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Pharm CPR > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

1
Q

What are the fast action potential cells in cardiac muscle?

A

Ventricular contractile cardiomyocytes
Atrial cardiomyocytes
Purkinje Fibers

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2
Q

What are the slow action potential cells in cardiac muscle?

A

SA node cells, AV node cells

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3
Q

What happens on an EKG when you block the K+ Channels?

A

QT widening

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4
Q

What happens on an EKG when you block the Na+ channel?

A

QRS widening and drop contractility

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5
Q

This drug has ganglion blocking properties and may reduce PVR causing hypotension, also has muscarinic activity

A

Procainamide

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6
Q

Define cinchonism

A

Tinnitus, hearing loss, confusion, delirum, psychosis involved in Quinidine

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7
Q

In quinidine what organ may be affected other than the heart?

A

Liver - hepatitis with fever

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8
Q

Someone was given a drug that caused them to have tachycardia, urinary retention, blurred vision, constipation, glaucoma when it was supposed to treat their ventricular arrhythmias?

A

Disopyramide

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9
Q

Class 1B drugs bind to…

A

The inactivated sodium channel

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10
Q

Lidocaine is administered…

A

IV because really fast first pass metabolism

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11
Q

What is the least toxic of all Class I drugs?

A

Lidocaine

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12
Q

What are the neurological side effects of lidocaine?

A

Paresthesia, tremor, slurred speech, convulsions

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13
Q

This drug is related to lidocaine. How is it administered and what is it used for?

A

Mexilitine - orally active, used for Vtach and relieving diabetic neuropathy or nerve injury due to chronic pain

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14
Q

Does Class C affect K+ channels?

A

Yes blocks certain ones

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15
Q

This class IC drug is used for refractory arrhythmias that are life threatening as well as supraventricular arrythmias

A

Fleicainide

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16
Q

This class of drugs binds to open, activated Na+ Channels

A

Class 1C

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17
Q

This Class 1C drug has weak B blocking activity and is used in supraventricular arrythmias

A

Propafenone, but can make the arrythmia worse too lol

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18
Q

What are the effects of beta blockers on the AV and SA node?

A

AV node = drops conductance to increase PR interval

SA node = drops HR to increase RR interval

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19
Q

What are the effects on the calcium curve for the beta blockers?

A
  1. Increased slope due to effects on If and T-type Ca2+ channels
  2. Reduced threshold due to effect on L-type Ca2+ channels

This decreases the responsiveness of the Ca2+ channels to depolarization so AP is less -

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20
Q

What are the 4 clinical uses of propranolol?

A
  1. Stress and thyroid storm
  2. Afib and flutter
  3. Paroxysmal Supraventricular Arrhythmias
  4. MI arrhythmias to drop mortality

PAMS

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21
Q

Esmolol is administered how?

A

IV admin with rapid onset and termination of its action

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22
Q

What is esmolol used for? (5)

A
  1. Supraventricular arrhythmias
  2. Arrythmias associated with thyrotoxicosis
  3. MI or acute MI with arrythmias
  4. Adjunct drug in general anesthesia to control arrhythmias in periop period

SAMA

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23
Q

What channels do Class III drugs block?

A

K+ channel and inactivated sodium channels

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24
Q

Does Amiodarone block CCBs?

A

Yes

25
Q

This Class III drug treats life threatening ventricular arrhtyhmias

A

Sotalol

26
Q

This class III drug treats recurrent Vtach and Afib

A

Amiodarone

27
Q

This Class III drug is used to restore sinus rhythm in patients with atrial fibrillation
This Class III drug is used to maintain the sinus rhythm after cardioversion in patients with atrial fibrillation

A

Both Dofetilide and Ibutilide

Just Dofetilide

28
Q

This drug specifically blocks the rapid component of the delayed rectifier potassium current

A

Dofetilide and ibutilide

29
Q

Explain what Class IV drugs block and what they’re active in?

A
  • Block L-type channels
  • Active in cells that exhibit pacemaker potential to decrease the slope of phase 0 and increase L-type Ca2+ threshold potential
30
Q

What is the effect of Class IV drugs on the SA and AV node?

A

Slow SA node depolarization to drop HR

Prolong conduction time in AV node

31
Q

These drugs can be used for paroxysmal supraventricular tachy and ventricular rate control in afib

A

Verapamil and Diltiazem

32
Q

This drug can cause constipation

A

Verapamil

33
Q

How does procainamide work on the nodes?

A

SA and AV node depression

34
Q

How does amiodarone work on the nodes?

A

Causes bradycardia and slows AV conduction

35
Q

What channels does adenosine act on?

A

Enhances K+ current and inhibit Ca2+ and funny current which causes hyperpolarization and suppresses action potentials in pacemaker cells

36
Q

What is the effect of Adenosine on the nodes?

A

Inhibits AV conduction and increases AV nodal refractory period

37
Q

What are the 4 drugs that can treat paroxysmal supraventricular tachycardia?

A

Adenosine, Verapamil, Diltiazem, Propranolol

DAVP

38
Q

What are the 5 adverse effects of adenosine?

A
  1. SOB
  2. Bronchoconstriction (A1 and A2B adenosine receptors)
  3. Chest burning
  4. AV block
  5. Hypotension
39
Q

What is CAST?

A

Terminated prematurely because flecainide and other class 1C drugs increased mortality by 2.5x

40
Q

What is pro-arrhythmia?

A

Drug induced significant arrhythmia or worsening of existing arrhythmia

41
Q

What should you do before starting antiarrhythmic therapy?

A
  1. Eliminate the cause
  2. Make a firm dx
  3. Consider underlying cardiac conditions and co-morbidities
  4. Consider nonpharm treatment of arrhythmias
42
Q

What are the nonpharm appropaches to treating arrhythmias?

A

Catheter ablation
Implantable cardioverter-defibrillator
Artificial cardiac pacemaker
Direct current cardioversion

43
Q

What are the antiarrhythmic drugs that promote torsades de pointes?

A

Class 1A and Class 3 Drugs leads to excessive slowing of repolarization

44
Q

What are the antiarrhythmic drugs that cause persistent Vtach?

A

Class 1A and 1C drugs

45
Q

An 80 YO patient has fatigue, weakness, decreased exercise tolerance, hypotension, pulmonary congestion, heart failure. What is the most common suspicion?

A

Afib

46
Q

How do we achieve rhythm control in afib?

A

DCC or Chemical cardioversion using:

  • Class 1C agents that block fast Na+ channels to drop retrograde conduction through damaged tissue to terminate reentry (only use these with Class 3 if LVEF >40%)
  • Class 3 agents that block K+ channels to keep cells in refractory period to prevent reentry (always use these even if LVEF < 40%)
47
Q

What is a reentry rhythm?

A

An obstruction must be there that leads to a circuit that exceeds refractory epriod
- One impulse reenters and excites areas of heart more than once

48
Q

Which is more effective - rhythm or rate control?

A

Rate because rhythm has more adverse effects associated with maintenance phase

49
Q

How do you treat with rate control in afib?

A

Assess LV function

  1. If No HF and LVEF > 40% then CCB or B blocker to amiodarone
  2. If HF and LVEF < 40% then B blocker to amiodarone

This helps with multiple waves of excitation hitting AV node it responds to fewer

50
Q

What is the CHAD score used for?

A

Out of 9 - to determine if patient needs to be on anticoagulant to prevent stroke in AFIB pts

51
Q

PSVT is characterized by… and the most common type?

A

Abrupt onset and termination

Most common: AVNRT

52
Q

What are the common symptoms in PSVT patients?

A

Palpitations, dizziness, lightheaded, dyspnea, chest pain

53
Q

What is the mechanism of PSVT?

A

Dual pathway with AV node with heterogenous electrophysiological properties allowing for re-entry circuit
Anterograde - slow
Retrograde - fast

54
Q

What does PSVT look like on EKG?

A

Narrow QRS, inverted P wave or not seen

55
Q

What is the protocol for PSVT?

A
  1. Try vagal maneuver
  2. Give adenosine
  3. If LVEF > 40% then diltiazem or verapamil, then B blocker MAP
  4. If LVEF < 40% of hx of heart failure then give digoxin then amiodarone then diltiazem
56
Q

Long QT syndrome aka

A

Torsades de Pointes

57
Q

What are the 2 ways you can get Torsade de Pointes?

A
  1. Congenital = due to K+ or Na+ mutations
  2. Acquired long QT = factors that prolong action potential duration like slow HR or electrolyte imbalances OR antiarrhythmic drugs acting on Class 1A and 3, antipsychotics, antibiotics
58
Q

Chloroquine and Hydroxychloroquine and Azithromycin for COVID leads to

A

TDP

59
Q

How do we treat TDP?

A
  1. Stop the drug
  2. Hemodynamically unstable: DCC
  3. Hemodynamically stable: correct metabolites, Magnesium sulfate by IV whether or not they need it, temporary pacemaker/isoproterenol IV

Pharm CPR (9 decks)

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