Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Multaq Phase One > Module 5 - Atrial Fibrillation Treatment Landscape > Flashcards

Module 5 - Atrial Fibrillation Treatment Landscape Flashcards

1
Q

Normal VS AF Action Potentials

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

AADs designed to treat AF act by one of two primary mechanisms:

A
  • Suppressing the initiating mechanism
  • Altering a reentrant circuit

Some drugs may suppress the initiator but promote reentry.

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

What is APD?

A

Action Potential Duration

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

The extent of sodium channel block depends on:

A
  • Heart rate and membrane potential
  • Drug-specific physicochemical characteristics that determine the time required to recover from a previous depolarization
  • pH

When sodium channels are blocked, greater membrane depolarization is needed to bring sodium channels from the rest state to the open state.

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

ACTION POTENTIAL PROLONGATION

A

Another mechanism by which AADs affect the heart is by changing the duration of the action potential. Action potential prolongation is often caused by block or inhibition of cardiac potas- sium channels, which also results in a reduction of normal automaticity.

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

Adverse Effects of Beta-blockade include:

A
  • Fatigue
  • Bronchospasm • Hypotension
  • Impotence
  • Depression
  • Aggravation of heart failure
  • Worsening of symptoms due to peripheral vascular disease
  • Masking of the symptoms of hypoglycemia in diabetic patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

A decrease in current or other functional modifications occurs because _______________ drugs bind to specific sites on the ion channel proteins.

A

a. Ion channel–blocking*

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

_________________ are thought to be as effective as agents with predominant sodium channel–blocking properties in both atrial and ventricular arrhythmias.

A

c. Amiodarone and sotalol*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

With most drugs, the action potential is prolonged by block- ing potassium currents. It can also be caused by enhanced ______________.

A

c. Inward sodium current*

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

Antiarrhythmic therapy is also approved by the FDA to _____________.

A

Reduce ventricular rate in atrial flutter or AF*

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

_________________ can increase the energy needed to fibrillate the heart, in acutely ischemic tissue.

A

Beta-blockers*

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

T/F: The class IA drug quinidine is rarely used today because of increased mortality rates observed in AF patients.

A

True

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

What were the main outcomes (1 or more) of the Flecainide Multicentre Atrial Fibrillation study?

A
  • Both treatment groups experienced high discontinuation rates.*
  • Both flecainide and quinidine were equally effective in preventing paroxysmal AF.*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Adverse effects related to propafenone usage include which one or more of the following?

A
  • Proarrhythmia*
  • Bradycardia*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The RAFT and ERAFT studies showed which (1 or more) of the following?

A
  • Higher propafenone doses result in longer times to AF recurrence.*
  • There was a dose-dependent increase in the occurrence of adverse events.*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the main indication for class IC drugs? (1 answer)

A

Paroxysmal AF and atrial flutter*

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

Match the antiarrhythmic drug with its drug class

Amiodarone

Propafenone

Quinidine

Dofetilide

A

Amiodarone – class III

Propafenone – class IC

Quinidine – class IA

Dofetilide – class III

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

The following agents are primarily used for rate control in AF. (Assign them to the correct class. )

Verapamil
Carvedilol
Bisoprolol

Diltiazem

A

Verapamil – calcium channel blocker Metoprolol – beta-blocker
Carvedilol – beta-blocker
Bisoprolol – beta-blocker

Diltiazem – calcium channel blocker

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

The indications for beta-blockers vary by country are generally approved by the FDA in which of the following (1 or more)?

A

a. Hypertension*
b. CHF*
c. LV dysfunction following MI*

d. MI*
e. Angina pectoris*

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

There have been 3 generations of beta-blockers. Assign the generation to the correct description.

First generation
Second generation
Third generation

A

First generation – Nonselective
Second generation – Beta1-selective (cardioselective)
Third generation – Nonselective and exhibit other properties

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

Which of the following best describes what the METAFER study showed?

A

Metoprolol reduced the risk of AF relapse after cardioversion in persistent AF patients.*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

A retrospective analysis of the US Carvedilol Heart Failure Trials Program showed which of the following?

A

Carvedilol improved ejection fraction in CHF patients with AF.*

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

Which of the following is correct?

  • Verapamil and diltiazem are approved by the FDA for rate control in AF patients.
  • Only verapamil is approved by the FDA for rate control in AF patients and diltiazem is not used in this indication.
  • Only verapamil is approved by the FDA for rate control in AF patients, but both are used in this indication.
A
  • Only verapamil is approved by the FDA for rate control in AF patients, but both are used in this indication.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Digoxin falls into which one of the Vaughan Williams AAD classes?

A

Digoxin does not fit into one specific class.*

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

Which of the following (1 or more) are true about digoxin?

a. It activates the inhibitory parasympathetic vagus nerves.
b. It reduces the heart rate.
c. It provides effective rate control during exercise.
d. It increases the contraction force of the heart (positive inotropism).

A

Which of the following (1 or more) are true about digoxin?

  • *a. It activates the inhibitory parasympathetic vagus nerves.*
    b. It reduces the heart rate.***
    c. It provides effective rate control during exercise.
  • *d. It increases the contraction force of the heart (positive inotropism).* **
26
Q

Which of the following are disadvantages of warfarin?

A
  • It has numerous drug-drug and food-drug interactions.*
  • It has a narrow therapeutic range.*
27
Q

The RE-LYTM trial found that ___________ 150 mg was associat- ed with lower rates of stroke and systemic embolism but similar rates of major hemorrhage relative to warfarin.

A

Dabigatran*

28
Q

State the 2 primary goals of AF treatment.

A

(1) To control symptoms by restoring and maintaining sinus rhythm or by controlling ventricular rate
(2) To prevent stroke, the major complication of AF

29
Q

Which type of endpoint is clinically relevant, but requires large sample sizes and long follow-up periods?

A

Mortality*

30
Q

Most prescriptions for AF treatments are written by:

A

Cardiologists*

31
Q

Which physician type is most likely to see patients who have few symptoms or who are elderly and have permanent AF?

A

Primary care physicians*

32
Q

Allosteric

A

pertaining to regulation of the rate of an enzymatic process

33
Q

Inotropic

A

influencing the contractility of muscular tissue

34
Q

Non-dihydropyridine

A

a calcium channel blocker that is not in the class of drugs characterized by a base molecule of pyridine with pharmacologic action as L-type calcium channel blockers

35
Q

Sympathomimetic

A

mimicking the stimulation of the sympathetic nervous system; an agent with this quality

36
Q

Vagolytic

A

an agent that has inhibitory effects on the vagus nerve

37
Q

Ionic Channel Blockers

A

These drugs act through electrophysiological mechanisms by blocking the ionic channels across cell membranes that create the action potentials. The different classes of AADs acton different phases of the action potential. By blocking ionic currents, AADs can alter the length of the action potential and hence influence the rhythm and rate of depolarization.

38
Q

Vaughn Williams Classifications

A
39
Q

AADs can be broadly divided into rhythm or rate-control agents based on their primary usage in AF. Class I and III AADs are mainly used as _______

A

rhythm-control agents in AF

40
Q

AADs can be broadly divided into rhythm or rate-control agents based on their primary usage in AF. ___________ are mainly used as rate-control agents.

A

Class II and class IV AADs

41
Q

Which drug does not fit neatly into the Vaughan- Williams classification and is also used as a rate-control agent in AF.

A

Digoxin

42
Q

RHYTHM-CONTROL DRUGS

A

Rhythm-control agents for the treatment of AF include class I and class III drugs.

Agents in this Class I include:

  • Flecainide
  • Propafenone

​

Agents in this Class III include:

  • Amiodarone
  • Sotalol
  • Dofetilide
43
Q

Effect of class I (types IA, IB, and IC) on the action potential

A

Class I agents bind to and block the activation of sodium channels that are responsible for phase 0 rapid depolarization. These drugs dissociate from these channels slowly, resulting in a greater effect at more rapid heart rates, known as use dependence. The inactivation of sodium channels results in a prolonged PR interval and widened QRS com- plex, which slows the sinus rate. These agents also have a significant negative inotropic effect.

Class IA AADs include quinidine and disopyramide.

44
Q

Class IA Agents are:

A
  • Quinidine (rarely used due to mortality increases)
  • Disopyramide
45
Q

Class IC AAD Agents are:

A
  • Flecainide
  • propafenone
46
Q

Risk of Atrial Flutter with IC Agents:

A

As with all class IC agents, there is risk of atrial flutter with 1:1 AV conduction. This is a serious side effect, in which all impulses from the atria are conducted to the ventricles. Normally the AV node filters impulses so that only a portion is transmitted to the ventricles. In 1:1 conduction, the ventricular rate becomes dangerously high.

47
Q

torsade de pointes and AAD’s

A

When the underlying heart rate is slow, many of AAD agents may disproportionately prolong cardiac action potentials and can cause torsade de pointes. This is usually seen with QT-prolonging AADs. In rare instances, however, it can occur with drugs that are not approved by the FDA for cardiac treatment. The incidence of torsade de pointes associated with treatment with AADs is significantly higher in women than in men. The reason for this is unknown.4

48
Q

SODIUM CHANNEL BLOCK

A

The extent of sodium channel block depends on:

  • Heart rate and membrane potential
  • Drug-specific physicochemical characteristics that determine the time required to recover from a previous depolarization
  • pH

When sodium channels are blocked, greater membrane depolarization is needed to bring sodium channels from the rest state to the open state.

49
Q

CALCIUM CHANNEL BLOCK

A

The major electrophysiological effects resulting from blockade of cardiac calcium channels are in:

  • Slow-response tissues
  • The sinus
  • AV nodes

There are only two agents that can effectively block calcium channels in cardiac cells at clinically used doses — verapamil and diltiazem. Generally, they slow the heart rate.

50
Q

BLOCK OF BETA-ADRENERGIC RECEPTORS

A

Beta-adrenergic stimulation has several physiological effects:

  • It increases the magnitude of the calcium current
  • It slows calcium current inactivation
  • It increases the magnitude of repolarizing potassium and chloride
  • currents
  • It increases pacemaker current (thereby increasing sinus rate)
  • It can increase afterdepolarization-mediated arrhythmias (under pathophysiological conditions)

Particularly in patients undergoing chronic diuretic therapy, plasma epinephrine increases are associated with severe stress (e.g., acute MI or resuscitation from cardiac arrest) and lower serum potassium. These effects are inhibited by beta-adrenergic receptor antagonists, which have the ability to produce antiarrhythmic effects by reducing heart rate, decreasing intracellular calcium overload, and inhibiting afterdepolarization-mediated automaticity.

51
Q

adverse effects related to beta-blockade

A

There are a number of adverse effects related to beta-blockade, including:

  • Fatigue
  • Bronchospasm
  • Hypotension
  • Impotence
  • Depression
  • Aggravation of heart failure
  • Worsening of symptoms due to peripheral vascular disease
  • Masking of the symptoms of hypoglycemia in diabetic patients
52
Q

Which Classes Act on Which Phases of The AP?

A
  • Class I (Rythym) Works on Phase 0 Which is Sodium Dependent
  • Class II (Rate) Works on Phase 4 Which is Calcium Dependent
  • Class III (Rythym) Works on Pase 3 Which is Potassium Dependent
  • Class IV (Rate) Works on Phase 2 Which is Calcium Dependent

(The AP Phases run clockwise 0-1-2-3-4)

(The Drug Classes run Counterclockwise 1-2-3-4)

53
Q

STRATEGIES FOR
TREATING ATRIAL FIBRILLATION

A
  1. Rate Control
  2. Rythym Control
  3. Preventtion of Thromboembolic Stroke
54
Q

AAD’s By Control Method

A

Rhythym Control

  • Class IA - Sodium Channel Blockers
    • Quinidine
    • Disopyramide
  • Class IIA - Potassium Channel Blockers
    • Flecainide
    • Propafenone

Rate Control

  • Class II - Beta Blockers
    • Metoprolol
    • Bisoprolol
    • Carvedilol
  • Class IV - Calcium Channel Blockers
    • Verapamil
    • Diltiazem
55
Q

Class IA Agents

A

Class IA AADs include quinidine and disopyramide. Because of their prolonging effect on QT interval, these drugs may be associated with proarrhythmia and torsade de pointes. Quinidine is one of the old- est AADs, but it has been associated with increased mortality in AF patients and is now rarely used.

56
Q

Class IC Agents

A

Flecainide and propafenone are classified as class IC antiarrhythmic agents, although they are known to have significantly different electro- physiological and other properties. These drugs have important use-dependent effects on the sodium channels in the heart. Their effect on conduction slowing is more pronounced at higher heart rates.

57
Q

Mnemonic:

Sodium Better Kill Calcium

A

the order of the Vaughn Williams classes:

I - Sodium (Na+) Channel Blockers

II - Beta Blockers

III - Potassium (K+) Channel Blockers

IV - Calcium (Ca+) Channel blockers

58
Q

Class III Agents are:

A
  • Amiodarone
  • Sotalol
  • Dofetilide
  • Ibutilide
59
Q

Class II Agents are:

A
  • Metoprolol
  • Bisoprolol
  • Carvedilol
60
Q

Class IV agents are:

A
  • Verapamil
  • Digoxin

Multaq Phase One (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions