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Block 4 - Cardio > Supraventricular and Ventricular Arrhthmias > Flashcards

Supraventricular and Ventricular Arrhthmias Flashcards

0
Q

What are the mechanisms of arrhythmias?

A

Automaticity due to changes in phase 4 depolarization
Single focus - drug toxicity
Triggered beats - rapid firing at single focus, triggered by beat before = early or late afterdepolarizations during phases 3 or 4, often single focus due to drug toxicity

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1
Q

What are escape beats?

A

Arise from ectopic focus and occur after pause in heart rhythm

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2
Q

What are the alpha and beta re entry pathways?

A

Alpha - typically slow conduction, short refractory period

Beta - typically fast conduction, long refractory period

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3
Q

What is the mechanism of symptoms of SVTs?

A

Degree of symptoms often correlates with HR and underlying cardiac abnormality
Decreased BP due to poor LV filling secondary to rapid rate –> weakness and light headedness
Pounding sensation due to cannon a waves - suggests AV nodal reentry

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4
Q

What is WPW?

A

EKG has delta wave, short PR interval and prolonged but narrow QRS
accessory pathway connecting atrium and ventricle - an AVRT
Orthodromic - ventricles activated down normal conduction system during tachycardia, no delta wave during tachycardia just at rest

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5
Q

How can you get a normal PR and QRS in WPW without a delta wave?

A

Premature atrial contraction may result in block in accessory pathway

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6
Q

What is antidromic?

A

Direction of AV reentry circuit that travels through AV node in opposite direction
AP in WPW activates first
Wide complex even though it is SUPRAventricular - less common

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7
Q

What is the mechanism of AV nodal reentrant tachycardia (AVNRT)?

A

Both reentrant circuits in AV node - EKG normal at sinus rhythm - looks like just fast pathway, only hints of p waves during tach
Slow and fast AV pathway
Premature atrial beat - fast pathway blocks resulting in prolonged PR from slow pathway
Rhythm continues until conduction block in one of pathways

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8
Q

What does atrial tachycardia result from?

A 
Reentry, automaticity, or triggered activity at distinct atrial focus 
Paroxysmal or show a warm up in rate
Tends to turn on and off
Usually 1:1 conduction to ventricles 
Different p wave from distant site
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9
Q

How can you use the p wave to differentiate between AVRT, AVNRT, and atrial tach?

A

P after QRS in AVRT
P in QRS in AVNRT (more common)
P before QRS in atrial tach

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10
Q

What is the most frequent type of atrial arrhythmia?

A

A fib

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11
Q

What is an important target for ablation in a fib?

A

Triggered activity and reentry originating in or around pulmonary veins

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12
Q

What are the different types of a fib?

A

Paroxysmal - self initiating and self terminating 7 days and requiring intervention to terminate
Chronic or permanent - accepted as final rhythm

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13
Q

When can atrial fibrillation be dangerous?

A

Occurring during WPW
In a fib, the accessory pathway causes rapid conduction to ventricles, resulting in low BP, syncope, or death
QRS complex is wide since ventricles activated via AP
= af with RVR (rapid ventricular response)

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14
Q

What are the possible complications of a fib?

A

Risk of atrial thrombus formation - most commons place for embolism is the brain –> ischemic stroke

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15
Q

When should you treat a fib with aspirin and when with warfarin or neither?

A

If CHADS score is 0 - treat with aspirin
If CHADS score is 1 - treat with aspirin or warfarin
If CHADS score is at least 2 - treat with warfarin

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16
Q

What are the CHADS score criteria?

A 
CHF - 1
HT - 1
Age at least 75 - 1
Diabetes - 1
Stroke or TIA in past - 2
17
Q

How are treatment decisions of rate vs rhythm control made in a fib?

A

Similar outcomes

Depends on symptoms

18
Q

What can drive a fib?

A

Hyperthyroidism
Drug or alcohol use
After cardiac surgery

19
Q

Where does the reentry happen in most a flutter?

A

Encircling tricuspid annulus

Impulse conducts up septum and down lateral right atrium

20
Q

What is the main complication and treatment for a flutter?

A

Atrial thrombus formation

Same treatment as a fib

21
Q

Which supraventricular tachycardias can be cured with ablation?

A

Ablate slow pathway in AVNRT or in a flutter has high success
A fib possible but less success

22
Q

When is a PVC more likely to precipitate a more serious ventricular arrhythmia?

A

Occurs during ventricular repolarization on a t wave

Particularly in setting of ischemia, MI, with prolonged QT interval

23
Q

How many PVCs constitute v tach?

A

3 or more

24
Q

What can sustained VT lead to?

A

Hemodynamic collapse, particularly in those with LV dysfunction

25
Q

What two manifestations of VT allow its identification and diagnosis?

A

AV dissociation
Fusion beats or capture beats - sometimes SA node can still conduct through to capture some or all of myocardium and you get fused or normal QRS complex

26
Q

What is outflow tract VT?

A

Repetitive monomorphic VT due to triggered activity
Originates from right or left outflow tract regions
Inferior axis - positive in leads II, III, and aVF
Typically occurs in setting of structurally normal heart

27
Q

What different morphologies does RVOT vs LVOT have?

A

RVOT - right ventricle depolarized firsts looks like LBBB

LVOT - left ventricle depolarized first looks like RBBB

28
Q

What is outflow tract vt sensitive to?

A

Adenosine and beta blockers

Treatable with ablation

29
Q

What is idiopathic left VT?

A

In normal ventricle due to macro reentrant circuit in LV septum that utilizes part of left fascicle
EKG has right bundle, superior axis morphology
Sensitive to verapamil but give with caution because can cause hemodynamic collapse in other VTs
Doesn’t occur in short bursts and not necessarily with exercise

30
Q

What is hereditary long QT syndrome?

A

AD disorder caused by mutations in genes encoding prominent ion channel complexes that control cardiac action potential
Usually in otherwise normal heart
10 gene abnormalities known - prolong phase III repolarization which increases likelihood of triggered activity that can lead to torsades de pointes
Negative genetic test doesn’t rule it out
Typical patient is 15-20 yrs old

31
Q

What is the EKG appearance of hereditary long QT syndrome?

A

Different depending on specific gene defect
Broad t wave in lqt1 - events due to exercise, esp swimming
Notching of t wave in lqt2 - events due to changes in arousal level, like waking up suddenly
Peaked t waves in lqt3 - events during rest or sleep
Torsades de pointes look like spiraling around azis

32
Q

What does therapy for hereditary long QT syndrome include?

A

Beta blockers in carrier or ICDs in patients with recurrent syncope or resuscitated cardiac arrest
Genotype specific therapy with mexilitine being explored for patients with sodium channel abnormalities

33
Q

What is brugada syndrome and how is it treated?

A 
Genetic disorder due to premature repolarization - opposite than LQT
Abnormality in cardiac sodium channel
increased risk for VF usually at night 
Therapy involves ICD implant 
Beta blockers may be harmful
34
Q

What does the EKG of brugada syndrome look like?

A

St elevation and t wave inversion in v1 and v2 often in setting of RBBB

35
Q

What drugs are particularly offending agents in development of drug induced LQTS and torsades de pointes?

A

Class Ia and III antiarrhythmics

Selected antipsychotic and antidepressants

36
Q

When is VF more common than VT due to abnormal LV function?

A

In absence of acute ischemic episode when altered channel function due to myocardial ischemia can change cellular refractoriness or automaticity

37
Q

When is VT more common than VF in LV dysfunction?

A

Absence of acute ischemia, reentrant VT more common due to reentry within scar due to prior MI

38
Q

What is the single greatest risk factor for SCD and what are other risk factors?

A

LV dysfunction with EF<30% is most robust marker
Presence of PVCs and nonsustained VTs increases risk
Survivors have increased risk

39
Q

What is the SCD paradox?

A

Individuals with fewer risk factors make up larger position of victims even though risk is low
Makes identifying populations that will benefit from ICD difficult

40
Q

What is the preferred preventative strategy for SCD in almost all situations?

A

Implantation of ICD

Block 4 - Cardio (15 decks)

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