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PHA321 > Antidysrhyrhmic Drugs > Flashcards

Antidysrhyrhmic Drugs Flashcards

1
Q

Arrhythmias are always symptomatic. True or false?

A

False. They may be symptomatic or asymptomatic.

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2
Q

Common symptoms of arrhythmia

A

sudden death
Syncopal attacks
Heart failure
Dizziness
Palpitations

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3
Q

Factors precipitating arrythmias:

A

MS HIDI

Mechanical injury
Stretching
Hypoxia
Ischemia
Drugs (anti-arrhythmics etc)
Imbalance of electrolyte / pH imbalance

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4
Q

Causes of Arrhythmias:

A

Atherosclerosis
Coronary artery spasms
Myocardial ischemia
Conduction block.

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5
Q

Types of arrhythmias

A

2SE2A2PV

Sinus tachycardia: HR > 100bpm
Sinus bradycardia: HR < 60bpm
Extrasystoles
Atrial flutter
Atrial fibrillation
Paroxysmal atrial tachycardia
Paroxysmal ventricular tachycardia
Ventricular fibrillation

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6
Q

Torsade de pointes occurs when

A

…a long QT causes undulating baseline/rapid asynchronous complexes on ECG.

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7
Q

Atrial rate in atrial tachycardia

A

100 - 250 bpm

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8
Q

What is so unique about PSVT?

A

Electrical signals, starting in the upper chambers fire irregularly, preventing the heart from having enough time to fill with blood before pumping out to the rest of the body

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9
Q

What on an ECG is indicative of ventricular tachycardia?

A

Widened QRS

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10
Q

What is the heart rate in ventricular tachycardia?

A

100 to 120bpm

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11
Q

What is the heart rate in PSVT?

A

120 to 230

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12
Q

Difference between V tach and V fib

A

In Vtach, spontaneous ventricular automaticity causes chaotic faster HR with widened QRS. Drugs like cocaine, meth, and structural heart dx are responsible.

In VFib, the ventricles contract rapidly and uncoordinatedly, causing sudden cardiac arrest and even death. It is caused by prior heart disease or electrolyte imbalance.

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13
Q

The four parameters explained in the electrophysiology of the heart include:

A

Automaticity
conduction
Excitability
refractory period

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14
Q

HIS/Purkinje fibres are specialised conducting tissues. True or false?

A

True

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15
Q

What are the automatic cardiomyocytes?

A
  • SAN
  • AVN
  • HIS/Purkinje
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16
Q

Non-pacemaker AP occurs in how many phases?

A

5

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17
Q

Give brief overview of events in Phases 0 to 4

A

0 - Na channels open (rapid depolarisation)
1 - Na channels close (early repolarisation)
2 - Ca channels open, fast K channels close (plateau)
3 - Ca channels close, fast K channels open (repolarisation)
4 - Resting potential

18
Q

What kind of abnormal conduction is seen in PSVT and WFW syndrome?

A

Reentry

19
Q

Give examples of conditions with micro entry circuit

A

Ventricular extrasystole
Ventricular tachycardia
V.fib

20
Q

What is a Conduction block?

A

Conduction from SA node to AV node could be slowed down by ischemia, causing partial to complete AV block or sick sinus.

21
Q

2nd degree AV block

A

Some supraventricular complexes are not conducted, missed beat.

22
Q

3rd degree AV block

A

No supraventricular complexes are not conducted, ventricles generate own impulse.

23
Q

What is the most common cause of conduction block?

A

Ischemia

24
Q

When are arrhythmias left untreated?

A

Simple arrhythmic agents e.g. Atrial extrasystole and ventricular extrasystole in a normal heart

25
Q

In what kind of arrhythmias are vigorous therapies required?

A
  • Life threatening conditions like Ventricular tachycardia.
  • Arrhythmias causing hypotension , breathlessness or heart failure.
  • Marked palpitation as in PSVT, sustained V.tach, Atrial fib, torsades de pointes.
26
Q

What are the classes of antiarrhythmic drugs?

A

Class I to V

27
Q

Class 1A antiarrhythmics

A

D-Disopyramide
P-Procainamide

28
Q

Class 1B antiarrhythmics

A

L-Lidocaine
M-Mexiletine

29
Q

Class 1C antiarrhythmics

A

Propafenone
Flecainide

30
Q

Class II antiarrhythmics

A

Esmolol
Sotalol
Propranolol

31
Q

Class III antiarrhythmics

A

Sotalol
Amiodarone
Dronedarone
Dofetilide

32
Q

Class IV antiarrhythmics

A

Verapamil
Diltiazem

33
Q

Class V antiarrhythmics

A

Adenosine
Digoxin
Magnesium sulfate

34
Q

Pharmacological action of quinidine

A

Decrease automaticity in purkinje fibers and other ectopic focus to extinguish extrasystoles and prophylaxis of re entrant arrythmias.

35
Q

How do class 1A drugs reduce membrane responsiveness?

A

Via anti-vagal action, it reduces the rate of 0 phase depolarization thereby reducing membrane responsiveness.

36
Q

ECG reading of class 1A

A

Increase PR and QR intervals, broaden QRS complex

37
Q

Pneumonic to know the drugs in anti-arrhythmic drugs and their classes

A

“Daring Paramedics Love Managing Potentially Fatal Episodes Since Patients Are Demanding Defibrillation Ventures Daily”

D - Disopyramide
P - Procainamide
L - Lidocaine
M - Mexiletine
P - Propafenone
F - Flecainide
E - Esmolol
S - Sotolol
P - Propranolol
A - Amiodarone
D - Dronedarone
D - Dofetilide
V - Verapamil
D - Diltiazem

38
Q

How many classes would amiodarone fit in?

A

Four - I, II, III, IV

39
Q

In what way is quinidine the opposite of digoxin?

A

It depresses myocardial contractility where digoxin increases it

40
Q

Lidocaine is effective for atrial tachyarrhythmia. True or false?

A

False. It affects ventricular re-entry only

PHA321 (12 decks)

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