Brainscape's Knowledge GenomeTM

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


See full index

MHD1/Pharm1 Exam 4 > (THER) Antiarrhythmic Agents I and II > Flashcards

(THER) Antiarrhythmic Agents I and II Flashcards

1
Q

What is the difference between pacemaker cells and regular myocytes?

A

They lack fast Na+ channels and as such their refractory period is determined by time, via a slow inward Na+ current (If = funny channels)

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

ALL arrhythmias result from what (3) things?

A
  1. Disturbed impulse formation
  2. Disturbed impulse conduction
  3. Combination of 1 and 2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

General symptoms from cardiac arrhythmias

A

Wide range from asymptomatic to severe hemodynamic consequences with reduced CO and death.

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

Types of Cardiac Arrhythmias (3)

A
  1. Too slow (bradycardia/bradyarrhythmia)
  2. Too fast (tachycardia/tachyarrhythmia)
  3. Asynchronous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In general, the aim of anti-arrhythmic therapy is to reduce…

A

Ectopic pacemaker activity and/or modify conduction characteristics to restore normal function.

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

What is one of the most dangerous potential side effects of anti-arrhythmic drugs?

A

The development of lethal arrhythmias because these drugs do not act specifically.

Depends on dosage or physciological conditions, such as faster heart rate, acidosis, electrolytes or presence of ischemia.

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

Are early afterdepolarizations usually at slow or fast heart rates? DAD’s?

A

EAD: slow

DAD: fast

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

What are the (3) requirements for reentry?

A
  1. Block (SA/AV block)
  2. Unidirectional conduction
  3. Slowed conduction through block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the (4) ways to regulate rate of pacemaker cells with abnormal automaticity?

A
  1. Reduction of phase 4 slope
  2. Increase of max Em
  3. Increase of threshold potential
  4. Increase of action potential duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How might a drug that affects the recovery time Na+ or Ca2+ channels effect arrhythmias?

A

Tachy-arrhythmias and premature beats (short cycle lengths) depend on the ability of Na+ channels to activate, inactivate and recover from inactivation RAPIDLY.

If a drug prolongs the recovery time of the Na+ channel (or Ca++ channel), then it may prevent re-entry, block tachycardias and prevent premature beats from occurring.

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

Describe the functioning of use-dependent or state-dependent drug action

A

They selectively block depolarized cells

They suppress channels that are used/inactivated frequently are more suceptible e.g. during fast tachy (when many channels are activated/inactivated) or in ischemic or infarcted tissues (more positive RMP).

Normal cells rapidly lose the drug during the resting phase

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

What drug is best for treatment of asymptomatic or minimally symptomatic arrhythmias?

A

TREATMENT SHOULD BE AVOIDED!

This is due to the potential of anti-arrhythmics to cause lethal arrhythmias

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

Name the Vaughan Williams Classification of Anti-Arrhythmic Drug Actions

A

Class I: Na+ channel blockers

Class II: B-adrenoceptor blockers

Class III: prolongation of the AP duration

Class IV: Ca2+ channel blockers

Other

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

Describe Class I Anti-Arrhythmics

What are they? What does their action depend on?

A

Na+ channel blockers (local anesthetic action)

Block fast Na+ channels. Actions depend on HR, Em and drug specific blocking kinetics

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

How do Na+ channel Blockers (Class I anti-arrhythmics) influence depolarization? repolarization?

A

Depolarization influence via: reduction of conduction velocity by reducing rate and magnitude of depolarization

Repolarization influence via: effects on K+ channels which may proong the AP duration

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

What are the (3) subclasses under type I anti-arrhythmics and which drugs full under which categories?

A

Class IA: intermediate kinetics, increases action potential duration (APD)

Drugs: Procainamide, Quinidine and Disopyramide

Class IB: Fast kinetics, decreases APD

Drugs: Lidocaine, mexiletine

Class IC: slow kinetics, no effect on APD

Drugs: Flecainide, Propafenone

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

Procainamide MOA and Effects

(what does it block? via what type of action? what is the electrical effect of its action? how does this effect rate?)

A

Blocks Na+ and K+ channels via use/state dependent action

This slows upstroke of AP and conduction, prolonging the QRS.

This has direct depressant actions on SA/AV nodes

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

Procainamide Indications

(also, what choice drug is it?)

A

Atrial and ventricular arrhythmias

2nd choice for vent. arrhythmias after acute MI

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

Procainamide route/half-life/ elimination

A

Route: PO/IV

t1/2: 3-4 hrs

elim: renal

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

Procainamide AEs (4)

A
  1. Torsades des pointes
  2. Hypotension
  3. Anticholinergic effects
  4. Lupus syndrome (long term use)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Quinidine is similar to what drug?

A

Procainamide

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

How does quinidine differ from procainamide?

A
  1. stronger anticholinergic effects
  2. cinchonism (headache, dizzines, tinnitus)
  3. it is rarely used because of cardiac/extra-cardiac AEs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Disopyramide is similar to what other drug?

A

Procainamide

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

How is disopyramide different from procainamide? (2)

A
  1. Much greater anticholinergic effects than procainamide and quinidine
  2. Negative inotropic effects which may induce heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Because of the anti-cholinergic effects of disopyramide, it requires co-administration of drugs that…

A

slow AV conduction

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

What is the only inducation that disopyramide is approved for?

A

It is a 1st or 2nd choice drug for ventricular arrhythmias

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

Lidocaine MOA/effects

(What does it do? What kind of drug action?)

A

Na+ channel blockade.

Use/state-dependent drug action

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

Lidocaine Indications

What is it not recommended for?

A
  1. Ventricular arrhythmias after MI
  2. 1st choice for V. tach/V. fib after cardioversion in setting of ischemia/infarction

Not recommended for prophylactic treatment (may increase mortality)

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

Lidocaine route/ metabolization/ t 1/2

A

Route: IV only

Metabolism: Extensive 1st pass metabolism

t1/2: 1-2 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Lidocaine AEs

A

Least cardiotoxic drug among Class I drugs

Neurological side ffects due to local anesthetic properties.

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

What is Mexiletine?

A

An oral lidocaine analogue. Actions/AEs are similar to lidocaine.

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

How is Mexiletine different from lidocaine?

(half-life? Other uses?)

A

t 1/2: 8-20 hours

Off-label use: chronic pain (diabetic neuropathy/nerve injury)

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

Flecainamide MOA

A

Na+ and K+ blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How does flecainamide affect AP duration and cholinergic effects?

A

Although K+ channel blocker, no effects on AP duration or anticholinergic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Flecainamide indications

A

Indication: supraventricular arrhythmias in patients with otherwise normal hearts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Flecainamide AEs

A

Increases mortality in patients with v. tach, MI, and ventricular ectopy (ALL CONTRAINDICATED)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Flecainamide 1/2 life and elimination

A

t 1/2: 20 hours

elmination: liver/kidney

38
Q

Propafenone MOA

What is it structurally similar to?

A

Potent blocker of Na+ channels; may also block K+ channels

Structurally similar to propanolol with weak B-blocking activity

39
Q

Indications for Propafenone

A

Used for supraventricular arrhythmias in patients with otherwise normal hearts.

40
Q

Propafenone AEs (4)

A
  1. Arrhythmogenic
  2. Sinus bradycardia/bronchospasm (B-blockade)
  3. Metallic taste
  4. Constipation
41
Q

Name the key non-selective B-blockers

A

PROPRANOLOL, sotalol and timolol

42
Q

Name the (relatively) “cardioselective” B-blockers

A

ESMOLOL and acebutolol

43
Q

Propranolol indications

A
  1. Prevention of recurrent infarction and sudden death after MI
  2. Atrial fibrillation
  3. Atrial flutter
  4. AV nodal reentry
44
Q

Propranolol AEs

A
  1. Bradycardia
  2. Reduced excercise capacity
  3. heart failure
  4. hypotension
  5. AV block

Contraindicated in patients with sinuse bradycardia and partial AV block

45
Q

What is the warning for propanolol for patients with asthma/COPD? Diabetics?

A
  • Bronchospasm caution in patients with asthma/COPD
  • May mask tachycardia associated with hypoglycemia in diabetic patients
46
Q

Key indication for esmolol

A

Supraventricular tachycardia (acute only)

47
Q

Esmolol half-life and route

A

t 1/2: 9 mins

route: IV only

48
Q

Amiodarone mechanism

A

Blocks K+ channels, as well as Na+ and Ca2+ channels and B-receptors.

Causes prolongation of AP duration, prolongs refractoriness and slows conduction, thereby suppressing abnormal automaticity.

49
Q

Amiodarone Indication (oral route? IV route?)

A

Oral:

  1. Recurrent v. tach or v. fib which is resistant to other drugs
  2. A. fib.

IV:

  1. 1st choice drug for out-of-hospital cardiac arrest
  2. termination of v. tach or v.fib
50
Q

Amiodarone half-life and route

A

3-10 days

Oral and IV

51
Q

Toxicities of Amiodarone (6)

Which is most important to watch out for?

A
  1. Accumulation in several organs (due to high lipophilicity)
  2. Bradycardia and heart block in patients with SA/AV node disease
  3. Pulmonary/hepatic toxicity
  4. Photodermatitis
  5. Cornea microdeposits
  6. Blocks T4 conversion so can cause thyroid issues

PULMONARY TOXICITY IS MOST IMPORTANT

52
Q

Dronedarone is a structural analogue of what? How is it different?

A

Amiodarone

It lacks the iodine atoms, thereby avoiding thyroxine metabolism

53
Q

Dronedarone Indications? Contraindications? 1/2 life?

A

Indications: A. fib/flutter

Contraindications: severe or recently decompensated symptomatic heart failure

t 1/2: 24 hrs

54
Q

Sotalol MOA

A

non-selective B-blcoker that inhibits delayed rectifyer and posisbly other K+ currents.

55
Q

Sotalol Indications

A
  1. Ventricular/ Supraventricular arrhythmias
  2. Maintenance of sinus rhythm in patients in patients with atrial fibrillation
56
Q

Verapamil MOA

A

Blocks activated and inactivated Ca2+ channels (L-type) primarily in the heart.

57
Q

Verapamil Effect

A

Use/state-dependent action

  1. Directly slows AV node conduction and increases AV node refractoriness
  2. Slows SA node automaticity

Lowers HR and increases PR interval

58
Q

Verapamil Indications (3)

A
  1. Supraventricular arrhythmias (1st choice)
  2. Re-entry arrhythmias/tachycardias involving the AV node
  3. Slows ventricular rate in atrial flutter/fibrillation
59
Q

Verapamil metabolization? Route? t1/2?

A

Extensive metabolism in the liver

Oral/IV

t1/2 = 7hrs

60
Q

General Adverse Effects associated with Verapamil

(After IV injection? Effects on inotropy? General effects to be wary of?)

A

Vasodilation after IV injection

Negative inotropic effects: hypotension and fibrillation

Generally must be carefully of arrhythmias/blocks in susceptible patients

61
Q

What can happen to patients on B-blockers if they take verapamil?

A

They have a high risk for heart block

62
Q

What drug is Diltiazem similar to? How is it different from this drug? (3)

A

Similar to Verapamil

  1. Lower cardioselectivity

Also used for 2. hypertension and 3. angina pectoris

63
Q

Adenosine MOA

A

Increases K+ conductance (hyperpolarization) and inhibits Ca2+ currents via purinergic receptors

64
Q

Effects of Adenosine (3)

(and where does it primarily work?)

A

Primarily acts on atrial tissues

  1. Slows AV node conduction
  2. Increases AV node refractoriness
  3. Produces transient cardiac arrest
65
Q

Adenosine indications

A

Conversion of paroxysmal (acute attack of) SVT to sinus rhythm

66
Q

Adenosine route/ t 1/2

A

Rapid IV bolus

t 1/2: seconds

67
Q

Adenosine interactions (2)/ AEs (2)

A

Interactions:

  1. Less effective with theophylline/ caffine
  2. Potentiated by dipyridamole

AEs:

  1. Flushing
  2. SOB
68
Q

Magnesium MOA

A

Mechanism unknown

(infuences Na/K+ and Ca channels/pumps to alter surface charge)

69
Q

Magnesium effect

A
  1. Anti-arrhythmic effects in some patients with normal Mg2+ levels.
  2. May inhibit afterdepolarizations
70
Q

Magnesium indications

A
  1. Digitalis induced arrhythmias with hypomagnesemia
  2. May be effective against torsades des points
71
Q

Magnesium Route of Admin

A

IV

72
Q

K+ MOA (in hyperkalemia? in hypokalemia?)

A

In hyperkalemia it depolarizes RMP

In hypokalemia it decreases K+ permeability

73
Q

K+ effects (in hyperkalemia? In hypokalemia?)

A

In hyperkalemia: slows conduction

In hypokalemia: enhances ectopic automaticity; lengthens AP duration

74
Q

K+ Indications

A

Maintains normal plasma K+

75
Q

K+ adverse effects

A
  1. May lead to reentry/Av block in hyperkalemia
  2. May lead to EADs (torsades de pointes) in hypokalemia
76
Q

K+ route

A

IV/PO

77
Q

Digitalis is what type of drug?

A

Cardiac Glycoside

78
Q

Digitalis MOA

A

Inhibit Na+/K+-ATPase, thereby increasing Na+Ca++ exchange, increase intracellular Ca++

79
Q

Digitalis effects (2)

A
  1. Positive inotropic actions (used widely in heart failure)
  2. Parasympathomimetic effects: (increase AV nodal refractoriness and slow AV node conduction.)
80
Q

Digitalis Indications

A
  1. Atrial arrhythmias (slow AV nodal conduction, thereby slowing excessively high ventricular rates)
  2. Heart Failure
81
Q

Digitalis t 1/2 and elimination

A

t 1/2: 40-160 hours

Renal elimination

82
Q

Digitalis AEs/toxicities

A
  1. Narrow therapeutic window may lead to DADs
  2. Visual disturbances (yellow-green)
  3. Drowsiness/depression
  4. GI issues
  5. Many drug interactions
83
Q

What physiological states may enhance the toxic effects of digitalis?

A

Hypokalemia/Magnesemia

84
Q

Severe digitalis toxicity can be reversed by…

A

Digoxin antibodies

85
Q

What patients are strictly contraindicated from use of verapamil?

A

Patients in V. Tach (due to the drugs negative inotropic effects)

86
Q

Name the non-pharmacologic anti-arrhythmic therapies (4)

A
  1. Vagal maneuvers
  2. Radiofrequency ablation/Cryoablation
  3. Electrical cardioversion
  4. Implantable Cardioverter-Defibrillator (ICD)
87
Q

Name the 1st and 2nd line drugs that should be used for:

Conversion to sinus rhythm

A
  1. Adenosine/ Amiodarone
  2. Flecainide
88
Q

Name the 1st and 2nd line drugs that should be used for:

Maintenance of sinus rhythm

A
  1. Amiodarone/Dronedarone
  2. Flecainide/Propafenone
89
Q

Name the 1st and 2nd line drugs that should be used for:

Ventricular rate control

A
  1. Diltiazem/verapamil
  2. Propanolol/Esmolol
90
Q

Name the drugs that should be used for:

V. tach/ V. fib in patients without heart disease

A
  1. Amiodarone
  2. Lidocaine
91
Q

Name the 1st and 2nd line drugs that should be used for:

A. fib

A
  1. Diltiazem/ Verapamil
  2. Propanolol
92
Q

Name the 1st and 2nd line drugs that should be used for:

Paroxysmal SVT

A
  1. Adenosine/Amiodarone
  2. Verapamil/Diltiazem/Propranolol

MHD1/Pharm1 Exam 4 (26 decks)

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