Brainscape's Knowledge GenomeTM

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


See full index

Cardio - Elam > Pathophysiology of Arrhythmias and Antiarrhythmic Drugs > Flashcards

Pathophysiology of Arrhythmias and Antiarrhythmic Drugs Flashcards

1
Q

What are the three types of enhanced automaticity?

A
  • Enhanced Normal
  • Enhanced Abnormal
  • Triggered
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of arrhythmia results from Digoxin Toxicity?

• what conditions will exacerbate this arrhythmia?

A
  • Digoxin causes INCREASED INTRACELLULAR Ca2+
  • Results in DELAYED AFTERDEPOLARIZATION
  • Exacerbated by: HYPOKALEMIA, CATECHOLAMINES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What triggers Torsade de Pointes?
• what type of arrhythmia is caused?
•What conditions will exacerbate this arrhythmia?

A
  • Prolonged QT interval leaves people susceptible to…
  • EARLY Afterdepolarization
  • Exacerbated by: HYPOKALEMIA and LOW HEART RATES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What areas of the heart may be affected by re-entry currents?
• Rate?
• Properties changed to end re-entry circuits

A

Areas
• Atrium = Flutter, Fibrillation
• AV node = Paroxymal Supraventricular Tachycardia
•Ventricle = Ventricular Tachycardia

Rate: typically more than 140 bpm

Properties:
• Conduction Velocity
• Refractory Period
• Convert Unidirectional Block to Complete block

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

What are the classes I through IV of Antiarrythmics?

• Drugs in each class?

A
  1. Na+ channel Blockers
    • Procainamide, Lidocaine
  2. Beta adrenoreceptor Blockers
    • Metoprolol, Atenolol
  3. K+ Channel Blockers
    • Amiodarone, Sotolol
  4. Ca+ Channel Blockers
    • Verapamil, Diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Class I antiarrhythmic agents
• How do they work?
• Cells that they act on?
• Net effect on AP?

A

MOA:

  1. Na+ channels are blocked
  2. Less Na+ allowed in the cell during depolarization
  3. INCREASED REFRACTORY PERIOD

Cells:
• Sodium Channel Dependence means only works on MYOCYTES in atria and ventricle

AP Effect:
• DECREASED phase 0 rise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q 
Differentiate between class IA, IB, and IC? 
• what is the root cause of these differences? 
• Drugs in each of these classes
A

Differences rooted in DIFFERENCES IN RATE OF DISSOCIATION from the Receptor - LONGER the drug is on the receptor the SHALLOWER the phase 0 slope

Class IA (intermediate dissociation const.): 
• also has K+ channel blocking properties that prologue AP
drugs: procaineamide, quinidine, disopyramide
Class IB (FAST dissociation const.): 
• good for antitachycardia
drugs: Lidocaine
Class 1C (SLOW dissociation const.): 
drugs: Flecanide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the ONLY drugs that both prolong phase 0 and prolong the overall AP?

A

• Class 1A sodium channel blockers

drugs: procaineamide, quinidine, disopyramide

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

How do Beta Blockers (class II antiarrhythmics) work as Antiarrhythmics?

A

• Slow ENHANCED AUTOMATICITY related to catecholamines and ischemia

these work really well to treat arrhythmias in patients with Coronary Heart Disease and Improves Survival

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

What arrhythmias are Beta Blockers used to treat?

A
  • Ventricular Pre-Mature Beats
  • EXCERCISE-INDUCED increases in VENTRICULAR rate and ATRIAL Fibrillation: slows AV nodes by blocking positive influence of Catecholamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do the Class III work?
• Arrythmia type?
• Risk?

A

MOA:

  1. K+ channel blockage
  2. less K+ escapes on depolarization
  3. LONGER EFFECTIVE REFRACTORY period
    * *Blockage in the SLOW conducting limb of the re-entry circuit**

Arrhythmia:
• Ectopic Pacemakers in Atria and Ventricles targeted

Risk:
• Prolonged QT => TORSADE DE POINTES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q 
How do class IV antiarrythmics work?
• Arrythmia type? 
• NAME THEM
A

Verapamil and Diltiazem (non-dihyropyridines)

MOA:

  1. Ca2+ channel blocked
  2. PACEMAKER cells can’t depolarize as easily

Arrythmia treated:
• blocks SA nodal AUTOMATICITY and AV nodal conduction

Risk:
• SA/AV BLOCK, impaired heart contractility

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

Class IV adverse effects and contraindications.

• Name them

A

Verapamil and Diltiazem

Risk:
• Complete SA or AV block
• Impaired Heart Contratility
• Hypotension

Contraindications:
• DO NOT GIVE TO PEOPLE WITH CHF, bradycardia, or AV block

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

How does digoxin work as an antiarrhythmic?
• Arrythmias treated?
•what patients is it most beneficial in?

A

In addition to effects of Na+/K+ channel inhibition leading to intracellular Ca2+ increases, DIGOXIN ALSO STIMULATES VAGAL ACTIVITY.

Effect:
•Reduction in SA nodal activity and AV nodal conductivity

Most beneficial in a CHF patient with Atrial Fibrillation

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

How does Adenosine work as an antiarrythmic?
• Arrythmias Treated
• Adverse Effects

A

MOA:
• HYPERPOLARIZATION of SA and AV nodes prevents heartbeat

Arrythmias Treated:
• Paroxysmal Supraventricular Tachy. (PSVT) by blocking AV node

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

You can make a DDx of two conditions using Adenosine. What two conditions does this include?
• why does this work?

A

DDx of Atrial Fibrillation/ Atrial Flutter vs. Paroxysmal Supraventricular Tachycardia

Adenosine ONLY works on SA/AV nodes - PSVT is a re-entry mechanism involving AV node while A. Fib. and A. Flutter are re-entry mechanisms involving only MYOCARDIAL tissue

If fibrillation doesn’t stop with adenosine then the arrhythmia was rooted in the SA or AV nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q 
Procainamide
• Class/MOA
• Tissues Affected
• SIDE EFFECTS 
• METABOLISM and excretion
• ADMINISTRATION
A

Procainamide

Class IA Na+ channel blocker, decreases phase 0 slope

MYOCARDIAL (atrial and ventricular tissues only affected)

Side Effects:
• DRUG INDUCED LUPUS
•TORSADES DE POINTES

**Hepatic Acetylation and Renal Excretion

***IV Administered b/c long term use give a HUGE chance of experiencing side effects

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

Why is there such a high risk of drug induced lupus for procainamide?
• Arrythmias treated

A

• 50% of the population are slow Acetylators putting them at a MUCH higher risk of Torsades de Pointes or Drug induced Lupus

***SHORT TERM TREATMENT FOR ATRIAL AND VENTRICULAR ARRYTHMIAS

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

A patient presents with arthralgia, skin rash, pleural and pericardial effusion. They were placed on an antiarrhythmic medication a few months ago. What is the name and MOA of the drug that caused this?
• What type of arrythmia were they probably being treated for?

A 
Procainamide: 
• Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels)

• Quinidine, Disopyramide

20
Q

A patient develops a low grade fever and petechiae over their extremities as a result of an antiarrhythmic, what drug is likely the cause?
• how does it work?

A 
Qunidine
• Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels)

• Procainamide and Disopyramide are the drugs in this class

21
Q

Quinidine
• Class/MOA
• Side effects
• Arryhthmias Treated

A 
Qunidine
• Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels) - works by slowing phase 0 depolarization

• Cause QT prolongation

Arryhthmias treated:
• Myocardial tissue based (a. fib, v. fib. etc)

Side Effects:
• DIARRHEA - severe and common
• AUTOIMMUNE THROMBOCYTOPENIA

22
Q

Disopyramide
• Class/MOA
• Side effects**
• Other drugs in class

A 
Qunidine
• Class 1A sodium channel blocker (since its class 1A it also blocks some K+ channels) - works by slowing phase 0 depolarization

• Cause QT prolongation

Side effects (IMPORTANT):
•PROMINENT VAGOLYTIC - atropine-like effects: URINARY retention, Dry Mouth, Blurred Vision
• May precipitate Heart failure

23
Q

A patient suffers a stoke as a result of atrial fibrillation. Would you use lidocaine to treat this patient?

A

NO, lidocaine is highly effective at treating v. fib. but NOT a. fib.

24
Q 
Lidocaine
• Class/MOA***
• Side effects
• Administration
• Arrythmias Treated
A

Class 1B
• 1B’s bind and block Na+ channels TRANSIENTLY
• Rapid dissociation means it has its GREATEST EFFECT ON ARRYTHMIC tissue due to rapid Kd

Side Effects:
• CNS (agitation, confusion, seizures)

Administration:
• MUST be given IV (b/c of 1st pass metabolism)

ONLY V. FIB treated

25
Q

Mexilitine
• Class/MOA***
• Side effects
• Administration

A

*Same as Lidocaine + frequent GI distress

Class 1B
• 1B’s bind and block Na+ channels TRANSIENTLY
• Rapid dissociation means it has its GREATEST EFFECT ON ARRYTHMIC tissue due to rapid Kd

Side Effects:
• CNS (agitation, confusion, seizures)

Administration:
• MUST be given IV (b/c of 1st pass metabolism)

ONLY V. fib treated

26
Q

Flecainide
• Class/MOA
• Arrythmias**

A

Class 1C
• Binds for a LONG TIME and blocks Na+ channels
• Increases Refractory Period in Atria and Ventricles

Side Effects:
• KILLS PATIENTS WITH COMPROMISED HEART - do not use under any circumstance

Arrythmias:
• A. Fib, A. Flutter
• SVT

27
Q

What Beta Blocker are used in treatment of Arrythmias?

A

AntiArryhMic PES

  • Atenolol
  • Acebutolol
  • Metoprolol
  • Propanolol
  • Esmolol
28
Q

Propanolol
• Cardioselective?
• arrythmia treated
• how?

A

NOT cardioselective

  • Ventricular Pre-mature Beats (VPBs)
  • Related to sympathetic activity
29
Q

Acebutolol
• Cardioselective?
• arrythmia treated
• how?

A

Cardioselective

• Treats premature beats related to Sympathetic activity

Safter in young People

30
Q

Metoprolol
• Cardioselective?
• arrythmia treated
• how?

A

Cardioselective

• Prevents SVTs by blocking the AV node

31
Q

Esmolol
• Cardioselective?
• arrythmia treated
• how?

A

Cardioselective

• SVTs - ULTRASHORT ACTING to block the AV node

32
Q

Atenolol
• Cardioselective?
• arrythmia treated
• how?

A

Cardioselective

• Used to control Atrial Flutter and Fibrillation AND prevent Paroxysmal Supraventricular Tachy. (PSVT)

LONG ACTING*

33
Q

What is the drug of choice in cardiac rescuscitation?

A

Amiodarone

34
Q

What is the second drug of choice in cardiac rescuscitation?

A

Lidocaine - was the drug of choice before it was replaced by amiodarone

35
Q

Amiodarone
• Class/MOA
• Arrythmias treated
• When is it used?

A

MOA:
Class III - Potassium Channel Blocker, blocks Na+, Ca2+, and Beta adrenergic receptors too

Arrthmias:
• Atrial and Ventricular Arrythmias

Use:
• Oral long term or IV in life threatening arrythmias (v. tach., v. fib.)

was created as an analogue to thyroid hormone

36
Q

Amiodarone:
• Administration
• Metabolism
• Elimination

A

Administration:
• Even if given orally an IV loading dose may be required

Metabolism:
• CYP3A4

Elimination:
• SLOW because T1/2 is 20-100 days

37
Q

Amiodarone:
• Side Effects
• Drug-Drug interactions

A

Amiodarone:
• PULMONARY FIBROSIS (5%) - if treating for V. Fib incidence is even higher

  • PHOTOSENSITIVITY DERMATITIS - gray-blue appearance
  • CORNEAL MICRODEPOSITS - visual halos
  • HYPOTHYROIDISM or HYPERTHYROIDISM

Drug-Drug:
• CYP3A4 metabolized so problems with Digoxin and Warfarin

38
Q

Sotalol
• Class/MOA
•Arrythmias treated
• Side Effects

A

Class III K+ blocker that also acts as a BETA blocker

Arrythmias Treated:
• Atrial, Ventricular, and AV nodal Arryhthmias

Side Effects: 
• TORSADE DE POINTE
• do not use if QT > 450 msec
• do not use with COPD, Asthma, CHF
• do not use with 2nd or 3rd degree heart block
39
Q

What are the Potassium Channel Blockers?
• Pure Blockers?
• Risk associated with all these drugs?

A

K+ blockers:
• Amiodarone
• Dronedarone
• Sotalol

PURE K+ blockers:
• Dofetilide
• Ibutilide

Risk:
• ALL can cause EARLY AFTER-DEPOLARIZATIONS leading to Torsade de Pointes - because their MOA is to prolong the QT

40
Q

Which of the K+ blockers is least likely to cause Torsade de Pointe?
• why?

A

Amiodarone - least likely to cause Torsade de Pointe because it acts on multiple channels decreasing cell ability to generate the Early Afterpotential needed to cause Torsade de Pointe

41
Q

Besides K+ channel blockers, what are some other drugs known to cause Torsade de Pointe?

A
  • Tricyclic Antidepressants
  • Na+ channel Blockers
  • non-sedating antihistamines
42
Q

what are two strategies used to control atrial Fibrillation/Flutter?
• Drug classes?

A

Rhythm Control
• These attempt to regain the original rhythm of the heart
• Class I and III antiarrythmics are used here (except for lidocaine - no atrial effect)

Rate Control
• Control how fast atrial impulses pass into the ventricle
• Class II and IV drugs work as well as Digoxin

43
Q

What drugs are effective in the treatment of Ventricular Tachycardia?

A

• ONLY class I and III drugs will be effective in treating V-tach.

If this were a recurrent V-fib. you would want to implant a defibrillator

44
Q

How do we treat Wolff-Parkinson-White?

• What drugs are DEFINITELY contraindicated in this syndrome?

A

WPW
Combination Therapy:
• Class Ia, II (usually procainemide, Beta-blocker)

Single Agent:
• Class III (amiodarone, sotolol) or CLASS IC (FeCanide)

DO NOT GIVE THE FOLLOWING: (b/c of opposite effects in atrial tissue)
• Digoxin
• Class IV drug (CCBs)
• Lidocaine (1B)

45
Q

What does the EKG for WPW look like?

A
  • Delta Wave

* Inverted T-wave

Cardio - Elam (4 decks)

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