8 Arrhythmias- Clinical aspects Flashcards

1
Q

What is this EKG showing?

A

Atrial fibrillation

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2
Q

What are some possible complications from atrial fibrillation?

A

Blood stasis in the atrium can lead to thrombus formation with risk of embolization and stroke

Patients with AF have 5x risk of stroke!!

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3
Q

How do you treat atrial fibrillation?

A
  • anticoagulation
    • acute at time of cardioversion
    • chronic based on CHADSVasc score
  • rate control
    • beta blocker
    • Ca channel blocker
    • digoxin
  • restoration of sinus rhythm
    • carioversion
    • antiarrhythmic drugs
    • catheter ablation
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4
Q

What are the criteria of the CHADSVASc score?

A
  • Congestive heart failure
  • Hypertension
  • Age >75 (2 points)
  • Diabetes
  • Stroke (2 points)
  • Vascular disease
  • Age >65
  • Sex Category (female= 1 point)

**0= no therapy, 1= aspirin or oral anticoagulant, 2+ = oral anticoagulant

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5
Q

What is the benefit of NOACs over warfarin?

A

Decreased stroke risk (significant decrease in hemorrhagic strokes specifically)

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6
Q

What do you expect to find on EKG post versus pre initiation of sotalol?

A

Heart rate slowed and QTc interval prolonged (can lead to EADs and/or Torsades de pointes)

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7
Q

What are 5 factors that can contribute to torsades de pointes?

A
  1. sotalol
  2. acute renal insufficiency
  3. hypokalemia
  4. hypomagnesemia
  5. azithromycin
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8
Q

How do you treat torsades des pointes?

A
  • Shock if sustained
  • Supplement electrolyte imbalances if nonsustained (will stop on its own)
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9
Q

What is this EKG showing?

A

SVT (no clear P wave/atrial activity, it’s hidden within the QRS)

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10
Q

What is the most common cause of SVT?

A

AVNRT (typically slow pathway is antegrade and retrograde reentrant circuit is over the fast pathway)

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11
Q

What is “concealed” AVRT?

A

When an AP conducts only retrograde (can still promote SVT), but it’s “concealed” because signal travels antegrade down the AV node/bundle of His as normal

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12
Q

What is ventricular pre-excitation syndrome?

A

When the AP conducts antegrade in AVRT, creating a delta wave on EKG due to the early excitation of the ventricle through the AP

**e.g. WPW

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13
Q

What is the difference between orthodromic and antidromic tachycardia?

A
  • orthodromic= retrograde conduction down AP (concealed)
  • antidromic= antegrade conduction down AP (delta wave)
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14
Q

What is the valsalva effect?

A
  • Forceful expiration against closed glottis
  • Increases intrathoracic pressure -> increased external pressure on heart and thoracic vessels -> vagal efferents stimulated -> slows heart
    • changes in HR are reciprocal to aortic pressures due to baroreceptor reflex
  • Used as an easy first attempt to correct reentrant SVT
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15
Q

What is a common medication used to treat SVT?

A

Adenosine

**rapid acting, short lived/short decrease in HR

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16
Q

What is the mechanism of adenosine?

A

Activates K channels to slow phase 4 depolarization in AV node and block cAMP enhanced Ca channel activity

**overall blocks AV node conduction

17
Q

What is this EKG showing?

A

Monomorphic V tach (typically wide QRS, rate >100 bpm)

18
Q

What classifies sustained VT?

A

Ventricular tachycardia lasting longer than 30 seconds… shock to treat

19
Q

What are some predisposing conditions to VT?

A
  • coronary disease (with ischemia/infaction)
  • congestive heart failure
  • ventricular hypertrophy
  • primary electrical disorders (e.g. long QT syndrome)
  • valvular disease
  • congenital heart disease
20
Q

What is monomorphic VT? What can cause it?

A
  • QRS complexes identical from beat to beat and rate is regular
  • sustained monomorphic VT typically results from reentry due to slowed conduction through surviving myocardial cells within areas of myocardial scar
21
Q

What is polymorphic VT? What can cause it?

A
  • QRS complex continually changes shape and rate varies from beat to beat
  • Caused by…
    • long QT with Torsades de pointes
    • acute ischemia/infarction
    • rare inherited abnormalities of cardiac ion channels/Ca handling

**may cause syncope/cardiac arrest if sustained

22
Q

How do you clinically manage VT?

A

**sustained VT= BAD (may degenerate into V fib)

  • acute therapy for unstable patient
    • cardioversion
  • acute therapy for stable patient
    • antiarrhythmic drugs (amiodarone)
    • sedate/cardioversion
  • long term
    • determine/correct aggravating factor
    • implantable cardioverter defibrillator (ICD)
    • maybe antiarrhythmic drugs or VT ablation
23
Q

What’s a major side effect of amiodarone?

A
  • long half life and high volume of distribution allows accumulation of metabolite desethylamiodarone
  • accumulates in…
    • lungs (usually)
    • liver, thyroid, nerves and skin
24
Q

What is this EKG showing?

A

Atrial flutter

**regular 2:1 atrial: ventricular depol and sawtooth pattern

25
Q

How do you treat atrial flutter?

A
  • similar to atrial fibrillation treatment (including anticoagulants and cardioversion to correct rhythm)
  • long term therapy=
    • ablation between the tricuspid annulus and IVC
    • antiarrhythmic drugs (flecanide)
  • A fib results ~50% of the time after atrial flutter ablation
26
Q

What is the common cause of atrial flutter?

A

Reentry around the tricuspid annulus in the right atrium

**typically counterclockwise rotation