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
Class 1A Action: Drugs:
Act: Moderate phase 0 Drugs: Quinidine, Procainamide
26
Class 1B Action: Drugs:
Act: No change phase 0 Drugs: Lidocaine
27
Class 1C Action: Drugs:
Act: Marked phase 0 Drugs: Flecainide
28
Class 2 Action: Drugs:
Act: Beta Adrenergic blockers Drugs: Propranolol, Esmolol
29
Class 3 Action: Drugs:
Act: Prolong repolarization Drugs: Amiodarone, Sotolol, Dofetalide, Ibuillide
30
Class 4 Action: Drugs:
Act: Ca+ channel blockers Drug: Verapamil, Diltiazem
31
``` 1A Quinidine MOA: Act: ECG: Effects: Use: Caution ```
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
``` 1A Procainamide MOA: Act: ECG: Use: Caution: ```
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
1B Lidocaine MOA: Use:
MOA: Pure Na+ channel blocker Use: ER, only works when heart speeds up, ventricular tachyarrhythmias
34
Oral version of Lidocaine?
Mexiletine
35
``` 1C Flecainide MOA: Action: Use: Caution: ```
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
``` Propanolol, Atenolol, Timolol MOA: Action: Use: Caution: ```
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
Esmolol | Use:
Use: supraventricular arrhythmias | very short 1/2 life
38
Amiodarone MOA: Use: Toxicity:
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
Sotalol MOA: Use:
MOA: K channel and B blocker Use: atrial flutter & fibrillations & ventricular tachycardias
40
What is the only antiarrythmic used in heart failure?
Amiodarone
41
``` Dronedarone Cardiac Effects: Uses: SE: Contraindicated: ```
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
``` Dofetilide MOA: Action: Use: Caution: ```
MOA: Selective K+ channel blocker Act: prolong AP duration Use: atrial fib, MI, HF Caution: Torsades
43
Ibutilide MOA: Use: Caution:
MOA: similar to dofetilide Use: convert atrial fib or flutters to normal rhythm Caution: Torsades
44
Verapamil, Diltiazem Action: Caution:
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
Adenosine | Use:
Very short 1/2 life, slows HR Slow AV conduction Acute Termination of re-entrant supra ventricular arrhythmias esp around AV
46
Atropine | Use:
Inc HR | Tx Vagal Bradycardia
47
Mg | Tx:
Tx: Torsades
48
Digitalis Action: Tx:
Act: Slow AV conduction Tx: atrial flutter, atrial fib esp during HF
49
What is the treatment of choice for unstable, life-threatening cardiac arrhythmias?
DC Cardioversion