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PHPY 304 > 11. Anti-arrhythmic Drugs > Flashcards

11. Anti-arrhythmic Drugs Flashcards

1
Q

What are the 2 goals of treatment for arrhythmia?

What are the 4 classes of mechanisms?

A

2 goals:

  1. Termination of an ongoing arrhythmia
  2. Prevention of an arrhythmia
4 classes:
Class 1- Na channel blockers
Class 2- Beta blockers
Class 3- K channel blockers 
Class 4- Ca channel blockers
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2
Q

Can anti-arrhythmic drugs cause arrhythmias too?

A

Yes with long term use

The function of the heart depends on its electrical activity- mediated by the action potential
The action potential depends on the activity of ion channels: Na ion channels, K ion channels, Ca ion channels
Anti-arrhythmic drugs alter activity of ion channels (if incorrectly used they can cause arrhythmias)

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3
Q

Review the heart diagram slide 6-7 Anti-arrhythmic drugs

A

Okay

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4
Q

What are the 2 types of cardiac tissue?

A
  1. That with which action potentials occur automatically
    - SA node (60-100bpm)
    - AV node (50-60bpm)
    - bundle of His (50-60bpm)
    - purkinje system (30-40bpm)
  2. That with which actions potentials do not occur automatically (received from automatic tissues and spread throughout)
    - atrial muscle
    - ventricular muscle
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5
Q

What are the 3 phases of the pacemaker action potential?

SA node AP

A

Phase 4- spontaneous If current- non-selective action channels (If current)- mainly carry Na in

Phase 0- rapid depolarization - inward Ca L type channels

Phase 3- repolarization - outward K current

Slide 9 anti-arrhythmic drugs

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6
Q

What are the 5 phases of action potential of cardiac myocytes?

A

Phase 0- rapid depolarization - inward Na - Ina current determines velocity if impulse conduction throughout ventricle

Phase 1- transient outward K current

Phase 2- (plateau) inward Ca current

Phase 3- repolarization - outward K current
(Phases 2/3 determine duration of AP and refractory period

Phase 4- resting phase, Na channels enter resting state from inactivated state

Slide 10 Anti-arrhythmic drugs

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7
Q

What are the 3 differences between pacemaker cells (SA node, AV node) and myocitic cells (atrial and ventricular muscle cells)?

A
  1. Pacemaker cells have automaticity (membrane starts to depolarizes slowly but spontaneously) while myocytes have no automaticity (membrane depolarizes when it receives AP from pacemakers)
  2. Pacemaker action potential has 3 phases, myocytes has 5 phases
  3. In pacemakers, Ca causes rapid depolarization in phase 0, in myocytes, Na causes rapid depolarization in phase 0

Slide 11 Anti-arrhythmic drugs

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8
Q

What is the serum K+ physiologic range?
What values are hypokalemic?
What values are hyperkalemic?

A

Serum K+ physiological range: 3.5 to 5 mM

Hypokalemia (<3.5mM)
Hyperkalemia (>5mM)

Both arrhythmogenic

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9
Q

What is hypokalemia?

How can they cause arrhythmias?

A

Serum K range of <3.5mM
Slows repolarization
Action potentials become wider (increased duration)

Cause arrhythmias by decreasing conductance of K channels, slow repolarization, K channel pores are blocked by Mg and polyamines, increase Na and Ca cause early and delayed after depolarizations, ectopic beats, ventricular tachycardia and fibrillation

Slides 12-14 anti-arrhythmic drugs

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10
Q

How can diuretics cause arrhythmias?

A

Diuretics (thiazides and loop) can cause hypokalemia and predispose to arrhythmias

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11
Q

What is hyperkalemia?

A

Serum K range of >5mM
Depolarizes membrane and slows conduction velocity
Renal failure can cause hyperkalemia and life threatening arrhythmias
Hyperkalemia decreases resting membrane potential (becomes more positive-depolarized)
Increases K channel conductance, faster repolarization

Decreases availability of Na channels responsible for phase 0 depolarization
At very high levels of K > 14mM conduction finals leading to cardiac arrest

Slides 15-16 anti-arrhythmic drugs

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12
Q 
What are the effects of class 1 anti-arrhythmic drugs?
Na channel blockers
A

Block Na channels in the open or inactive state
Decrease re entry and prevent arrhythmia

In atrial and ventricular muscle:
Decrease depolarization in phase 0, decrease conduction velocity

In SA node:
- decrease spontaneous Na channel opening in phase 4, decrease heart rate and automaticity

Slide 18 anti-arrhythmic drugs
Slide 27 AAD

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13
Q

What is class IA of Na channel blockers?
Uses?
Adverse effects?

A

IA- procainamide: class IA sodium channel blocker that prefers binding to open state

Used to treat supraventricular and ventricular arrhythmias (ex: atrial fibrillation)

Adverse effects: chronic treatment may cause lupus like syndrome

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14
Q

What is class IB of Na channel blockers?
Uses?
Adverse effects?

A

Lidocaine
Exhibits use dependant block (blocks Na channels in their open and inactive states)
Works best in depolarized or rapidly driven tissues (found in ischemic myocardium)
Also has local anesthetic action

Adverse effects: tremor, dysarthria, confusion, dizziness, seizures (due to block of CNS Na channels)

Used for acute IV treatment of ventricular arrhythmias. NOT useful in atrial arrhythmias
(Don’t think I have to know this use)

Slides 29-30 AAD

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15
Q 
What are the common therapeutic effects of Na channel blockers?
Who are class I drugs restricted to?
A

To treat supraventricular and ventricular arrhythmias (atrial flutter or fibrillation) and maintain sinus rhythm
To prevent ventricular tachycardia and fibrillation

Class I drugs restricted to patients with structurally normal hearts (can cause arrhythmias I’m not normal hearts)

Slide 31 AAD

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16
Q 
What are the effects of class 2 anti-arrhythmic drugs?
β blockers
A

Block β1 and β2 receptors in heart

In SA, AV nodes:

  • decrease spontaneous Na channel opening in phase 4, decrease heart rate
  • decrease Ca channel opening and depolarization in phase 0, decrease automaticity and conduction velocity at AV node

In ventricular muscle:
- decrease contractility (different mechanism)

Slide 19 AAD
Slide 32 AAD

17
Q

What are the therapeutic uses of β blockers?
(4 of them)
Adverse effects?

A

Widely used, decrease mortality after myocardial infarction
Terminate re-entry arrhythmias involving AV node
Control the ventricular rate in atrial flutter and fibrillation
To suppress stress induced arrhythmias
Control arrhythmias induced by Na channel blockers

Adverse effects: can cause severe bradycardia and even AV block

18
Q 
What are the effects of class 3 anti-arrhythmic drugs?
K channel blockers
Adverse effects?
A

Block K channels

In atrial and ventricular muscle:
- decrease repolarization in phases 2 and 3, increase action potential duration (wider), increase refractory period, decrease re entry, prolonged repolarization

No effect in SA node

Adverse effects: increased risk of early after hyperpolarizations and torsades de pointes

Slide 20 AAD
Slide 34 AAD

19
Q

What is the K channel blocker Amiodarone?

Adverse effects?

A

Blocks K channels, inactivated Na channels, Ca channels, and β receptors
Increases action potential duration, decreases conduction velocity, increases refractoriness in all cardiac tissues
Used for recurrent ventricular tachycardia or fibrillation resistant to other drugs

Adverse effects: (with higher doses and long term therapy) pneumonitis, pulmonary fibrosis, hyper or hypothyroidism

Slide 35 AAD

20
Q

What is the K channel blocker sotalol?

Adverse effects?

A

Blocks K channels in all cardiac tissue (increases action potential duration)
Blocks β channels (decrease automaticity, decrease AV conduction, increase AV refractory period)
Used for ventricular tachyarrhythmias, atrial flutter and fibrillation

Adverse effects: fatigue, bradycardia, risk of torsades de pointes (with high dose and low plasma K)

Slide 36 AAD

21
Q 
What are the effects of class 4 anti-arrhythmic drugs?
Ca channel blockers
A

Block L TYPE calcium channels in the heart

In AV node:
- decrease Ca channel opening and depolarization in phase 0, decrease automaticity and conduction velocity at AV node

In SA node:
- decrease depolarization in phase 0, decrease heart rate

Slide 21 AAD

22
Q

What are the uses and adverse effects of Ca channel blockers?

A

Uses: supraventricular tachyarrhythmias, AV re-entrant tachycardia, decrease ventricular rate in atrial flutter and fibrillation, parental verapamil and diltiazem for rapid conversion of PSVTs to sinus rhythm

Adverse effects: bradycardia or AV block, hypotension, constipation
Do not combine non-DHPs with β blocker (can precipitate heart failure)

Slide 40 AAD

23
Q

What are the 6 causes of arrhythmias?

A
  1. Defects in impulse formation- increase sympathetic or parasympathetic activity
  2. Electrolyte disturbances- hypo or hyperkalemia
  3. Drugs that increase action potential duration (decrease K currents, EADs, and DADs)
  4. Defects in impulse conduction- re entry, conduction block
  5. Damage to myocytes- myocardial infraction (mostly ventricular tachycardia and fibrillation)
  6. Structural defects
24
Q

What are the 5 types of arrhythmias?

A
  1. Sinus tachycardia- SA node rate 100-180bpm
  2. Paroxysmal supraventricular tachycardia (PSVT)- atrial rate 140-250bpm
  3. Atrial flutter- atrial rate 280-300bpm
  4. Atrial or ventricular fibrillation- rate >300bpm
    Atrial fibrillation can be fine for many years
    Ventricular fibrillation is emergency
  5. Torsades de Pointes (twisting of points around the baseline in an ECG)- results from after depolarizations when action potential duration is increased (some have prolonged QT syndrome) - slide 37-38 AAD
25
Q

What do we do if something is wrong with pacemaker in an arrhythmia?
What do we do if something is wrong with conduction of action potential in an arrhythmia?

A

Something wrong with pacemaker- increase or decrease rate- use drugs that alter heart rate (pacemaker activity)

Something wrong with conduction of action potential:
In AV node, use drugs that alter conduction velocity in AV node
In atrial and ventricular smooth muscle, use drugs that alter conduction velocity (depolarization through Na channels) or refractory period (determines by K channel and APD)

33
Q

How do you pick anti-arrhythmic drugs if they’re from atrial myocytes and ventricular myocytes?

A

Atrial myocytes- drugs that decrease conduction velocity and increase action potential duration (refractory period):
Na channel blockers and K channel blockers

Ventricular myocytes- drugs that decrease conduction velocity and increase action potential duration (refractory period):
Na channel blockers and K channel blockers

Slide 25 AAD

34
Q

How do you pick anti-arrhythmic drugs from the SA node and AV node?

A

SA node- drugs that decrease automaticity:
β blockers, Ca channel blockers, and Na channel blockers

AV node- drugs that decrease automaticity (rate) and AV conduction velocity:
β blockers, Ca channel blockers, and Na channel blockers

Slide 25 AAD

35
Q

What is the problem with applying anti-arrhythmic drugs to atrial flutter?

A

At atrial rate of 300bpm ratio of impulses reaching ventricles 2:1 or 4:1 which makes ventricular rate 150bpm or 75bpm which means it can still pump blood efficiently
Adding anti-arrhythmic drug reduces flutter rate from 300 to 200bpm without ventricular protection
So atrial rate is at 200bpm with 1:1 ventricle impulse ratio so ventricle is at 200bpm which isn’t good to pump blood efficiently

Slide 26 AAD

PHPY 304 (12 decks)

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