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Cardiovascular > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

What do any arrhythimc drugs generally do?

A

Inhibit specific ion channels with the intention of suppressing abnormal electrical activity

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2
Q

What is the vaugh williams classification?

A

Classified pharmacologically based upon their cardiac action potential

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3
Q

What are the classes of anti-arrhythmic drugs?

A 
1, 2, 3 and 4 with class 1 subdivided into subclasses 1a, 1b and 1c 
The drugs in the Vaughn Williams class act upon different parts of the AP
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4
Q

What anti-arrhythmic drugs don’t fit into the Vaughn Williams classification?

A

Adenosine

Digoxin

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5
Q

What do class 1 drugs do?

A

They block voltage-activated sodium channels. This will have effects upon APs whose upstroke depends on the opening of Na+ channels. These are found in atrial and ventricular muscle and the purkinje system - although the all act on Na+ channels, they all have slightly different mechanisms

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6
Q

What is the major difference between all the class 1 drugs?

A

The major difference is the rate at which the drugs bind/associate with the voltage activated Na+ channels and the rate at which they unbind from it

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7
Q

What is the action of lignocaine (class 1B)?

A

A rapidly acting drug that will rapidly bind and unbind from Na+ channels - this will prevent premature beats.
1B agents help to stop one action potential rising too quickly after another action potential - they increase the amount of time between APs

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8
Q

What is the action of disopyramide (class 1A)?

A

It acts in a similar manner to class 1B drugs but will bind and unbind at a slower rate (moderate rate). 1A agents slow the rate of rise of the AP and prolong the duration of the action potential - increase the amount of time that Na+ channels spend in the refractory period increasing the time between AP dischrage

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9
Q

What is the action of flecainide (class 1C)?

A

The action is similar to all other class 1 agents but they bind and unbind very slowly and will greatly depress the rise of the upstroke but has little effect on the time between APs

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10
Q

What is the action of metoprolol (class 2 drug)?

A

Beta-adrenoceptor (acts as agonist) which decrease the rate of depolarisation in SA and AV nodes. They are particularly useful in stress induced arrhythmias that is caused by an excess sympathetic drive

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11
Q

What is the action of amiodarone (class 3 drug)?

A

They block voltage-activated K+ channels preventing the repolarisation phase to increase the refractory period

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12
Q

What is the action of verapamil (class 4 drug)?

A

They block voltage-activated calcium channels that suppress the upstroke of AP in nodal tissue and reduce the amount of calcium that enters muscle cells

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13
Q

What do voltage-activated Na+ channels cycle between?

A

Resting, open and inactivated (refractory) states. Relative proportions of time spent in each depend upon firing frequeny

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14
Q

What is the proportion of each Na+ channel state during high frequency (tachyarrhythmias)

A

The Na+ channels spend relatively more time in the open and inactivated states. Whenever the membrane is depolarised for a prolonged period of time, the Na+ will be locked in the inactive state, in order for them to conduct the resting membrane potential must be restored by repolarisation.

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15
Q

What effect do class one agents have on resting Na+ channels?

A

They work preferentially on open and inactive states but little effect on resting Na+ channels. Some class 1 agents bind to Na+ channels in the open state and make it non-conducting. Some bind to the inactive state to slow the transition from the inactive to resting state. They stabilise the channel in this non-conduction inactive state

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16
Q

What is the state of the Na+ channels during tachycardia?

A

There is less time in the resting state and more time in the open/inactivated states. Since the anti-arrhythmic class 1 channels work on open/inactive channels they will target the sodium channels that are being opened more frequently. Class 1 agents have little effect upon myocardium that is beating at a normal frequency because the time avaliable for them to act on open/inactive channels is low. In tachycardia, the class 1 agents work preferentially on those open/inactive channels

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17
Q

What does AF look like on an ECG?

A

Absence of P waves with an irregularly irregular rhythm
Ventricular rate is dependent upon: AV nodal conduction, sympathetic and parasymapthetic tone, presence of drugs that act on AV node)

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18
Q

What is AF?

A

Chaotic and disorganised atrial activity that produces an irregular heartbeat

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19
Q

What are the 3 types of AF?

A

Paroxysmal
Persistent
Permanent (chronic)

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20
Q

What are the changes cellularly that causes AF?

A

There is an increased parasympathetic tone which decreases atrial refractory periods, shortening the wavelength making it easier for AF to sustain itself

21
Q

Where do the ectopic foci originate in AF?

A

In the muscle sleeves in the ostia of the pulmonary veins

Multiple wavelets of reentry do not allow the atria to organise themselves

22
Q

How can AF be treated pharmologically?

A

Drugs such as flecainide, sotalol and amiodarone can terminate and prevent AF

23
Q

How can AF be treated non-pharmacologically?

A

DC conversion to revert back to sinus rhythm

24
Q

What is paroxysmal AF?

A

It lasts less than 48 hours and is often recurrent

25
Q

What is persistent AF?

A

An episode of AF that lasts longer than 48 but can still be cardioverted to sinus rhythm. It is unlikely in persistent AF that the heart will spontaneously revert to sinus rhythm

26
Q

What is permanent AF?

A

There is an inability of pharmacological or cardio-version to restore sinus rhythm

27
Q

What can cause AF?

A 
Hypertension
CHF
Sick sinus synrome 
CHD
Obesity 
Thyroid disease 
Familial 
Valve disease 
Alcohol abuse
Congenital heart disease 
COPD, pneumonia
Septicaemia
Pericarditis, tumours
28
Q

What is idiopathic AF?

A

AF in the absence of any heart disease and no evidence of ventricular dysfunction. This is a diagnosis fo exclusion

29
Q

What are the symptoms of AF?

A 
Palpitations 
Pre-syncope (dizziness) 
Syncope
Chest pain
Dyspnea (SOB)
Sweatiness
Fatigue
30
Q

What are the management objectives for AF?

A

Rhythm control: maintain SR
Rate control: Accept AF but control ventricular rate
Always anti-coagulate if high risk for thrombus

31
Q

What are drugs that can control AVN conduction?

A

Digoxin
Betablockers
Verapamil, diltiazem
Adenosine

32
Q

How can NSR (normal sinus rhythm) be restored?

A

Anti-arrhythmic drugs = amiodarone, flecainide, sotalol

Direct current cardioversion

33
Q

How can NSR be maintained?

A

Anti-arrhythmic drugs

Catheter ablation of atrial focus / pulmonary veins

34
Q

What is the aim of cardioversion?

A

To terminate the arrhythmia by the delivery of a dose of electrical current to the heart at a specific moment in the cardiac cycle

35
Q

What generally do anti-arrhythmic drugs (AADs) do?

A

They act through electrophysical mechanisms by blocking the ionic currents across cell membranes that create the action potentials

36
Q

What channel does class 1 AADs block?

A

Sodium channel in action potential phase 0 (rapid depolarisation). Controls rhythm in AF (lidocaine, flecoainide, hydroquinidine)

37
Q

What channel does class 2 AADs block?

A

Beta-receptors in phase 4 of the action potential (refractory period of stable action potential). Controls rate in AF (beta blokcers)

38
Q

What channel does class 3 AADs block?

A

Potassium channels in phase 3 of the action potential preventing the repolarisation of the membrane potential. Rhythm control in AF (amiodarone, sotalol, dronedarone)

39
Q

What channel does class 4 AADs block?

A

Calcium channels in the plateau phase (phase 2) of the action potential preventing cardiac contraction. Rate control in AF (amlodipine, verapamil, diltiazen)

40
Q

What are the risk factors for thromboembolism?

A 
Valvular heart disease 
Age > 75 
Hypertension 
Heart failure 
Previous thromboembolism / stroke 
Coronary artery disease
Thyrotoxicosis
41
Q

What are the indications of anti-coagulation in AF?

A 
Valvular AF (mitral valve disease) 
Age > 75
Hypertension 
HF
Previous stroke
CAD
Diabetes
42
Q

What are the anti-coagulants used in AF?

A

Warfarin (vitamin K inhibitor)

Rivaroxiban (directly inhibits Xa)

43
Q

How is radiofrequency ablation in AF used to maintain NSR?

A

By ablating the AF focus (usually in the pulmonary veins)

44
Q

How is radiofrequency ablation used in rate control?

A

Ablation of he AVN to stop fast conduction to the ventricles

45
Q

What is atrial flutter?

A

Rapid and regular form of atrial tachycardia which is usually paroxysmal. This is sustained by a macro-reentrant atrium

46
Q

What chronic atrial flutter lead to?

A

Atrial fibrillation which may result in thrombo-embolism

47
Q

What are the ECG changes in atrial flutter?

A

Saw tooth F wave
Normal QRS complex
Conduction is normal but physiologic 2:1 and the rhythm is regular but may be variable `

48
Q

How can atrial flutter be treated?

A

RF ablation
Pharmacologic treatment (slows ventricular rate, restore sinus rhythm and to maintain sinus rhythm once converted)
Cardioversion
Warfarin to prevent thromboembolism

Cardiovascular (27 decks)

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