Lecture 12, 13 Flashcards

1
Q

Where are impulses initiated?

A

SA Node

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2
Q

What follows SA Node depolarization?

A

Atrial Activation

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3
Q

After Atrial Activation, where do impulses go through?

A

AV Node

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4
Q

What kind of conduction is AV?

A

Slow

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5
Q

After AV node, what is activated?

A

His Purkinje System

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6
Q

After His Purkinje, where does the impulse spread?

A

Ventricular myocardium

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7
Q

Antiarrythmia drugs work by modulating the ____ & ____ to change how the heart works

A

ligand, voltage channels

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8
Q

What is the order of phases of the fast cardiac action potential?

A

4, 0, 1, 2, 3, 4

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9
Q

Action potential starts in diastole, MP is at -90

A

Phase 4 (1st one)

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10
Q

Normally, the Na+ channels are closed, in depolarization they rapidly open & Na floods in, cell goes from -90 to +55 in less than a second

A

Phase 0

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11
Q

Na channels close, Voltage Ca2+ (L-type) channels open, Ca2+ keeps cell at positive potential, cell stays depolarized for longer time

A

Phase 1

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12
Q

Open K+ channels, K+ leaves, makes cell become negative again

A

Phase 2

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13
Q

Repolarization, voltage gated K+ channel opens

A

Phase 3

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14
Q

Cell is still repolarizing, Na+ inside cell, K+ outside, Na+/K+ ATPase pump fixes it

A

Phase 4 (last one)

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15
Q

Effect of Local Anesthetics on the Fast Cardiac AP:

A
  1. Block Na+ channels, so slope of phase 0 less steep= longer to get to +55
  2. Longer refractory period due to slower recovery from inactivation
  3. Increased threshold – Stabilize the membrane
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16
Q

Effect of drugs that block K+ Channels:

A
  1. AP takes longer to repolarize
  2. Increase APD
  3. Decrease HR by increasing refractory period by blocking K+ channels
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17
Q

P wave

A

Atrial Depolarization

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18
Q

QRS complex

A

Ventricular Depolarization

speed of conduction

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19
Q

T wave

A

Ventricular Repolarization

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20
Q

PR interval

A

Atrial & AV conduction time

21
Q

QT interval

A

Action Potential duration

22
Q

What happens to ECG if a drug slows AV conduction by DECREASING slope of phase 0?

A

Increase PR

23
Q

What happens to ECG if a drug slows conduction of a ventricle by decreasing slope of phase 0? What drug does this?

A

Increase QRS width

Local Anesthetics

24
Q

What happens to ECG if a drug blocks K+ channels?

A

Lengthen QT

Increase AP duration of the ventricle

25
Q

Class 1A
Action:
Drugs:

A

Act: Moderate phase 0
Drugs: Quinidine, Procainamide

26
Q

Class 1B
Action:
Drugs:

A

Act: No change phase 0
Drugs: Lidocaine

27
Q

Class 1C
Action:
Drugs:

A

Act: Marked phase 0
Drugs: Flecainide

28
Q

Class 2
Action:
Drugs:

A

Act: Beta Adrenergic blockers
Drugs: Propranolol, Esmolol

29
Q

Class 3
Action:
Drugs:

A

Act: Prolong repolarization
Drugs: Amiodarone, Sotolol, Dofetalide, Ibuillide

30
Q

Class 4
Action:
Drugs:

A

Act: Ca+ channel blockers
Drug: Verapamil, Diltiazem

31
Q
1A Quinidine
MOA:
Act:
ECG:
Effects:
Use:
Caution
A

MOA: block Na+ & some K+ channels

Act: slows CV in ventricle, APD increases

ECG: Widened QRS & QT

Effects: Vagolytic action, makes supra ventricular tachycardias worse

Use: Wide, atrial flutter, fibrillation, ventricular tachycardias

Caution: Proarrhythmic, increase in QT cause Torsades

32
Q
1A Procainamide
MOA:
Act:
ECG:
Use:
Caution:
A

MOA: block Na+ & some K+ channels

Act: slows CV in ventricle & atria, APD increases

ECG: widened QRS & QT

Use: wide, atrial flutter, fibrillation, ventricular tachycardias

Caution: Proarrhythmic, not used long term, lupus

33
Q

1B Lidocaine
MOA:
Use:

A

MOA: Pure Na+ channel blocker

Use: ER, only works when heart speeds up, ventricular tachyarrhythmias

34
Q

Oral version of Lidocaine?

A

Mexiletine

35
Q
1C Flecainide
MOA:
Action:
Use:
Caution:
A

MOA: Blocks Na+ & K+ channels – better in atria K channels

Action: Long binding constant -> stays on channel long -> marked phase 0, tonic & rate dependent block

Use: Atrial flutter & fibrillation

Caution: Proarrhythmic

36
Q
Propanolol, Atenolol, Timolol
MOA:
Action:
Use:
Caution:
A

MOA: B1/B2 blocker

Action: Slow AV conduction, HR decreased

Use: Sympathetic sinus tachycardias, re-entry rhythms in & around AV

Caution: with other drugs that lengthen AV conduction time – Ca+ blocker, digitalis, asthma, diabetic

37
Q

Esmolol

Use:

A

Use: supraventricular arrhythmias

very short 1/2 life

38
Q

Amiodarone
MOA:
Use:
Toxicity:

A

MOA: Block Na, K, Ca channels, B receptors – long 1/2 life

Use: wide, supra ventricular arrhythmias, post MI, HF

Tox: cholesterol in eye, blue skin, pulmonary, hepatic, thyroid

39
Q

Sotalol
MOA:
Use:

A

MOA: K channel and B blocker

Use: atrial flutter & fibrillations & ventricular tachycardias

40
Q

What is the only antiarrythmic used in heart failure?

A

Amiodarone

41
Q
Dronedarone
Cardiac Effects:
Uses:
SE:
Contraindicated:
A

CE: same as Amiodarone, lacks an Iodine & less fat soluble

Use: prevent recurrence of atrial fibrillation/ flutter – not good at converting atrial fib/ flutter

SE: Bradycardia, long QT, Torsades, metabolized by antifungals

Contrain: HF

42
Q
Dofetilide
MOA:
Action:
Use:
Caution:
A

MOA: Selective K+ channel blocker

Act: prolong AP duration

Use: atrial fib, MI, HF

Caution: Torsades

43
Q

Ibutilide
MOA:
Use:
Caution:

A

MOA: similar to dofetilide

Use: convert atrial fib or flutters to normal rhythm

Caution: Torsades

44
Q

Verapamil, Diltiazem
Action:
Caution:

A

Act: Like B blocker
- dec. slope of phase 0 (Ca++), slow conduction through AV node

  • inc. refractory period in AV node
  • break re-entry rhythms around AV node.
  • dec. slope of phase 4 in SA node to slow HR

Caution: drugs that slow AV conduction, HYPOtension

45
Q

Adenosine

Use:

A

Very short 1/2 life, slows HR

Slow AV conduction
Acute Termination of re-entrant supra ventricular arrhythmias esp around AV

46
Q

Atropine

Use:

A

Inc HR

Tx Vagal Bradycardia

47
Q

Mg

Tx:

A

Tx: Torsades

48
Q

Digitalis
Action:
Tx:

A

Act: Slow AV conduction

Tx: atrial flutter, atrial fib esp during HF

49
Q

What is the treatment of choice for unstable, life-threatening cardiac arrhythmias?

A

DC Cardioversion