Arrhythmias Flashcards

1
Q

Types of Channels

A
  • Fast sodium channel
  • Potassium channels
  • Calcium channels
  • “Funny” sodium channels (If channels)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Fast sodium channel

A
  • Voltage dependent

- Lets sodium in, keeps potassium from going out and keeps calcium from blocking channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Potassium channels

A

Contribute to regulation of action potential duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Calcium channels

A
  • T-type channels initiate action potential (short)

- L-type channels sustain action potential (long)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

“Funny” sodium channels (If channels)

A

In SA and AV nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Voltage clocks influenced by?

A

Autonomic Nervous System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Divisions of Autonomic Nervous System and their function?

A
  1. Sympathetic: increases activity

2. Parasympathetic: decreases activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Antiarrhythmic drugs are used to

A
  • decrease or increase conduction velocity
  • alter the excitability of cardiac cells by changing the duration of the effective refractory period
  • suppress abnormal automaticity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Antiarrhythmic drugs treat which arrhythmias?

A
  • Supraventricular arrhythmias: atrial fibrillation

- Ventricular arrhythmias: ventricular fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Class I do what?

A
  • Fast sodium channel blockers

- Slows Phase 0 depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Example of Class I?

A

lidocaine

quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Class II do what?

A
  • Beta blockers

- Suppresses Phase 4 depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Example of Class II?

A

metoprolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Class III do what?

A
  • Repolarization prolongation

- Prolongs Phase 3 repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Example of Class III?

A

amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Class IV do what?

A
  • calcium channel blockers

- shortens action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Example of Class IV?

A

verapamil

diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Class V do what?

A
  • calcium accumulation

- vagal effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Example of Class V?

A

digoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Quinidine uses

A
  • Atrial tachyarrhythmias

- AV-junctional and ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ADR of Quinidine

A
	Diarrhea
	Hemolytic anemia, thrombocytopenia
	Aggravate heart failure
	Liver failure
	Digoxin interaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How Quinidine works

A

Slow Phase 0 depolarization, prolong action potential, slow conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What Vaughn Williams class is Quinidine

A

IA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

uses for Lidocaine

A

Ventricular arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ADR of Lidocaine

A

 Worsen certain arrhythmias
 Seizures
 CNS effects
 Contraindicated in second degree or complete heart block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How Lidocaine works

A

Shorten Phase 3 repolarization and decrease duration of action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What Vaughn Williams class is Lidocaine

A

Vaughn-Williams-IB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Dose for Lidocaine

A

Prefilled syringe of 100 mg IV bolus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

uses for Propafenone (Rhythmol™)

A
  • Life-threatening ventricular tachycardia or ventricular fibrillation
  • Refractory supraventricular tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How Propafenone (Rhythmol™)works

A

Slow Phase 0 depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What Vaughn Williams class is Propafenone (Rhythmol™)

A

Vaughn-Williams-IC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Prescription for Propafenone (Rhythmol™)

A

225 mg

One tablet every 8 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

ADR of Propafenone (Rhythmol™)

A
  • Potential to worsen heart failure

- Prone to drug-drug interactions that can raise warfarin and digoxin levels

34
Q

What type of metabolism for Propafenone (Rhythmol™)?

A

o Extensive 1st pass metabolism –> CYP2D6 (genetic differences)
 Concern with drugs that inhibit CYP2D6 activity
 Dose adjustment in patients with liver impairment

35
Q
  1. What are the Beta Blockers?

2. What Class

A
  1. Metoprolol (Lopressor™)

2. Esmolol (Brevibloc™)

36
Q

Metoprolol (Lopressor™) prescription for maintenance dose

A

50 mg

One tablet twice a day

37
Q

Metoprolol (Lopressor™) prescription for ED

A

o 2.5-5 mg IV push q. 2-5 mins.
o After ~15 mins, shouldn’t have repeated more than 3 times
o Max dose = 15 mg

38
Q

Metoprolol (Lopressor™) prescription for On floors for HTN

A

o 5 mg IV q. 6 hours PRN HTN (Optimal BP or HR…etc.)

- Also tell nurses when to not give

39
Q

How does Metoprolol work?

A

o Selective inhibitor of beta1 receptors

 Metabolized by CYP2D6; extensive first pass effect (smaller IV dose)

40
Q

Contraindications for Metoprolol

A

 Can treat acute myocardial infarction except if: (Don’t use ↓)
• Heart rate less than 45 bpm
• Greater than first-degree heart block
• Systolic blood pressure less than 100 mm Hg
• Moderate to severe heart failure

41
Q

Esmolol (Brevibloc™) administration

A

Loading dose(s) and continuous infusion

42
Q

How Esmolol (Brevibloc™) works

A
o	Selective inhibitor of beta1 receptors
	Very short elimination half life
•	Onset of action in 6 to 10 minutes
•	Action ceases approximately 20 minutes after infusion stop
	For immediate beta receptor blockade
43
Q

How Beta blockers work in general

A

o Diminish Phase 4 depolarization (↓ functional refractory period)
 Depresses automaticity
 Prolongs AV conduction
 Decreases heart rate and contractility
***Control rates!

44
Q

Prescription of Amiodarone

A

 Amiodarone
200 mg
One tablet daily
 maintenance dose, once > 400 mg –> side effects

45
Q

How Amiodarone works

A

 Predominantly block the potassium channels, thereby prolonging repolarization.
 Controls Rhythm

46
Q

Uses of Amiodarone

A

Supraventricular arrhythmias, atrial fibrillation/flutter, prevent recurrence of ventricular tachycardia or ventricular fibrillation

47
Q

ADR of Amiodarone

A

 Dose dependent
 Pulmonary toxicity: Respiratory arrest (infiltration, fluid)
• Get pulmonary function tests; make sure patient knows S/S
 Photosensitivity
 Possible bradycardia
 Thyroid Toxicity: inhibits T3  T4 and gives iodine. Both Hypo/hyper possible
• Monitor TSH levels

48
Q

How initiate therapy of Amiodarone

A
  • Big loading dose (1400-1600 mg)  tapper down to maintenance dose
  • Do in hospital with telemeter so can monitor
49
Q

How Dofetilide (Tikosyn) works

A
  • Prolongs action potentials in atria and ventricles

- Blocks rapid potassium channels only

50
Q

How initiate therapy of Dofetilide (Tikosyn)

A

o Initiate in Hospital for 3 days

51
Q

Kinetics of Dofetilide (Tikosyn)

A

 Renal excretion –> adjust based on creatinine clearance
 3 strengths based on CrCl
• 500, 250, 125 mcg q. 12 hours
 CYP3A4 metabolism –> drug interactions

52
Q

ADR of Dofetilide (Tikosyn)

A

QTc prolongation leading to torsades

≥ 500 msec. or ↑by 15% = bad

53
Q

How Sotalol works

A

 L-isomer exhibits non-selective beta blocking activity
 Increase in action potential duration in both atria and ventricles
• Decreased sinus rate and AV conduction

54
Q

Kinetics of Sotalol

A

Renal excretion –> adjust based on creatinine clearance

55
Q

ADR of Sotalol

A

QTc prolongation leading to torsades

56
Q

When is Sotalol Contraindicated

A

heart block

57
Q

Prescription for Diltiazem

A

20 mg IV bolus now and infuse intravenously at a rate of 10 mg per hour

58
Q

Uses for Diltiazem

A

Treatment of PSVT, atrial fib/flutter

59
Q

How Diltiazem works

A
  • Inhibit calcium-dependent slow action potentials in the SA and AV nodes
    • Slow diastolic depolarization both nodes (Phase 4 spontaneous depolarization)
    • Reduction of ventricular responses to atrial fibrillation
60
Q

ADR of Diltiazem

A

 Avoid in advanced heart disease or hypotension
 Bradycardia, hypotension
 Contraindicated in WPW and atrial fibrillation

61
Q

Kinetics of Diltiazem

A

 IV push, infusion- peak effect in 15 minutes

62
Q

Uses for Verapamil

A

slows ventricular response to atrial fib/flutter, terminates PSVT

63
Q

Dose for Verapamil

A

5 mg vials (max), 2.5 mg next lowest

IV push

64
Q

The longer you give a Calcium channel blocker…

A

the more refractory your body becomes to the drug

o Why it is stopped after 24 hours

65
Q

Prescription for Adenosine

A

o Adenosine
6 mg IV bolus
Repeat dose at 12 mg if first dose ineffective
o Give in left arm because it’s closest to the heart
 Rapid half-life (8 seconds

66
Q

Administration for Adenosine

A

o Rapid bolus with immediate flush (0.9% NaCl)

67
Q

Uses for Adenosine

A

o Treatment of paroxysmal supraventricular tachycardia associated with WPW
o Get rapid resolution

68
Q

ADR of Adenosine

A

o Chest pressure, flushing, tightness in throat

69
Q

Contraindication for Adenosine

A

o Second/third degree heart block

70
Q

2 major factors for Atrial fibrillation

A

 The electrical trigger that initiates the arrhythmia

 Abnormal myocardial substrate that allows atrial fibrillation to be maintained

71
Q

What is the risk associated with Atrial fibrillation

A

Embolism –> stroke (2-7x’s ↑)

72
Q

Stroke pneumonic

A
  • F- Face
  • A- arms
  • S- Slurred speech
  • T- Time
73
Q

Drugs to treat Atrial fibrillation

A
  1. Amiodarone 100 to 400 mg
  2. Sotalol 160 to 320 mg
  3. Dofetilide 500 to 1000 mcg
  4. Propafenone 450 to 900 mg
74
Q

Acute therapy for Supraventricular Tachycardia

A

Responsive to adenosine, beta blockers or calcium channel blockers

75
Q

Long-term Therapy for Supraventricular Tachycardia

A

 Associated with frequent recurrences and adverse effects
• Without structural cardiac disease
o propafenone or flecainide

76
Q

Ventricular Arrhythmias classes?

A

All classes may have application

77
Q

Class I in Ventricular Arrhythmias

A

• proarrhythmic effect

78
Q

Class II in Ventricular Arrhythmias

A

• efficacy in reducing morbidity and mortality more evident

79
Q

Class III in Ventricular Arrhythmias

A

• proven efficacy with lower proarrhythmic effect than the Class IA agents

80
Q

Class IV in Ventricular Arrhythmias

A

• no appreciable effect on conduction velocity or repolarization and tend to increase sympathetic activation

81
Q

Role in therapy for Ventricular Arrhythmias

A
  • CAST study/ESVEM study and beta blockers
  • Amiodarone: no increased survival and no increased risk of sudden death?
  • Heart failure patients: Class IA and IC “out” and amiodarone “in”?