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Cardiology II > Atrial Fibrillation and Cardiac Arrythmias > Flashcards

Atrial Fibrillation and Cardiac Arrythmias Flashcards

1
Q

what are clinical presentations of arrhythmias?

A
  • palpitations
  • chest pain
  • shortness of breath, exercise intolerance
  • lightheadedness, dizziness
  • syncope
  • caridac arrest
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2
Q
  • fever, pain, anemia, hypoxemia, anxiety, hyperthyroidism, pheochromocytoma
  • treat the patient not the pulse rate
  • inappropriate tachycardia: underlying cause is ruled out, consider beta-blocker, ablation procedure
A

sinus tachycardia

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3
Q
  • macro-reentrant arrhythmia around a functional or anatomical circuit
  • most common type of flutter
  • atrial rate is 240-340bpm
  • often counterclockwise
  • leads II, III, AVF- negative; V1 positive
A

typical atrial flutter

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4
Q
  • macro-reentrant circuit is unknown
  • atrial rate is typically faster (340-430bpm)
  • similar acute and chronic mangament but different ablation strategy
A

atypical atrial flutter

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5
Q

what diagonostic maneuver is used for atrial flutter?

A
  • adenosine or valsalva maneuver- will not terminate the tachycardia
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6
Q

acute management of atrial flutter?

A

Rate control

  • Beta blockers
  • calcium channel blockers
  • +/- digoxin

Anticoagulation

  • heparin/ low molecular weight heparin
  • warfarin
  • dabigatran/ rivaroxaban/ apixaban/ edoxaban
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7
Q

when is cardioversion safe in atrial flutter?

A
  • if less than 48 hours—> cardioversion (pt must be on IV heparin)
  • if longer than 48h–> adequate anticoagulation x 3 weeks–> cardioversion
  • if no appropriate anticoagulation—> TEE to exclude an atrial clot
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8
Q

what types of cardioversion methods are there?

A

electrical cardioversion
chemical cardioversion (IV ibutilde, amiodarone)

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9
Q

chronic management of atrial flutter

A

If patient is asymptomatic

  • rate control with beta blockers, calcium channel blockers +/- digoxin
  • anticoagulation

If patient is symptomatic

  • Anti-arryhthmics (e.g, felcainide, propafenone, amiodarone)
  • electrophysiology study with RF ablation
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10
Q
  • Includes several types of tachycardia that originate in the atria
  • atrial rate usually in the 140-240bpm range
  • p waves have different morphology than sinus P waves
  • different mechanisms: automatic, triggered, reentrant
A

atrial tachycardia

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11
Q

medical management of atrial tachycardia?

A

rate control

  • beta blockers, calcium channel blockers +/- digoxin
  • anti-arrythmics (e.g, flecainide, propfane, amiodarone)

If refractory to medical therapy

  • electrophysiology study with RF ablation
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12
Q
  • dual AV node physiology with a slow and fast pathway
  • during tachycardia there is conduction through the slow and fast pathways in opposite directions
  • ECG: narrow QRS without P waves or they are present at the end of QRS
  • it can terminate with Valsalva maneuvers or adenosine
A

AV nodal reentrant tachycardia

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13
Q

Medical treatment for AV nodal re-entrant tachycardia?

A

Medical Therapy

  • Beta-blockers
  • calcium channel blockers
  • anti-arrhythmics

Invasive therapy

  • EP study and RF ablation
  • indicated if refractory to medical therapy or intolerance to medication
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14
Q
  • Accessory pathway or bypass tract between the atrium and the ventricle
  • pathways are located around the tricuspid or mitral annulus
  • multiple pathways can co-exist in a single patient
  • ECG indicates the presence of a short PR-interval and a delta wave
  • the delta wave represnet early activation of the ventricles through the accessory pathway or bypass tract
A

Wolf-Parkinson-White syndrome

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15
Q

when do patients have narrow QRS in WPW? when do they have wide?

A
  • Narrow QRS tachycardia is the most frequently observed arrythmia
  • patients can develop a wide QRS tachycardia if there is anteroretrograde conduction through the accessory pathway
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16
Q

managment of WPW?

A
  • best therapy of tachycardias involving a bypass tract is an EP study with RF ablation
  • Avoid AV nodal blocking agents (beta blockers, calcium channel blockers, digoxin) as they can lead to preferential conduction through the accessory pathway
  • anti-arrythmic agents (class I, III) have relative limited efficacy
17
Q
  • wide QRS complex tachycardia originated from the ventricles
  • there is AV dissociation on the ECG
  • two types: in the presence of structural heart disease, in the absense of structural heart disease
A

Ventricular Tachycardia

18
Q
  • its origin can be in the right ventricle or left ventricle
  • patients present with palpitations and dizziness, frequently related to exercise
  • sudden death is very rare
  • tx: Beta blockers, calcium channel blockers
  • final therapy: EP study with RF ablation
  • ICD implantation is not indicated
A

VT in the “normal” heart

19
Q
  • most occur in the presence of ischemic heart disease
  • reentrant mechanism around a scar in the ventricle
  • patients present with syncope, very symptomatic/hypotensive or with sudden death
  • treatment: ICDs with the option of anti-arrhythmics (amiodarone, sotalol mexiletine)
  • pallative therapy with EP study and RF ablation
A

VT in structural heart disease

20
Q

indications for pacemakers?

A
  • symptomatic bradycardia
  • high grade heart block (mobitz type II, complete)
  • symptomatic sinus pauses/sick sinus syndrome
  • inappropriate chronotropic response to exercise
  • presence of bradycardia and need to add beta-blockers and/or calcium channel blockers for treatment of concomitant cadiovascuar disease (e.g, coronary artery disease)
21
Q
  • the most common sustained cardiac arrhythmia
  • irregularly irregular supraventricular tachycardia
  • ECG: fine oscillations of the baseline
  • absence of organized atrial activity
  • atrial rate 400-600bpm
A

atrial fibrillation

22
Q

what types of atrial fibrillation are there? define them

A
  • Lone: “afib for a day or two- no triggering factor”; paroxysmal, persistent or permanent without evidence of heart disease
  • paroxysmal (40%): self termination within 7 days (usually < 24hrs) +/- recurrent
  • persistent: fails to self terminate, lasts > 7 days. requires termination (medical or electrical)
  • permanent: persistent af > 1 year (refractory to cardioversion or cardioversion never tried)
23
Q

Management of stable atrial fibrillation

A

Rate control

  • Rate control with beta blockers or non-DHP calcium. channel blockers
  • digoxin may be used when beta blockers or calcium channel bockers are contraindicated
24
Q

management of unstable atrial fibrillation? what long-term management is available for Afib?

A
  • Direct current (synchronized) cardioversion

Long term management

  • rate control usually preferred over rhythm control for long-term management
  • direct current (synchronized cardioversion)
  • radiofrequency catheter ablation or surgical “MAZE” procedure
  • anticoagulation: similar CHAD2D2-VASc) for nonvalvular atrial fibrillation in patients at risk for embolization
25
Q

what does the CHA2DS2-VASc calculate the risk for? when would anticoagulation therapy be recommended?

A
  • measures the risk of embolization in nonvalvular atrial fibrillation patients

Recommended therapy

  • score greater than > 2: Moderate to high risk: chronic oral anticoagulation recommended
  • 1= low risk: based on clinical judgement, consideration of risk to benefit assesment & discussion with patient, anticoagulation may be recommended
  • 0 = very low risk: no anticoagulation needed

Cardiology II (12 decks)

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