Brainscape's Knowledge GenomeTM

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


See full index

medicine block (y3) > Week 4: Cardiology (5) (antiarrhythmic) > Flashcards

Week 4: Cardiology (5) (antiarrhythmic) Flashcards

1
Q

rationale for antiarrhythmics

A

prevent dangerous and restore normal sinus rhythm and conduction
o Decrease conduction velocity
o Change duration of the effective refractory period (ERP)
o Supress abnormal automaticity

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

classification system of antiarrhythmics

A

vaughan williams classification

1B

1C

II

III

IV

V

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

class IB

A

action: sodium channel blockers (no change in phase 0)
e. g. lidocaine

]

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

class IC

A

action: sodium channel blockers (marked phase 0)
e. g. flecainade and propafenone

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

class II

A

action: B blocker
e. g. bisoprolol, metoprolol, propranolol

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

class III

A

action: potassium channel blockers- prologed repolarisation
e. g. amiodarone, sotalol

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

class IV

A

action: calcium channel blcoker
e. g. verapamil, dilitiazem

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

class V

A

action: variable
e. g. adenosine, digoxin, atropin, ivabradine

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

most efficacious drug

A
  • Amiodarone is the best
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

most tolerable drug

A

B blockers most tolerable, amiodarone least (e.g. sunburn and breathlessness)

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

when are class 1B agents used e.g. lidocaine

A
  • Ventricular tachycardia (in relation to a scar in the heart- ischaemia)
  • Not used in atrial arrhythmias or AV junctional arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ventricular tachycardia and class 1B agents e.g. lidocaine

A
  • Damaged areas of myocardium may be depolarised and fire automatically
  • More Na+ channels are open in depolarised tissue
    • Lidocaine blocks these sodium channels
    • Preventing automatic firing of depolarised ventricular tissue
  • Effect on cardiac activity
    • Fast binding offset kinetics
    • In normal tissue
      • No change in phase 0 (no tonic block)
      • ADP slightly decreased
    • Fast beating or Ischaemic tissue
      • Increase threshold for Na
      • Decrease phase 0 conduction
    • Effect on ECG
      • None in normal
      • In fast beating or ischaemic = increase QRS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

adverse drug repsonse clas 1B agents

A
  • Less proarrhythmic than Class 1A (less QT effect)
  • CNS effect: dizziness, drowsiness
  • Abdominal upsets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

when are class 1C agents used e.g. flecainide

A
  • Wide spectrum
    • Supraventricular arrhythmias
      • Atrial fibrillation
      • Atrial flutter
    • Premature ventricular contractions
    • Wolff- Parkinson-White syndrome (ectopic beats)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MOA of class 1C agents e.g. flecainide

A
  • Na+ channel blocker
  • Effect on cardiac activity
    • Very slow binding offset kinetics (>10s)
    • In normal tissue
      • Decreased phase 0 (Na+)
      • Decreased automaticity
    • In rapidly depolarising atrial tissue
      • Increased APD (K+) and increased refractory period
    • Effect on ECG (beware of Torsades de Pointe)
      • Increase PR
      • Increase QRS
      • Increase refractory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

ADR class 1C e.g. flecainide

A
  • Pro-arrhythmia and sudden death especially with chronic use and ins structural hear disease
  • Increase ventricular response to supraventricular arrhythmias (flutter)
  • CNS and GI effects like other local anaesthetics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

contraindication of class 1C

A
  • Coronary heart disease
  • Structural heart disease e.g. previous MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

when are class 2 agents used e.g. B blockers

A
  • Treating sinus and catecholamine dependent tachycardia e
  • Converting repentant arrythmias at AV node
  • Protecting the ventricles from high atrial rates (slow AV conduction) in atrial flutter or atria fibrillation
19
Q

MOA of class 2 agents e..g b blockers

A
  • Inhibition of sympathetic influences on cardiac electrical activity i.e. B1 antagonists- blocking NA binding (also reduce sympathetic stimulation of aberrant pacemaker activity- ectopic foci)
  • Reduction in influx of calcium
    • Effect on cardiac activity
    • Increase Action Potential Duration and refractory period
    • Decrease phase 4 depolarisation (catecholamine dependent)
    • Blocking arrhythmias caused by re-entry
  • Effect on ECG
    • Increase PR
    • Decrease HR
20
Q

ADR of class 2 agents

A
  • Bronchospasm
  • Hypotension
21
Q

contraindication of class 2 agents e.g. propanolol

A
  • Don’t use if partial AV block or acute heart failure
  • Asthma
22
Q

uses of class 3 agents e.g. amiodarone

A
  • Very wide spectrum- effective for most arrhythmias
23
Q

MOA of class 3 agents e.g. amiodarone

A
  • Block potassium channels
    • Class effects of 1,2,3 and 4
  • Reduction in influx of calcium
  • Effect on cardiac activity
    • Increase APD and refractory period and increase APD (K+)
    • Decrease phase 0 and conduction (Na)
    • Increase threshold for AP
    • Decrease phase 4 depolarisation (B block and Ca2+ block)
    • Decrease speed of AV conduction
  • Effect on ECG
    • Increase PR
    • Increase QRS
    • Increase QT
    • Decrease HR
24
Q

ADR for class 3 agents

A
  • Pulmonary fibrosis
  • Hepatic injury
  • Thyroid disease
  • Photosensitivity (factor 50)
  • Optic neuritis (transient blindness)
25
Q

contraindication of type 3 agents

A

may need to reduce dose of digoxin and monitor warfarin

26
Q

sotalol (oral) is used for

A
  • Wide spectrum: Supraventricular and ventricular tachycardia
27
Q

MOA of sotalol

A
  • Block potassium channels
    • Class effects of 1,2,3 and 4
  • Effect on cardiac activity
    • Increase APD and refractory period in atrial and ventricular tissue
    • Slow phase 4 (B blockers)
    • Slow AV conduction
  • Effect on ECG
    • Increase QT
    • Decrease HR
28
Q

adr sotalol

A
  • Proarrhythmic
  • Fatigue
  • insomnia
29
Q

class 4 agents uses e.g. verapamil and diltiazem

A
  • Control ventricles during supraventricular tachycardia
  • Convert supraventricular tachycardia (re-entry around AV)
  • Used with people who have asthma (cant use B blockers)
30
Q

MOA of class 4 agents

A
  • Calcium channel blockers
  • Effect on cardiac activity
    • Slow conduction through Av (Ca2+)
    • Increase refractory period in AV node
    • Increase slope of phase 4 in SA to slow HR
  • Effect on ECG
    • Increase PR
    • Decrease HR (or increase depending on baroreceptor reflex)
31
Q

ADR class 4 agents e.g. verapamil

A

GI problems (constipation)

32
Q

contraindication of class 4 agents e.g. verapamil

A
  • AV block- can get asystole if B blocker is on board
    • Don’t give B blockers and CBB together
  • Hypotension
33
Q

NEVER give …… with……

A
  • Don’t give B blockers and CBB together
34
Q

example of class 5 antiarrhythmis agents

A

ivabradine

digoxin

atropine

35
Q

ivabradine

A

Drug name: Ivabradine

  • Oral

Uses

  • Reduce inappropriate sinus tachycardia
  • Reduce heart rate in heart failure and angina (avoiding blood pressure drops)

Mode of actions

  • Blocks If ion current highly expressed in sinus node
  • Cardiac effect
    • Slows sinus node but does not affect blood pressure

Adverse drug reaction

  • Flashing lights
  • Teratogenicity not known (avoid in pregnancy)

Contraindication

  • Pregnancy
36
Q

digoxin (cardiac glycoside)

A

Uses

  • Treatment to reduce ventricular rates in AF and flutter

Mode of actions

  • Enhances vagal activity (increases k+ current, decreases calcium current and increases refractory period)
  • Slows AV conduction, slowing HR
37
Q

atropine

A

Uses

  • Vagal Bradycardia

Mode of actions

  • Selective muscarinic antagonist
  • Blocks vagal activity to speed AV conduction and increase HR
38
Q

Which IV drug would you use first for VT

A

Depends on which drugs that are already on

  • Intravenous metoprolol/bisoprolol
    • If BP low- cardiovert electrically
    • If BP okay just metoprolol
  • If already on B blocker
    • IV lignocaine or oral mexiletine
  • Or Amiodarone (IV central line)
39
Q

Should flecainide be used alone for atrial flutter?

A

No- give AV nodal blocking drugs to reduce ventricular rates in atrial flutter

  • Can be used alone in atrial fibrillation
40
Q

Best drug for WPW?

A
  • Flecainide or amiodarone
  • Avoid AV nodal blocking drugs (B blockers) due to risk of pre-excited AF and therefore VF
41
Q

drug used in re-entrant SVT in the acute setting

A

adenosine

verapamil

flecainide

42
Q

drug used in re-entrant SVT in the chronic setting

A

bisoprolol, verapamil

sotalol

flecainide

amiodarone

43
Q
  1. Which drugs would be used for ectopic atrial tachycardia?
  • First line- bisoprolol (safest
  • Next line- CCB
  • Lastly: Flecainide, sotalol, amiodarone
A
  • First line- bisoprolol (safest
  • Next line- CCB
  • Lastly: Flecainide, sotalol, amiodarone
44
Q

which drugs for sinus tachycardia

A

ivabradine if not drop in BO

bisorpolol, verapamil

medicine block (y3) (38 decks)

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