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MD2 Cardio > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

How can ECG monitoring be achieved over 24 hours?

A

Holter monitor

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2
Q

How can ECG monitoring be achieved over a week?

A

Event recorder

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3
Q

How can ECG monitoring be achieved over months to years?

A

Loop recorder

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4
Q

When does the holter monitor work?

A

Continuously; records every beat while the pt keeps a symptom diary

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5
Q

What is the drawback of holter and event recorders?

A

Susceptible to artifact

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6
Q

When does the event recorder work?

A

When triggered by patient (retains 20 minutes of memory pre-trigger)

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7
Q

How long can the loop recorder record for?

A

Up to 3 years

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8
Q

How is a loop recorder applied?

A

Via a small operation (will leave a scar - look out for this!)

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9
Q

What investigations should be ordered for palpitations?

A

ECG (prolonged ECG monitoring if indicated)
Echo
Stress testing/coronary angiography (if ischaemia suspected)
Electrophysiology study

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10
Q

How is an electrophysiology study performed?

A

Minimally invasive test, performed in cardiac cath lab by an electrophysiologist (cardiologist highly specialised in diagnosing and treating arrythmias); try to provoke arrythmia to assess

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11
Q

How can arrhythmias be managed?

A

Drugs to control rate or rhythm

Catheter ablation

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12
Q

What are the management implications for a patient experiencing premature ventricular/atrial complexes (“ectopics”)?

A

Usually benign; provide reassurance and recommend cutting down on caffeine intake
If very frequent and symptomatic may require treatment with B-blockers/Ca2+ channel blockers

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13
Q

How might a patient experiencing premature ventricular/atrial complexes describe their palpitations?

A

Feeling of “skipped beats”

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14
Q

How might a patient with AF describe their palpitations?

A

Intermittent irregular tachyarrhythmia with shortness of breath +/- chest pain, especially during exertion
NB May be asymptomatic

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15
Q

Why is AF important to recognise?

A

Associated with increased risk of stroke or peripheral embolus

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16
Q

How is AF managed?

A

Look for underlying precipitants and causes, treat these

Evaluate rate vs. rhythm control, and stroke vs. bleeding risk

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17
Q

Identify 3 methods of rhythm control in AF

A

Antiarrhythmic agents
Electrical cardioversion
Catheter ablation (selected patients whose symptoms persist despite medical therapy)

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18
Q

Give 3 examples of specific antiarrhythmic agents for AF

A

Sotalol
Flecainide
Amiodarone

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19
Q

What anticoagulant agents are available to treat increased risk of bleeding?

A

Warfarin
Dabigatran
Rivaroxiban
Apixiban

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20
Q

What is the safest approach to managing AF?

A

Rate control; rhythm controlling agents can precipitate other significant arrhythmias (e.g. VT)
Often need to involve cardiologist

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21
Q

What are the risks of using rhythm control to manage AF?

A

Increased risk of other significant arrhythmias e.g. VT

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22
Q

What are the common sites for catheter ablation for AF?

A

Around the pulmonary veins (“pulmonary vein isolation”)

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23
Q

What is the success rate of catheter ablation in Australia?

A

70-80%

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24
Q

What is the aim of catheter ablation in AF?

A

To maintain sinus rhythm by preventing signals propagating from AF origin sites

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25
Q

How might a patient with SVT describe their palpitations?

A

Sudden onset regular tachyarrhythmia at rest, resolving suddenly (can become persistent)

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26
Q

What are the main causes of SVT?

A

AV nodal re-entrant tachycardia (90%)

Wolff-Parkinson-White syndrome

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27
Q

What is the target for treatment in SVT?

A

AV node (involved in almost all SVTs)

28
Q

How is SVT managed acutely?

A

Vagal manoeuvres
Adenosine
Verapamil

29
Q

How is adenosine administered in the acute setting to treat SVT? What is the mechanism of action?

A

6-12mg IV, followed by saline flush (patient will flush and feel terrible for a few seconds, but adenosine half life is

30
Q

How is verapamil administered in the acute setting to treat SVT?

A

IV in 1mg increments

31
Q

What ECG pattern suggests WPW? What causes this pattern?

A

Slurred upstroke of QRS complex (delta wave) in praecordial leads
Large “macro” re-entrant pathway bypassing the AV node causes the ventricle to be excited earlier than normal

32
Q

How can SVT be managed long term?

A

If symptoms are rare or if isolated episode, no Rx required
Otherwise Rx usually involves B-blockers or Ca2+ channel blockers (“pill-in-pocket” approach)
Catheter ablation achieves success rates >95%

33
Q

How would a patient with VT describe their palpitations?

A

Regular tachyarrhythmia +/- SOB and lightheadedness

34
Q

How should VT be managed in the acute setting?

A

Continuous cardiac monitoring
If haemodynamically unstable, immediate DC reversion is required
If sustained and haemodynamically stable, try pharmacological reversion with amiodarone, or sedate patient to administer DC shock

35
Q

What are 2 possible underlying causes of VT? What Ix should be performed to assess for these?

A

Cardiac ischaemia e.g. post-MI (ECG, troponin, angiogram)

Significant underlying cardiac disease e.g. cardiomyopathy (echo)

36
Q

What are the Class I indications for a permanent pacemaker?

A

Sinus node dysfunction (symptomatic sinus bradycardia, sinus pauses >2s during day or >2.5s at night)
Symptomatic 2nd or 3rd degree AV block
Intermittent 3rd degree AV block

37
Q

How is sinus node dysfunction defined?

A

Symptomatic sinus bradycardia

Sinus pauses >2s (day) or >2,5s (night)

38
Q

How might a patient with tachy-brady syndrome (“sick sinus syndrome”) describe their palpitations?

A

Episodes of sinus bradycardia or pauses, other episodes of AF with tachyarrhythmia

39
Q

How should tachy-brady syndrome be treated?

A 
With PPM (difficult to treat without; can't control tachycardias without worsening bradycardias)
Can use AV node blocking agents (B-blockers or Ca2+ channel blockers) to control tachyarrhythmia, but ONLY after PPM implanted (if concerned about possible tachy-brady syndrome wait for Holter monitor results before starting AV nodal blocking agents)
40
Q

What is catheter ablation?

A

Invasive procedure used to remove or terminate a faulty cardiac conduction pathway in those prone to developing arrhythmias (e.g. AF, atrial flutter, SVT, Wolff-Parkinson-White syndrome)
Catheter ablation involves advancing several flexible catheters into the patient’s blood vessels, usually either in the femoral, internal jugular or subclavian vein
Electrical impulses are used to induce the arrhythmia and local heating or freezing is used to ablate (destroy) the abnormal tissue that is causing it

41
Q

When are palpitations concerning?

A 
Documented cardiac arrhythmia at time of symptoms
Severe symptoms
Evidence of cardiac disease on baseline tests (e.g. echo)
PHx of cardiac disease
FHx of SCD
High risk work environment
High level sporting activities
Before/during pregnancy
42
Q 
25 year old woman
Fit and active
Feeling of "skipped beats"
Felt mostly when in bed in evening
ECG shows ventricular and atrial ectopics
Significance?
A

Usually benign
Provide reassurance
Cutting down on caffeine may help
If frequent and symptomatic, consider treating with B blockers or Ca2+ channel blockers

43
Q

72 year old woman
Episode of irregular palpitations 2 years ago
Recently, intermittent irregular palpitations with racing heart beat, exertional dyspnoea
No chest pain

A

ECG shows atrial fibrillation

44
Q

Risk factors for AF

A

Age

Known CVD or CV risk factors

45
Q

42 year old man
Occasional palpitations: sudden onset and offset, at rest, regular, 5-10 minutes, resolve spontaneously
Further episode lasting >1 hour, called ambulance

A

ECG showed SVT

46
Q

List 5 vagal manoeuvres that can be used to treat SVTs

A 
Valsalva
Lying on back with legs vertical
Breath-holding
Coughing
Face into cold water (dive reflex)
Carotid sinus massage
47
Q

What is the mechanism of action of the valsalva manoeuvre?

A

Increases intra-thoracic pressure and affects baroreceptors in aorta

48
Q

55 year old man
PHx: T2DM, HTN, hyperlipidaemia
FHx: CAD
2 previous episodes of regular palpitations
Now more prolonged episode with SOB and light-headedness

A

ECG showed broad complex tachycardia (ventricular tachycardia until proven otherwise)

49
Q

76 year old woman
PHx: HTN
Rx: perindopril 10mg daily
3 episodes in previous week of LOC

A

?

50
Q

AF precipitants

A

Hyperthyroidism
Infection
Others?

51
Q

AF causes

A

Cardiomyopathy

Others?

52
Q

What are the 2 separate management decisions to be made in AF?

A

Rhythm vs rate control

Stroke risk vs bleeding risk

53
Q

How does rate control for AF work?

A

Slows conduction at the AV node

54
Q

Why is the myocardium around the pulmonary veins more prone to becoming AF origin sites?

A

Dunno lol

55
Q

What does broad complex regular tachycardia suggest?

A

VT until proven otherwise

56
Q

What are the most common causes of syncope?

A

Neurocardiogenic (vasovagal)
Cardiac
Postural hypotension
Neurological (less common)

57
Q

What is the definition of syncope?

A 
Transient LOC
Self-limiting
Relatively rapid onset
Leads to fall
Recovery complete, rapid and spontaneous
58
Q

What factors of a syncope Hx are important to elicit?

A

Prodrome
Context
Collateral Hx/witnesses (specific length of LOC, pallor, jerks, length of recovery)
Hx of previous episodes

59
Q

What features may assist in distinguishing neurocardiogenic from cardiac syncope?

A

Neurocardiogenic: presyncopal symptoms include diaphoresis, headache, nausea, visual changes; signs include facial pallor, yawning, pupillary dilatation; precipitating events include fear, emotional distress, instrumentation, prolonged standing
Cardiac: may be no warning symptoms; rapid LOC often associated with injury; may be exertional or occur when supine; associated features may include chest pain or palpitations; family Hx of SCD; background of known structural cardiac disease (e.g. reduced LV systolic function)

60
Q 
76 year old woman
PHx: HTN
Rx: perindopril 10mg daily
3 episodes in previous week of LOC
No warning, grazed knees bilaterally
1) What would you look for on examination?
2) What further Ix should be done?
A

1) Pulse rate (rate, rhythm), standing and lying BP (assess for postural drop), CV examination (assess for murmurs)
2) ECG abnormalities (looking for signs of sinus node disease including sinus bradycardia and pauses, and signs of AV conduction block, rarely WPW pattern or long QT interval)

61
Q

Characteristic pattern of first degree AV block

A

PR interval of >0.2 second

Every P wave followed by a QRS complex

62
Q

Characteristic pattern of second degree AV block, Mobitz type I (Wenckebach)

A

Progressive lengthening of PR interval and shortening of RR interval until a P wave is dropped
PR interval after dropped beat is shorter than preceding PR interval

63
Q

Characteristic pattern of second degree AV block, Mobitz type II

A

Intermittently blocked P waves

PR interval on conducted beats is constant

64
Q

Second degree, high grade AV block

A

Conduction ratio of 3:1 or more

PR interval of conducted beats is constant

65
Q

Third degree AV block

A

Dissociation of atrial and ventricular activity

Atrial rate is faster than ventricular rate, which is of junctional or ventricular origin

66
Q

Rate control agents for AF

A

B blockers
Ca2+ channel blockers
Digoxin

MD2 Cardio (11 decks)

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