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EP Board Review Flashcards

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USMLE® Step 1 flashcards
1
Q

What class AAD is contraindicated in PVC treatment?

A
  • Class Ic agents
  • CAST trial (1991)
    • increased mortality in patients with structural heart disease
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2
Q

What is the treatment of digoxin toxicity?

A
  • correction of potassium/magnesium
  • Bradycardia
    • Atropine or
    • Pacing
  • VT/VF
    • Lidocaine
  • Refractory VT/VF and Hyperkalemia
    • Fab antibody or
    • Digoxin immune Fab (in setting of complete heart block)
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3
Q

Describe the findings

A

Pre-excited A-fib

  • varying R-R intervals and variable QRS width
  • This occurs due to competition between the AV node and the accessory pathway, resulting in varying degrees of QRS fusion with wider QRS complexes due to predominant accesory pathway conduction and narrower QRS complexes due to AV nodal conduction
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4
Q

Define Permanent AF

A

Patient and clinician make a joint decision to stop attempts to restore and/or maintain sinus rhythm

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5
Q

What is the reversal agent:

  • Warfarin
A
  • Vitamin K
  • FFP
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6
Q

When can Droneaderone be used in A-fib?

What are the major contraindications?

A
  • Paroxysmal AF + CAD + normal LVEF
  • Contraindications:
    • decreased LVEF
    • Persistent AF
    • CHF
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7
Q

Describe ARVC

A
  • Fibrosis and fibrofatty replacement of ventricular myocardium progresses from epicardium to endocardium
    • involving the RV and less commonly the LV
  • Prevalence 1:5,000
  • Autosomal dominant (most common)
  • ​typically presents between 20-50 years of age
  • mutations in gene coding for desmosomal proteins
    • plakoglobin, plakophilin-2, desmin, desmocollin, desmoglein-2
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8
Q

Why are canon A waves seen in pacemaker syndrome?

A
  • ventriculo-atrial conduction –>
  • contraction of the atrium with a closed AV valve
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9
Q

Determine QRS axis: Right superior axis ( -90 to 180)

A
  • Lead I –> negative
  • Lead aVF –> negative
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10
Q

What are clinical and EP features associated with an increased risk of SCD in WPW pattern patients?

A
  • Younger age
  • EPS:
    • inducible AVRT
    • multiple accessory pathways (AP’s)
    • AP capability to conduct rapidly to the ventricles
      • SPERRI during AF « 250 ms
      • short antegrade ERP of AP « 250 ms​
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11
Q

What is the first diagnostic step in patients with symptomatic PVC’s?

A

assess PVC burden –> 24 hour Holter monitor

  • ► 25% can lead to PVC induced cardiomyopathy
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12
Q

Describe EKG findings of Bi-V pacing

A
  • qR or QS complexes in I and aVL
    • indicate ventricular activation is starting in the posterolateral LV (typical location of LV pacing via coronary sinus lead)
    • conducting away from the LV and toward the RV
  • rS complex or R waves (positive) in V1-V3
    • reflects activation starting posterolaterally in the LV –>
    • conducting anteriorly toward the RV
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13
Q

What is the definition of chronotropic incompetence in the setting of bradycardia?

A
  • HR < 100 bpm (peak)

and

  • < 70% age-predicted maximum heart rate
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14
Q

Describe the findings and the next best step in therapy:

  • 40 year old female with palpitations
  • Tachycardic, hypotensive –> cardioversion
  • Labs and Echo - normal
  • Cardiac MRI - no LGE or structural abnormalities.
A
  • Sustatined monomorphic VT
  • Treatment: VT supression
    • BB - Propanolol
    • Antiarrhythmic drugs
    • Catheter ablation
  • ​​Preventitive therapy in a structurally normal heart + VT
  • All may be considered first line therapy
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15
Q

What is the recommended treatment strategy for symptomatic WPW?

A

Catheter ablation

  • high success rate
  • low complication rate
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16
Q

What is the differential for polymorphic VT (rapid VT with changing morphology)?

How do you distinguish between them?

A
  • Polymorphic VT
    • Torsades des pointes
    • Ischemia
  • TdP
    • starts with a late-coupled VPC (late R-on-T) and
    • QT interval is prolonged
  • Ischemia
    • early-coupled VPC (early R-on-T)
    • QT interval is normal
    • ST segment may be elevated
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17
Q

What are factors that can enhance AV nodal conduction?

A

Exercise

  • cause predominantly more of the ventricles to be activated in the normal fashion such that the delta wave will diminish with exercise
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18
Q

What medications can be used for PVC management in patients with structural heart disease (LV dysfunction)?

A

Class III agents

  • Sotalol
  • Amiodarone
  • Dofetilide
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19
Q

What disease processes are particularly associated with Monomorphic VT (MVT)?

A
  • ARVC
  • Chagas disease
  • Sarcoidosis

Less Likely (usually MVT and PVT):

  • Hypertrophic cardiomyopathy
  • Ventricular noncompaction
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20
Q

What are common causes of low voltage on EKG?

A
  • COPD
  • Obesity
  • Myxedema
  • Pericardial effusion
  • Pleural effusion
  • Restrictive / infiltrative cardiomyopathy
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21
Q

When coding - Sinus arrhythmia:

  • Unecessary to code
A

sinus rhythm

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22
Q

What class of medications is utilized for “pill-in-pocket” approach?

Why?

A
  • Class Ic antiarrhythmics (flecainide, propafenone)
  • Use dependence
    • ​block open sodium channels (INa)
    • slow conduction velocity in the myocardium
    • slowly dissociate from sodium channels during diastole –> more effective at rapid heart rates
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23
Q

Define Persistent AF

A

AF > 7 days in duration

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24
Q

Describe the findings

A
  • Katz-Wachtel phenomenon
  • Congenital heart disease with biventricular hypertrophy
  • EKG:
    • large amplitude, equiphasic (R = S) complexes in mid-precordial leads
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25
Q

What is one concern regarding RV apical pacing in patients with intact LV systolic function?

A

increased incidence of AF

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26
Q

What are the recommendations for anticoagulation during cardioversion for AF?

A

► 4 weeks after cardioversion

  • recommended when ► 48 hours or unknown AF duration
  • regardless of CHADSVasc score
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27
Q

What is the most common cause of PMVT?

A

Ischemia

​

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28
Q

What is the definition of VT storm?

A

> 3 episodes of VT in 24 hours

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29
Q

What type of pacing is contraindicated in the setting of permanent AF?

A

dual chamber pacing

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30
Q

What are the currently available DOAC’s for stroke prevention?

A
  • Dabigatran
    • Anti-factor IIa - Direct Thrombin Inhibitor
  • Apixaban, Rivaroxaban, Edoxaban
    • Factor Xa inhibitors
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31
Q

What is the most common pattern of aberrantly conducted PAC’s?

A

RBBB

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32
Q

What is the next step in evaluation/management of VA’s in patients with:

  • PVC’s
  • Structural heart disease
A
  • Medical therapy
    • BB
    • Amiodarone
    • Sotalol
  • Catheter ablation if:
    • failed medical therapy
    • single/dominant PVC morphology
    • reversible cardiomyopathy (probable)
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33
Q

What are common sites for focal AT’s?

A
  • Right atrium:
    • Crista terminalis
    • Coronary sinus ostium
  • Left atrium:
    • LAA
    • mitral valve annulus
    • Pulmonary veins
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34
Q

What are the treatment options:

  • Brugada Syndrome (confirmed)
  • Without Cardiac arrest or recent unexplained syncope
A
  • Lifestyle changes

and

  • Observe without therapy or
  • EP study for risk stratification (Class IIb)
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35
Q

What is an interpolated beat?

A
  • premature contraction of the ventricles which is not followed by a compensatory pause
  • does not disturb the dominant rhythm of the heart
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36
Q

Which phase of the cardiac action potential distinguishes it from a neuronal action potential?

A

Phase 2

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37
Q

What are the class I recommendations for risk stratification in WPW?

A
  • Exercise stress test or
  • Holter or
  • EPS

****How well does the accessory pathway conduct?****

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38
Q

What is the diagnosis and most likely mechanism leading to SCD?

  • SCD in a young person while swimming
A
  • Long QT syndrome type 1
  • Mutation in the IKs potassium channel
    • ​loss of function and thus a delay in membrane repolarization
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39
Q

What is the anticoagulant recommendation with antifungals?

A
  • Contraindicated:
    • ​Dabigatran
    • Rivaroxaban
    • Apixaban
  • Edoxaban 30mg daily
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40
Q

What lead can be used to confirm acute inferior or lateral Q wave MI?

What are the findings?

A
  • Inferior –> aVL
  • Lateral –> aVF
  • ST-depression
    • there will always be recriprocal ST-depression even if the ST segment elevation in other leads is minimal
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41
Q

What are the recommendations for ICD placment:

  • ARVC
A
  • Class I
    • SCD (resuscitated)
    • RVEF or LVEF « 35%
  • Class IIa
    • Syncope (presumed due to VA)
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42
Q

What is the threshold for PVC cardiomyopathy?

A

PVC burden > 10-20%

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43
Q

What is the next best test in a patient with CAD + Syncope?

A

EPS (after negative ischemia evaluation)

  • Evaluate for:
    • Sinus node dysfunction
    • AV node dysfunction
    • Ventricular arrhythmias –> ICD implantation
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44
Q

Describe classic criteria for VT

A
  • Brugada’s sign
    • distance from onset of the QRS complex to the nadir of the S-wave is 100ms
  • Josephson’s sign
    • notching near the nadir of the S wave
  • Fusion beats
  • AV dissociation
  • Capture beats
  • Extreme axis (“northwest”)
  • Wide QRS ( > 160 ms)
  • RSR’ complexes
    • taller “left rabbit ear”
    • most specific sign of VT
  • Absence of typical RBBB or LBBB morphology
    • RBBB > 140
    • LBBB > 160
  • Positive or negative concordance (all precordial leads)
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45
Q

What statin can increase the risk of rhabdomyolysis when used in combination with Amiodarone?

What are alternative options?

A

Simvastatin

  • due to Amiodarones inhibition of CYP3A4

Rosuvastatin or Pravastatin

  • neither utilize CYP3A4
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46
Q

What is the site of therapy in A-flutter ablations?

A

Cavotricuspid isthmus

  • located between the IVC and the tricuspid annulus (IVC-TA isthmus)
  • creation of a line of ablation from the TA to the IVC is an obligatory route for typical flutter
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47
Q

EKG definition: incorrect electrode placement

A
  • Reversal of right and left limb leads, resulting in:
    • I, aVL - negative P wave and QRS axis
    • aVR - positive P wave and QRS axis
  • Reversal of two precordial leads, resulting in:
    • sudden decrease in R wave progression with a marked return in the R wave on the ensuing precordial lead

****most commonly seen with these two

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48
Q

What are the indications for ICD placement in Brugada syndrome?

A
  • Confirmed Brugada syndrome (BrS type 1)

and

  • Cardiac arrest or Recent unexplained syncope
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49
Q

Differential diagnosis for:

  • Inverted P-wave in Lead I
A
  • PAC’s
  • Atrial rhythm
    • EAT
    • MAT
    • SVT
  • PJC’s
  • Dextrocardia
  • Limb lead reversal
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50
Q

What is the diagnosis:

  • Narrow QRS tachycardia (QRS « 120 ms)
  • Regular
  • Visible P waves
  • Atrial rate > ventricular rate
A
  • Atrial flutter
  • Focal AT
  • AVNRT (rare)
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51
Q

What is the next step in evaluation/management of VA’s in patients with:

  • PVC’s
  • Abnormal initial evaluation
A
  • Holter monitor –> assess PVC burden
  • Cardiac MRI (consider)
  • Treatment if:
    • PVC > 10,000 in 24 hours
    • Symptom limiting
    • Interfering with CRT delivery
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52
Q

What are the treatment options:

  • Brugada Syndrome (confirmed)
  • Cardiac arrest or recent unexplained syncope
A
  • ICD (Class I)
  • Quinidine or Catheter ablation (Class I)
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53
Q

Describe the findings and mechanism for inititation of this heart rhythm

A

Prolonged QT + Polymorphic VT (Torsades de pointes)​ –> VF

  • Triggered activity due to early afterdepolarizations
  • ​Medications (Azithromycin) can prolong QT interval and predispose patients with a long QT syndrome to this event
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54
Q

Describe the findings and best treatment option:

A
  • Typical A-flutter
  • Catheter ablation
    • ​95% success rates
    • drug therapy (prophylaxis or as the occasion arises with drugs that block AV nod or antiarrhythmic drugs) is rarely effective or helpful
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55
Q

What medications used in A-fib can cause increased serum Digoxin levels when used concomitantly?

A
  • Verapamil
  • Amiodarone
  • Dronedarone
  • Quinidine
  • Rivaroxaban
  • Apixaban
  • Erythromycin, Clarithromycin
  • Cyclosporine
  • Ketoconazole
  • Itraconazole

****P-glycoprotein inhibitors (in bold)

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56
Q

What are the steps in assessing symptomatic PVC’s?

A
  • 24 hour Holter monitor
    • Assess PVC burden
    • ► 10-25% can lead to PVC cardiomyopathy
  • Echo
    • Ventricular size and function
      • LV –> PVC-CM or ischemia
      • RV –> ARVD
  • EKG (12 lead)
    • if same PVC present in multiple leads –> potential site of VT origin
  • ​Cardiac MRI
    • exclude ARVD, scar-related VT (myocarditis, sarcoidosis)​
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57
Q

Based on response, what is the diagnosis of Narrow complex Tachyardia (QRS < 120 ms) in the setting of adenosine administration:

  • Sudden termination
A
  • AVNRT
  • AVRT
  • Sinus node re-entry tachycardia
  • Triggered Focal AT (DAD’s)
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58
Q

What is the origin of the PVC’s?

A

Idiopathic ​LV outflow tract PVC’s

  • Left-bundle, inferior axis morphology
    • precordial R-wave transition (totally positive QRS complexes in lead V3) is earlier than is typically seen in RVOT VT
    • LVOT (sinuses of Valsalva specifically) is posterior and inferior to the RVOT –> results in more positive voltage and earlier transition in the precordial leads
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59
Q

What is the diagnostic criteria for Brugada Syndrome?

A

► 1 lead among the right precordial leads V1-V2 positioned in the “high pre-cordial position” (2nd, 3rd, or 4th intercostal space)

+

  • BrS type 1 - ST-segment elevation with type 1 (coved) morphology ► 2 mm; on the resting EKG

or

  • BrS type 2 or type 3 - ST-segment elevation + provocative drug test with IV administration of Class I antiarrhytmic drugs –> a type 1 BrS EKG morphology
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60
Q

Describe the findings

A
  • RSR’ pattern
  • Suggestive of SVT with RBBB
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61
Q

What did SCD-HeFT trial (2002) show in regards to Amiodarone?

A

amiodaorne did not improve survival compared to placebo

in heart failure patients

  • Single-lead, shock-only ICD therapy reduces mortality by 23% compared to conventional therapy or amiodarone in stable NYHA class II or III HF with EF <35%.
  • Amiodarone conferred no survival benefit compared to placebo.
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62
Q

What are the recommendations for ICD placment:

  • CPVT
A

Class I

  • Recurrent VT or syncope while on maximal medical therapy (BB, Flecainide)
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63
Q

How can P waves help differentiate types of SVT?

A
  • AVNRT
    • Retrograde (caudocranial) atrial activation
    • negative P waves in inferior leads
  • ​AT (some times)
    • Craniocaudal activation
    • positive P waves in inferior leads
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64
Q

Describe the HASBLED score

A
  • Validated bleeding risk score for AF
  • HASBLED score:
    • Low risk = 0-2
    • High risk = ► 3
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65
Q

Describe symptom onset for:

  • AVNRT
  • AVRT
  • AT
A
  • AVNRT and AVRT
    • sudden, abrupt onset and termination without any clear inciting factor
  • AT
    • gradual onset and resolution (although this may not be a consistent finding)
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66
Q

What is manifest pre-excitation? What does it mean?

A
  • presence of a delta wave on EKG
  • WPW pattern
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67
Q

What are symptoms of pacemaker syndrome?

What is treatment for pacemaker syndrome?

A
  • Symptoms:
    • SOB
    • DOE
    • fatigue
    • palpitations in a patient with sinus rhythm
    • single-chamber, ventricular device
  • Upgrade to dual-chamber device
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68
Q

When coding - Incorrect electrode placement:

  • Unecessary to code
A

Axis deviation

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69
Q

What is the differntial diagnosis for VT arising fom the RVOT?

A
  • Idiopathic VT
  • ARVC
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70
Q

When coding - Incorrect electrode placement:

  • Inorrect to code
A

Axis deviation

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71
Q

What will happen in orthodromic or antidromic AVRT with AV nodal blockade?

A

termination of the tachycardia

  • dependent on AV node for propagation of the arrhythmia
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72
Q

What medication may increase serum levels of dabigatran in vivo?

A

Amiodarone

  • inhibits P-glycoprotein –> increased serum levels
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73
Q

Differential diagnosis for:

  • Inverted P-wave in Lead II
A
  • PAC’s
  • Atrial rhythm
    • EAT
    • MAT
    • SVT
  • Retrograde activation
    • PJC’s
    • PVC’s
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74
Q

Describe the findings:

A
  • NSR
  • PAC’s
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75
Q

When coding - LAFB:

  • Unecessary to code
A

LAD

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76
Q

Describe phase 1 of the action potential

A

Phase 1

  • “initial” or “early” rapid depolarization
  • caused by:
    • inactivation of Na+ current (INa)
    • activation of transient outward current (Ito) potassium channels –> carried mostly by K+ ions
      • Ito is composed of two components Ito1 and Ito2
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77
Q

What is the next step if conservative measures fail in the treatment of vasovagal syncope?

A
  • ILR
    • if a marked cardio-inhibitory response (asystole) shown
  • PPM can be considered
    • only if prolonged periods of asystole
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78
Q

What PVC burden can lead to PVC-induced cardiomyopathy?

A

► 25%

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79
Q

What RP interval is considered short?

What is the most common diagnosis in this scenario?

A

< 70 ms

AVNRT

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80
Q

What are independent predictors of failure of BB therapy in LQTS?

A
  • QTc ► 500 ms
  • early occurrence of life-threatening ventricular arrhythmias (before 7 years of age)
  • LQTS 2 and LQTS 3 genotype
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81
Q

What is the least commonly encountered PSVT?

A

Atrial tachycardia

  • accounts for 10% of cases of PSVT
  • single automatic or micro-re-entrant focus that is firing independently of the sinus node
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82
Q

What are the class II recommendations for surgery in infective endocarditis?

A
  • Mobile vegetation > 10 mm
    • with or without embolization
  • Recurrent embolization after appropriate antibiotic therapy
  • Persistent vegetation after antibiotic therapy
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83
Q

Describe the findings:

A

QRS fragmentation - Brugada syndrome

  • one or more QRS notches (arrows) may indicate heterogeneous electrical conduction
    • heterogeneous: of or denoting a process involving substances in different phases (solid, liquid, gas)
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84
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Polymorphic VT/VF
  • Initial evaluation
A
  • Urgently treat ACS if present
  • Similar initial evaluation as other VA’s
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85
Q

When coding - Atrial tachycardia:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • SVT
  • Inorrect to code
    • Atrial enlargement
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86
Q

What are distinct EKG features of SVT?

A
  • r’ at the end of QRS comlex in V1
    • 30% of cases
  • retrograde P waves just before the QRS complex - evident as negative P waves in II, III, aVF
    • 25% of cases
  • retrograde p waves occur within QRS complex and are not visible on EKG
    • 45% of cases
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87
Q

What are ways to noninvasively affect AV nodal and His-Purkinje conduction?

A
  • Carotid massage (parasympathetic stimulation)
    • slows sinus rate
    • worsens AV nodal conduction –> worsen AV block
    • protective effect on distal conduction system –> His-Purkinje system may improve
  • Exercise (sympathetic stimulation)
    • increases sinus rate
    • improves AV nodal conduction
    • decreases His-Purkinje conduction
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88
Q

What pharmacologic property explains why Amiodarone is initiated with a load (higher dose for several days or weeks)?

A

Large volume of distribution

  • requires greater dosage administrated early on
  • Although, increasing dose of the drug early on, does not allow the achievement of a steady state any faster
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89
Q

What is the cause of a “pause” when an extra P wave is present between QRS complexes?

A
  • Atrial prematurity –> PAC’s
  • 2nd degree AV block
    • prolongation of PR interval leading to blocked P wave –> Type I (Wenckebach)
    • constant PR intervals leading to and following the blocked P wave –> Type II
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90
Q

What is the benefit of rate control in permanent A-fib in regards to optimal HR?

A

No additional benefit between conservative vs. aggressive control (if asymptomatic)

  • RACE-II Study compared patients with permanent AF (asymptomtic)
    • target HR < 80 bpm vs. target HR < 110 bpm
    • similar rates of major adverse events with both strategies
    • additional medications –> increased side effects –> without clear benefits in a low-risk, asymptomatic patient
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91
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Polymorphic VT/VF
  • Abnormal initial evaluation
A
  • If revascularization for ACS:
    • re-evaluate LVEF as appropriate for ICD candidacy
  • Assess for inherited arrhythmia syndrome
  • Consider cMRI
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92
Q

What is one clinical scenario in which anticoagulation is recommended for stroke prophylaxis regardless of CHADSVasc score?

A

Hypertrophic Cardiomyopathy + AF/Flutter

  • Class I recommendation
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93
Q

What are Long R-P tachycardias / SVT’s?

A
  • Atrial tachycardia
  • AVRT
  • Atypical AVNRT
  • PJRT (permanent junctional reciprocating tachycardia)
    • form of AVRT, slow conducting pathway
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94
Q

How is Vascular disease defined in the CHADSVasc risk score?

A
  • CAD (prior MI)
  • PAD
  • Aortic plaque
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95
Q

What is the diagnosis and next step in management:

  • 77 year old female with syncope
  • No warning symptoms
  • Meds: ASA and Amlodipine
A
  • Mobitz II, AV block
  • PPM
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96
Q

What are important interactions with Adenosine?

A
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97
Q

Describe the findings:

A

Typical (isthmus-dependent) Atrial flutter

  • utilizes a large macroreentrant pathway in the RA
  • EKG:
    • inverted flutter waves in II, III, aVF
    • upright flutter waves in V1 (may appear as upright p waves)
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98
Q

Describe the findings:

A
  • SVT
  • Right axis deviation
  • Electrical alternans
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99
Q

What is the reversal agent:

  • Apixaban
  • Rivaroxaban
A

Andexanet alfa (Andexxa)

  • modified factor Xa molecule
  • only approved for Apixaban and Rivaroxaban currently - may be useful for other Factor Xa agents
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100
Q

Describe the differential/algorithm for narrow QRS tachycardia (QRS < 120 ms)

A
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101
Q

What are indications for PPM in AV Node Disease - Class IIb

A
  • AV block of any degree in the setting of neuromuscular disease with or without symptoms
  • AV block in the setting of drug toxicity that may recur even when drug is withdrawn
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102
Q

Describe the findings:

A
  • NSR
  • RAD
  • RVH
  • RBBB, complete
  • ST and/or T wave abnormalities secondary to hypertrophy
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103
Q

What medications have demonstrated reduction in the risk of ICD shocks and mortality in patients with:

  • structural heart disease
  • reduced EF
  • secondary prevention ICDs (history of ventricular arrhythmias or syncope with inducible ventricular arrhythmias)
A

Sotalol and Amiodarone

  • OPTIC trial
    • Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients study
  • Sotalol ICD
    • Sotalol as Adjunctive Therapy to ICD’s in Heart Failure Patients study
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104
Q

What is one concern regarding RV apical pacing in patients with impaired LV systolic function?

A

deleterious effect of prolonged RV pacing –>

worsening of LV function and heart failure

  • Supporting trials:
    • DAVID (Dual Chamber and VVI Implantable Defibrillator)
    • MOST (Mode Selection Trial)
    • DANISH (Danish Study to Assess the Efficacy of ICDs in Patient with Non-Ischemic Systolic Heart Failure on Mortality)
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105
Q

What are indications for PPM in Sinus Node Disease - Class IIa

A
  • HR < 40 bpm and symptoms consistent with bradycardia
    • but clear association between bradycardia and symptoms is undocumented
  • Unexplained syncope and abnormal sinus node function on EPS
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106
Q

What is the mechanism for VT:

  • Torsades des pointes
  • Prolonged QT syndrome
A

Triggered activity - Early AfterDepolarizations (EADs)

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107
Q

What are the recommended lifestyle changes for patients with known or suspected Brugada Syndrome?

A
  • Avoid precipitating drugs
  • Treat Fever
  • Avoid excessive alcohol
  • Avoid Cocaine
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108
Q

What percentage of patients with WPW experience tachycardia?

A

70%

  • 70% - SVT (ORT or ART)
  • 30% - A-fib
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109
Q

Describe the findings and treatment:

  • 30 year old, healthy, relatively asymptomatic patient
A

Idiopathic LV (fascicular) VT

  • Re-entrant tachycardia involving most commonly the left posterior fascicle
  • EKG
    • mildly wide complex tachycardia
    • RBBB-like morphology
    • superior or left axis
  • Treatment:
    • Verapamil
    • rhythm is highly sensitive to verapamil
    • low-risk tachycardia –> catheter ablation of fascicle is usually curative
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110
Q

EKG definition: Juvenile T waves

A
  • localized TWI in right precoridal leads (V1-V3)
    • not symmetrical or deep
  • Commonly seen in children and adolescents
    • occassional normal variant in adult women
    • rarely seen in men
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111
Q

What is the treatment/recommendations for PVT and VF within 48 hours of MI/revascularization?

A
  • Do not confer a long-term risk
  • Long term therapy with antiarrhythmics or ICD is generally not required
  • ICD should be considered for patients:
    • sustained PVT that is not due to a reversible cause and
    • expectation of survival, with acceptable functional status ► 1 year
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112
Q

What is the differential and distinguishing features for non-conducted P-waves?

A
  • DDx: nonconducted P-waves –> grouped beating
    • PAC’s (blocked)
    • Mobitz I, 2nd degree AV block
    • Mobitz II, 2nd degree AV block
  • Differentiating between them:
    • PAC’s –> irregularlarity of P-P interval
    • Mobtiz I –> PR interval prolongation
    • Mobitz II –> PR interval constant

*****Mobitz II –> further supported by bifascicular block / block distal to the AV node

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113
Q

What is the difference in phase 0 between SA and AV nodal tissues?

A

depolarization is carried mainly by T- and L-type Ca2+ channels

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114
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Polymorphic VT/VF
  • No SHD or historical high-risk features
A
  • Assess for reversible cause
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115
Q

What are indications for PPM in Sinus Node Disease - Class IIb

A
  • Minimally symptomatic patients with chronic HR < 40 bpm while awake
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116
Q

Describe the proarrhythmic effects of Digoxin:

  • mechanism
  • most common arrhythmias
A
  • intracellular calcium overload –> delayed after depolarizations (DAD’s) and triggered activity
  • Most common:
    • atrial tachycardia with AV block
    • bidirectional VT
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117
Q

When coding - LPFB:

  • Unecessary to code
A

RAD

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118
Q

What are key situations that require bridging anticoagulation therapy in A-fib?

A
  • Mechanical Valve
  • Prior stroke/TIA
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119
Q

What does a “delta wave” represent?

A

“fusion” of impulses activating the ventricles via both the AV node and the accessory pathway

  • only present if accessory pathway can conduct antegradely
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120
Q

What are the characteristics of common accessory pathways?

A
  • short, rapidly conducting accessory pathways across mitral or tricuspid annulus
    • Left sided –> structurally normal hearts (most common)
    • Right sided –> Ebstein’s anomaly
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121
Q

Describe the findings and next step:

  • 84 year old woman with syncope (without prodrome), regained consciousness after 20s with contusion on her cheek
  • PMH: paroxysmal AF, HTN
  • EKG: NSR, RBBB and LAFB
  • Echo: Normal LVEF
  • MPI: negative for ischemia
A

Dual-chamber PPM

  • EP study is appropriate given high likelihood of a mlaignant etiology of her symptoms with negative standard evaluation
  • EP study:
    • prolonged HV interval (normal 35-55 ms)
  • Indications:
    • Class I - syncope + prolonged HV interval
    • Class IIa - unexplained syncope + bifascicular block
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122
Q

Describe the differences between 2nd degree AV block

  • PR interval
  • QRS duration
A
  • Mobitz I - 2nd degree AV block
    • PR interval –> progressive lengthening
    • Block at the level of the AV node –> narrow QRS
  • Mobitz II - 2nd degree AV block
    • PR intervals are constant
    • Block at/below the bundle of His –> wide QRS (in 80% of cases)
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123
Q

Describe Atypical AVNRT

A
  • 1-5% of AVNRT
  • Slow (antegrade) - Slow (retrograde) conduction
    • left atrial fibers for retrograde conduction
  • Often confused with ST as P wave before QRS complex
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124
Q

Describe the findings:

A

2nd degree AV block - with periods of 2:1 AV block

  • likely indicates that the site of block is below the AV node (at the level of the His bundle) and more likely to progress to complete heart block
  • 3rd strip - may show Mobitz type 1 block with PR prolongation prior to the blocked beat
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125
Q

What is the difference between rate and rhythm control in A-fib?

  • stroke
  • mortality
  • hospitalizations
A
  • stroke –> No difference
  • mortality –> No difference
  • hospitalizations –> less hospitalizations with rate control
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126
Q

Describe phase 2 of the action potential

A

Phase 2

  • “plateau” of the action potential
    • can be several hundred msec long in some cardiac cells (Purkinje)
  • most complex phase due to many small amplitude currents and several ion channels
  • caused by:
    • Inward (depolarizing) current:
      • INa - late inactivating Na+ channels
      • ICa-L - L-type Ca2+ channels
    • Outward (repolarizing) current:
      • K+ channels
        • Ito - inactivation
        • IKr rapidly - slow activation
        • IKs slowly - activating delayed-rectifier K+ channels
  • Occurs through electrogenic transmembrane transporters:
    • Na+ - Ca2+ exchange
    • Na+ - K+ exchange
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127
Q

Why is it important to diagnose RVOT VT early?

A

Highly amenable to catheter ablation

  • no ischemic workup required
  • unless other risk factors present
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128
Q

What is the diagnosis and next best step?

  • 30 year old male with syncope (x2 in the last year while exercising)
  • No medical problems or medications
  • FH: Uncle died at 34 in drowning accident
    *
A
  • Brugada syndrome
  • EKG with high precordial leads
    • ​recording V1 and V2 in second and third intercostal space can assist in the diagnosis of borderline cases
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129
Q

What are indications for PPM in Sinus Node Disease - Class III

A
  • SND in asymptomatic patients
  • SND in patients with symptoms documented in absence of bradycardia
  • Symptomatic bradycardia due to non-essential drug therapy
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130
Q

Describe the findings:

A
  • Atrial tachycardia
  • Nonspecific ST and/or T wave abnormalities
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131
Q

What sports/activities are athletes with definite diagnosis of ARVC allowed to participate in?

A

Class 1A sports - Golf

  • sports low in static and dynamic loads
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132
Q

What is the diagnosis:

  • Narrow QRS tachycardia (QRS « 120 ms)
  • Regular
  • Visible P waves
  • Ventricular rate > Atrial rate
A
  • High septal VT
  • JET (junctional ectopic tachycardia)
  • AVNRT (rare)
  • Nodoventricular/fascicular-nodal re-entry (rare)
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133
Q

What did the LEGACY trial show?

A

Weight management is associated with a reduction in AF symptom burden

  • “Long-Term Effect of Goal-Directed Weight Management in AF Cohort Trial”
    • 335 patients with BMI > 29
    • ► 10% reduction body weight resulted in a sixfold greater probabilty of arrhythmia-free survival at 5 years

References

Pathak RK, Middeldorp ME, Meredith M, et al. Long-term effect of goal-directed weight management in an atrial fibrillation cohort: a long-term follow-up study (LEGACY). J Am Coll Cardiol 2015;65:2159-69

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134
Q

When is catheter ablation recommended for atypical A-flutter?

A

After failure of at least 1 antiarrhytmic agent

  • ablation is much more difficult for atypical A-flutter
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135
Q

When coding - MAT:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • SVT
  • Inorrect to code
    • Atrial enlargement
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136
Q

What are methods that can be utilized to assist or “unmask” Brugada syndrome in borderline cases?

A
  • Sodium channel blocking agent –> type I pattern
    • flecainide, ajmaline, procainamide
  • “High” precordial leads
    • recording leads V1 and V2 in the 2nd and 3rd intercostal space to improve diagnostic accuracy
    • should be performed during drug testing and during 12-lead Holter monitoring
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137
Q

What are the Class I recommendations for genetic testing in LQTS?

A

Class I

  • Comprehensive or LQTS 1-3 targed genetic testing (KCNQ1, KCNH2, SCN5A) for patients with:
    • strong clinical suspicion for LQTS and QT prolongation
    • asymptomatic adult patients with QTc > 500 (adults) or > 480 ms (prepubescents) in the absence of other clinical conditions that might prolong the QT interval
  • Mutation specific genetic testing for:
    • first-degree relatives of individuals with LQTS + an identified causitive mutation

Class IIb

  • Comprehensive or LQTS 1-3 targed genetic testing (KCNQ1, KCNH2, SCN5A) for patients with:
    • Asymptomatic patients with otherwise idiopathic QTc > 480 (adults) or > 460 (prepubescents) on EKG
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138
Q

What are the major causes/concerns of dyspnea following ablation?

A
  • Pulmonary vein stenosis
    • ​all PVS until proven otherwise
  • Atrial arrhythmias
  • Tamponade
    • ​pericarditic feature (should be resolved by day 3)
  • Less common/severe:
    • Atelectasis
    • Volume overload
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139
Q

What trials support the use of catheter ablation in AF and HF?

A

CASTLE-AF

  • Catheter Ablation vs. Standard Conventional Therapy in Patients with LV Dysfunction and A-Fib)
  • AF (paroxysmal or persistent) + symptomatic HFrEF (NYHA II-IV, LVEF « 35%)
  • Catheter ablation is associated with:
    • 16.1% absolute reduction in death or hospitalization
    • greater improvement in LVEF
    • greater improvement in long-term maintenance of sinus rhythm
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140
Q

What are chronic medical conditions that contribute to AF development/burden?

A
  • HTN
  • OSA
  • Obesity
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141
Q

What DOAC’s have the highest hepatic metabolism?

A

Apixaban and Rivaroxaban

  • CYP3A4 metabolism
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142
Q

When coding - VT:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • Axis deviation
    • IVCD
  • Inorrect to code
    • LVH
    • RVH
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143
Q

Describe the findings and diagnosis

A

ARVD

  • Epsilon waves
  • TWI in V1-V3
  • Prolonged S-wave upstroke of 55 ms in V1-V3 (95% of patients)
  • Localized QRS widening of 110 ms in V1-V3
  • Paroxysmal episodes of VT with LBBB morphology
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144
Q

What are causes of bidirectional VT?

A

Calcium overload

  • Digoxin toxicity
  • CPVT
  • Andersin-Tawil (long QT syndrome)
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145
Q

What are the preferred antiarrhythmics for A-fib in patients with structural heart disease?

A
  • Class I
    • Sotalol
    • Dofetilide

If medication failure:

  • Class I
    • Ablation
  • Class IIa
    • Amiodarone
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146
Q

Describe the findings and origin of the arrhythmia?

A

RV Outflow tract VT

  • NSR with NSVT
  • LBBB morphology
  • inferior axis (large positive deflections int he inferior leads 2, 3, aVF)
  • late precordial transition at V5 (point at which the vector changes from negative to positive)
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147
Q

EKG definition:

  • Nonspecific ST and/or T wave abnormalities
A
  • Mild, < 1 mm of ST-T segment depression or elevation, and/or
  • Slightly inverted ( < 2 mm) or flattened T wave
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148
Q

What is the most common cause of Polymorphic VT (PVT)?

A

acute myocardial ischemia

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149
Q

Describe termination of typical AVNRT

A
  • block in the antegrade slow pathway
  • P wave that blocks in the AV node with no R wave
  • Abrupt termination of tachycardia
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150
Q

Define AVRT

A
  • macro-re-entrant tachycardia (diameter > 2 cm)
  • requires participation of at least one accessory pathway
    • electrical connection between atria and ventricles that bypass the normal conduction system
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151
Q

In patients with ARVC, what lifestyle modifications are recommended regarding physical activity?

A

​Limit competitive sports participation

  • physical activity may accelerate structural progression of ARVC
    • in a study of heterozygous plakoglobin-deficient mice, enduracne training accelerated the developement of arrhythmias and RV dysfunction
  1. Corrado D, Basso C, Rizzoli G, Schiavon M, Thiene G. Does sports activity enhance the risk of sudden death in adolescents and young adults? J Am Coll Cardiol 2003;42:1959-63.
  2. Kirchhof P, Fabritz L, Zwiener M, et al. Age- and training-dependent development of arrhythmogenic right ventricular cardiomyopathy in heterozygous plakoglobin-deficient mice. Circulation 2006;114:1799-806.
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152
Q

Determine QRS axis: LAD (-30 to -90)

A
  • Lead I –> positive
  • Lead aVF –> negative
  • Lead II –> negative
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153
Q

When does dose reduction of Apixaban occur?

A

When > 2/3 are present:

  • Age ► 80 years
  • Weight <= 60 kg
  • Creatinine ► 1.5 mg/dL
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154
Q

What are the recommendations for ICD placment:

  • Cardiac Sarcoidosis
A
  • Class I
    • SCD (resuscitated)
    • VT (sustained)
    • LVEF « 35%
  • Class IIa
    • Syncope
    • Myocardial scar by MRI or PET
    • Positive EPS for inducible VT
    • Indication for PPM
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155
Q

Describe phase 3 of the action potential

A

Phase 3

  • “final rapid repolarization” phase
  • caused by:
    • inactivation of depolarizing currents
    • progressive activation of repolarizing K+ currents:
      • IKr
      • IKs
      • IK1 - inward rectifier K+ current
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156
Q

Describe features of Timothy Syndrome

A
  • Timothy syndrome (TS-LQT8)
    • high mortality ( > 80%) with complex phenotypes
    • marked QT prolongations + AV block + congenital heart defects
    • syndactyly + developmental disorders (autism) + reduced immune response
    • CACNA1c (gain of function) –> ICa (alpha subunit of L-type calcium channels)
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157
Q

What is a contraindication to the use of DOACs?

A

Advanced or ESRD

  • particularly those on dialysis
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158
Q

What is one way to differentiate ARVC from Cardiac Sarcoidosis by rhythm?

A

AV block favors sarcoidosis

  • both will present with RV outflow tract VT
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159
Q

How is Dofetilide eliminated?

A

Kidneys (80% in urine)

  • occurs by both glomerular filtration and cationic renal (active tubular) secretion
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160
Q

What did the CAST trial show?

A
  • Encainide, Flecainide, Morizicine (Class IC)
    • increased mortality in post-MI patients with PVC and/or NSVT
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161
Q

Describe Ashman’s phenomenon

A
  • aberrant ventricular conduction
  • usually RBBB morphology
  • follows a long-short R-R interval pattern
    • long R-R interval –> short R-R interval –> aberrant conductio
  • Commonly seen in A-fib
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162
Q

Describe the findings:

A
  • NSR
    • first two beats with narrow QRS
  • Accelerated idioventricular rhythm ~ 75 bpm
    • AV dissociation can occur with AVIR and complete heart block
    • can be distinguished by atrial and ventricular rates
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163
Q

What antibiotics are used for SBE prophylaxis prior to procedures?

A
  • Oral
    • Amoxicillin
  • NPO
    • Ampicillin
    • Cefazolin
    • Ceftriaxone
  • Allergic to PCN or Ampicillin (oral)
    • Cephalexin
    • Clindamycin
    • Azithromycin or Clarithromycin
  • Allergic to PCN or Ampicillin (NPO)
    • Cefazolin
    • Ceftriaxone
    • Clindamycin
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164
Q

What antiarrhythmics effect defibrillation thresholds (DFT’s)?

A
  • Amiodarone and Class Ic
    • ​increase DFT’s
  • Class III (except Amiodarone)
    • ​decrease DFT’s
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165
Q

In the setting of polymorphic VT, what usually points to the cause being prolonged QT?

A
  • Prolonged QTc on baseline EKG
  • Preceding:
    • pause or
    • transient slowing of the heart rate
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166
Q

Based on response, what is the diagnosis of Narrow complex Tachyardia (QRS < 120 ms) in the setting of adenosine administration:

  • Gradual slowing then reacceleration
A
  • ST
  • Automatic Focal AT
  • JET
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167
Q

Describe typical AVNRT

A
  • short R-P tachycardia ( < 70 ms)
  • abrupt onset (without warning)
  • conduction down (anterograde) a slow pathway and up (retrograde) a fast pathway
  • EKG:
    • P waves are often hidden - embedded in previous QRS
    • Pseudo r’ wave may be seen in V1
    • Pseudo S waves may be seen in leds II, III or aVF
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168
Q

Describe the Brugada Criteria

A
  • Absence of RS complex in all precordial leads (pic)
    • Positive or Negative concordance
  • R to S interval > 100ms in any precordial lead
  • AV dissociation
  • Morphology criteria (RBBB or LBBB) for VT

****If yes to any questions –> VT

****No to all questions –> SVT

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169
Q

Why is Holter monitoring beneficial in Brugada syndrome diagnosis?

A
  • type 1 EKG is intermittent
  • fequently not present on baseline EKG
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170
Q

What is a medication that precludes the use of Dofetilide?

Why?

A

HCTZ

  • Pharmacokinetic and Pharmacodynamic interactions
    • Dofetilide 500 mcg BID and HCTZ 50mg daily –>
      • increase in dofetilized AUC by 27% and Cmax by 21%
      • pharmacodynamic effect of dofetilide increased by 197% (as measured by the QTc increase over time) and a 95% increase in the maximum QTc increase
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171
Q

Differential diagnosis for:

  • Multiple P-wave morphologies
A
  • Wandering atrial pacemaker (rate < 100 bpm)
  • MAT (rate > 100 bpm)
  • Sinus or atrial rhythm with multifocal PAC’s
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172
Q

What is the anticoagulant recommendation with HIV Protease inhibitors?

A

All contraindicated

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173
Q

What mechanism do Epsilon waves (in ARVC) represent?

A

delayed activation of RV

  • accounts for all EKG changes
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174
Q

What is the appropriate intervention in CRT-D when pseudofusion is seen?

A

AV delay may be programmed to a shorter delay

  • allows for LV pre-excitation
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175
Q

EKG definition:

  • Premature atrial complexes (PAC’s)
A
  • Premature P wave, usually of differing morphology than sinus P wave, with normal appearing QRS complex
  • PAC’s typically will conduct back into the SA node, resetting the node and causing a temproary pause in sinus activity
    • “post-extrasystolic pause”
    • not equal to double the preceding RR interval (not a “full compensatory pause”)
176
Q

What are the current recommended uses of Quinidine in Brugada Syndrome?

A
  • ICD and multiple shocks
  • ICD implantation is contraindicated
  • SVT’s
177
Q

What frequently precedes polymorphic VT due to QT prolongation / acquired long QT syndrome on EKG?

A
  • sinus pause
  • transient slowing of the heart rate
178
Q

What antiocagulants require dose adjustment with Diltiazem?

A
  • Rivaroxaban + kidney disease

**consider decreased dose

179
Q

What percentage of patients with WPW pattern will develop an arrhythmia related to their AP?

What arrhythmias?

A
  • 20% (1 out of 5)
  • AP arrhythmias:
    • AVRT (80%)
    • AF (20%)
    • AVNRT
    • AT
180
Q

What is considered early PVE?

What is most likely cause of PVE?

A
  • < 60 days after surgery
  • nosocomial infections
181
Q

What are signs of phrenic nerve palsy (diaphragm paralysis) post A-fib cryoablation?

A
  • Elevated R > L hemidiphragm
  • Asymptomatic in most
  • Highly symptomatic in some
  • Usually resolves
  • Symptoms
    • SOB, recurrent pneumonia, anxiety, insomnia, morning headache, excessive daytime somnolence, orthopnea, fatigue, and difficulty weaning from mechanical ventilation
182
Q

What is the differential when classifying narrow QRS tachycardia’s (QRS < 120 ms) by RP interval?

A
  • Short (RP < RP) + RP « 90 ms
    • Typical AVNRT
    • Focal AT
    • JET (junctional ectopic tachycardia)
    • AVRT (rare)
  • Short (RP < PR) + RP > 90 ms
    • AVRT
    • Atypical AVNRT
    • Focal AT
  • Long (RP ► 90 ms)
    • Focal AT
    • AVRT
    • Atypical AVNRT
183
Q

When coding - RBBB:

  • Inorrect to code
A

Posterior MI (acute or old)

184
Q

Describe initiation of orthodromic AVRT

A
  • abrupt in onset
  • often associated with an ectopic beat:
    • PAC’s
      • may cause delay in the AV node or ategrade block in the pathway –> allowing enough time to permit retrograde accessory pathway conduction to set up a macro re-entrant circuit
    • PVC’s
      • may block regrograde in the AV node –> but conduct to the atrium via the accessory pathway and return to the ventricle via the AV node to initiate the tachycardia
185
Q

Describe the findings

A

Initiation of Atrial tachycardia

  • Sinus beat (S) followed by a long RP tachycardia with different P wave morphology
  • P wave is negative in the inferior leads
186
Q

What is the best way to differentiate between dextrocardia and lead reversal?

A

Precordial leads

  • dextrocardia –> reverse R wave progression in precordial leads
  • Lead reversal –> normal R wave progression in precordial leads

***Both will present with –> QRS in aVR > aVL

187
Q

When is the probability for genetic testing greatest in assessment of LQTS?

A

QTc > 480 msec

  • 70-80% accurate
  • especially in the setting of positive family history
  • 20-25% of these individuals will have normal QTc
188
Q

What is first line therapy in a patient presenting with:

  • LQTS
  • Arrhythmic syncope (suspected)
A

Beta-blockers (nadolol)

189
Q

Define electrical alternans on EKG

What are common causes?

A

Beat to beat variability in the amplitude or direction of the P, QRS, and/or T waves

  • Pericardial effusion
    • ​only 33% of patients with electrical alternans have pericardial effusion
    • only 12% of patients with pericardial effusion have electrical alternans
  • HTN
  • CAD
  • Severe CHF
  • SVT
  • VT
  • Deep respirations
190
Q

What medications may alter Dofetilide (Tikosyn) metabolism and increase its toxicity?

A

Verapamil

and

HCTZ

191
Q

Describe the findings:

A

Normally and aberrantly conduced PAC’s

  • Aberrantly conduced PAC (aVL and aVF)
    • could be mistaken as a PVC - however, it is preceded by an abnormal P wave
  • Normally conducted PAC also present in the rhythm strip
192
Q

Describe the difference in ablation success/outcomes for AVRNT:

  • Radiofrequency
  • Cryoablation
A
  • RF
    • more durable lesion –> 90-95% success rate with slow pathway modification of AVNRT
    • higher risk of inadvertant permanent injury (complete AV block)
  • Cryoablation
    • ​80% success rate
    • lower risk of heart block
193
Q

EKG definition - LPFB

A
  • RAD with mean QRS axis between 100-180 degrees
    • No other factor is responsible for RAD
  • QRS duration between 0.08 - 0.12 ms
  • rS in leads I and aVL
  • qR in leads II, III, aVF
194
Q

What are Short R-P tachycardias / SVT’s?

A
  • Typical AVNRT
  • Orthodromic AVRT (rare)
  • ****sometimes atrial tachycardia****
  • JET
195
Q

When is catheter ablation of VT associated with improved outcomes?

A

Structural heart disease

196
Q

What anticoagulants require dose adjustment with Dronedarone?

A
  • Dabigatran –> contraindicated
  • Rivaroxaban 15 mg
  • Edoxaban 30 mg
  • Warfarin
197
Q

What are the major DOAC trials which established use for stroke prevention in AF?

  • Dabigatran
  • Apixaban
  • Rivaroxaban
  • Edoxaban
A
  • Dabigatran –> RE-LY
  • Apixaban –> ARISTOTLE
  • Rivaroxaban –> ROCKET AF
  • Edoxaban –> ENGAGE AF
198
Q
A

Macro-reentrant tachycardia - Atrial flutter

  • linear ablation lines (for A-fib) in the LA –> higher incidence of A-flutter
199
Q

What determines the morphology and rate of the A-flutter wave?

A
  • Morphology
    • determined by the exit site of the advancing wavefront
  • Rate
    • determined by the size of the re-entrant circuit
200
Q

EKG Definition:

  • Posterior MI age recent, or probably acute
A
  • V1-V3
    • Horizontal ST segment depression ► 1 mm with upright T waves
  • Tall Broad R waves > 30 ms
  • Dominant R wave (R/S ratio > 1) in V2
  • Posterior MI is usually seen in the setting of acute inferior or inferolateral MI, but may also occur in isolated lateral MI
  • Inferfere with the diagnosis of posterior MI
    • RVH
    • WPW
    • RBBB
201
Q

What are “low atrial ectopics”?

A
  • PAC’s arising close to the AV node
  • activate the atria retrogradely
  • produce an inverted “P” wave with a relatively short PR interval ( ►120 ms)
    • PR interval < 120 ms = PJC
202
Q

Which DOACs are metabolized by C-P450?

A
  • Apixaban
  • Rivaroxaban
203
Q

Which trial demonstrated the benefit of Warfarin over Dabigatran in mechanical heart vales?

A

The RE-ALIGN trial (2013)

  • Dabigatran versus Warfarin in Patients with mechanical Heart valves
  • increased rates of thrombembolic as well as bleeding complications with Dabigatran
204
Q

What is the next step in evaluation/management of VA’s in patients with:

  • PVC’s
  • No SHD or Historical High-risk features
A
  • Reassurance
  • Ambulatory rhythm monitoring
  • Treat only if symptoms are limiting
205
Q

Describe localization of VT site of origin on EKG

A

QRS morphology = VT circuit exit site

  • V1
    • LBBB morphology
      • RV or
      • Septum
    • RBBB morphology
      • LV

Precordial leads = sagittal plane origin

  • V3, V4, V5
    • R waves dominant
      • Basal
    • S waves dominant
      • Apical

QRS axis = coronal plane origin

  • Axis (inferior leads)
    • Inferior axis (Positive inferior leads)
      • Anterior or
      • Lateral
    • Superior axis (Negative inferior leads)
      • Inferior
206
Q

What is the next best step:

  • Post-op patient
  • Meds: lidocaine, propofol
  • EKG: type 1 or type 2 Brugada pattern
A

Reassurance

  • benign finding and will resolve
207
Q

What medications are contraindicated with use of dofetilide?

A
  • HCTZ
  • Ketoconazole
  • Trimethoprim
  • Megestrol
  • Verapamil
  • Prochlorperazine
208
Q

Describe the different types of AVRT

A
  • Orthodromic AVRT
    • antegrade conduction down the AV node
    • retrograde conduction up the accessory pathway
  • Antidromic AVRT
    • antegrade conduction down the accessory pathway
    • retrograde conduction up the AV node
209
Q

What are common drug-drug interactions with amiodarone?

A
210
Q

What is the effect of Sotalol on mortality in patients with LVEF < 40%?

A

increased risk of mortality

  • increased risk of mortality in patients with diminished LVEF without defibrillators
  • less effective than amiodarone + BB for suppression of appropriate ICD shocks in patients with reduced LVEF

****SWORD (Survival with Oral D-Sotalol)

*****OPTIC (Optimal Pharmacological Therapy in Cardioverter-Defibrillator Patients)

211
Q

What is the mechanism for VT:

  • fascicular VT’s
A

Abnormal Automaticity

212
Q

What is the mutation associated with CPVT?

A
  • CPVT1 –> Ryanodine receptor
  • CPVT2 –> Calsequestrin
213
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Sustained VT
  • SHD
A
  • ICD if indicated
  • Medical therapy:
    • BB
    • Amiodarone
    • Sotalol
    • Mexilitene
  • Catheter ablation
    • informed by VT location and underlying substrate
214
Q

How often does Amiodarone-induced thyrotoxicosis occur?

A

3% of Amiodarone treated patients in North America

  • may be up to 10% of patients living in iodine depleted areas
215
Q

Who should undergo testing in asymptomatic pre-excitation patterns?

A
  • High-risk occupation (military, airline pilot, etc.)
  • Competitive athletes
216
Q

What are signs of chronic infarct remodeling:

  • EKG
  • Clinically/Laboratory
A
  • Q waves
  • “demand ischemia”
    • low-level elevations in cardiac biomarkers of myocyte injury during rapid SVT
217
Q

What is the electrophysiologic mechanism responsible for slow A-fib in young, highly condiditioned individuals?

What channels are activated in this process?

A
  • Parasympathetically (vagally) mediated A-fib
  • IKACh potassium channels (SA node and Atria)
    • vagal stimulation –> muscarinic receptors –> which are coupled to IKACh channel by a G protein
    • leads to slowing of the sinus rate –> decrease in AV nodal conduction –> ***decrease in the duration of the action potential in the atrium**
    • commonly occurs during sleep
218
Q

What percentage of patients develop LAA thrombi after ► 2 days of AF?

A

5-14%

  • 2-40 mm in size
  • Following 1 month of wafarin –> 75% of LAA thrombi resolve
219
Q

What is the best way to differentiate:

  • Complete heart block
  • AIVR
A
  • Complete heart block
    • sinus rate >> ventricular rate
  • AIVR
    • ventricular rate >> sinus rate

*****Both can demonstrate –> AV dissociation

220
Q

What are the recommendations for ICD placment:

  • Hypertrophic Cardiomyopathy
A
  • Class I
    • SCD (resuscitated)
    • Spontaneous VT with syncope
  • Class IIa
    • LV wall thickness ► 30 mm
    • 1st degree relative with SCD caused by HCM
    • Syncope (unexplained)
  • Class IIb
    • NSVT (on ambulatory monitoring) without other risk factors
221
Q

Describe localization of AP using surface EKG

A
222
Q

EKG definition: SA exit block

A

Failure of sinus impules to escape SA node - 4 types

  • First degree
    • not detectable on surface EKG
  • Second degree Mobitz I
    • group beating
    • shortening P-P interval
    • constant P-R interval
    • P-P pause interval less than twice the usual P-P interval
  • Second degree Mobitz II
    • constant P-P interval
    • P-P pause interval being approximately a precise multiple (within 0.10s) of the usual P-P interval
  • Third Degree
    • not detectable on surface EKG
223
Q

What did the AVID trial show?

A

superiority of an ICD for survival over antiarrhythmic drugs in patients with ventricular arrhythmia

  • AVID trial (Antiarrhythmics vs. ICD) enrolled
    • VF (resuscitated)
    • sustained VT with syncope
    • sustained VT with an LVEF < 40% associated with severe symptoms (HF, angina)
  • About 10% of the AVID population underwent revascularization, and the benefit of an ICD was independent of revascularization
224
Q

What is the difference in stroke reduction:

  • Warfarin
  • ASA
A
  • Warfarin –> 60%
  • ASA –> 20%
225
Q

Describe “northwest” axis

When is this seen?

A
  • Extreme axis deviation
  • QRS positive in aVR
  • Negative in I and aVF
  • VT
226
Q

Describe the findings:

A
  • Precordial S waves only
  • Negative concordance in all precordial leads –> VT
227
Q

What populations of patients do the CHADSVasc and HASBLED scores not apply to?

A
  • MS (moderate-severe)
  • Mechanical heart valve
  • Hypertrophic cardiomyopathy
228
Q

What are risk factors for arrhythmia in Brugada Syndrome?

A
  • Fever
    • SCN5A channel is temperature sensitive
  • Alcohol (heavy use)
  • Cocaine
  • Precipitating medications
    • Fluoxetine
    • Sodium channel blockers (INa)
    • Propofol
    • Lithium
    • Antihistamines
    • TCA’s
    • Trifluoperazine
    • Heavy metals
229
Q

When coding - 2nd degree AV block (type I or II):

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • 1st degree AVB
  • Inorrect to code
    • Sinus pause
230
Q

What are causes/interventions of CRT nonresponse?

A
  • LV noncapture
    • reprogram device
    • revise LV lead
  • Low % CRT pacing - A-fib
    • AV nodal blockade
    • Rhythm control
  • Low % CRT pacing - frequent PVC’s
    • catheter ablation
  • LV scar burden
    • consider multipoint LV pacing
  • Phrenic nerve capture
    • reprogram device
    • revise LV lead
231
Q

When coding - Early repolarization, normal variant:

  • Inorrect to code
A

ST-T injury

232
Q

What additional channel do class Ia antiarrhythmics block

A

IKr - rapidly activating potassium channel

  • manifests on surface EKG as QT prolongation
233
Q

When coding - Hypertrophic cardiomyopathy:

  • Unnecessary to code
  • Inorrect to code
A
  • Unnecessary to code
    • LVH
    • ST-T hypertrophy
  • Inorrect to code
    • MI (acute or old)
234
Q

Define:

  • Inferior MI, age indeterminant or probably old
A
  • pathological Q waves in at least two inferior leads (II, III, or aVF) - must be:
    • QS complex or
    • ► 30 ms wide and 0.1 mV deep in amplitude
  • No evidence of acute or evolving myocardial injury
    • i.e. no ST-elevation
235
Q

What are the acute treatment recommendations for pre-excited AF?

A
  • Hemodynamically unstable
    • Synchronized Cardioversion (Class I)
  • ​Hemodynamically stable
    • IV Ibutalide or Procainamide (Class IIa)
    • IV Flecainide or Propafenone (Class IIb)
236
Q

Describe the findings and next step:

  • 20 year old male with palpitations x 2 hours
  • PMH: none
  • Meds: none
  • VS: BP 108/66, HR 190
A
  • Pre-excited A-fib (AF + WPW)
  • Ibutilide or Procainamide
    • both medications decrease ventricular rate by slowing conduction over the accessory pathway
237
Q

Describe the findings:

A

Blocked PAC

  • hidden PAC gives a “peaked” or “camel hump” appearance to the T wave (circled)
    *
238
Q

Define Paroxysmal AF

A

AF terminates < 7 days with or without intervention

239
Q

What arrhythmia can become life threatening after administration of Adenosine?

A

Pre-excited AF

  • can lead to 1:1 conduction via the accessory pathway which deteriorates rapidly to VF
240
Q

When coding - Brugada syndrome:

  • Unnecessary to code
  • Inorrect to code
A
  • Unnecessary to code
    • Nonspecific IVCD
  • Inorrect to code
    • Complete or incomplete RBBB
241
Q

What is the result of PAC’s in the setting of SA entrance block?

A
  • SA entrance block –> preventing conduction back into the SA node, the node will not reset and either:
    • an interpolated beat (extra QRS complex between otherwise constant R-R intervals) or
    • full compensatory pause will occur
242
Q

What is the prevalence of patients presenting with VT after ToF repair?

A

5% of patients

  • due to re-entry through regions of scarring in the area of the repair
243
Q

Based on response, what is the diagnosis of Narrow complex Tachyardia (QRS < 120 ms) in the setting of adenosine administration:

  • No response
A
  • Inadequate dose/delivery
  • High septal VT
244
Q

Describe EKG changes with hypokalemia:

A
  • Prominent U waves
  • Prolonged QT/QU interval (occassionally)
  • ST-T segment depression and flattened T waves
  • Various degrees of AV block
  • VT and VF
245
Q

Describe the EKG findings, diagnosis and management in a patient with:

  • PPM interrogation: no intrinsic activity at VVI 40 bpm
  • exercise intolerance and neck pulsations
A
  • Pacemaker syndrome
  • EKG
    • Regular VVI pacing at 60 bpm
    • P waves seen just following each paced QRS complex due to retrograde conduction through the AV node
  • Upgrade to dual-chamber PPM
    • ​will restore AV synchrony and improve symptoms
246
Q

77 year old female with HTN presents with syncopal episode at home. Prior to the event she had been standing in the kitchen preparing dinner feeling well and denies any warning symptoms. The event was unwitnessed. She only recalls awakening on the floor. There is no prior history of syncope.

  • Meds: ASA, Amlodipine
  • EKG shown
  • Patient remains asymptomatic and labs unremarkable

What is the next step?

A

PPM insertion

247
Q

What proportion of strokes does AF account for?

  • strokes in US
  • > 80 years of age
  • cryptogenic stroke
A
  • > 15% of strokes in US
  • > 33% of strokes in patients > 80 years
  • 20% of cryptogenic stroke where clear vascular etiology is not present
248
Q

When coding - SVT:

  • Inorrect to code
A

Atrial enlargement

249
Q

What is considered structural heart disease in A-fib management?

A
  • CAD
  • Decreased LVEF
250
Q

What amount of pacing is needed for CRT?

A

> 90% Bi-V pacing

251
Q

Define Long-standing persistent AF

A

Continuous AF > 12 months

252
Q

What is considered valvular AF (for anticoagulation purposes)?

A
  • Bioprosthetic or mechanical valve (in any location)
  • Mitral Vavle Repair
  • Rheumatic MS
253
Q

Describe LBBB morphology in VT

A
  • V1-V2 appearance
    • Dominant S-wave in V1
    • 3 features are diagnostic of VT:
      • RS interval (time from R wave onset to S wave nadir) > 60-70 ms
      • Notching/slurring of the S wave (Josephson sign)
      • Initial R wave > 30-40 ms
  • V6 appearance
    • LBBB-pattern + Q waves in V6 = VT
    • 2 possible patterns:
      • QS waves (as with RBBB-like patterns)
        • very specific for VT
      • qR complex in V6
        • small q wave, large R wave
254
Q

Describe features of Anderson-Tawill sydndrome

A
  • Andersen-Tawil syndrome (ATS-LQT7)
    • QT prolongation + large U waves + frequent PVC’s and NSVT
    • facial dysmorphic features + hypokalemic periodic paralysis
    • KCNJ2 mutation –> IK1 potassium channel
255
Q

When coding - Afib:

  • Unecessary to code
A

A-flutter

256
Q

What is the treatment for idiopathic LV (fascicular) VT?

A

Verapamil

  • rhythm is highly sensitive to verapamil
  • low-risk tachycardia –> catheter ablation of fascicle is usually curative
257
Q

What are causes of prominent U waves?

A
  • Most commonly found with:
    • Hypokalemia
    • Bradycardia
  • Less common causes:
    • Hypocalcemia
    • Hypomagnesemia
    • Hypothermia
    • HCM
    • Elevated intracranial pressure
    • LVH
    • Drugs
      • Digoxin
      • Class Ia (Quinidine, Procainamide)
      • Class III (Amiodarone, Sotalol)
258
Q

What are the indications for antibiotic prophylaxis for bacterial endocarditis?

A
  • Previous endocarditis
  • Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
  • Cardiac transplantation recipients who develop cardiac valvulopathy
  • Congenital heart disease
    • Unrepaired cyanotic CHD
      • including palliative shunts and conduits
    • Repaired CHD
      • Completed with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
      • Incomplete with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
259
Q

Describe RBBB morphology in VT

A
  • V1-V2 appearance
    • 3 patterns indicative of VT:
      • Smooth monophasic R-wave
      • Notched downslop to the R wave - the taller left rabbit ear
      • qR complex (small Q wave, tall R wave) in V1
  • V6
    • QS complex
      • completely negative complex with no R wave
    • R/S ratio < 1
      • small R wave, deep S wave
      • indicates VT only if LAD also present
260
Q

What are unique findings of AVNRT?

A
  • Short RP ( < 70 ms)
  • Pseudo R’ waves in V1 and/or V2
  • Pseudo S waves in II, III, aVF
    • not present when converted to NSR
261
Q

What are the class I indications for surgery in infective endocarditis?

A
  • Heart failure (valvular dysfunction)
  • Heart block
  • Abscess
  • Resistant organism (fungal)
  • Relapsing PVE (prosthetic valve endocarditis)
  • Persistent infection (positive surveillance cultures)
262
Q

75 year old presents with syncope and hemodynamically unstable VT –> defibrillation. He is found to have severe MVCAD and LVEF 35-40% and undergoes CABG x3. What is the best treatment of VT prior to discharge?

A

ICD prior to discharge

  • secondary prevention criteria
  • Class I recommendation - for VT + structural heart disease
  • AVID trial (Antiarrhythmics vs. ICD) showed superiorority of ICD for survival over antiarrhythmic drugs
263
Q

What trials demosntrated superiority of Amiodarone to Lidocaine in VT and VF?

A

ARREST and ALIVE

264
Q

When coding - LBBB:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • LVH
  • Inorrect to code
    • MI (acute or old)
265
Q

What are indications for PPM in Sinus Node Disease - Class I

A
  • Symptomatic sinus bradycardia and pauses
  • Symptomatic sinus bradycaria due to required therapy
  • Symptomatic chronotropic incompetence
266
Q

What are indications for PPM in AV Node Disease - Class I

A
  • CHB or ASDB with:
    • bradycardia and symptoms or ventricular arrhythmias due to block
    • arrhythmias or other conditions requiring drug therapy resulting in bradycardia
    • pause > 3s, escape rate < 40 bpm or below the AV node
    • A-fb and pauses > 5s
    • after catheter ablation of the AV junction
    • after cardiac surgery not expected to resolve
    • associated with neuromuscular disorders
  • CHB or HR > 40 bpm in the setting of:
    • cardiomegaly
    • LV dysfunction
    • site of block is below the AV node
  • 2nd degree AV block of any type with symptomatic bradycardia
  • 2nd or 3rd degree AV block with exercise without ischemia
  • Asymptomatic Mobitz II block with wide QRS
267
Q

What medication interactions result in increased Digoxin toxicity?

A
  • Amiodarone
  • Dronedarone
  • Verapamil
268
Q

What should be avoided in the evaluation of atrial-esophageal fisutla?

A

Endoscopy

  • Insufflation –> air emboli in the left atrium
269
Q

What two trials demonstrated use of the WATCHMAN device?

A
  • PROTECT AF
    • demonstrated that WATCHMAN was noninferior to warfarin therapy for prevention of ischemic or hemorrhagic stroke and eventually superior in long term follow up
  • PREVAIL
    • did not demonstrate noninferiority of WATCHMAN
270
Q

EKG definition:

  • Prominent U waves
A
  • U wave amplitude > 1.5mm
271
Q

What is a major distinguishing feature between Idiopathic LV and RV outflow tract VT?

A

Precordial transition point

  • LVOT VT
    • early precordial transition or
    • broad initial R wave in V1, V2
  • RVOT VT
    • late precordial transition, typically leads V3-V4

**** LBBB morphology + Inferior axis in both

272
Q

When is Dronedarone contraindicated in A-fib treatment?

What studies support these findings?

A
  • Permanent A-fib

or

  • NYHA class IV heart failure
  • NYHA class II or III heart failure with a recent decompensation requiring hospitalization
  • ANDROMEDA trial
  • PALLAS trial
273
Q

What are causes of PPM - undersensing?

A
  • acute MI
  • scar tissue or edema at the interface between the lectrode tip and myocardium
  • mechanical problems:
    • lead fracture
    • lead dislodgement
    • insulation break
    • pulse generator malfunction
    • inappropriate reprogramming
274
Q

What antiarrhythmics effect pacing thresholds?

A

Class Ic - increased pacing threshold

  • may precipitate loss of capture
275
Q

Describe the findings:

A
  • Sinus arrhythmia
  • Prominent U waves
  • Hypokalemia

***Patient has type I (distal) RTA –> defective acid secretion in the distal tubule of the kidney

****Variable potassium balance, including hypokalemia, is common. K = 1.6 mEq/L –> prominent U waves

276
Q

How is HF defined in the CHADSVasc risk score?

A
  • EF < 40% or
  • Recent decompensated HF (regardless of EF)
277
Q

What is the diagnostic criteria for LQTS?

A
  • LQTS score ≥ 3.5 + absence of a secondary cause for QT prolongation and/or
  • Pathogenic mutation in one of the LQTS genes
  • QTc ≥ 500 ms (for HR using Bazett’s formula) in the absence of secondary causes
  • QTc 480-499 ms in repeat EKGs + unexplained syncope + absence of secondary causes for QT prolongation + absence of a pathogenic mutation
278
Q

Describe Atypical A-flutter

A
  • “non-isthmus-dependent”
  • macroreentrant atrial arrhythmia that does not utilize the cavo-tricuspid circuit
  • “clock-wise” reentry
    • upright flutter waves in II, III, aVF
    • inverted flutter waves in V1
  • Arises from circuits elswhere in the RA or LA and may occur in a variety of clinical settings:
    • congenital heart disease
    • cardiac surgery (after)
    • catheter ablation of AF
    • ASD repair
279
Q

Describe Quinidine:

  • MOA
  • indications
  • toxicity
A
  • blocks (Ito) potassium current
  • J-wave syndromes
    • Brugada syndrome
    • Early repolarization syndrome
  • Digoxin toxicity <– reduces renal clearance of digoxin
    • P-glycoprotein inhibitor
280
Q

EKG definition: Dextrocardia (mirror image)

A
  • P wave, QRS complex, and T wave in leads I and aVL are inverted or “upside down”
  • Reverse R wave progression
    • R wave amplitude is largest in V1 and gets smaller as you move towards V6

****Lead reversal can appear similar –> reverse R wave progression will no exist in lead reversal

281
Q

What is the next best step:

  • 67 year old male with history of CABG 5 years ago and asymptomatic (exercises 4x per week)
  • Echo with LVEF 25%
  • Meds: ASA, Atorvastatin, Carvedilol, Lisinopril
  • EKG: NSR, RBBB, QRS 138ms
A

ICD implant

  • Primary prevention criteria - MADIT-II trial
    • In post-MI patients with systolic dysfunction (EF ≤30%), prophylactic ICD reduced all-cause mortality compared to standard medical therapy.
    • (14.2% vs. 19.8%; P=0.016; NNT=18)
  • Class III recommendation for:
    • Bi-V pacing or CRT in NYHA I or II + non-LBBB pattern + QRS < 150 ms
282
Q

What is the first line treatment for PVC’s?

A

BB or CCB

283
Q

Describe the metabolism of Dabigatran

A
  • Dabigatran etexilate is a prodrug, which converts to the active drug dabigatran via hydrolysis within the liver following ingestion
  • Eliminated primarily via the kidneys
    • Renal impairment –> increased risk for hemorrhage due to higher circulating levels
  • Substrate for P-glycoprotein transport system
    • susceptible to interactions with inducers/inhibitors
284
Q

What is the more effecitve therapy in patients with structural heart disease + SCA or hemodynamically unstable VT?

A

ICD therapy is superior to antiarrhythmics

  • Secondary prevention studies:
    • AVID (1997)
    • CIDS (2000)
    • CASH (2000)
285
Q

What are the recommendations for ICD placment:

  • LQTS
A

Class I

  • SCD (reuscitated)
  • High risk patients in whom BB is ineffective or not tolerated
    • < 40 years of age
    • Females with LQTS 2
    • LQTS 2 and 3
    • onset of symptoms < 10 years of age
    • prior cardiac arrest or recurrent syncope
    • QTc > 500 ms

Class IIb

  • Asymptomatic patients, QTc > 500 ms on BB
286
Q

Describe the findings and next step:

  • 56 year old woman with NICM (LVEF 20%) and CRT-D presents with progressive DOE
  • Meds: Carvedilol, scubitril/valsartan, furosemide, spironolactone
  • PE: trace edema
  • CXR: mild vascular congestion
A
  • EKG: LBBB which is consistent with RV pacing only
  • Device interrogation
    • ​assess for LV pacing and capture
287
Q

In patients with intact sinus node function, what PPM settings can result in suboptimal hemodynamics?

A
  • VVI
  • VVIR
288
Q

What type of arrhythmia is associated:

  • Re-entry circuit within the triangle of Koch
A

AVNRT

289
Q

What is P-glycoprotein?

A

transporter responsible for the absorption of digoxin through the intestines as well as its elimination in the kidneys

290
Q

What is the treatment for patients with hyperthyroidism who present with tachycardia?

A

Propylthiouracil or Methimazole

  • BB are also first line therapy
291
Q

What is the definition of ST-elevation (that is suggestive of acute myocardial ischemia)?

A
  • New ST-elevation at the J-point in 2 contiguous leads with the cutoff point:
    • ► 1 mm in all leads other than leads V2-V3
    • V2-V3 cutoffs:
      • ► 2 mm in men ► 40 years
      • ► 2.5 mm in men < 40 years
      • ► 1.5 mm in women regardless of age
292
Q

What antiarrhythmic should be avoided in a 59 year old woman with no structural heart disease and persistent symptomatic AF?

A

Dronedarone

  • higher mortality in patients with persistent AF
293
Q

What trials support the use of catheter ablation in AF?

A

CABANA

  • “Effect of Catheter Ablation vs. Antiarrhythmic Drug Therapy on Mortality, Stroke, Bleeding, and Cardiac Arrest Among Patients with A-Fib”
  • Symptomatic AF (paroxysmal, persistent, long-standing persistent)
    • Catheter ablation
    • Rhythm control
  • Results:
    • No difference in death, disabling stroke, serious bleeding or cardiac arrest
    • Improved CV related hospitalizations, quality of life and symptom burden with AF
294
Q

Describe the findings:

A
  • NSR
  • Sinoatrial exit block
    • grouped beating + absence of P-wave during the dropped interval
295
Q

What anticoagulants require dose adjustment with Verapamil?

A
  • Dabigatran
  • Edoxaban

***decrease dose

296
Q

What is the definition for low voltage:

  • Limb leads
  • Precordial leads
A

entire amplitude of the QRS (R + S) must be:

  • Limb leads
    • < 5mm
  • Precordial leads
    • < 10 mm
297
Q

What are indications for PPM in AV Node Disease - Class III

A
  • Aysmptomatic
    • 1st degree AV block
    • Mobitz I
  • AV block that is expected to resolve
    • reversible drug effect
    • Lyme disease
    • transient increase in vagal tone or during hypoxia and sleep apnea
298
Q

What is one timing relationship that is helpful in differentiating SVT’s?

A
  • Long R-P
  • Short R-P
299
Q

What is the diagnosis?

  • RAD
  • TWI in V1-V2
  • inferior Q waves
A

Posterior Infarction

300
Q

Who is most likely to benefit from CRT therapy?

A

LBBB

+

QRS > 150 ms

  • RBBB or nonspecific IVCD are less likely to benefit
301
Q

Describe the findings and next step:

  • 30 year old female with syncope (lightheaded and nauseous before)
  • EKG (baseline): NSR with RBBB (QRS 128 ms)
  • Echo: normal LV function, mild RV enlargment and dysfunction, mild TR
  • GXT: multiple runs of rhythm below
  • FH: negative for syncope, CAD, arrhythmia, SCD
A
  • Monomorphic VT
  • Cardiac MRI
302
Q

What does the presence of a delta wave on baseline ECG in a patient with PSVT indicate?

A

97% specific for AVRT

303
Q

What are the patient characteristics that increase the risk of an arrhytmic cause of syncope?

What is the next step? Why?

A
  • Age > 60
  • CAD

Echo is next step to evaluate for structural heart disease

304
Q

What is the treatment of PMVT (Torsades des pointes)?

A
  • Magnesium
  • Isoproterenol
  • Overdrive pacing

***Avoid bradycardia, which increases vulnerability to R on T

305
Q

When coding - Acute pericarditis:

  • Inorrect to code
A

ST-T injury

306
Q

In what clinical scenario should atenolol be held?

A

Acute renal failure (oliguria)

  • Atenolol is a water-soluble BB and has a prolonged half-life in the setting of renal failure
  • It can accumulate to toxic levels in the setting of renal failure –> SND, bradycardia
307
Q

54 year old woman presents to the clinic with frequent palpitations and lightheadedness. She has a history of hypertension and takes lisinopril. She denies any family history of cardiac disease. She was recently seen in the ED and an ECG was obtained (figure 1).

  • Adenosine 6mg was administered with no change in rhythm with atrial activity seen during the transient period of AV block. her palpitations resolved and a second ECG was obtained (Figure 2)
A

Abnormal ectopic atrial foci

  • P waves before QRS in a “long RP tachycardia”
  • P wave is somewhat different from sinus
  • Adenosine is unlikely to convert atrial tachycardia but will reveal P waves during AV block
308
Q

What is a common arrhythmia complication of hyperthyroidism?

A

Atrial Fibrillation

  • 5-15% of cases
309
Q

What is the next step in evaluation/management of VA’s in patients with:

  • NSVT
  • SHD
A
  • ICD if indicated
  • Medical therapy
    • BB
    • Amiodarone
    • Sotalol
    • Mexilitene
310
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Sustained VT
  • Abnormal initial evaluation
A
  • Treat SHD as appropriate
  • Consider:
    • Cardiac MRI
    • EPS
    • ICD
      • optimization for ATP termination
  • VT suppression
311
Q

What are the two most common types of SVT?

A
  • AVNRT (60%)
  • AVRT (30%)
312
Q

What is the appropriate periprocedure anticoagulation management strategy?

  • 76 year old male with Dual-chamber PPM presents for generator change
  • PMH: A-fib, HTN, DM, CVA (2 months prior)
  • Meds: Lisinopril Metformin, Metoprolol, Warfarin
A

Continue Warfarin

  • BRUISE CONTROL 1 trial (2013)
    • 80% fewer pocket hematomas when warfarin continued

References:

Birnie DH, Healey JS, Wells GA, et al.; BRUISE CONTROL Investigators. Pacemaker or defibrillator surgery without interruption of anticoagulation. N Engl J Med 2013;368:2084-93.

313
Q

Describe the findings:

A

RV VT with LBBB morphology / ARVD

314
Q

When and How does atrial-esophagela fistula present post-ablation?

A

1-4 weeks

  • Asymptomatic before major event
  • CNS confusion/CVA
  • Esophageal symptoms
  • Fever/chills
  • GI bleeding
315
Q

EKG definition: RVH in setting of a RBBB

A

R prime amplitude > 15 mm

316
Q

What is the effect of PSVT’s and increasing age?

A
  • AVNRT and AT –> Increase
  • AVRT –> Decrease
317
Q

What maneuvers can enhance the effectiveness of Valsalva in termination of PSVT?

A

abrupt change from sitting to supine with legs elevated after forced expiration

  • enhanced more than two-fold with this maneuver
318
Q

What is the MOA of digoxin?

A

blocks the sodium-potassium adenosine phosphatase –>

  • increased intracellular calcificaiton (release from SR)
  • increased vagal tone
    • vagolytic effect
    • minimal direct inhibition of SA or AV node (except at toxic levels)
  • Sensitizes baroreceptors
    • decreases activation of the sympathetic nervous system and RAAS
319
Q

Describe the findings (Leads II, V2, V5):

A

LQTS 2

320
Q

What is the recommended medication adjustment when using Amiodarone and Warfarin?

A

Warfarin dose reduction 25-33%

  • Amiodarone inhibits CYPC9, which is important in the metabolism of warfarin
321
Q

Describe monitoring for Amiodarone induced thyrotoxicosis

A
  • FT4 and TSH checked:
    • before initiation of therapy
    • 3 month intervals while taking
    • ► 1 year after discontinuing
322
Q

What percentage of RV pacing is concerning for pacemaker cardiomyopathy and development of heart failure ?

A

> 20%

  • 12% of patients will develop heart failure
323
Q

When coding - Torsades de pointes:

  • Unnecessary to code
A

VT or VF

324
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Sustained VT
  • No SHD or Historical High-risk features
A
  • VT suppression
  • Ambulatory rhythm monitoring
325
Q

What is the mechanism for SCD in WPW pattern patients?

A

AF that conducts rapidly to the ventricles over the AP –> VF

326
Q

When an accessory pathway is not present on EKG due to longer conduction time through the accessory pathway, What can precipate AVRT in this situation?

A
  • AV nodal conduction decreases/decrements
    • HR increases
    • PAC
327
Q

Describe the findings and next step:

  • 40 year old female with palpitations and worsening exercise intolerance
  • Holter monitor: runs of NSVT
  • Echo: technically limited due to body habitus
  • FH: uncle died of “rhythm problem”
  • PE: normal
A
  • EKG:
    • PVC’s of multiple morphologies
    • PVC’s with right bundle morphology (namely positive in V1) but with different amplitudes in the late precordial leads
    • PVC’s likely arising from the LV, but different locations
  • Cardiac MRI
    • ​imaging to assess for possible cardiomyopathy (echo suboptimal)

*****Dx: LV noncompaction

328
Q

Describe the findings:

A
  • Precoridal R waves only
  • Positive concordance in all precordial leads –> VT
329
Q

Define electrical alternans

A

beat to beat variability in the amplitude or direction of the P, QRS, and/or T waves

330
Q

Describe the findings:

A
  • Sinus tachycardia
  • Dextrocardia, mirror image
    • P-waves in lead I, suggesting either an ectopic atrial rhythm, limb lead reversal or dextrocardia
    • RAD –> limb lead reversal vs. dextrocardia
    • absence of R wave progression –> dextrocardia
331
Q

What is the recommended medical therapy in a patient with:

  • Brugada syndrome
  • ICD and shocks
  • Recurrent VT
A

Quinidine or Catheter Ablation

  • Class Ia antiarrhythmic
    • Ito and IKr blocker effects
  • Class I recommendations
332
Q

What is the current QTc recommendation for initiation of Dofetilide (Tikosyn)?

A
  • QTc < 440 msec
  • QT interval or QTc < 500 msec in patients with an intraventricular conduction delay
333
Q

What is the next step in evaluation/management of VA’s in patients with:

  • NSVT
  • No SHD or Historical High-risk features
A
  • VT suppression guided by symptoms
  • Ambulatory rhythm monitoring
334
Q

What are predictors of improved outcomes after catheter ablation of VT in structural heart disease?

A
  • Noninducibility on EPS
  • EF > 30%
335
Q

Describe the findings (Leads II, V2, V5):

A

LQTS 3

336
Q

What is the mechanism for VT:

  • CAD
A

scar-mediated re-entrant VT

337
Q

What is the management of VT storm?

A
  • Amiodarone (1st line), Lidocaine (2nd line)
  • Electrolytes (Mg, K)
  • Precipitant drug?
  • Reduce sympathetic tone
    • BB (Esmolol, Metoprolol)
    • Sedation/intubation - general anesthesia
    • Stellate ganglion block and thoracic epidural anesthesia
  • Cardiac cath if ischemia driven
338
Q

When coding - LBBB + ST-T injury:

  • Inorrect to code
A

Acute MI

339
Q

What is the next step in evaluation/management of VA’s in patients with:

  • NSVT
  • Abnormal Initial Evaluation
A
  • Tread SHD as appropriate
  • Consider:
    • EPS
    • Cardiac MRI
  • VT suppression guided by symptoms
340
Q

Describe Amiodarone induced hyperthyroidism

A
  • Type 1 AIT
    • normal thyroid at baseline
    • destructive thyroiditis
    • most common
  • Type 2 AIT
    • Hyperthyroid at baseline
    • Exacerbation by iodine (Jod-Basedow effect)
341
Q

Define RBBB, complete

A
  • QRS duration:
    • Adults: ► 120 ms
    • Children (4-16 years): ► 100 ms
    • Children ( < 4 years): ► 90 ms
  • rsR’, rsr’, or rSR’ complexes in V1 or V2, with the secondary R wave (r’ or R’) usually wider than the initial R wave (r)
    • a minority of patients may have a wide and often notched R wave pattern in lead V1 and/or V2
  • S wave of greater duration than R wave or > 40 ms in leads I and V6 = “slurred S wave”
  • Normal R peak time in leads V5 and V6 but > 50 ms in lead V1

***first 3 should be present to make the diagnosis.

****When a pure dominant R wave with or without a notch is present in V1, the 4th criteria should be satisfied.

342
Q

What is the annual adjusted stroke rate in A-fib patients?

A
343
Q

When coding - Acute MI:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • ST-T injury
  • Inorrect to code
    • ST-T ischemia
344
Q

Describe the findings and next step:

A
  • Mixed vasodepressor and cardio-inhibitory vagal response
    • Vaso-vagal syncope
  • Emphasize fluid and salt intake
    • ​patient reassurance, education, physical counterpressure maneuvers are also recommended
345
Q

Differential diagnosis for:

  • Irregularly, irregular baseline
A
  • A-fib
  • Artifact due to tremor
  • MAT
346
Q

What are distinctive forms of LQTS in which their clinical manifestations extend beyond the cardiac phenotype?

A
  • Jervell and Lange-Nielsen syndrome (JLN1 and JLN2)
    • congenital sensorineural deafness
    • KCNQ1 or KCNE2 gene mutations
  • Andersen-Tawil syndrome (ATS-LQT7)
    • preesent = QT prolongation + large U waves + frequent PVC’s and NSVT + facial dysmorphic features + hypokalemic periodic paralysis
    • KCNJ2 mutation –> IK1 potassium channel
  • Timothy syndrome (TS-LQT8)
    • high mortality ( > 80%) with complex phenotypes
    • marked QT prolongations + syndactyly + AV block + congenital heart defects + developmental disorders (autism) + reduced immune response
    • CACNA1c (gain of function) –> ICa (alpha subunit of L-type calcium channels )
347
Q

EKG definition:

  • Atrial tachycardia
A
  • Abnormal P waves different in morphology from sinus P waves
  • Differs from PAC’s in that there are at least 3 beats in succession
  • Typical atrial rate is 100-180 bpm
  • Usually results in a normal QRS complex (similar to that seen in sinus rhythm) following each P wave, unless the QRS complex is aberrantly conducted
348
Q

What is the next step in management if ARVC is suspected on EKG with normal Echo?

A

CT or MR

349
Q

What medication is contraindicated in Brugada Syndrome?

A

Beta-blockers

  • can increase ST-segment elevation
350
Q

Describe the findings and next step:

  • 64 year old, asymptomatic male
  • PMH: HTN
  • Labs: TSH normal
A
  • EKG:
    • NSR
    • Mobitz type 2
  • Carotid sinus massage
    • ​noninvasive vagal and sympathetic maneuvers can help to distinguish one from the other:
      • Mobitz 1 - usually AV nodal
      • Mobitz 2 - usually His-Purkinje system
351
Q

Describe initiation of AVNRT

A
  • PAC that blocks in the fast pathway and
  • Conducts down the slow pathway
  • With a long PR interval
  • Followed by tachycardia

***Atria and ventricles are activated nearly simultaneously

352
Q

Describe the findings:

A

Intracardiac electrogram

  • Polymorphic VT –> VF
  • Acute myocardial ischemia
353
Q

Describe class Ib antiarrhythmics:

  • examples
  • MOA
  • toxicity
  • elimination
A
  • Lidocaine and Mexilitene
  • block sodium channels with preferential action in ischemic tissue
  • CNS side effects
    • tinnitus, tremor, blurred vision, nausea, dysphoria, dizziness –> seizures, AMS, coma
  • Liver (mostly) and kidneys
    • CYP2D6 (absent in 7% of Caucasian population)
    • Dose reduction in renal failure
354
Q

When should Sotalol be dose-adjusted?

A

CrCl < 60

  • administered at an interval of 24 hours
  • starting at a low dose (80mg daily)
355
Q

What is the most common mechanism of VT in patients with CAD?

A

scar-mediated re-entrant VT

  • EKG
    • WCT, monomoprhic
    • positive concordance across the precordial leads
    • monophasic R wave in V1
356
Q

What is the most common ablation target for AVNRT catheter ablation?

A

Posterior slow pathway

  • facilitated by reliable anatomic and eletrophysiologic landmarks of Koch’s triangle
  • carries the lowest risk of AV block
  • preserves the fast pathway function (and a normal PR interval postablation)
357
Q

What is the recommened treatment for recurrent symptomatic PSVT?

A

Catheter ablation

  • 95% success rate in good centers
358
Q

What is the explanation in the presence of an accessory pathway if a delta wave is not present on EKG?

A
  • Concealed pathway
    • incapable of conducting antegradely
  • Accessory conduction << than AV nodal conduction
    • due to brisk AV nodal conduction or
  • Large distance between the origin of the atrial impulse (such as the sinus node) and the AV accessory pathway –> left free-wall accessory pathway
359
Q

Describe the prevalence of LQTS, mutations involved and channels involved in the mutations

A

90% of cases (1:300-7,000)

  • LQT1 (KCNQ1)
    • encoding for the potassium current IKs
  • LQT2 (KCNH2)
    • encoding for the repolarizaing potassium current IKr
  • LQT3 (SCN5A)
    • encoding for the alpha subunit of the sodim channel that conducts the depolarizing sodium current INa
360
Q

What causes variation in the heart rate during Atrial flutter?

A

variable conduction block within the AV node

  • may be due to intrinsic conduction system disease or
  • action of AV nodal blocking agents
361
Q

Determine QRS axis: RAD ( > 90)

A
  • Lead I –> negative
  • Lead aVF –> positive
362
Q
A
363
Q

Describe the findings and most likely etiology:

  • 43 year old male who presented with chest pain
  • PMH: tobacco use, HTN
  • FH: father died suddenly at age 50
  • Troponin negative
A
  • VF
    • ongoing chest pain with normal EKG can be seen with acute CFx occlusion
  • Acute myocardial ischemia
    • ​most common cause of VF and polymorphic VT
364
Q

What will the result of:

  • BBB
  • Orthodromic AVRT
A
  • lengthening of macro-re-entrant circuit over which tachycardia has to travel
  • Ipsilateral BBB –> increase in RP interval = diagnostic of orthodromic AVRT
  • Localizes pathway to right or left, depending on BBB morphology
365
Q

What is the initial evaluation of PVC’s, NSVT, Sustained VT?

A
  • Careful assessment of personal and family history for:
    • syncope
    • SCD
    • cardiomyopathy
  • Physical exam
  • EKG
  • Echo
366
Q

When coding - WPW Pattern:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • Axis deviation
    • IVCD
    • ST-T abnormality
  • Inorrect to code
    • LVH
    • RVH
    • MI (acute or old)
367
Q

EKG definition: AV junctional rhythm/tachycardia

A
  • Consistently occuring, usually narrow, QRS complex:
    • 40-60 bpm = junctional rhythm
    • > 60 bpm = junctional tachycardia
  • QRS complex can be wide in the presence of aberrancy or a pre-existing IVCD
  • P wave, typically with a superior and leftward axis, if seen, may be seen immediately before or after the QRS complex
368
Q

What is the difference in terms of mortality between rate and rhythm control in AF?

A

no difference in mortality

  • Safety and efficacy of rhythm vs. rate control have been evaluated in several randomized, prospective trials
    • AFFIRM trial (Atrial Fibrillation Follow-up Investigation of Rhythm Management)
    • RACE-I trial (Rate Control versus Electrical Cardioversion for Presistent Atrial Fibrillation)
369
Q
  • What is one medication in glaucoma patients that can lead to bradycardia?
  • What are medication interactions/mechanism that are commonly seen in the elderly?
A
  • Timolol
  • Paroxetine (SSRI, anti-depressant)
    • both metabolized by cytochrome P450 2D6
    • when co-administered, can increase concentration of the other drug
370
Q

What diagnoses can mimick RVH?

A
  • Posterior MI
  • Inferoposterolateral MI
371
Q

Describe the findings (Leads II, V2, V5):

A

LQTS 1

372
Q

What are the recommendations for ICD placment:

  • Brugada Syndrome
A

Class I

  • Cardiac arrest or recent unexplained syncope

+

  • spontaneous type 1 EKG pattern
373
Q

EKG definition:

  • RVH
A
  • Mean QRS axis ►100 degrees (RAD)
  • Precordial leads (or)
    • R/S ratio in V1 > 1
    • R/S ratio in V5 or V6 < 1
    • qR complex in V1
    • R wave > 7 mm in V1
  • Secondary ST-T segment changes (ST depression or TWI) in right precordial leads
374
Q

When is Dofetilide (Tikosyn) contraindicated in CKD?

A

CrCl < 20 mL/min

375
Q

Describe the findings:

A
  • NSR
  • 2nd degree AV block - Mobitz II
  • LAD
  • LVH
  • LAFB
  • RBBB, complete
  • ST and/or T wave abnormalities secondary to hypertrophy
376
Q

What are the components of the risk score for LQTS?

A
  • ► 4 = high probability
  • 2-3 = intermediate probability
  • « 1 = low probability
377
Q

What are the EKG features of ARVD?

A
  • ​Localized QRS widening of 110 ms in V1-V3
  • Epsilon waves
    • ​most specific finding, seen in 30% of patients
  • Prolonged S-wave upstroke of 55 ms in V1-V3
    • 95% of patients
  • Paroxysmal episodes of VT with LBBB morphology
  • TWI in V1-V3
    • 85% of patients
378
Q

Describe the findings and diagnosis

A
  • AV dissociation
  • VT
379
Q

Based on response, what is the diagnosis of Narrow complex Tachyardia (QRS < 120 ms) in the setting of adenosine administration:

  • Persisting AT with transient High-grade AV block
A
  • A-flutter
  • Micro-re-entrant AT
380
Q

What are cutoffs for ST-elevation in leads V2-V3?

A

New ST-elevation at the J-point in 2 contiguous leads with the cutoff point in V2-V3:

  • ► 2 mm in men ► 40 years
  • ► 2.5 mm in men < 40 years
  • ► 1.5 mm in women regardless of age
381
Q

What are causes of early afterdepolarizations (EADs)?

A

Prolonged action potential duration

  • Drugs
    • Class Ia and III antiarrhythmics
    • Many noncardiovascular drugs (Azithromycin)
  • Gene mutations that cause LQTS
  • Clinical conditions
    • hypokalemia
    • hypomagnesemia
    • Ischemia
382
Q

When coding - 3rd degree AV block:

  • Inorrect to code
A
  • Incorrect to code
    • 1st degree AV block
    • 2nd degree AV block (type I or II)
383
Q

What is the mechanism for VT:

  • idiopathic outflow tract VT
A

Triggered activity - Delayed AfterDepolarizations (DAD’s)

384
Q

When coding - 2:1 AV block:

  • Unecessary to code
  • Inorrect to code
A
  • Unecessary to code
    • 1st degree AV block
  • Inorrect to code
    • 2nd degree AV block (type I or II)
385
Q

What is the best way to differntiate SA exit block and 2nd degree Mobitz 1 (Wenckebach) on EKG?

A

P-wave activity during dropped interval

  • SA exit block –> no P-wave activity

****Both will have group beating

386
Q

Describe the findings and next step in management

  • BP 100/60
A

VT

  • RBBB, WCT
  • V1 large monophasic R wave
  • V6 has qs pattern
  • Extreme Northwest axis (negative in V1 and aVF)

Procainamide

  • Good choice for hemodynamically stable VT
387
Q

Define RBBB, incomplete

A
  • QRS duration:
    • Adults 110-120 ms
    • Children (4-16 years) 90-110 ms
    • Kids ( < 8 years) 86-90 ms
  • Rest of criteria are the same as RBBB, complete
388
Q

When coding - Dextrocardia:

  • Unnecessary to code
A

RAD

389
Q

What are the four categories of syncope?

A
  • Arrhythmias
  • Structural obstructions
  • Hypotensive failure
  • Reflex responses
390
Q

What percentage of the population has WPW pattern on EKG?

A

0.25%

391
Q

Describe the findings:

A

​Atypical atrial flutter

  • macroreentrant atrial arrhythmia that does not utilize the cavo-tricuspid circuit
  • “non-isthmus-dependent”
392
Q

Define capture beats

When are these seen?

A
  • occur when the SA node transiently ‘captures’ the ventricles, in the midst of AV dissociation
  • produces a QRS complex of normal duration
  • VT
393
Q

Describe Amiodarone induced hypothyroidism:

A
  • Hypothyroid at baseline
  • Worsened by hypothyroidism
  • “Failue to escape” from Wolff-Chaikoff effect
394
Q

Define pacemaker undersensing

A
  • failure to sense native cardiac electrical events
  • results in pacer spikes being inserted at inappropriate times, usually prematurely
  • Causes of failure to sense:
    • acute MI
    • scar tissue or edema at the interface between the lectrode tip and myocardium
    • mechanical problems
      • lead fracture
      • lead dislodgement
      • insulation break
      • pulse generator malfunction
      • inappropriate reprogramming
395
Q

When do you check an Echo after valve surgery?

A

2-4 weeks

396
Q

Describe the findings:

A
  • Sinus tachycardia (HR > 100 bpm)
  • VT (nonsustained)
  • RBBB, incomplete
397
Q

What is one scenario where digoxin is contraindicated?

A

Ventricular pre-excitation (WPW pattern)

398
Q

What are two arrhythmias that can occur in the setting of Digoxin toxicity?

A
  • Atrial tachycardia with block
  • Bidirectional VT
399
Q

What is the relationship between cardioversion and thrombus formation?

A
  • Cardioversion –> atrial stunning
    • can promote thrombus formation
  • Return of atrial systole –> thrombus dislodgement
  • High risk of thrombus formation/stroke up to 1 month after cardioversion
400
Q

What is the reversal agent:

  • Dabigatran
A

Idarucizumab (Praxbind)

  • monoclonal antibody that can completely reverse the anticoagulant effect of dabigatran within minutes
401
Q

Describe the findings and next best step

A

Metoprolol

  • PVC’s that are not related to pacing
  • no evidence of pacemaker lead malfunction, as there is appropriate sensing and ventricular capture
  • trial of antiarrhythmic, such as BB, should be attempted and if unsuccessful, and he remains highly symptomatic, PVC/VT ablation could be considered
402
Q

What is the MOA of Class III antiarrhythmics that can be proarrhythmic?

What trials demonstrated these effects?

A
  • block outward potassium channels (IKr) and (IKs)
  • prolong refractoriness –> prolongation of the action potential
  • predisposes to early after-depolarizatons (EAD’s) and “triggered” activity –>
  • PVT (torsades de pointes) and VF
  • SWORD (Survival with Oral D-Sotalol)
    • increased mortality in patients treated with D-sotalol (sotalol without the beta-blocking action)
403
Q

How can the proarrhythmic effect of Class I antiarrhythmics be assessed?

A

Exercise treadmill test

  • increasing the heart rate while on medical therapy
404
Q

What are indications for use of Disopyramide (Norpace)?

A
  • Bradycardia-induced AF
    • due to anticholinergic effects
  • Hypertrophic Cardiomyopathy
    • due to negative inotropic effects
405
Q

What is the dose adjustment of Dofetilide based on QTc changes after initiation of therapy?

A
  • QTc ► 15% increase –> decerase dose by 50%
  • QTc > 500 ms after second dose –> discontinue
406
Q

What are the presentations that involve accessory pathways?

A
  • Orthodromic AVRT
  • Antidromic AVRT
  • Pre-excited tachycardias
407
Q

What is the diagnosis and next step:

  • 30 year old female with palpitations and lightheadedenss x 1 hour
  • BP 120/70, HR 180 bpm
  • Adenosine 6mg and 12mg with not change
A
  • Idiopathic LV (fascicular) VT
    • re-entrant tachycardia (most commonly) involving the left-posterior fascicle –>
      • wide complex tachycardia
      • RBBB morphology
  • Verapamil
    • ​highly sensitive to verapamil
    • low-risk tachycardia –> catheter ablation of fascicle involved is usually curative
408
Q

What are the procedures which require antibiotic prophylaxis for SBE?

A
  • Dental procedures that involve manipulation of:
    • gingival tissue
    • periapical region
    • perforation of oral mucosa
  • Active infection present:
    • GI
    • GU
    • Skin
409
Q

Describe phase 0 of the action potential

A

Phase 0

  • ​“upstroke” or “rapid depolarization” of the action potential
  • INa channels
    • dominated by Na ions entering through voltage-gated Na channels
  • peak voltage may reach +30 to + 40 mV
410
Q

Describe the findings/diagnosis and treatment:

A
  • EKG:
    • Atrial tachycardia at 160 bpm
    • 3:2 Wenckebach conduction
      • physiologic due to high atrial rate
    • RBBB
  • Treatment:
    • Acutely –> IV Metoprolol
    • Chronic –> catheter ablation
411
Q

What are the manifestations of SND?

A
  • symptomatic bradycardia
  • sinus pauses due to:
    • sinus arrest
    • sinoatrial exit block
  • chronotropic incomepetence
412
Q

When coding - Juvenile T waves:

  • Inorrect to code
A

ST-T ischemia

413
Q

Describe the findings and next step:

  • 50 year old male underwent routine appendectomy
  • Briefly unresponsive with the following tracing
  • Stress Echo - normal (6 months prior)
A
  • EKG
    • NSR x 5 beats
    • PVC –> polymorphic VT
    • VF
  • Coronary angiography
    • ​most likely due to myocardial ischemia
414
Q

What is the differential diagnosis in narrow QRS (QRS « 120 ms), irregular tachycardia?

A
  • Focal AT with variable conduction
  • A-flutter with variable conduction
  • A-fib
  • MAT
415
Q

Describe the findings

A

Typical EKG with RV pacing

416
Q

Describe the findings:

A
  • Incorrect electrode placement
    • significant RAD
    • QRS in aVR > aVL (vector moving towards right side of heart)
    • R wave progression is normal in precordial leads (rules out dextrocardia)
  • PAC’s
  • AV junctional rhythm/tachycardia
417
Q

What are two arrhythmias for which cardiac sympathetic denervation can be effective?

A
  • CPVT
  • LQTS
418
Q

What is the next step in evaluation/management of VA’s in patients with:

  • Polymorphic VT/VF
  • SHD
A
  • Consider ICD
  • Medical therapy:
    • BB
    • Selected antiarrhytmics in selected syndromes
  • Consider ablation:
    • PVC triggers or
    • Purkinje potentials if failed medical therapy
419
Q

What are causes of RAD?

A
  • Dextrocardia
  • Ostium secundum ASD
  • Lead reversal
  • LPFB
  • Lateral MI
  • Vertically positioned heart
  • COPD
  • PE
420
Q

What is the best way to differentiate between 2nd degree AV block?

A

compare the PR intervals immediately before and after the blocked P wave

  • PR interval
    • Mobitz I –> progressive lenthening
      • different PR intervals before and after
    • Mobitz II –> fixed PR interval
      • constant PR intervals
421
Q

What is the likely mechanism that explains the pathophysiology of sudden cardiac death?

  • 18 year old female
  • no past medical history
  • normal physical exam
  • SCD while swimming
A

LQTS 1 - loss of function of potassium channel

  • mutation in the IKs potassium channel
  • loss of function –> delay in membrane depolarization
  • Class I recommendation
    • avoidance of competitive sports
422
Q

Describe the findings:

A
  • NSR
  • AV junctional rhythm/tachycardia
  • 3rd degree AV block
  • Low voltage, limb leads
  • Inferior MI, age recent or probably acute
423
Q

When coding - Ventricular pacing:

  • Unnecessary to code
  • Inorrect to code
A
  • Unnecessary to code
    • Axis deviation
    • IVCD
  • Inorrect to code
    • LVH
    • RVH
    • MI (acute or old)
424
Q

What are indications for PPM in AV Node Disease - Class IIa

A
  • CHB with HR > 40 bpm in asymptomatic individuals without cardiomegaly
  • Asymptomatic 2nd degree AV block with intra- or infra-Hisian block found on EPS
  • 1st or 2nd degree AV block with symptoms
  • Asymptomatic Mobitz II block with narrow QRS
425
Q

What percentage of AT’s are responsive to adenosine?

A

15-20%

426
Q

Determine QRS axis: normal variant (0 to -30)

A
  • Lead I –> positive
  • Lead aVF –> negative
  • Lead II –> positive
427
Q

19 year old asymptomatic male patient presents for further evaluation based on baseline ECG which demonstrates intermittent pre-excitation at HR 57 bpm; what is the preferred approach?

A

Reassurance

  • intermittent blocking of the accessory pathway at low HR’s
  • will not conduct at fast HR’s
428
Q

When coding - Inferior MI (acute/old):

  • Inorrect to code
A

LAFB

429
Q

What are causes of electrical alternans?

A
  • Pericardial effusion
    • only about 33% of patients with QRS alternans have a pericardial effusion
    • only about 12% of patients with pericardial effusions have electrical alternans
  • CAD
  • CHF (severe)
  • Deep respirations
  • HTN
  • SVT
  • VT
430
Q

Describe features of Jervell and Lange-Nielsen syndrome

A
  • Jervell and Lange-Nielsen syndrome (JLN1 and JLN2)
    • congenital sensorineural deafness
    • KCNQ1 or KCNE2 gene mutations
431
Q

What arrhythmias have high cure rate with catheter ablation therapy. And therefore is considered first line therapy?

A
  • PSVT
  • Atrial flutter
  • WPW
  • Idiopathic PVC’s
  • Idiopathic VT
432
Q

How can SVT’s be differentiated?

A
  • rate
  • regularity
  • mode of initiation and termination
  • effect of AV block
    • (vagal maneuvers during tachycardia)
433
Q

What is the differential for negative P waves in lead I?

A
  • Ectopic atrial tachycardia
  • Limb lead reversal
  • Dextrocardia
434
Q

Describe the findings and origin of PVC’s:

A

​PVC’s originating from the Left coronary cusp

  • NSR with PVC’s
  • LBBB morphology
  • inferior axis (large positive deflections in inferior leads 2, 3, aVF)
  • early precordial transition at V2
435
Q

Describe Uncommon AVNRT

A
  • 10% of AVNRT
  • Fast (antegrade) - Slow (retrograde) conduction
  • EKG:
    • QRS - P - T complexes
    • P waves are visible between the QRS and T
436
Q

Describe the phases of the cardiac action potential

A

Medical (69 decks)

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