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4 - CPT > Cardiac Arrhythmia Drugs > Flashcards

Cardiac Arrhythmia Drugs Flashcards

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1
Q

State the common causes of arrhythmias

A
  • Arrhythmia due to disturbances in pacemaker impulse formation (SA/AV node), contraction impulse conduction (bundle of His) or a combination of the two
  • Results in rate/timing of contraction of heart muscle that is insufficient to maintain normal cardiac output
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2
Q

Describe how abnormal impulse generation leads to arrhythmias

A
  • Can be automatic rhythms
    • Enhanced normal automaticity - increased action potential from SA node (such as when scared)
    • Ectopic focus - action potential arises from sites other than SA node
      • Can occur in areas of infarcts where damaged myocardium becomes depolarised and spontaneously active
  • Triggered rhythms
    • Delayed afterdepolarisation - arises fro the resting potential
    • Early afterdepolarisation - arises from the plateau phase commonly with a prolonged plateau phase
  • Drugs should either decrease funny current slope or increase the threshold
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3
Q

Describe how abnormal electrical conduction can lead to arrhythmias

A
  • Conduction block (1st, 2nd, 3rd degree)
    • When the impulse is not conducted from the atria to the ventricles
    • Treated by pacemakers
  • Re-entry loop
    • Wolff-Parkinson-White syndrome (WPW)
      • An accessory pathway in the heart called Bundle of Kent can cause a constant re-entry loop
  • Drugs should either decrease conduction velocity or increase refractory period
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4
Q

Briefly describe the effects of blocking the different channels with anti-arrhythmic drugs

A
  • Blocking Na channels
    • Marked slowing conduction in tissue (phase 0) - shifts curve to right
      • Minor effects on action potential duration
  • Beta-blockers
    • Diminish phase 4 depolarisation and automaticity
    • Increase action potential duration
    • Decrease slope of pacemaker potential in SA and slow conduction at AV node
      - Reduce funny current and reduce opening of Ca channels
  • Blocking potassium channels
    - Increase action potential duration by prolonging refractory period
  • Blocking calcium channels
    • Calcium channel blockers decrease inward calcium currents resulting in a decrease of phase 4 spontaneous depolarisation
    • Increases refractory period of SA node action potentials - slows down action potentials
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5
Q

Describe the effect of class 1A agents on the heart

A
  • Eg. Procainamide, quinidine, disopyramide
  • Effects on cardiac activity
    • Decrease conduction by decreasing depolarisation in ventricular cells
    • Increase refractory period (increase action potential duration and sodium inactivation) - indirect effect on potassium channels
    • Decrease automaticity (decrease slope of funny current)
    • Increase threshold of sodium
  • Effects on ECG - increase QRS interval, increase QT interval
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6
Q

Describe the uses and side effects of class 1A agents

A
  • Uses
    • Wide spectrum
    • Quinidine - maintain sinus rhythms in atrial fibrillation and flutter and to prevent recurrence
    • Procainamide - acute IV treatment of supraventricular and ventricular arrhythmias
  • Side effects
    • Hypotension, reduced cardiac output
    • Proarrhythmia - if AF causes a usual 2:1 AV node response (ie 150bpm if 300bpm from SA node), a sudden decrease in SA node potential frequency causes 1:1 AV node response, thus leading to ventricular fibrillation
      • Torsades de Points - longer QT interval leading to arrhythmia
    • Dizziness, confusion, insomnia, seizure (high dose)
    • GI effects
      • Lupus-like syndrome (especially procainamide)
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7
Q

Describe the effects of class 1B agents on the heart

A
  • Effects on cardiac activity
    • Increased threshold of sodium
    • Decreased sodium depolarisation in fast beating or ischaemic tissue
    • Decreases length of refractory period and action potential
  • Effects on ECG
    - Increase QRS in fast beating or ischaemic tissue only
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8
Q

Describe the uses and side effects of class 1B agents

A
  • Eg. Lidocaine (IV), mexiletine (oral)
  • Uses
    • Acute - ventricular tachycardia especially during ischaemia
    • Not used in atrial arrhythmias or AV junctional arrhythmias
  • Side effects
    • CNS effects - dizziness, drowsiness
      • Abdominal upset
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9
Q

Describe the effects of class 1C agents on the heart

A
  • Eg. Flecainide, propafenone
  • Effects on cardiac activity
    • Substantially decreases sodium depolarisation
    • Decrease automaticity (increases threshold)
    • Increased action potential duration and increased refractory period (lower increase compared to 1A)
  • Effects on ECG
    - Increased PR interval, increases QRS, increased QT
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10
Q

Describe the uses and side effects of class 1C agents

A
  • Uses
    • Wide spectrum
    • Used for supraventricular arrhythmias (fibrillation and flutter)
    • Premature ventricular contraction - if no ischaemic tissue
    • Wolff-Parkinson-White syndrome
  • Side effects
    • Proarrhythmia and sudden death with chronic use
    • Increase ventricular response to supraventricular arrhythmias
      • CNS and GI effects
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11
Q

Describe the effects of class II agents on the heart

A
  • Effects on cardiac activity
    • Increase action potential duration and refractory period in AV node to slow AV conduction velocity due to opening of calcium channels
    • Decrease funny current depolarisation to slow conduction at SA and AV nodes
  • Effects on ECG
    - Increased PR interval, decreased heart rate
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12
Q

Describe the uses and side effects of class II agents

A
  • Eg. Propanolol (ß1,ß2, oral, IV), bisoprolol (ß2, oral), metoprolol (oral, IV), esmolol (IV)
  • Uses
    • Treat SA node and catecholamine dependent tachycardia
    • Converting reentrant arrhythmias at AV node as reduces AV node entry
    • Protecting the ventricles from high atrial rates (slows AV conduction)
  • Side effects
    • Bronchospasm
    • Hypotension
      • Do not use in partial AV block or ventricular (heart) failure
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13
Q

Describe the effects of amiodarone on the heart

A
  • Effects on cardiac activity
    • Increase refractory period and increases action potential duration
    • Decrease depolarisation and sodium conduction
    • Increase threshold
    • Amiodarone also a ß-blocker and Ca channel blocker - decrease funny current
    • Decrease speed of AV conduction
  • Effects on ECG
    • Increase PR, QRS, QT
    • Decreased heart rate
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14
Q

Describe the uses and side effects of amiodarone

A
  • Uses
    • Very wide spectrum
    • Effective for most arrhythmias
    • Wolff-Parkinson-White syndrome
  • Side effects - BITCH
    • Bradycardia
    • Interstitial lung disease (pulmonary fibrosis) - monitor lung function
    • Thyroid (hypo and hyper)
    • Corneal/cutaneous
      • Hepatic injury - monitor liver function/hypotension
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15
Q

Describe the effect of sotalol on the heart

A
  • Effects on cardiac activity
    • Increase action potential duration and refractory period in atrial and ventricular tissue
    • Slow funny current (ß blocker)
    • Slow AV conduction
  • Effects on ECG
    - Increase QT, decrease heart rate
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16
Q

Describe the uses and side effects of sotalol

A
  • Uses
    • Wide spectrum
    • Supraventricular and ventricular tachycardia
  • Side effects
    - Proarrhythmia, fatigue, insomnia
17
Q

Describe the effects of class IV agents on the heart

A
  • Eg. Verapamil (oral, IV), diltiazem (oral)
  • Effects on cardiac activity
    • Slow conduction through AV node by blocking calcium channels
    • Increased refractory period in AV node
  • Effects on ECG
    • Increased PR
    • Heart rate may increase or decrease depending on blood pressure response and baroreflex
18
Q

Describe the uses and side effects of class IV agents

A
  • Uses
    • Control ventricles during supraventricular tachycardia
    • Convert supraventricular tachycardia (re-entry around AV)
  • Side effects
    • Caution when partial AV block is present - can get asystole if ß-blocker is used
    • Hypotension - further decrease cardiac output
      • GI problems
19
Q

Describe the mechanism and effect of adenosine

A
  • Rapid IV bolus - heart is stopped when given and metabolised, then starts again
  • Mechanism
    • Natural nucleoside binds A1 receptors and activates K currents in AV and SA node
    • Decreases action potential duration and causes hyperpolarisation, which decreases heart rate
    • Decreases calcium currents - increase refractory period in AV node
  • Effects on cardiac activity
    - Slows AV conduction
20
Q

Describe the uses of adenosine

A
  • Convert re-entrant supraventricular arrhythmias
  • Hypotension during surgery
  • Diagnosis of coronary artery disease - MRI scan of heart and see difference when perfusion re-established
21
Q

Describe the mechanism of digoxin (cardiac glycosides)

A
  • Digoxin blocks Na/K ATPase
  • By blocking Na/K ATPase, sodium concentration inside increases
  • NCX activity decreases leads to increase in calcium concentration inside
  • Calcium becomes stored in SR via SERCA
  • Increase calcium available to be released in action potential and increase force of contraction
  • Glycosides also act on neurones in cardiac control centre to increase vagal activity
    • Increase potassium currents, decrease calcium currents and increases refractory period
      • Slows AV conduction and slows heart rate
22
Q

Describe the uses of digoxin

A
  • Treatment to reduce ventricular rates in atrial fibrillation and flutter
  • Used in adjunction to other drugs
23
Q

State the preferred drugs used to treat supraventricular arrhythmias

A
  • Rate control - slow heart rate by slowing AV node conductance
    • Adenosine - can be used after beta blocker unlike verapamil
    • Digoxin - slows ventricular response to AF and atrial flutter
    • Verapamil - useful in slowing ventricular response to AF but need to watch out if beta blocker given alongside
    • Beta blocker - control ventricular rate
  • Rhythm control
    • Procainamide
    • Amiodarone
    • Sotalol
      • Flecainide
24
Q

State the preferred drug used to treat Wolff-Parkinson-White syndrome

A
  • Amiodarone

- Flecainide

25
Q

State the preferred drugs used to treat supraventricular and ventricular arrhythmias and ectopic beats

A
  • Amiodarone - slows AV node conductance and ventricular response
  • Beta blockers - slow AV node conductance
  • Sotalol - increase refractory period in atrial and ventricular tissue, slow AV conductance
  • Flecainide - decrease depolarisation of ventricular tissue
  • Procainamide - decrease conductance and increase refractory period in ventricular tissue
26
Q

State the preferred drugs used to treat ventricular arrhythmias

A
  • Lidocaine - decrease ventricular tissue conductance in ischaemic tissue
  • Amiodarone
  • Beta blocker
  • Flecainide
  • Procainamide

4 - CPT (23 decks)

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