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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
How might a patient with SVT describe their palpitations?
Sudden onset regular tachyarrhythmia at rest, resolving suddenly (can become persistent)
26
What are the main causes of SVT?
AV nodal re-entrant tachycardia (90%) | Wolff-Parkinson-White syndrome
27
What is the target for treatment in SVT?
AV node (involved in almost all SVTs)
28
How is SVT managed acutely?
Vagal manoeuvres Adenosine Verapamil
29
How is adenosine administered in the acute setting to treat SVT? What is the mechanism of action?
6-12mg IV, followed by saline flush (patient will flush and feel terrible for a few seconds, but adenosine half life is
30
How is verapamil administered in the acute setting to treat SVT?
IV in 1mg increments
31
What ECG pattern suggests WPW? What causes this pattern?
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
How can SVT be managed long term?
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
How would a patient with VT describe their palpitations?
Regular tachyarrhythmia +/- SOB and lightheadedness
34
How should VT be managed in the acute setting?
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
What are 2 possible underlying causes of VT? What Ix should be performed to assess for these?
Cardiac ischaemia e.g. post-MI (ECG, troponin, angiogram) | Significant underlying cardiac disease e.g. cardiomyopathy (echo)
36
What are the Class I indications for a permanent pacemaker?
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
How is sinus node dysfunction defined?
Symptomatic sinus bradycardia | Sinus pauses >2s (day) or >2,5s (night)
38
How might a patient with tachy-brady syndrome ("sick sinus syndrome") describe their palpitations?
Episodes of sinus bradycardia or pauses, other episodes of AF with tachyarrhythmia
39
How should tachy-brady syndrome be treated?
``` 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
What is catheter ablation?
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
When are palpitations concerning?
``` 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
``` 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? ```
Usually benign Provide reassurance Cutting down on caffeine may help If frequent and symptomatic, consider treating with B blockers or Ca2+ channel blockers
43
72 year old woman Episode of irregular palpitations 2 years ago Recently, intermittent irregular palpitations with racing heart beat, exertional dyspnoea No chest pain
ECG shows atrial fibrillation
44
Risk factors for AF
Age | Known CVD or CV risk factors
45
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
ECG showed SVT
46
List 5 vagal manoeuvres that can be used to treat SVTs
``` Valsalva Lying on back with legs vertical Breath-holding Coughing Face into cold water (dive reflex) Carotid sinus massage ```
47
What is the mechanism of action of the valsalva manoeuvre?
Increases intra-thoracic pressure and affects baroreceptors in aorta
48
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
ECG showed broad complex tachycardia (ventricular tachycardia until proven otherwise)
49
76 year old woman PHx: HTN Rx: perindopril 10mg daily 3 episodes in previous week of LOC
?
50
AF precipitants
Hyperthyroidism Infection Others?
51
AF causes
Cardiomyopathy | Others?
52
What are the 2 separate management decisions to be made in AF?
Rhythm vs rate control | Stroke risk vs bleeding risk
53
How does rate control for AF work?
Slows conduction at the AV node
54
Why is the myocardium around the pulmonary veins more prone to becoming AF origin sites?
Dunno lol
55
What does broad complex regular tachycardia suggest?
VT until proven otherwise
56
What are the most common causes of syncope?
Neurocardiogenic (vasovagal) Cardiac Postural hypotension Neurological (less common)
57
What is the definition of syncope?
``` Transient LOC Self-limiting Relatively rapid onset Leads to fall Recovery complete, rapid and spontaneous ```
58
What factors of a syncope Hx are important to elicit?
Prodrome Context Collateral Hx/witnesses (specific length of LOC, pallor, jerks, length of recovery) Hx of previous episodes
59
What features may assist in distinguishing neurocardiogenic from cardiac syncope?
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
``` 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? ```
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
Characteristic pattern of first degree AV block
PR interval of >0.2 second | Every P wave followed by a QRS complex
62
Characteristic pattern of second degree AV block, Mobitz type I (Wenckebach)
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
Characteristic pattern of second degree AV block, Mobitz type II
Intermittently blocked P waves | PR interval on conducted beats is constant
64
Second degree, high grade AV block
Conduction ratio of 3:1 or more | PR interval of conducted beats is constant
65
Third degree AV block
Dissociation of atrial and ventricular activity | Atrial rate is faster than ventricular rate, which is of junctional or ventricular origin
66
Rate control agents for AF
B blockers Ca2+ channel blockers Digoxin

MD2 Cardio (11 decks)

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