Brainscape's Knowledge GenomeTM

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


See full index

CPT > Session 7 Cardiac Arrhythmia Drugs > Flashcards

Session 7 Cardiac Arrhythmia Drugs Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

What are arrhythmias?

A

Heart condition where disturbances in:

  • pacemaker impulse formation
  • contraction impulse conduction
  • combination of the two
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What do arrhythmias results in? (Refer to rate etc)

A

Results in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal cardiac output

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

What is meant by resting potential and what is it caused by?

A

= a transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell

Caused by unequal distribution of ions inside vs outside ell

  • Na+ higher outside than inside cell
  • Ca+ much higher outside than inside cell
  • K+ higher inside cell than outside

Maintenance by ion selective channels, active pumps and exchangers

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

What are the effects of class 1 drugs?

What do they block?

A

Block Na+ channels

= marked slowing conduction in tissue (phase 0 - the steep upward stroke)

Plus minor effects on action potential duration

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

What are the effects of class 2 beta-blockers?

A

They diminish phase 4 depolarisation and automaticity

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

Effect of class 3 drugs?

what do they block?

A

Block K+ channels

= increase action potential duration

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

What are the effects of class 4 drugs?

What do they block?

A

Calcium blockers

= calcium channel blockers DECREASE INWARD Ca2+ currents .. this results in a DECREASE of phase 4 spontaneous depolarisation

= they affect plateau phase of action potential

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

What drugs affect automaticity?

A

Beta agonists - increase the slope at phase 4 (i.e. make it steeper)

Muscarinic agonists, adenosine - decrease slope at phase 4

(Check this)

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

What are the two classes of rhythms associated with abnormal impulse generation?

NB: think about flow chart in slides

A
  1. Automatic rhythms

2. Triggered rhythms

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

What can automatic rhythms be broken down into (class wise)?

A

Enhanced normal automaticity —> increased AP from SA node

OR

Ectopic Focus —> AP arises from sites other than SA node

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

What can ‘triggered rhythms’ be broken down into?

A

delayed afterdepolarisation

OR

Early afterdepolarization

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

When referring to abnormal conduction, what two classes of problems come under this?

A 
Conduction block (1st, 2nd or 3rd degree) 
 =when the impulse is not conducted from the aria to the ventricles

Reentry (circus movement or reflection)

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

What is wolf-Parkinson-white syndrome?

A

An example of abnormal anatomic conduction that is present only in small populations

It leads to preexcitation

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

What are the actions of drugs either;

A) if there is abnormal generation

B) if there is abnormal conduction

A

Abnormal generation

  • decrease of phase 4 slope (in pacemaker cells)
  • raises the threshold

Abnormal conduction

  • decrease conduction velocity
  • increase EPR (so the cell wont be reexcited again)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Why do arrhythmias occur? 2

A

Automatic or triggered activity

Re-entry due to scar, anatomy of AV node slow and fast pathway/WPW

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

What is the goal for anti-arrhythmic drugs?

A

To restore normal sinus rhythm and conduction and to prevent more serious and possible lethal arrhythmias from occurring

These drugs are used to
A) decrease conduction velocity
B) change the duration of ERP
C) suppress abnormal automaticity

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

Class 1A drugs:

Action

Drug example

A

Action = moderate phase 0

Drugs = Quinidine, procainamide

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

Class 1B drugs

Action

Drug name

A

Action = no change in phase 0

drug name = lidocaine

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

Class IC drugs

Action

Drug name

A

Action = marked phase 0

Drugs = flecainide, propafenone

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

Class II drugs

Action

Drugs

A

Action = beta-adrenergic blockers

Drugs = bisoprolol, metoprolol, propranolol (esmolol)

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

Class III drugs

Action =

Drugs =

A

Action = prolong repolarisation

Drugs = amiodarone, sotalol

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

Class IV drugs

Action

Drugs

A

Action = calcium channel blockers

Drugs = verapamil, diltiazem

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

Class 1A agents

Absorption and elimination?

A

Oral or IV

24
Q

Class 1A agents

Effects on cardiac activity?

A

Decrease conduction (decrease phase 0 of the action potential (Na) )

Increase refractory period (increase APD (K+) and increase Na inactivation)

Decrease automaticity (decrease slope of phase 4, fast potentials)

Increase threshold (Na+)

25
Q

Class 1A agents

Effects on ECG?

A

Increase QRS

+/- PR

Increase QT

26
Q

Uses of class 1A drugs?

A

Wide spectrum

Quinidine = maintain sinus rhythms in atrial fibrillation and flutter and to prevent recurrence, Brugada syndrome

Procainamide = acute IV treatment of supraventricular and ventricular arrhythmias

27
Q

Side effects of class 1A drugs?

A

Hypotension

Reduced CO

Proarrhythmia (generation of a new arrhythmia)
E.g. Torsades de Points (increased QT interval)

Dizziness, confusion, insomnia, seizure (at high doses)

GI effects (common)

Lupus-like syndrome (particularly with procainamide)

28
Q

Class 1B agents

Absorption and elimination?

A

Lidocaine = IV only

Mexiletine = oral phase

29
Q

Class 1B agents.

Effects on cardiac activity

A

Fast binding offset kinetics

No change in phase 0 in normal tissue (no tonic block)

APD slightly decreased (normal tissue)

Increase threshold - Na+

Decrease phase 0 conduction in fast beating or ischaemic tissue

30
Q

Class 1B agents

Effects on ECG?

A

None in normal

In fast beating or ischaemic

Increase QRS

31
Q

Class 1B agents

Uses

A

Acute: ventricular tachycardia (esp during ischaemia)

NB: Not used in atrial arrhythmias or AV junctional arrhythmias

32
Q

Class 1B agents

Side effects?

A

They’re less pro-arrhythmic than class 1A (less QT effect)

CNS effects: dizziness and drowsiness

Abdominal upset

33
Q

Class 1C agents

Absorption and elimination?

A

Oral or IV

34
Q

Class 1C agents

Effects on cardiac activity

A

Very slow binding offset kinetics (>10 s)

Substantially decrease phase 0 (Na+) in normal

Decrease automaticity so increase threshold

Increase APD (K+) and increase refractory period

35
Q

Class 1C agents

Effects on ECG?

A

Increase PR

Increase QRS

Increase QT

36
Q

Class 1C agents

Uses?

A

Wide spectrum

Supraventricular arrhythmias (fibrillation and flutter)

Premature ventricular contractions

WPW syndrome does

37
Q

Class 1C drugs

Side effects

A

Pro arrhythmias and sudden death especially in chronic disease

structural heart disease - there is Increased ventricular response to supraventricular arrhythmias (flutter)

38
Q

Class 2 agents

Absorption and elimination =

Cardiac effects =

Effects on ECG =

Uses =

Side effect =

A

Absorption and elimination

  • propranolol = oral or IV
  • metoprolol 5mg IV (oral too)
  • bisoprolol = oral
  • esmolol = IV ONLY (very short acting - half life is 9 mins)

Cardiac effects

  • increase APD and refraction period in AC node to slow AV conduction velocity
  • decrease phase 4 depolarisation (catecholamine dependent)

Effects on ECG

  • increase PR
  • decrease HR

Uses

  • treating sinus and catecholamine dependent tachycardia
  • converting reentrant arrhythmias at AV node
  • protecting the ventricles from high atria rates (slow AV conduction) in atrial flutter or atrial fibrillation

Side effect

  • bronchospasm
  • hypotension
39
Q

Class III agents - AMIODARONE

Absorption and elimination =

Cardiac effects =

Effects on ECG =

Uses =

Side effect =

A

Absorption and elimination = oral or IV (half life is about 3 months)

Cardiac effects

  • increase refractory period and increase APD
  • decrease phase 0 and conduction
  • increase threshold
  • decrease phase 4 (beta blocker and calcium block)
  • decrease speed of AV conduction

Effects on ECG

  • increase PR
  • increase QRS
  • increase QT
  • decrease HR

Uses
* very wide spectrum! Effective for most arrhythmias

Side effect

  • serious ones that increase with time!
  • pulmonary fibrosis
  • hepatic injury
  • increase LDL cholesterol
  • thyroid disease
  • photosensitivity
  • optic neuritis (transient blindness)
40
Q

Class III = SOTALOL

Absorption

Cardiac effects

ECG effects

Uses

Side effects

A

Absorption = oral

Cardiac effects

  • increase APD and refractory period in atrial and ventricular tissue
  • slow phase 4 (beta blocker)
  • slows AV conduction

ECG effects

  • increases QT interval
  • decreases HR

Uses

  • wide spectrum!
  • supraventicular and ventricular tachycardia

Side effects

  • proarrhythmia
  • fatigue
  • insomnia
41
Q

Class IV agents : verapamil and diltiazem

Absorption

Cardiac effects

ECG effects

Uses

Side effects

A

Absorption / administration

  • verapamil = oral or IV
  • diltiazem = oral

Cardiac effects

  • slow conduction through AV (calcium)
  • increase refractory period in AV node
  • increases slope of phase 4 in SA to slow HR

ECG effects

  • increases PR interval
  • can increase OR decrease HR depending on BP response and baroreflex

Uses

  • control ventricles during supraventricular tachycardia
  • convert supraventricular tachycardia (re-entry around AV)

Side effects

  • caution when partial AV block is present as can get asystole if beta blocker being used
  • caution when hypotensive, decrease CO or sick sinus
  • some GI problems e.g. constipation
42
Q

Adenosine

Administration

Mechanism

Cardiac Effects

Uses

A

Administration
* rapid IV bolus (very short half life - seconds!)

Mechanism

  • natural nucleoside that Indus A1 receptors an activates K+ currents in AV and SA node
  • decrease APD and hyperpolarisation can lead to decreased HR

Cardiac Effects
* slows AV conduction

Uses

  • convert re-entrant supraventricular arrhythmias
  • diagnosis of coronary artery disease (scans)
43
Q

Vernakalant

Admin

Mechanism

Cardiac effects

Side effects

Uses

A

Vernakalant

Admin = IV bolus over 10 minutes

Mechanism = blocs atrial specific K+ channels

Cardiac effects = slows atrial conduction
* increased potency with higher heart rates

Side effects

  • hypotension
  • AV block
  • sneezing and taste disturbances

Uses
* convert recent onset atrial fibrillation to normal sinus rhythm

44
Q

Ivabradine

Administration

Mechanism

Cardiac effects

Side effects

Uses

A

Admin = orally in 2.5 mg bolus dose up to 10mg

Mechanism = blocks If ion currently that is highly expressed in Sinus node

Cardiac effects = slows the sinus node but does not affect BP

Side effects = flashing lights / teratogenicity not known so avoid in pregnancy

Uses = reduce inappropriate sinus tachycardia
* reduce HR in heart failure and angina - as it avoids BP drops

45
Q

Digoxin

Mechanism

Uses

A

Mechanism

  • enhances vagal activity - increased K+ currents, decreases Ca2+ currents and increases refractory period
  • slows AV conduction and slows HR

Uses
* treatment to reduce ventricular rates in atrial fibrillation and flutter

46
Q

Atropine

Mechanism

Cardiac effects

Uses

A

Mechanism = selective muscarinic antagonist

Cardiac effects = block vagal activity to speed AV conduction and increase HR

Uses = treats vagal bradycardia

47
Q

Which anti-arrhythmic drug has the most efficacy?

A

Amiodarone

48
Q

Which anti arrhythmic drug is the worst in terms of safety and tolerability? And the best?

A

Worst = amiodarone

Best = beta blockers

49
Q

Which drugs should be used in AF?

A
  • rate control - slow conduction though AV node to reduce heart back to normal levels
    = bisoprolol
    = verapamil
    = diltiazem +/- digoxin
  • rhythm control
    = sotalol
    = flecainide with bisoprolol
    = amiodarone
50
Q

Which drugs for VT?

A

Depends on what drugs already prescribed!

  • metoprolol/bisoprolol
  • lignocaine/mexiletine
  • amiodarone

IV metoprolol/lignocaine or amiodarone

51
Q

Should flecainide be used alone in atrial flutter?

A

No

Give AV nodal blocking’s drugs to reduce ventricular rates in atrial flutter

52
Q

Best drug for treatment of WPW?

A

Flecainide

Amiodarone

53
Q

List drugs that could be used in re-entrant NCT

A

Acutely (IV)

  • adenosine
  • verapamil
  • flecainide

Chronic (repeated episodes - orally)

  • bisoprolol, verapamil
  • sotalol
  • flecainide, procainamide
  • amiodarone
54
Q

Which drugs for ectopic beats?

A
  • bisoprolol = first line

Then flecainide, sotalol or amiodarone

55
Q

Which drugs to treat sinus tachycardia?

A
  • Ivabradine (no drop in BP!)

* bisoprolol, verapamil

CPT (23 decks)

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