ACCSAP Arrhythmias Flashcards

1
Q

What CHADSVASc score in patients with HCM requires anticoagulation?

A

Any afib/flutter necessitates AC regardless of chadsvasc score due to high rate of thromboembolism.

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2
Q

What is classical manifestation and cause of long QT syndrome type 1?

A

Sudden cardiac death while swimming, this is a loss of function mutation in the Inward K+ channels that are responsible for membrane repolarization, and therefore produce long QT

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3
Q

What is the most common cause of VF or polymorphic VT?

A

Ischemia

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4
Q

What are the EKG appearances of type I and type II Brugada pattern? How do you prove someone has this syndrom?

A

Type 1 ST-segment changes, “coved,” are diagnostic of the syndrome whereas type 2 “saddle back” ST changes are equivocal, as seen in this ECG (Figure 2). To make a definitive diagnosis, type 1 ST-segment elevations must be observed following superior placement of precordial leads (V1 and V2) in the second intercostal space or after administration of sodium channel blocking drugs.

There is no clear role for genetic testing in Brugada syndrome.

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5
Q

What are diagnostic criteria for Long QT syndrome?

A

Long QT syndrome (LQTS) is diagnosed in the presence of corrected QT interval (QTc) = 500 msec or LQTS risk score = 3.5 when secondary causes have been excluded or in the presence of a pathogenic mutation in one of the LQTS genes. It can also be diagnosed when the QTc is 480-499 msec in a patient presenting with syncope.

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6
Q

What is the mechanism of Na channel blockers in treating rapid arrhythmias?

A

“Use dependence” Class I antiarrhythmics block inward sodium channels and slow conduction velocity in the myocardium. Class I drugs exhibit a phenomenon called “use dependence” in which the extent of channel block is increased at a higher heart rate. These drugs therefore block the sodium channels to a greater degree at faster heart rates.

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7
Q

How do you diagnose sinus node dysfunction with chronotropic incompetence?

A

SND with chronotropic incompetence as evidenced by her heart rate response during exercise, with a peak heart rate <100 bpm and <70% age-predicted maximum heart rate.

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8
Q

Which beta blocker can accumulate in patients with renal dysfunction?

A

Atenolol.

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9
Q

Where is the typical location of Mobitz 1 vs mobitz 2 block?

A

Mobitz 1 is usually AV nodal and mobitz 2 is typically in the His-Purkinje system. If there is 2:1 block you can use noninvasive vagal and sympathetic maneuvers to distinguish one from the other. Carotid sinus massage typically slows AV conduction and will worsen AV clock. Can also use exercise to improve AV nodal conduction and worsen HIS-Purkinje conduction.

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10
Q

What is QTC cutoff felt to be most predictive of a a positive genetic screen for LQTS?

A

The probability of a positive genetic test for LQTS is greatest when the QTc is >480 msec, especially in the setting of a positive family history

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11
Q

What are the class I indications for ICD and for BiV pacing?

A
Class I indication for defibrillator includes an EF of 35% or less with NYHA class II or III symptoms.
Class I indication for biventricular pacing with class II, III, or ambulatory IV heart failure, LBBB, and QRS duration of 150 ms or greater
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12
Q

Define paroxysmal, persistent, and permanent afib

A

Persistent if the episode is >7 days. Longstanding persistent if >12 months. Permanent AFib is defined by cessation of attempts to control rhythm (decision with pt/provider)

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13
Q

CPVT - Catecholaminergic polymorphic VT.

What is the mutation most commonly involved?

A

Ryanodine receptor

Characterized by VT induced by exercise or emotional stress

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14
Q

Familial thoracic aortic aneurysm diseases.

What is the mutation most commonly involved?

A

TGF-beta (transforming growth factor-beta) mutations

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15
Q

Marfan syndrome.

What is the mutation most commonly involved?

A

Fibrillin mutations

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16
Q

Dilated CM and hypertrophic CM

What is the mutation most commonly involved?

A

Myosin heavy chain mutations

17
Q

ARVC

What is the mutation most commonly involved?

A

Plakophilin mutation

18
Q

What is the weight loss needed to reduce AFib burden per the LEGACY trial?

A

Weight loss of ≥10% of body weight resulted in a sixfold greater probability of arrhythmia-free survival at 5 years.

19
Q

What is a common asthma therapy known to prolong QT?

A

Albuterol!

20
Q

What are patient factors that favor a cardiac cause of syncope?

A

Age >60, male sex, known ischemic heart disease.
In patients with unexplained syncope, TTE is reasonable to look for LV dysfunction as this significantly increases likelihood of cardiac syncope.

21
Q

What is EKG finding most common with fascicular VT?

A

Mildly prolonged QRS in a RBBB-like morphology, in a young healthy patient without structural heart disease. VERY responsive to verapamil and catheter ablation is usually curative.

22
Q

Who requires screening once a family member is diagnosed with Brugada syndrome with +genetic mutation?

A

First- and second-degree relatives of patients with Brugada syndrome and positive genetic screen are recommended to undergo genetic testing even in the setting of a normal baseline ECG.

Brugada syndrome = SCN5A mutation.

In the absence of a genetic mutation, could consider an exercise stress test to induce ST segment changes suggestive of brugada pattern.

23
Q

What are meds used to treat pre-excited afib? (Pt with WPW)

A

IV procainamide, IV ibutilide, or synchronized cardioversion.

Agents that slow conduction through the AV node (BB, CCB, or Amio) can lead to VF.

24
Q

What is best antiarrhythmic for a patient with Brugada syndrome and frequent VT/ICD shocks?

A

Quinidine (class 1c agent). Currently used for patients with ICD and multiple shocks, patients who cannot get ICD, or to treat SVTs in pts with brugada pattern.

Do NOT use procainamide or flecainide (these are used to unmask brugada pattern on EKG)

Amiodarone is PROARRHYTHMIC in Brugada syndrome.

Beta blockers increase St segment elevation and are contraindicated

25
Q

What is the diagnostic threshold for chronotropic incompetence?

A

Failure to reach 80% maximum predicted HR with exercise.

26
Q

Suspected diagnosis?

Exercise-induced VT, RV enlargement on TTE, and RBBB on EKG.

A

Suspect ARVC.
In order to meet criteria for ARVC, there should be two major criteria, or one major and two minor criteria, in the categories of ventricular dysfunction, tissue characterization, arrhythmias, and ECG de/repolarization criteria.

Cardiac MRI is helpful. If confirmed, family screening indicated as this is typically an autosomal dominant condition.

27
Q

What is the mechanism of torsades in long QT syndrome?

A

Early afterdepolarizations

28
Q

What are indications for ICD in a patient with HCM?

A

Sudden death in a first-degree relative, maximal septal thickness >30 mm, unexplained syncope, low blood pressure during treadmill stress testing, and nonsustained ventricular tachycardia (NSVT) on Holter.

29
Q

Treatment of sustained MMVT in structurally normal heart?

A

beta-blockers, calcium channel blockers, and antiarrhythmic medications as well as catheter ablation are considered first-line therapies

30
Q

What is the suspected mechanism of syncope AFTER using propafenone to abort pAF?

A

Propafenone and flecainide can exacerbate underlying conduction system disease, unmasking sinus node dysfunction, atrioventricular block, or infrahisian block, and increases in the P-R and QRS intervals of ≤25% over baseline values are commonly seen with the use of these drugs.

31
Q

What is EKG pattern of RVOT VT?

A

left bundle appearance and inferior axis. Can be seen in structurally normal hearts.

If there is suspicion for ARVC - there is a class I recommendation for cardiac magnetic resonance imaging (MRI) to establish the diagnosis and for risk stratification. ARVC is characterized by progressive ventricular myocyte loss with replacement by fatty or fibrous tissue, and is associated with progressive ventricular dysfunction that may involve both ventricles.

32
Q

Mechanisms of ventricular arrhythmia - describe

  1. enhanced normal automaticity,
  2. abnormal automaticity,
  3. triggered activity induced by early or late afterdepolarizations
  4. re-entry.
A

Re-entry around a scar is the mechanism of monomorphic VAs in patients with ischemic heart disease.

33
Q

What is EKG pattern of RVOT VT?

A

left bundle appearance and inferior axis

34
Q

What antiarrhythmic drugs have use dependence characteristics?

A

Class Ic - making them more effective at rapid heart rates. (propafenone, flecainide).

Reverse use dependence = more effective at slower heart rates ie SOTALOL

35
Q

What is a water soluble beta blocker that should be discontinued in the setting of renal failure?

A

Atenolol