> slows AV conduction velocity

PHARMACOKINETICS:

  • propanolol PO or IV; esmolol IV only, bisoprolol PO
  • ECG = lengthened PR interval, reduced heart rate

INDICATIONS:

  • treatment of sinus and catecholamine dependent tachyarrhythmias
  • converting re-entrant arrhythmias in AVN
  • protecting ventricles from high atrial rates (flutter and AF) by slowing AV conduction

ADRs:

  • bronchospasm (contraindicated in asthma)
  • hypotension —> exacerbates partial AV block and ventricular failure
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12
Q

Describe the mechanism of action and pharmacokinetics associated with class 3 anti-arrhythmics. Give some examples of drugs in this class.

A

e.g. amiodarone, sotalol, dofetalide, ibutilide

MECHANISM OF ACTION:

  • block K+ efflux in phase 2 and 3
  • increases refractory period —> increases AP duration
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13
Q

Describe the mechanism of action, pharmacokinetics, indications, and ADRs associated with amiodarone.

A

MECHANISM OF ACTION:

  • reduces phase 0 conduction
  • increases threshold
  • reduces phase 4 conduction
  • reduces AV conduction

PHARMACOKINETICS:

  • PO or IV (t1/2 = ~ 3 months; give large divided loading dose IV over 24hrs —> redistributes into body —> maintenance doses)
  • ECG = lengthened PR interval, QRS interval, QT interval; reduced heart rate

INDICATIONS: effective for most arrhythmias

ADRs:

  • pulmonary fibrosis
  • reversible hepatic injury (monitor LFTs)
  • increased LDL cholesterol
  • hypothyroidism (monitor TFTs)
  • photosensitivity (wear sunscreen)

note: may need to reduce doses of digoxin, class 1 anti-arrhythmics, and warfarin (CYP450 interactions)

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14
Q

Describe the mechanism of action, pharmacokinetics, indications, and ADRs associated with sotalol.

A

MECHANISM OF ACTION:

  • increases refractory period —> increases AP duration
  • reduces phase 4 conduction
  • reduces AV conduction

PHARMACOKINETICS:

  • PO
  • ECG = lengthened QT interval, reduces heart rate

INDICATIONS: supraventricular and ventricular tachycardias

ADRs:

  • proarrhythmic (due to lengthened QT interval)
  • fatigue
  • insomnia
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15
Q

Describe the mechanism of action and pharmacokinetics associated with class 4 anti-arrhythmics. Give some examples of drugs in this class. When are they indicated? Give some examples of ADRs associated with these drugs

A

e.g. verapamil, diltiazem

MECHANISM OF ACTION:

  • blocks Ca2+ influx
  • slows AV conduction
  • increases refractory period at AVN
  • increases phase 4 slope in SAN —> slows heart rate

PHARMACOKINETICS:

  • verapamil PO or IV; diltiazem PO
  • ECG = lengthened PR interval, reduced heart rate (can also increase dependency on BP and baroreceptor response)

INDICATIONS:

  • controls ventricles during supraventricular tachycardia
  • converts supraventricular tachycardia by preventing re-entry around AVN

ADRs:

  • asystole when taking beta-blocker in partial AV block
  • caution req. when hypotensive, reduced cardiac output, sick sinus syndrome
  • GI disturbances e.g. constipation
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16
Q

What is sick sinus syndrome?

A

Types of arrhythmias caused by SAN malfunction

17
Q

Give some examples of drugs in class 5 of the Singh-Vaughan Williams classification system.

A

Adenosine

Digoxin

Atropine

Magnesium

18
Q

Describe the mechanism of action and pharmacokinetics associated with adenosine. When is it indicated? Give some examples of ADRs associated with adenosine.

A

MECHANISM OF ACTION:

  • binds to alpha-1 receptors and activates K+ currents in SAN and AVN —> reduces AP duration
  • hyperpolarisation —> reduces heart rate
  • reduces Ca2+ currents —> increases refractory period in AVN
  • slows AV conduction

PHARMACOKINETICS:
- rapid IV bolus during episode of arrhythmias (right atrium —> ventricles —> lungs)

INDICATIONS:

  • covert re-entrant supraventricular arrhythmias
  • hypotension during surgery
19
Q

Describe the mechanism of action of digoxin. When is it indicated?

A

MECHANISM OF ACTION:

Inhibits Na+/K+-ATPase —> increase in [Na+]i (initial increase in rate of APs) —> NCE reverses —> increase in [Ca2+]i (+ve ionotropy and increased K+ conductance) —> lengthens phase 4 and 0 (refractory period) —> reduced heart rate

  • enhances vagal activity
  • –> increases K+ currents
  • –> reduces Ca2+ currents
  • ———–> increases refractory period
  • slows AV conduction (increased in atria)
  • slows heart rate (-ve chronotropy)

INDICATIONS: treat AF and atrial flutter

20
Q

Describe the mechanism of action of atropine. When is it indicated?

A

MECHANISM OF ACTION:

  • selective muscarinic antagonist
  • blocks vagal activity
  • –> increases AV conduction
  • –> increases heart rate

INDICATIONS: vagal bradycardia e.g. vasovagal syncope, whilst waiting to put in a pacemaker

21
Q

Describe the mechanism of action of magnesium. When is it indicated?

A

Stabilise receptors in the heart

Treat tachycardia resulting from long QT/torsades de pointes

22
Q

Contrast the differences between muscle types regarding dependency on calcium to contract.

A

CARDIAC MUSCLE =

  • influx of Ca2+ required to contract
  • lots of mitochondrial Ca2+ recycling

SKELETAL MUSCLE =
- nAChR stimulates Ca2+ release from stores in mitochondria

VASCULAR SMOOTH MUSCLE =

  • influx of Ca2+ required
  • limited mitochondrial Ca2+ recycling
23
Q

Give examples of ADRs associated with digoxin.

A
  • N&V
  • diarrhoea
  • arrhythmias
  • conduction disturbances
  • dizziness
  • blurred/yellow vision
  • rash
  • eosinophilia
  • renal impairment (digoxin toxicity increased in hypokalaemia)
24
Q

What are the treatment options for atrial fibrillation?

A

Warfarin
- reduce risk of thromboembolism due to stasis of blood in atria

Statins
- reduce CVS risk

Rate-controlling drugs (AVN):

  • beta-blockers
  • OR Ca2+ channel blockers
  • OR digoxin (PO loading dose of 0.75mg-1.5mg over 24hrs in divided doses, then maintenance of 125-250 micrograms)

Rhythm-controlling drugs (SAN):

  • class 3 anti-arrhythmics e.g. amiodarone, soletal
  • class 1 anti-arrhythmics

Cardioversion:
- young patients with re-entrant loops AND rate-controlling has not been successful/failed to control symptoms

25
Q

What are the most common causes of atrial fibrillation?

A 
Hypertension
Coronary artery disease e.g. MI
Hyperthyroidism 
PE 
Chest infection 
Rheumatic fever ---> mitral stenosis 
Cardiomyopathy 
Congenital defect 
Idiopathic 
Alcohol

Pharmacology & Therapeutics (18 decks)

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