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Flashcards in Cardio: Antiarrhythmics Deck (29)
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1

Na+ Channel blockers - Antiarrhythmics

Block fast Na+ channels
thereby reducing the rate of Phase 0 depolarization
prolonging the effective refractory period
increasing the threshold of excitability
and reducing Phase 4 depolarization

  • (3) Class I antiarrhythmics
    • Class IA
    • Class IB
    • Class IC

2

Class IA: Drugs

  • Quinidine (Muscarinic and α antagonist = Atropine)
    • SEx: reflex tacycardia 
    • Used for Atrial Fibrillations
    • Digitilize pt. w/ Digoxin to slow AV node conduct.
  • Procainamide
  • Disopyramide
     
  • "The Queen Proclaims Diso's pyramid"

3

Class IA: Mechanism

  • Moderate block of Na+ channels; prolong APs
  • Fast Na+ Channels
  • Slow Conduction → 
    APD - action potential duration
  •  ERP = effective refractory period
  • Prolongation of the QRS and  QT interval
    • ​→ Torsades
  • Possible Heart block
     
  • At low doses, anticholinergic (vagolytic) effects predominate, and may increase conduction velocity in the AV node and accelerate HR

4

Class 1A: Clinical Use

  • Both Atrial Fibrillation to prevent passage to ventricular arrhythmias (use w/ Digoxin)
  • especially re-entrant and ectopic SVT and VT and can be used to maintain Sinus rhythm

5

Class IA: Toxicity

  • Cinchonism (Quinidine =  tinnitus, ringing of the ears and dizziness, headache, GI dysfunction, ocular disfunction)
  • Procainamide = Reversible SLE-like syndrome (w/ slow acyelators = +ANA, +Antihistone)
    • Hematotoxity (CBCs monitored), Torsades
  • Heart Failure (Disopyramide)
  • Thrombocytopenia
  • Torsades de pointes due to increased QT interval
    • "Twisting of the spikes"
  • ​w/ Digoxin → monitor ECG
  • w/ Hyperkalemia → enhances effects

6

Class IB: Drugs

  • Lidocaine (Only used IV due to first-pass)
    • Post-MI
    • Open-Heart Surgery
    • Digoxin toxicity
    • SEx: CNS toxicity, Least Cardiotoxic!!
       
  • Mexiletine (Oral)
  • Tocainide (Oral)

7

Class IB: Mechanism

  • Fast Na+ Channels (↓ INa)
  • Shorten the duration of the Refractory period
    Blocks inactivated channels (slow conduction in hypoxic and ischemic heart)
    → ↓ APD - due to slow Na channels during the plateau phase - plateau gets shorter - more narrow
  • Preferentially affect ischemic or depolarized Purkinje and Ventricular tissue
  • Phenytoin can also fall into the class IB category

8

Class IB: Clinical Use

  • Suprress Acute ventricular arrhythmias
    (especially post-MI)
    • IB is Best post-MI
  • Little effect on conduction velocity so it has little effect on atrial function
  • Digitalis-induced arrhythmias

9

Class IB: Toxicity

  • CNS stimulation / depression
  • Cardiovascular depression

10

Class IC: Drugs

  • Flecainide (Tambocor)
    • Limited use because of its proarrhythmogenic effects leading to sudden cardiac death
  • Propafenone
     
  • Class IC:
  • "Can I have Fries Please"

11

Class IC: Mechanism

  • Strongly blocks fast Na+ and K+ channels
    • especially His-Purkinje tissue
    • No effect on APD
    • No ANS effects
  • Significantly prolongs refractory period in AV node
  • Minimal effect on AP duration

12

Class IC: Clinical Use

  • ULTIMATE - Last ditch use
  • Treat SVTs
  • Including Paroxysmal Atrial fibrillation and Atrial flutter
  • Only as a last resort in refractory VT

13

Class IC: Toxicity

  • Flecainide = Proarrhythmic actions --> use of these drugs is limited, cautious use is recommended may cause SCD
  • Contraindicated in post-MI
    • Structural and Ischemic
       
  • IC is Contraindicated in structural and ischemic heart disease

14

Class II: Drugs

ß-blockers

  • Propranolol (non-selective)
     
  • Carvedilol
  • Metroprolol
  • Esmolol (Selective)
  • Atenolol
  • Timolol
     
  • "PC MEAT"

 

15

Class II: Mechanism

  • β-adrenoceptor antagonists and act by reducing sympathetic stimulation
  • Depress automaticity
  •  SA and AV nodal activity by decreasing cAMP
  • decreased Ca2+ currents
  • ↓ slope of phase 4 (repolarization)
  • AV node particularly sensitive
    • Increase PR interval
    • Esmolol very short acting

16

Class II: Clinical Use

  • Prophylaxis post-MI - neg. inotropic effect ↓ O2 demand
  • SVTs
  • Prevent reflex tachycardia produced by vasodilationg agents
  • Used for Digitalis toxicity
  • Esmolol (IV) in acute SVT
  • Slowing ventricular rate during Atrial Fibrillation and Atrial Flutter

17

Class II: Toxicity

  • Bradycardia
  • AV block
  • CHF
  • Impotence
  • Exacerbation of COPD and Asthma (bronchospasm)
  • CNS (Sedation, Sleep alterations)
  • Masks sings of Hypoglycemia
  • Metoprolol: can cause dyslipidemia
  • Propanolo: exacerbate vasopasm in Prinzmetal angina
  • Contraindicated: in cocaine users (unopposed 
    α-adrenergic receptor agonist activity) Tx: glucagon

18

Class III: Drugs

K+ channel blockers

  • Amiodarone
    • Mimics classes I, II, III, IV
    • Used w/ ANY Arrhythmias
    • t1/2 = 80 days, forever to reach half lives
  • Ibutilide
  • Dofetilide
  • Sotalol
  • "Three(III) letters took him to his final resting place... AIDS"

19

Class III: Mechanism

  • ↓ IK - ↓ outward K+ - currents or slow inward Na+ currents
  • ↑ APD
  • ↑ ERP
  • Used when other antiarrhythmics fail
  • Prolong QT interval

20

Class III: Clinical Use

  • Atrial fibrillation
  • Atrial flutter
  • Ventricular tachycardia (amiodarone, sotalol)

21

Class III: Toxicity

  • Amiodarone: Pulmonary fibrosis, Hepatotoxicity, Hypo/Hyper-thyroidism (40% iodine by weight), Corneal deposits, Blue/gray skin deposits - photodermatitis, neuro effects, constipation, cardio (bradycardia, heart block, CHF)
    • Remember to check PFTs, LFTs, and TFTs
    • Class I, II, III, and IV effects and alters lipid membrane - hapten - triggers immune responses
  • Ibutilide: Torsades de pointes
  • Dofetilide: None
  • Sotabol: Torsades de pointes, excessive ß-blockade

22

Class IV: Drugs

L-type Ca2+ Channel blockers

  • Verapamil
  • Diltiazem
     
  • Use with SVTs

23

Class IV: Mechanism

  • Blocks Slow L-type Ca2+ channels 
  • ↓ Phase 0
  • ↓ Phase IV
  • ↓ SA, ↓ AV nodal activity
  • Decrease conduction velocity
  •  ERP
  • ↑ PR interval

24

Class IV: Clinical Use

  • Reentrant Supraventricular Tachycardia (reSVT)
  • Prevention of nodal arrhythmias (e.g. SVT)
  • Rate control of Atrial fibrillation and Atrial Flutter

25

Class IV: Toxicity

  • Constipation (Verapamil)
  • Flushing, dizziness
  • Edema
  • Additive AV blocks w/ β-blockers (↑ PR interval)
  • Verapamil displaces digoxin from binding sites
  • Sinus node depression)
  • May be exacerbated in individuals taking β-adrenoceptor antagonists
  • Should not be used w/ WPW pts.

26

Adenosine antiarrhythmics
(Class V drugs)

  • ↓ SA and AV nodal activity
  • Acts through a specific Purinergic (P1) receptor
  • Gi-coupled - ↑ K+ efflux --> hyperpolarizaing the cell ↓ ICa (Calcium influx) --> Hyperpolarizes the cell
  • Tx: DOC and paroxysmal Supraventricular tachycardia (pSVT) (WORST EVER) including WPWs
  • Very short acting (~10 - 15 seconds)
  • SEx: flusing, sedation, dyspnea (bronchospasm, must warn pts.), hypotension, angina
  • Antagonized by Methylxanthines (Theophylline (COPDs) and Caffeine)

27

Mg2+ antiarrhythmics

  • Competes with Ca2+
  • Tx: Torsades de pointes - ↓ K+ efflux - long complex
    • Drugs causing Torsades de pointes​
      • K+ channel blockers ('AIDS')
      • Antipsychotics (Thioridazine)
      • Tricyclic antidepressants
      • Anti-histimines
  • Digoxin toxicity
  • Seizures - Pregnancy

28

Antiarrhythmic Classes

  • Class I: Na+ channel blockers
  • Class II: ß-blockers
  • Class III: K+ channel blockers
  • Class IV: Ca2+ channel blockers
  • Others: Adenosine, Mg2+, Digoxin

29

Atropine

  • Blocks the effects of Acetylcholine
  • Elevates Sinus rate and AV nodal and SA conduction
  • Decreases refractory period
  • Used to treat Bradyarrhythmias that accompany MI
  • Adverse effects include:
    • Dry mouth, Mydriasis (dilation of pupil), and Cycloplegia (loss of accomodation of eye)
    • May induce arrthythmias