Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm Test 4 :( > Antiarrhythmic Drugs > Flashcards

Antiarrhythmic Drugs Flashcards

0
Q

after-depolarization

A

Arrhythmia mechanism

Early- Arises from prolonged action potentials (K channel blockers)
Delayed -arises from baseline conditions of Ca overload

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

Ectopic pacemaker

A

Arrhythmia mechanism
-Spontaneous generation of action potentials by tissue that does not normally display automaticitiy

Caused by tissue depolarization, following ischemia

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

Arrhythmias result from:

A

Abnormal initiation of cardiac action

  • ectopic pacemaker
  • after-depolarization

Abnormal conduction pathway (reentry)

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

Reentry

A

Impulse travels in a loop sending depolarizing impulses to the rest of the heart each time it goes around the loop

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

How to treat reentry Arrhythmias

A

Lengthen action potential, thus lengthening the refractory period so the action potential is extinguished by entering refractory tissue

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

Premature ventricular beat

A

Premature beat, often due to delayed after-polarization (lots of Ca)

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

Atrial/ventricular tachycardia

A

Due to reentry or ectopic pacemakers

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

Supraventricular tachycardia

A

Tachycardia originating in the SA node, AV node

Types:
AV nodal reentry
Wolff-Parksinson White
Accessory AV node

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

Paroxysmal tachycardia

A

Rapid abnormal beats

Sudden onset and offset

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

Flutter

A

Rapid regular contractions
Due to reentry
Can degenerate into fibrillation

Tx: dampen transmission at AV node-give time for ventricles to fill
Ca channel blocker

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

Fibrillation

A

Self-sustaining, random waves of depolarization which prevent coordinated blood-pumping contractions

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

Torsade de pointes

A

Rotation of the QRS vector on the EKG

Acquired: due to drug induced early after-depolarization (K channel blockers)

Congenital: long QT syndrome

  • mutation of Na channels that reduces inactivation so channels remain active longer, extending the plateau.
  • mutation of K channels so K can’t exit the cell, prolonging the action potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Class 1 drugs

A

Na channel blockers

1a: Na and K channel block
1b: block Na in depolarizes tissue
1c: potent and selective Na channel blockers

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

Class 1a drugs

A

1a: Na and K channel blocker

Na: decreases excitability and conduction velocity
K: prolong action potential by inhibiting repolarization

Quinidine
Procainamide

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

Class 1b dugs

A

1b: block Na in depolarizes tissue

Lidocaine

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

Class 1c drugs

A

1c: potent and selective Na channel blockers

Flecamide

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

Class II drugs

A

Beta blocker
Blocks NE stimulation of CA channels

Propranolol

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

Class III drugs

A

K channel blockers

Amiodarone, sotalol, dofetilide

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

Class IV drugs

A

Ca channel blockers

Vermapil, diltiazem

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

Adenosine

A

K channel activator

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

Quinidine

A

Class 1a: Na and K blocker

A. Flutter, a fib, supra ventricular Arrhythmias
V. Tachycardia

Not first line due to side effects

Cardio toxicity:
Lengthens QRS interval

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

Quinidine syncope

A

Lightheadedness and fainting caused by quinidine induced torsade de pointes

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

Quinidine side effects

A

Cardio toxicity
GI disturbances
Cinchonism (tinnitus, dizziness, blurred vision, HA)
Rare:thrombocytopenia, hepatitis,

23
Q

Procainamide

A

Class 1a: Na and K channel blockers

Metabolized to NAPA in liver- increased K channel blocking effects

Used for atrial and ventricular Arrhythmias, not good for long term use due to Lupus

24
Procainamide side effects
Torsades de pointes less common than quinidine Increases w/ elevated NAPA Hypotension Lupus erythematosus
25
Lidocaine
Class 1b drug: Na channel blocker in depolarized fast tissue Blocks open and inactivated Na channels more than closed channels * stronger effects on unhealthy, depolarized tissue - use after Arrhythmias (ectopic pacemakers) after an MI, w/ ischemia, digitalis toxicity
26
Lidocaine side effects
Affects CNS: parenthesis, prickling, drowsiness, tinnitus, blurred vision
27
Prophylaxis of lidocaine with patients thought to have an MI _____survival
Decreases | -maybe due to enhanced likelihood of heart block or HF
28
Flecainide
Class 1c: potent and selective Na channel blockers Strong effects on His/Purkinje fiber system *tx of supraventricular Arrhythmias (ex) A fib
29
Flecainide side effects
Significantly pro arrhythmic - greater increase of death with prolonged use
30
Propranolol and beta blockers
Blocks beta receptor stimulation of Ca channels *ventricular Arrhythmias due to exercise and emotion after MI to prevent infarction (Decrease AV nodal conduction, thereby decreasing ventricular rate) Slows upstroke of action potential in slow tissue (SA/AV nodes) Decreases excitability and slows conduction velocity -negative ionotrophic and chronotrophic effects (less contraction, and slower rate)
31
Beta blockers ______ long term survival
Increase
32
Metapropalol and other beta blockers also improve mortality in patients with mild to moderate_______
Heart failure
33
Amiodarone
Blocks K channels -> prolonged action potential duration Highly effective for supraventricular and ventricular tachyarrhythmias Many side effects, but still widely used, doesn't increase mortality
34
Amiodarone side effects
Extensively tissue bound -long half life: Concentration in tissues Skin deposits leading to photosensitivity GI, neurological, cardiovascular, hepatotoxic, thyroid Increases plasma level of other antiarrhymic drugs
35
Sotalol
Racemic mix of D- and L- isomers D: blocks K channels ( prolonging action potential) L: beta blocker (decreased AV transmission) Used to tx atrial flutter and fibrillation (rate reducing)
36
Sotalol side effects
Torsades de pointes | Same effects as other beta blockers
37
Beta blocker side effects
SA and AV block Sudden withdrawal may worsen angina and Arrhythmias Dyspnea
38
Dofetilide
Selective blocker of delayed rectifier K channels in heart Few extra cardiac effects High risk of Torsades de pointes Clinics must have training on how to monitor
39
Verapamil and Diltiazem
Class IV drugs: Ca channel antagonists Blocking Ca channels suppresses upstroke of phase 0 in slow tissue -slows excitability and conduction velocity Direct action on SA node generally slows HR ``` First choice (w/adenosine) for supraventricular tachycardia due to AV nodal reentry ( reduce ventricular rate in atrial flutter) ```
40
Verapamil and diltiazem side effects
Cardiac V. Fibrillation and hypotension if ventricular tachycardia is mid diagnosed as supraventricular tachycardia Constipation AV block, negative ionotrophic effects
41
Adenosine
Adenosine receptor agonist leads to opening of K channels which hyperpolarizes AV nodal tissue Terminates paroxysmal supraventricular tachycardia Short time of action
42
Digoxin
Cardiac glycoside ``` Used to treat CHF Positive ionotrophic effects -inhibits Na/K ATPase Increases intracellular Ca -> increased force of contraction -> Increased CO Not first line tx ``` Reduces ventricular rate in presence of a. A. Tachy, a. Flutter, a. Fib Acts like a beta blocker
43
One problem with digoxin and bacteria
Intestinal bacteria in 10% of patients degrade digoxin, so antibiotic tx can lead to a sudden increase in digoxin availability and toxicity
44
Digitalis toxicity
Low toxic dose Toxicity due to K+ depletion (diuretics) 1. V tachycardia and v. Fib 2. AV block 3. AV junctional rhythm 4. GI effects 5. Neurological effects
45
Diuretics
Reduce salt and water retention thereby reducing ventricular after load and preload -loss of K
46
ACE inhibitors
Block conversion of angiotensin I to angiotensin II | Reduce salt and water retention and reduce preload and after load
47
Angiotensin receptor agonist
Block the actions of angiowtrnsin II on AT1 receptors Reserved for pts that don't tolerate ACE inhibitors well
48
Beta blockers
Improve mortality by reducing ventricular
49
Vasodilators
Reduce after load | *hydralazine
50
K channel blockers mechanism
Lengthen action potential which lengthens refractory period and can interrupt re-entry Arrhythmias * Torsade de pointes Quinidine Procainamide (NAPA) Sotalol Dofetilide
51
Ca channel inhibition mechanism
Reduces excitability of slow AV nodal and SA nodal tissue -used for reducing ventricular rate during atrial tachyarrhythmias * SA and AV nodal block -too much dampening * negative ionotrophic effect
52
Na channel inhibition mechanism
Inhibits excitability in fast tissue -used for ventricular supraventircular arrythimias Lengthened QRS intervals Potent Na channel blockers are pro arrythmic
53
Used for re-entry arrythimias
K channel blockers
54
Used for reducing ventricular rate during atrial tachyarrhythmias
Ca channel blockers
55
Used for ventricular or supraventricular arrythimias involving fast tissue
Na channel blockers

Pharm Test 4 :( (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions