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Year 1 Cardiology > Aryythmias > Flashcards

Aryythmias Flashcards

1
Q

Causes of arrhythmias

A

Impulse formation

Impulse conduction

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2
Q

Where do supraventricular arrhythmias originate from?

A

Atria, SA and AV node

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3
Q

What is overdrive suppression?

A

As the SA node fires at the highest frequency its impulses mask those of the other nodal tissue specifically the AV and purkinje fibres

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4
Q

What is a latent pacemaker?

A

AV node or purkinjes fibres these are nodal tissues that can initiate the impulses but as they fire at a lower rate are masked by the SA node

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5
Q

What is an escape beat or rhythm

A

When a latent pacemaker initiates a contraction outside off vagus rhythm

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6
Q

What is an ectopic beat or rhythm?

A

When a latent pacemaker fires at an intrinsic rate faster than the SA node

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7
Q

Reasons for at ectopic heart beat?

A

Ischeamia , hypokalaemia, increased sympathetic activity

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8
Q

What heart rate is associated with early afterdepolarisations?

A

Slow

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9
Q

What are afterdepolarisations and what two types of them are there?

A

Abnormal oscillations in membrane potential

Early and delayed afterdepolarizations occur

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10
Q

In what tissues of the heart do early afterdepolarisations generally occur in?

A

Purkinje or bundle of His fibres, areas with a pronounced phase 1 and 2

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11
Q

What arrhythmia is related too early after depolarisations?

A

Torsades de pointes- life threatening

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12
Q

When do delayed afterdepolarisations occur?

A

Upon complete depolarisations in Phase 4 due to increased Ca2+

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13
Q

What heart rate are delayed AD likely to occur?

A

Fast

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14
Q

What are the risks associated with?

A

Increasing duration of Action potential decreases the risk as less Ca2+ so longer phase 2

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15
Q

What two drugs increase likelyhood of delayed AD

A

Catecholamines , digoxin both increase intracellular conc of Ca2+

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16
Q

What two things allow are re-entry cycle to occur?

A

An alternate pathway to the AV node e.g. bundle of Kent

Or an area of unconducting scarred tissue due to an MI etc

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17
Q

Why does an re-entry occur

A

If one side of the unconducting tissue only allows conductance to occur in one direction then when the wave of depolarisation passes around the scarred tissue it can pass back up.
If long enough has passed the tissue can repolarise above the scarred tissue allowing the depolarisation to pass back down and trigger a second contraction out of sinus rhythm.
This circuit can continue around the unconducting tissue

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18
Q

What is partial block

A

First degree AV node block

Tissue conducts all impulses but at a slower rate

19
Q

ECG reading of First degree AV node Block

A

Prolonged gap between P wave and QRS complex

20
Q

What is intermittent block?

A

Second degree AV node block

Node conducts some but not all of the impulses

21
Q

Mobitz type 1

A

PR interval gradually increases from cycle to cycle until AV node fails completely so ventricular QRS wave is not present

22
Q

Mobitz type 2

A

PR interval is consistent but every nth QRS cycle is missed

23
Q

In what mobitz type is atropine used?

A

ONLY type 1

24
Q

What is complete block?

A

Tissue conductance doesn’t occur

Third degree AV node block

25
Q

What happens in third degree block?

A

Atria and ventricles beat independently, purkinje fires take over as dominant pacemaker

26
Q

Clinical aspects of third degree block?

A

Bradychardia and very low CO

27
Q

Atrial fibrillation symptoms

A

SOB, palpitations, dizziness, loss of consciousness, faintness, sudden cardiac death, angina, heart failure

28
Q

Treatment for Tachy-Brady

A

Pacemaker to prevent bradychardia, beta blockers to prevent tachychardia

29
Q

Sinus Bradychardia

A

Atropine if acute

Pacemaker if harm-dynamic compromise

30
Q

Sinus Tachychardia >100bpm

A

Anxiety fever hypotension anaemia

treatment with beta blockers

31
Q

Atrial Ectopic beats

A

generally no treatment can burn of areas inducing
B adrenergic blockers may help
avoid stimulants e.g. coffee caffein

32
Q

Regular Superventricular tachychardia

A

Acute- increased vagal tone, valsalva manoeuvre carotid massage
- Iv adenosine and Ca2+ blockers
Chronic- radio frequency ablation, avoid stimulants, beta blockers and antiarrythmic drugs

33
Q

Paroxysmal

A

Last less than 48 hours often reccurent

34
Q

Persistant

A

last 48 hours

35
Q

Permanent

A

Constant

36
Q

Lone Idiopathic

A

Absence of any. heart disease and no supporting evidence

often genetic and increased risk of strokes

37
Q

What drugs are used for Atrial Fibrillation?

A

Diltiazem or verapamil - Rate slowing Ca2+ channel Beta blockers
Digoxin

38
Q

What treatment is used in younger AF sufferers

A

Ablation radiofrequency is used to destroy tissue creating impulses

39
Q

Which antiarrythmic should never be used with digoxin?

A

Amiodarone

40
Q

What anti-arrythmic drugs are used?

A

Na+ blockers- slows phase 0
K+ blockers - slows repolarisation
Amiodarone- blocks everything

41
Q

How can you monitor the antiarrythmic drugs?

A

Using an ECG
Na+ blockers- wider QRS
K+ blockers - wider QT interval

42
Q

Treatment for ventricular tachychardia/fibrillation

A

Implantable cardioverter-defibrillator

Ablation - has better outcomes

43
Q

What drug is used in the treatment of ventricular tachycardia

A

Amiodarone

Year 1 Cardiology (17 decks)

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