Brainscape's Knowledge GenomeTM

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


See full index

Cardio Week 2 > ICL 2.5: Antiarrhythmics > Flashcards

ICL 2.5: Antiarrhythmics Flashcards

1
Q

what are the 4 classes of antiarrhythmics?

A

CLASS I: membrane stabilizers = Na channel blockers

CLASS II: B Blockers

CLASS III: K+ channel modifier (prolongs AP)

CLASS IV: Ca++ channel blockers

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

what are the subcategories of class I antiarrhythmics?

A

class I antiarrhythmics = membrane stabilizers = Na+ channel blockers

1(A) –> moderately decrease velocity of phase 0

1(B) –> little decrease in velocity of phase 0

1(C) –> marked decrease in velocity of phase 0

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

which drugs are class 1(A) antiarrhythmic drugs?

A
  1. quinidine
  2. procainamide
  3. disopyramide

moderately decrease velocity of phase 0 and prolongs action potential duration

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

which drugs are class 1(B) antiarrhythmic drugs?

A
  1. lidocaine
  2. mexiletine

little decrease in velocity of phase 0 and may shorten action potential duration

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

which drugs are class 1(C) antiarrhythmic drugs?

A
  1. propafenone
  2. flecainide

marked decrease in velocity of phase 0 and may prolong action potential duration n

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

which drugs are class II antiarrhythmic drugs?

A

B blockers!

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

which drugs are class III antiarrhythmic drugs?

A

K+ channel modifier agents that widen AP

  1. amiodarone
  2. dronedarone
  3. dofetilide
  4. ibutilide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

which drugs are class IV antiarrhythmic drugs?

A

calcium channel blockers

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

which drugs are used for PSVT?

A
  1. adenosine

2. digoxin

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

which drugs are used for AV block?

A
  1. isoprenaline and other sympathomimetics

2. atropine and other anticholinergics

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

which conditions is digoxin used for?

A
  1. Afib
  2. atrial flutter
  3. PSVT

used to control ventricular rate

adenosine is used more clinically for PSVT because digoxin is slower

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

what is triggered activity?

A

a normal AP is interrupted/followed by an abnormal depolarization aka a triggering rhythm

this can be due to either a delayed after depolarization or an early after depolarization

delayed after depolarization is due to Ca+2 overload and can be caused by digoxin toxicity, myocardial ischemia, adrenergic stress or heart failure

early after depolarization is due to interruption in phase 3 depolarization and can be caused by slow heart rate, hypokalemia and drugs prolonging the QT interval (quinidine, stall, procainamide)

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

what is tornado de pointes?

A

due to marked prolongation of AP depolarization

you’ll see long QT interval and frequent changing of QRS

seen in polymorphic ventricular tachycardia

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

what is reentry?

A

when the tachycardia is initiated by an ectopic beat but sustained by a closed loop or re-entry circuit

a multidirectional arrhythmia where there’s a scar area and the normal propagation of electricity is disrupted

most tachycardia-arrhythmias are due to re-entry around ischemic/scarred areas

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

which antiarrhythmic drug class is sotalol?

A

it’s a class III K+ channel blockade but it also has na+ channel blocking ability!!

so it’s great for atrial and ventricular arrhythmia treatment

it can effect repolarizaiton so it effects APD by increasing it similar to class III antiarrhythmics

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

what are the effects of class I antiarrhythmic drugs?

A

Na+ channel blockers

decrease in conduction velocity manifests as widening of WRS duration

increase action potential threshold = decreased automaticity/acing threshold

slight decrease in AP duration = QT interval

negative inotropy = lowers Na+ permeability through the channel which means less Na+ in the cell –> more Na/Ca exchange since the exchanger lets Na+ in and Ca+2 out –> less intracellular Ca+2 and less contractility

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

how do class IA antiarrhythmic drugs effect AP?

A

moderate Na+ channel blockers

increases AP duration

increases effective refractory period

IA are the only ones that prolong QT

effect atrial, perkinje and ventricular cardiomyocytes

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

how do class IB antiarrhythmic drugs effect AP?

A

weak Na+ channel blockers

decreases AP duration and effective refractory period

effect perkinje and ventricular cardiomyocytes; don’t effect atrial cells!

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

how do class IC antiarrhythmic drugs effect AP?

A

strong Na+ channel blockers

no effect on AP duration or effective refractory period

effect atrial, perkinje and ventricular cells

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

what are the adverse effects of class IA antiarrhythmic drugs?

A
  1. pro-arrhythmic
    can cause tornado de pointes
  2. negative inotropic effect (quinidine)
  3. systemic lupus erythematosus (procainamide)
  4. anticholinergic side effects (disopyramide) –>mad as hatter, dry as a bone
21
Q

what are the adverse effects of class IB antiarrhythmic drugs?

A
  1. lidocaine –> seizures

2. mexilitine –> GI upset

22
Q

what are the adverse effects of class IC antiarrhythmic drugs?

A
  1. proarrhythmic

2. propafenone –> metalic taste

23
Q

what is the MOA of class II antiarrhythmic drugs?

A

decrease depressed SA node automaticity and prolong the refractoriness of the AV node

may prevent shortening of refractoriness at all levels in the heart

they also block adrenergic activation of Ca+2 channels = decreased force of contraciton

may suppress non-sustained ventricular arrhythmias especially in patients with an underlying adrenergic mechanism –> they’re the DOC in exercise-induced arrhythmias and in patients with long QT syndrome

B2 receptors are implicated in ischemia dependent ventricular fibrillation which may be prevented by nonselective blockade

24
Q

what are the benefits of B blockers?

A
  1. anti-ischemic effects

2. decrease force of the contraction and HR = decreased oxygen demand!!

25
Q

what are the clinical uses of B blockers?

A
  1. Afib
  2. atrial flutter
  3. atrial tachycardia
  4. PVCs
  5. recent MI
  6. adjunctive to NSVT an VT
26
Q

what are the side effects of B blockers?

A
  1. sinus bradycardia
  2. heart pauses
  3. can block/pause AV node
  4. heart failure
  5. CNS = fatigue, sedation, sleep disturbance, sexual dysfunction
  6. dyspnea/bronchospasm from B2 blocking
  7. hypoglycemia unawareness; blocks the symptoms of low BG
27
Q

when are B blockers contraindicated?

A
  1. cocaine toxicity
  2. pheochromocytoma

this would lead to unopposed alpha receptor stimulation = severe HTN, aortic dissection, coronary spasm or MI

28
Q

what are the antidotes to B blockers?

A
  1. atropine
  2. glucagon
  3. fluids
29
Q

how does glucagon act as an antidote to B blockers?

A

B blocker is blocking B receptor but glucagon can bypass that and still increase cAMP through activating a different receptor

30
Q

how do class I vs. III antiarrhythmics effect QRS complex length?

A

class I = Na+ channel blocker –> effect phase 0 which directly effects depolarization and would increase QT interval and QRS complex

class III = K+ channel blockers = effects phase 3 –> this is the repolarization so it wouldn’t effect the QRS complex but it would prolong the QT interval

31
Q

what is the MOA of class III antiarrhythmics?

A

increased APD = increased QT interval

many K+ channel blockers have a reverse use dependent effect and bind to resting channels –> AP prolongation is greater at slower rather than faster heart rates

there is increased risk of triggered activity due to prolonged phase 3 = early active depolarization

32
Q

which drugs are mixed vs. pure class III antiarrhythmics?

A

MIXED

  1. amiodarone
  2. dronedarone
  3. sotalol

PURE

  1. ibutilide
  2. dofetilide
33
Q

how does amiodarone work?

A

K+ channel blocker effects phase 3 and prolongs AP duration and refractory period in both atrial and ventricular cardiomyocytes

it has noncompetitive inhibition of alpha and B adrenergic receptors

reduces automaticity of automatic cells

34
Q

what are the EKG changes you would see with amiodarone?

A
  1. eduction of Sinus rate only by 15-20%
  2. increased PR and QT duration (prolongs)
  3. U waves and NS (nonspecific) Twave changes
35
Q

what are the clinical used of amiodarone?

A
  1. atrial flutter
  2. atrial fibrillation
  3. ventricular arrhythmias
36
Q

how would you treat stable ventricular tachycardia?

A
  1. IV amiodarone
  2. cardioversion with moderate sedation
  3. post EKG
  4. expert an expert
37
Q

what are the side effects of amiodarone?

A
  1. acute pulmonary toxicity = hypersensitivity pneumonitis
  2. long term toxicity = interstitial alveolar pneumonitis
  3. abnormal thyroid function test or thyrotoxicosis –> hypo or hyperthyroidism!
  4. abnormal liver function tests
  5. optic neurotis
  6. photosensitivity
  7. avoid grapefruit juice because prolonged QT
  8. caution with digoxin
38
Q

how would you treat ventricular tachycardia after an MI?

A

amiodarone

if that doesn’t work, use lidocaine or procainamide

then DC cardioversion

chronic reaction use ICD with or w/o amiodarone

39
Q

how would you treat ventricular tachycardia w/o structural heart disease?

A
  1. B blockers
  2. verapamil

chronically, use B blockers

40
Q

how would you treat ventricular fibrillation?

A

treat with defibrillation 1st

amiodarone 2nd to prevent recurrence

then lidocaine and procainamide

41
Q

what are class IV antiarrhythmic drugs?

A

they are effective in arrhythmias that must traverse Ca-dependent cardiac tissue like the AVN

they cause a use-dependent selective depression of calcium current in tissues that require the participation of L-type Ca channels

AV conduction velocity is decreased and effective refractory period increased by these drugs

PR interval is consistently increased

42
Q

what are the effects of Ca+2 channel blockers?

A
  1. inhibit the SA and AVN and tissue with abnormal automaticity dependent on Ca+2 channels
  2. generally little effect on the APD
  3. stops triggered activity like EAD and DAD
  4. slows HR and decreases contractility
  5. EADs due to oscillatory depolarizations due to waves of Ca+2 channel reactivation

DADs result from Ca+2 overload of the cell

43
Q

what are the clinical uses of Ca+2 channel blockers?

A
  1. SVTs
  2. atrial fibrillation
  3. certain ventricular arrhythmias
44
Q

what are the side effects of Ca+2 channel blockers?

A
  1. AV blocks

2. heart failure

45
Q

how does adenosine work?

A

binds to Adenosine receptors AV node

blocks Ca++ entry

blocks K+ channels –> hyperpolarizes cells

46
Q

what are the clinical uses of adenosine?

A

diagnosing atrial arrhythmias

47
Q

how does digoxin work?

A

blocks Na/K ATPase pump which allows more Ca+2 in the cell which increases force of contraction

it also increases vagal activity which decreases AV conduction and decreases HR –> decreases HR in both SA and AV nodes

toxicity = atrial tachycardias with AV node block

48
Q

what are the antidotes to digoxin?

A
  1. digibind

2. magnesium

Cardio Week 2 (6 decks)

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