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Cardio Week 3 > Lecture 25: Drugs Affecting Cardiac Rhythm > Flashcards

Lecture 25: Drugs Affecting Cardiac Rhythm Flashcards

1
Q

What are the Class I drugs?

A

Local anesthetics
Procainamide
Lidocaine
Flecainide

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2
Q

What is the targets for the local anesthetics?

A 
Class I drugs
Procainamide (class IA) = Na and K channels
Lidocaine = Na channels
Flecainide = Na channels
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3
Q

What are class II drugs?

A

Beta blockers

Example: Atenolol

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4
Q

What are the targets for beta blockers?

A

Class II drugs

Atenolol = beta receptor (calcium, potassium and funny currents)

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5
Q

What are the class III drugs?

A 
Called class III drugs lol
Example: Dofetillide, amiodarone
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6
Q

What is the mechanism of Class III drugs?

A

Changes the potassium current

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7
Q

What are the class IV drugs?

A

Calcium channel blockers

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8
Q

What are examples of calcium channel blockers?

A

Verapamil

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9
Q

What is verapamil?

A

A Ca channel blocker

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10
Q

What are drugs that inhibit AV nodal reentry?

A
  1. atenolol (class II)
  2. Verapamil (class IV)
  3. Digoxin
  4. Adenosine
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11
Q

What are the drugs used to treat atrial fibrillation?

A
  1. Class I drugs

2. Class III drugs

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12
Q

What are the drugs used to treat AV reentry?

A
  1. Atenolol
  2. Class III drugs
  3. Class I drugs
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13
Q

What are the drugs used to treat AV nodal reentry?

A
  1. Digoxin
  2. Adenosine
  3. Class IV (Verapamil)
  4. Atenolol
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14
Q

What are the three rhythm mechanisms affected by drugs?

A
  1. reentrant tachycardias
  2. Automaticity
  3. Tachycardia due to early afterdepolarizations
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15
Q

What are the drug effects on reentrant tachycardias?

A
  1. Effects excitability, ERP and conduction velocity

Acts at tachycardias in atrial, ventricular, AVN and mixed

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16
Q

What are drug effects on automaticity?

A
  1. sinus node automaticity

2. drug that affects phase 4 depolarization

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17
Q

What are drug effects on early afterdepolarizations?

A

Sites = torsade des pointes in ventricle

Drugs that prolong ventricular APD

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18
Q

What is APD?

A

Action potential duration

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19
Q

What are drugs used to slowdown fast response tissue?

A 
Class I (Lidocaine, Procainamide, Flecainamide, all of which are amides because of two “I’s”)
Class III (Dofetilide)
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20
Q

What do class I drugs do to fast response tissue?

A

Lidocaine, Flecainamide and Procainamide
All decrease conduction velocity and excitability of fast response tissue through blockage of Na channel
Procainamide blocks K channel as well
Fast response tissue = everything in the heart except for SA and AV node

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21
Q

What do Class III drugs do to fast response tissue?

A

Dofetilide blocks K channel

Increases Action Potential duration (APD) by increasing effective repolarization period

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22
Q

What are the factors that modify the strength of sodium channel blockade? Significance?

A
  1. Different strength of different subclasses
    IC is most potent (Flecainide)
    IA is intermediate (Lidocaine)
    IB is least potent
  2. more potent cells with depolarized resting potential
  3. more potent at fast heart rates
    Lidocaine (weakest) is used when heart rate is very fast, or else it won’t be effective
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23
Q

What are factors that increase the effect of K+ current blockade on action potential depolarization?

A
  1. Slow heart rates
  2. Low extracellular K (increases APD)
  3. Low magnesium
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24
Q

What are the drugs that are used to target slow response tissue for tachy treatment?

A
  1. beta blockers (class II)
  2. Class 4 (calcium channel blockers)
  3. Digoxin
  4. Adenosine
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25
Q

What are the pathways for drug action in slow response tissue?

A
  1. Beta receptor blocker (decreases calcium channel)
  2. Direct channel blocker blocker
  3. Enhanced vagal response and muscarinic receptor
  4. Adenosine agonist
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26
Q

What are the effects of atenolol, verapamil, digoxin, adenosine on slow response tissue?

A

All of it the same
Decrease sinus rate by
i. increasing AVN ERP
ii. Decreasing AVN excitability

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27
Q

What is the effect of calcium channel blockers on sinus rate?

A

It slows the sinus rate

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28
Q

What is ERP?

A

Effective refractory period

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29
Q

What is the biggest determinant of APD in fast response tissue?

A 
Potassium channel 
IA drugs and class III drugs
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30
Q

What is the biggest determinant of APD in slow response tissue?

A

Calcium channel

So calcium channel blockers will prolong SA and AV node

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31
Q

What are the Ca blockers that act on cardiac muscle?

A
  1. Verapamil
  2. Diltiazem
    Unlike Nifedipine which does NOT do shit to cardiac muscle
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32
Q

Out of the drugs that act on slow response tissue, what lasts the longest?

A

Atenolol
(1 day)
Atenolol = only drug that cannot be given IV also (only oral)
Digoxin also lasts over 1 day

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33
Q

Out of the drugs that act on slow response tissue, what lasts the shortest?

A

Adenosine (only seconds)
Can only be given IV
Most suitable for acute AVNRT

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34
Q

Out of the drugs that act on slow response tissue, what has a positive inotropic effect?

A

Digoxin

Atenolol, verapamil and adenosine have NEGATIVE inotropic effects so decrease in cardiac output

35
Q

What are the three characteristics of WPW ECG?

A
  1. wide QRS
  2. short PR interval
  3. delta wave (which depends where the reentry pathway is)
36
Q

What are the two types of reentry tachycardias?

A
  1. reentry in a fixed circuit

2. reentry with multiple shifting wavefronts

37
Q

What are the characteristics of reentry in a fixed circuit?

A
  1. ventricular tachycardia in a healed infarct
  2. AV nodal reentry tachycardia
  3. AV reentry using a bypass tract
38
Q

What are the types of reentry with multiple shifting wavefronts?

A
  1. atrial fibrillation

2. ventricular fibrillation

39
Q

What are conditions needed for reentry?

A
  1. Potential path
  2. unidirectional block
  3. slow conduction
40
Q

What are the two mechanisms by which drugs cause CONDUCTION BLOCK to stop tachycardia?

A
  1. Class I drugs
    i. decrease excitability (making one portion of circular tissue literally inexcitable)
    ii. fixed bidirectional block by blocking sodium channels
    Example: Lidocaine, flecainamide and procainamide
  2. Class IA or III drugs by increasing effective refractory period
    i. increase effective refractory period (ERP) by blocking potassium channels
    ii. block due to refractoriness
    Example: Dofetilide and Procainamide
41
Q

What is the excitable gap?

A

The distance between between the propagating wave and the refractory tissue in a loop

42
Q

How does the length of the excitable gap affect termination by IA or III drugs?

A

The shorter the excitable gap (smaller the distance between refractory period and depolarized tissue), the easier it is for IA and III drugs to block reentry
If the excitable gap is too long, then the drugs will not be able to fill up enough of the gap with refractory tissue

43
Q

When are Class IA and III drugs used to terminate reentry?

A

When there is a short excitable gap

May lead to long APDs and early afterdepolarizations

44
Q

When are class I drugs used to terminate reentry?

A

Low safety factor (so you can make small zone inexcitable without spreading to whole heart)
However, by giving something increases refractoriness, you might promote reentry

45
Q

What are the strategies for terminating reentry?

A
  1. prolong the effective refractory period to cause refractory block
  2. decreased excitability to cause fixed block
    What is the fast response circuit of reentry?
46
Q

What are the target sites in AVRT?

A
  1. Bypass tract (use fast response drugs)
  2. AV node (use slow response drugs)
  3. ablation of bypass tract
    So you can use both adenosine (slow response drug) and procainamide in combination
47
Q

What is the slow response circuit of reentry?

A

AV node

48
Q

In AV reentry tachycardia, what do the p waves look like?

A

Inverted ninja (as seen above)
Also, if you give Class III drug (sotalol) and you block the tachycardia, where is the block occurring?
In the accessory tract because the fast tissue is blocked by the drug and then last contraction to occur is the ventricle (and cant get back up to the atria)

49
Q

What are the key characteristics of ventricular tachycardia post MI?

A

MoA = reentry in fast response tissue
Substrate = loop of surviving fibers around scar
Slow conduction due to poor coupling

50
Q

What is drug target for ventricular tachycardia post MI?

A 
Fibers with poor coupling in infarct area
Thus you want to use FAST response tissue drugs (because these guys are the ones that don’t affect SA/AV node)
Examples = class I and III
51
Q

What are the drugs that are used for ventricular tachycardia post MI?

A 
Procainamide
Flecainide
Amiodarone
Sotalol
DO NOT USE LIDOCAINE for long term treatment only for short term
52
Q

What are the electrophysiologic effects of Class I and III drugs in treating ventricular tachycardia?

A

Increase ventricular effective refractory period and decrease excitability

53
Q

What are the key characteristics of AV nodal reentry?

A

Mechanism = reentry
Substrate = loop due to dual AV nodal pathways
-slow conduction is normal in the AV node

54
Q

What is the drug target in AV nodal reentry?

A

AV nodal tissue

Therefore you want to use slow tissue drugs like verapamil, atenolol, digoxin and adenosine

55
Q

What are drugs used to target AV nodal reentry?

A 
Acute termination
1. adenosine
2. verapamil
Prevention of tachycardia
1. verapamil
2. atenolol
3. digoxin
56
Q

What is the relationship between wavelength and refractory period?

A

Wavelength = ERP * Conduction velocity

Time it takes to get through one cycle of depol-repol

57
Q

What are the key characteristics of atrial fibrillation?

A 
MoA = multiple wavelet reentry
Substrate = atrial enlargement and short atrial ERP
58
Q

What are the two target sites of atrial fibrillation?

A
  1. atrial muscle (to stop atrial fibrillation)
    -fast tissue drugs
  2. AV node (slow ventricular rate)
    -slow tissue drugs
    So you can use class I and III drugs + verapamil, digoxin, adenosine and atenolol
59
Q

What are drugs that target atrial muscle in atrial fibrillation?

A
  1. Procainamide
  2. Amiodarone
  3. Sotalol
  4. Dofetilide
  5. Flecainide
    Used to increase wavelength by increasing atrial ERP
60
Q

What are the drugs that target the AV node?

A
  1. atenolol
  2. digoxin
  3. verapamil
    Used to slow ventricular rate by prolong AV nodal ERP
61
Q

How does alcohol affect ERP?

A

Shortens refractory period

62
Q

What are the key characteristics of Torsades des Pointes?

A 
Mechanism = triggered activity due to EADs (early after depolarizations)
Substrate = long APD (QT) due to slow heart rate, low K, Mg, Class IA and III drugs and ion channel defects
63
Q

What are the drugs that prolong ventricular Aps that lead to Torsades?

A

Class I and III drugs because these guys are the ones that act on fast response tissue

64
Q

What are the target sites for Torsades des Pontes drugs?

A

Ventricular Action potentials

Purkinje fiber action potentials

65
Q

What are the drugs used to treat Torsades des Pointes?

A

Remove IA and III drugs
Isoproterenol to increase HR
Isoproteronol is a beta1/beta2 agonist which increases inotropy/chronotropy
Pacing devices that increase HR and decrease QT

66
Q

What are drugs that affect cardiac rhythm used for nonarrhythmic indications?

A 
Calcium channel blockers and beta receptor blockers for HTN
	-class II and IV drugs slow down slow tissue (SA node and AV node)
Beta receptor blockers (like carvedilol) and digoxin for systolic dysfunction
	-Class II and digoxin slow down slow tissue (SA node and AV node)
Beta blockers and calcium channel blockers for ischemia
	-class II and IV slow down slow tissue (SA node and AV node
67
Q

What are conditions that raise the risk of using antiarrhythmic drugs?

A
  1. Prolonged QT especially with low K and Mg
    • risk of Torsade de Pointes with Class IA and III drugs
  2. Sick sinus node
    • risk of worse sinus bradycardia with amiodarone (what grandma is tacking), class II and IV, and digoxin
  3. AV block
    • exacerbated by class II and IV drugs (whereas I and II slow junctional pacemaker)
  4. Poor systolic function
    • Class I, II and IV are all negatively inotropic
68
Q

What class of drugs are negatively inotropic?

A

Class I
Class II
Class IV

69
Q

What is the drug that only specifically inhibits potassium channels?

A 
Dofetilide
This is why “Class III” is not negatively inotropic (not including the other class III drugs that Frame did not really touch upon)
70
Q

How does low K exacerbate drug administration?

A

Makes you at greater risk for digoxin toxicity

Also, Class I and III drugs have a greater response (fast response tissue)

71
Q

What is sotalol?

A 
A class III drug
Also a beta blocker but think of it as the former
72
Q

What is amiodarone?

A 
A class III drug
Has a shitload of toxicities because it binds everywhere
73
Q

When do you want to avoid using lidocaine?

A

In tissue with normal resting potential or is easily excitable

74
Q

What is the potassium current blocked by Class IA and III?

A

The delayed rectified potassium current

75
Q

What are purinergic receptors?

A

Receptors that bind to adenosine

76
Q

When a patient has normal LV function and angina, should you use atenolol or digoxin to increase coronary perfusion?

A

Atenolol because the negative inotropic effect shouldn’t impair LV function that much
-will help treat ischemia

77
Q

When a patient has CHF and is hypotensive, should you use atenolol or digoxin?

A

Digoxin because you are trying to do everything you can to maximize cardiac output
-atenolol may decrease contractility and increase mortality

78
Q

When a patient has atrial fibrillation with severe COPD, do you choose sotalol or amiodarone to slow down the atrial muscle?

A

Class III drugs

Choose sotalol because amiodarone has pulmonary toxicity which would be contraindicated in a COPD patient

79
Q

Explain why dofetilide is an effective drug for treating atrial fibrillation but should be avoided in a patient with a QTc interval of 500 msec, a serum potassium of 3.5 mM and periods of sinus bradycardia to 40 bpm. Include in your answer the drug class, receptors or channels it targets, electrophysiologic effects, mechanism of arrhythmia, mechanisms of antiarrhythmic action and basis for risk of proarrhythmia.

A 
Dofetilide = class III
Effective because it blocks delayed rectified potassium channel which prolongs ERP and thus prolongs APD
Ineffective for patients with long QT because increasing ERP may lead to occurrence of early after-depolarizations which may lead to torsades de pointes
Also, since the patient has sinus bradycardia, prolonging the ERP would decrease sinus rate and a) make the patient go into heart failure because not enough CO or b) make another part of the heart start a junctional escape rhythm if sinus is too slow, thus setting the stage for arrhythmia
80
Q

Explain why lidocaine is an effective drug for treating ventricular tachycardia during acute ischemia but Procainamide or flecainide are more likely to be effective in treating recurrent ventricular tachycardia months to years after a myocardial infarction

A

Lidocaine is effective for acute ischemia because it decreases excitability and slows conduction velocity in atrial muscle, ventricular muscle and His-Purkinje system. In normal tissue, decreasing excitability and conduction velocity will have a neglibible effect on cardiac excitation
However in DISEASED tissue, the excitability is low to begin with (hyperpolarized) so if you block more sodium channels, it will be that much harder for tissue to become excitable
-therefore lidocaine leads to conduction block in diseasd tissue only
Procainamide and flecainmide also decrease excitability by blocking sodium and potassium (in the cass of procainamide) channels but do so with much more potency. That’s why you use these guys to treat healthy tissue months after the MI

81
Q

In treating atrial fibrillation name two of the prototype drugs that could slow the ventricular response and two drugs that could be used to terminate the fibrillation. Mention the pertinent electrophysiologic effects and target tissue.

A

Two drugs that slow ventricular response in atrial fibrillation:
i. atenolol
ii. verapamil
These two slow ventricular response by increasing the ERP of the AV node
Two drugs that terminate the fibrillation
i. procainamide
ii. dofetilide (also sotalol and amiodarone)
These two drugs terminate the fibrillation by prolonging the ERP in the atria

82
Q

Amiodarone was not used as one of the prototype drugs but does appear in Table II. Explain the statement that it is a class III that has actions characteristic of all four Singh-Vaughan Williams Classes.

A

Amiodarone is a class III drug in the sense that it inactivates the delayed rectifier potassium channel. However, it shares actions characteristics of Class I drugs because it blocks sodium channels as well; is like class II drugs because it is an antagonist of both alpha and beta receptors; and is like class IV drugs because it blocks calcium channels.

83
Q

A 25 year old women presents to the emergency room and is found to be in AV nodal reentry tachycardia. What drugs would you consider to terminate the tachycardia.

A

AV nodal = slow response tissue
I would use adenosine for acute resolution, then verapamil, atenolol or digoxin for maintenance
You can also use ablation therapy

Cardio Week 3 (10 decks)

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