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SP - Week 3 > Anti- Arrhytmic Drugs Pt. 2 > Flashcards

Anti- Arrhytmic Drugs Pt. 2 Flashcards

1
Q

AUTONOMIC REGULATION OF HEART RATE

A

-Nodal tissue innervation
- Parasympathetic nervous system (Muscarinic M 2
receptors)
- Sympathetic nervous system (Adrenergic β 1
receptors)

-SNS: Increases HR
• Increase ICa(L), Increase I k , Increase I f

-PNS: Decreases HR
• Decrease I Ca(L) , Decrease I K ,, Decrease I f, Produces I k(Ach)

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2
Q

Mode of action

CLASS II: β-BLOCKERS

A
  • Decrease SA and AV nodal activity
  • Decrease slope of phase 4 (diastolic currents) of action potential in pacemakers
  • Increase the refractory period of the AV node and can prevent recurrent SVT: restore sinus rhythm
  • Reduce ventricular rate in Afib
  • Many dysrhythmias are due to sympathetic activation
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3
Q

CLASS II: β-BLOCKERS

Examples

A
  • Propranolol (non-selective), with minor class I activity
  • Metoprolol (β 1 -selective)
    -Esmolol (β1 -selective: used in acute SVT via IV route: very short-acting)
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4
Q

Clinical uses of Class II

A
  • to reduce mortality after MI
  • to prevent recurrence of tachyarrhythmias (paroxysmal afib) induced by increased symp. activity
  • in managing hyperthyroidism while control of anti thyroid drugs is being established
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5
Q

CLASS III: K+ CHANNEL BLOCKERS
Mode of Action

A
  • Block K+ channels, including the outward
    (delayed) rectifier current
  • Significantly prolong APD
  • Greater refractory period may interrupt
    reentrant arrhythmias and suppress
    ectopic beats
  • Especially active in Purkinje and ventricular
    fibers
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6
Q

CLASS III: K+ CHANNEL BLOCKERS

Pro-arrhythmic adverse effects

A

-Prolonged APD (prolonged QT interval) may
lead to torsade de pointes (polymorphic form of VT)
- Increased risk with antipsychotics,
especially K+ hypokaelemia, hypercalcaemia or hereditary prolonged QT
- Important to monitor electrolyte levels,

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7
Q

CLASS III: K+ CHANNEL BLOCKERS
Examples

A
  • Amiodarone
  • dronedarone
  • Sotalol
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8
Q

-AMIODARONE Pk PD

A
  • Very effective
  • Extensively bound to tissues
  • Long half-life: 10-100 days
  • Accumulates in the body during repeated dosing
  • Loading dose needs to be used and needs to be
    given IV
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9
Q

AMIODARONE: ADVERSE EFFECTS

A
  • Photosensitive skin rashes
  • Slate-grey/bluish discoloration of the skin
  • Thyroid abnormalities
  • Pulmonary fibrosis (late in onset but may be
    irreversible)
  • Corneal deposits
  • Neurological and GI disturbances, including hepatitis
  • Cardiovascular effects
    •Bradycardia, heart block, heart failure
    • Torsades de pointes and VT are very unusual
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10
Q

Dronedarone
Clinical uses + AE

A

 Lacks iodine: designed to be less lipophilic
than amiodarone to reduce thyroid and pulmonary toxicity
 Improved survival in high-risk patients with Afib
 Increased mortality in patients with severe CHF

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11
Q

-Sotalol

A

 Use: life-threatening VT
 Also non-selective β-blocker
 Less effective than amiodarone in prevention of
chronic VTs
 Can cause torsades de pointes
Used in paroxysmal Supraventricular dysrhythmias and suppresses ventricular ectopic beats and short runs of ventricular tacchycardia

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12
Q

Amiodarone clinical use

A

Tachycardia ass. W/ Wolff-Parkinson- White syndrome. Also effective in many other supraventricular and ventricular tachyarrhythmias but has serious AE.

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13
Q

CLASS IV: CALCIUM CHANNEL BLOCKERS
Ex.

A

Verapamil

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14
Q

CLASS IV: CALCIUM CHANNEL BLOCKERS
Decrease which phases

A

Decrease phases 0 and 4 in the SA and AV nodes
- Slow conduction in the SA and AV node
- Increase ERP
- Terminate SVT by causing partial AV block and increasing AV nodal refractoriness (increased PR interval)

Decrease phase 2 in fast-response fibers
-Shorten the plateau of the AP
-Decrease contractility
-Reduce after-depolarization: suppresses premature ectopic beats

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15
Q

Verapamil
Uses+ roA

A
  • Main drug in this class
  • Uses: prevention of paroxysmal SVT, Afib (reduce
    ventricular rate)
  • Oral preparations
  • IV: previously used to terminate SVT: dangerous and
    very rarely needed
    -> Adenosine is safer for this
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16
Q

Verapamil CI

A

-Wolff-Parkinson-White-Syndrome
- VTs

17
Q

Verapamil AE

A

Constipation (verapamil), dizziness, flushing,
hypotension, AV block, edema

18
Q

Important drug interactions
With verapamil

A

-Additive AV block with β-blockers and digoxin
- Verapamil displaces digoxin from tissue-binding sites check digoxin levels and reduces its renal elimination thus predisposing to digoxin toxicity
- Co-prescription with digoxin: reduce digoxin dose and

19
Q

-ANTI-ARRHYTHMIC DRUGS NOT CLASSIFIED

A

Atropine -> Sinus bradycardia
Adenosine -> SVT
Digoxin -> Afib

20
Q

-ATROPINE

Mechanism of Action

A

Muscarinic receptor antagonist
- Inhibits the effects of excessive vagal activation on the heart, which is manifested as sinus bradycardia and AV nodal block

21
Q

Atropine Clinical use + roA

A

Clinical Use: Temporarily reverts sinus bradycardia to a normal sinus rate and reverses AV nodal block

Mode of administration: IV

22
Q

Atropine
AE

A

anti-cholinergic
- Tachycardia, pupil dilation, dry mouth, urinary retention, inhibition of sweating (anhidrosis), blurred vision, constipation.

‘(DUMBBELLS?)

23
Q

Adenosine MoA

A

Produced endogenously

Mode of action:
- Adenosine receptor (A1)
- Gi-coupled decrease in cAMP
- Increases K outward current (I KAch) and decreases Ca inward current
- Hyperpolarization
- Decreases SA and AV nodal activity

24
Q

Adenosine Clinical use

A

Clinical use: SVT termination (IV)
- Shorter-lived effect than verapamil, thus safer
- Effects only last 20-30s after a bolus, metabolized quickly

25
Q

Adenosine

Short-lived adverse effects:

A

chest pain, SOB (shortness of breath), dizziness,
nausea, flushing

26
Q

-Clinically important interactions w/ Adenosine

A

 Theophylline and other xanthines (caffeine) block adenosine receptors and thus inhibit the actions of adenosine
 Dipyridamole blocks the nucleoside uptake mechanism potentiating adenosine and prolonging its adverse effects

27
Q

Ivabradine is NOT anti-arrhythmic

MoA

A

Selective inhibitor of I f channels
 Prolongs slow depolarization phase
 Decreases SA node firing
 Reduces oxygen demands

28
Q

Ivabradine clinical uses

A

-Chronic stable angina
- Chronic heart failure for patients
•In sinus rhythm; HR ≥70bpm
•LVEF≤35%
•Who are either on a maximum tolerated dose of beta-blocker or have a contraindication to a beta-blocker

29
Q

Ivabradine AE

A

bradycardia, visual disturbances, hypertension,
long QT, atrial fibrillation

SP - Week 3 (2 decks)

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