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Cardiology > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

Treatment for torsades

A
  • Pulseless torsades should be defibrillated.
  • IV MAGNESIUM is the first-line pharmacologic therapy in Torsades de Pointes. Magnesium has been shown to stabilize the cardiac membrane, though the exact mechanism is unknown. The recommended initial dose of magnesium is a slow 2 g IV push.1
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2
Q 
Which of the following IV antiarrhythmic drugs are absolutely contraindicated for the acute management of VT?
A. Lignocaine 
B. Verapamil 
C. Procainamide
D. Amiodarone 
E. Sotalol
A

B. Verapamil

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3
Q 
Which of the following is not a long term treatment for this scar-related ventricular tachycardia?
A. Amiodarone 
B. ICD 
C. Sotalol 
D. Catheter ablation 
E. Mexiletine
A

B. ICD- - it treats risks but doesn’t treat the VT

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4
Q

Features of VT

A
  • AV dissociation (capture and fusion beats) - hallmark of VT
  • QRS > 140
  • Extreme axis/north west axis
  • RSR complexes with a taller “left rabbit ear”
  • Positive or negative concordance
  • Josephson’s sign
  • Brugada’s sign

Other causes of extreme axis/north west axis: emphysema, hyperkalaemia, ventricular pacing

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5
Q

Medications that cause QT prolongation

A 
Clarithromycin 
Erythromycin 
Metoclopramide
Haloperidol 
Methadone 
Droperidol
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6
Q

Management of VT

A
  • Unstable: urgent cardioversion
  • Stable: amiodarone, lidocaine, procainamide, sotalol
  • Generally these patients (>90%) have advanced structural heart disease with poor LV ejection fraction (prior MI) so no flecainide, verapamil, metoprolol - VERAPAMIL SHOULD NOT BE USED IN VT as can cause hypotension and MI
  • ICD for primary/secondary prevention - this is to treat the treat the risk of sudden cardiac death, not to prevent VT recurrence
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7
Q

What do you have to be wary of in inferolateral STEMI?

A

RV infarction

  • STE in V1
  • STE in lead III > lead II
  • ST depression in V2
  • Presence of STE in the right sided leads (V3-V6)

Preload sensitive and can develop hypotension when nitrates are given

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8
Q

What is bifascicular block and trifascicular block?

A

Bifascicular Block

  • Sinus
  • Left axis deviation
  • RBBB

Trifascicular Block

  • Left axis deviation
  • RBBB
  • First degree AV block
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9
Q

What arteries are affected in the following STEMI

  • Lateral
  • Inferior
  • Anterior/Septal
A

Lateral: LCx or diagonal of LAD

Inferior: RCA

Anterior/Septal: LAD

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10
Q

What is long QT 1,2,3 precipitated by?

A

LQT1 - exercise (supervise swimming)
Genetic defect decreases activity of the slow-acting K current
Beta blockers
KCNQ1

LQT2 - loud noise (avoid loud noises, alarm, clocks)
Affect potassium
Beta blockers
KCNH2

LQT3 - during sleep
Allow Na influx to continue to a greater degree, prolonging the action potential, give flecanide
SCN5A

QT> 500 represents greatest risk of symptomatic arrhythmias

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11
Q

Brugada Syndrome

A
  • Autosomal dominant
  • More common in SE Asia
  • Typical ECG findings
    Coved ST segment elevation in lead V1-V3 + at least one of the following
    Personal or family hx of syncope
    Ventricular arrhythmias
    Similar ECG findings in other family members
  • Sodium channel gene defect - SCN5a where the sodium channel is underactive. “LOSS OF FUNCTION” mutations affecting sodium channel activity

To bring out brugada, you do a flecanide challenge

  • May be polygenic
  • Polymorphic VT and VF

ICD indicated for prior syncope or documented ventricular arrhythmias

Tx:

  • Avoid sodium channel blockers
  • ICD if syncope, VT
  • Treat fevers with paracetamol
  • Quinidine may be useful with recurrent arrhythmia
  • Trials of ablation for VT storms
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12
Q

AF rhythm management - new onset

A
  • Reasonable to revert if <48 hours
  • If > 48 hours or uncertain
    TOE, revert and anticoagulate for at least 6 weeks
    Anticoagulate for 4-6 weeks and then revert
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13
Q

Rhythm control of AF

A
  • Sotalol: effect but least well tolerated
    Very poor at reverting AF
  • Amiodarone: most effective but multiple SE
    Thyroid toxicity (hypo 6%, hyper 2%)
    Pulmonary toxicity
    Hepatic toxicity
    Ocular toxicity - photosensitivity, corneal depositis

Flecanide: GI and some dysthesia
Risk of organisation to atrial flutter and 1:1 conduction so you add on beta blocker

AF ablation - pulmonary vein isolation

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14
Q

Atrial Flutter

A
  • Rapid, regular atrial depolarisation from MACRO RE-ENTRY CIRCUIT WITHIN ATRIUM, dependent on cavo-tricuspid isthmus - between IVC and tricuspid valve.
  • Typical counter-clockwise around the tricuspid valve pattern of downward p wave in II, III, aVF

Tx:
- Ablation treatment of choice - successful in 90%
But with increased incidence of subsequent AF
- Calcium channel blocker, eg: diltaizem, verapamil
- Bea blockers: propanolol, metoprolol, atenolol

  • Usually occurs in patients with structural heart disease or post surgical or post ablation
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15
Q

NOACs and creatinine clearance

A
  • Dabigatran: CrCl >30
  • Apixaban: CrCl >15
  • Rivaroxaban: CrCl >15
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16
Q

When do you dose reduce apixaban?

A

At least 2 of the following
Age > 80
Weight < 60kg
Cr >133

17
Q

AVNRT - AV nodal re-entrant tachycardia (60-70% of paroxysmal SVT)

A
  • Typical (slow-fast, short R-P) and atypical (fast-slow, long R-P)
    Typical: p wave is hidden in QRS complex or after QRS, 90% of all cases
    Atypical: p wave before QRS
  • Originates above the Bundle of His and is the most common cause of palpitations in patients with structurally normal hearts.

Typical AVNRT – ‘slow-fast’
Initiated by PAC > antegrade down slow > retrograde up fast
Atypical AVNRT – ‘fast-slow’
Initiated by VEB > antegrade down fast > retrograde up slow

Treatment

  • Therapies which slow AV node conduction, block circuit and allow normal conduction from SA node
  • Carotid massage, vagal manoeuvres, leg lift
  • Adenosine

Prevention

  • Verapamil
  • EPS
18
Q

Arrhythmogenic right ventricular cardiomyopathy

A
  • Autosomal dominant genetic disorder of myocardium in which there is fatty infiltration of the right ventricular free wall, predisposing to paroxysmal ventricular arrhythmias, sudden cardiac death, and biventricular failure
  • Mutations in desmosomal “cell glue”
  • Second most common cause of sudden cardiac death in young people (after HOCM), accounting for up to 10% of sudden cardiac deaths in patients < 65 yrs of age
  • Prevalence ~ 1 in 5000
  • ARVC causes symptoms due to ventricular ectopic beats or sustained VT (with LBBB morphology), and typically presents with palpitations, syncope or cardiac arrest precipitated by exercise
  • The first presenting symptom may be sudden cardiac death
  • Over time, surviving patients develop features of right ventricular failure, which may progress to severe biventricular failure and dilated cardiomyopathy

ECG FINDINGS:
Epsilon wave
T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
T-wave inversion in precordial and inferior leads, without RBBB pattern
Widening of QRS in V1-V3 (>110ms)

Epsilon Wave:
Small positive deflection (“blip” or “wiggle”) buried in the end of the QRS complex
Best seen in ST segment of V1 and V2, they are usually present in leads V1 through V4
Caused by post-excitation of myocytes in the right ventricle

19
Q

AVRT - atrioventricular re-entrant tachycardia

Pre-excitation syndromes

A
  • Mediated by an accessory pathway/bypass tract, connection between the atria and the ventricles in one of the AV rings
  • AVRT are further divided into orthodromic or antidromic conduction based on direction of re-entry conduction and ECG morphology
  • Ventricular activation via AV node (orthodromic) is more common than via accessory tract (antidromic)
  • Usually short RP, uncommon long RP, rarely no RP
  • In orthodromic AVRT anterograde conduction occurs via the AV node with retrograde conduction occurring via the accessory pathway. This can occur in patients with a concealed pathway
  • In antidromic AVRT anterograde conduction occurs via the accessory pathway with retrograde conduction via the AV node. Much less common than orthodromic AVRT occurring in ~5% of patients with WPW.
20
Q

Wolff Parkinson White

A
  • Wolff-Parkinson White: pre-excitation (delta wave) + tachyarrhythmia
  • In WPW, the accessory pathway is often referred to as the Bundle of Kent or atrioventricular bypass tract
  • Impulses travel at a greater conduction velocity across the bundle of Kent → bypassing AV node
  • ECG shows – early ventricular depolarisation in the form of slurring of the QRS complex – delta wave.
    PR interval < 120ms
    Delta wave: slurring slow rise of initial portion of the QRS
    QRS prolongation > 110ms
  • Type A (left sided pathway): right axis, dominant R wave in V1
    Positive delta waves in all precordial leads with R/S >1 in V1
  • Type B (right sided pathway): left axis, non dominant R wave in V1
    Negative delta wave in leads V1 and V2 - indicates right sided accessory pathway
21
Q

Conditions associated with WPW

A
  • HOCM
  • Mitral valve prolapse
  • Ebstein’s abnomaly: congenital heart defect in which the septal and posterior leaflets of the tricuspid valve are displaced towards the apex of the right ventricle of the heart.
  • Thyrotoxicosis
  • Secundum ASD
22
Q

Management of WPW

A

Definitive Management: radiofrequency ablation of the accessory pathway

Medical Therapy: sotalol, amiodarone, flecanide

  • Sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and
  • Verapamil and digoxin should be avoided as they may precipitate VT or VF
23
Q

AF and WPW

A
  • Feared complication of WPW
  • Rapid conduction of AF down accessory pathway with very short refractory time

Stable: IV flecanide
Unstable: DC cardioversion

24
Q

Catecholaminergic polymorphic VT

A
  • Catecholaminergic Polymorphic Ventricular Tachycardia is a congenital disease that leads to exercise induced ventricular arrhythmias and / or syncope and carries an increased risk of sudden death.
  • Fam history
  • Multiple and frequent ventricular arrhythmias on stress testing

Tx: Flecainide

25
Q

2nd degree heart block

A

Mobitz Type 1: The PR interval slowly increases and then there is a dropped QRS complex (beat)

  • Usually benign
  • Normally in young and fit
  • No indication for PPM

Mobitz Type 2: If the PR interval is fixed but there are dropped beats

  • No variation in PR interval
  • Significant risk to progress to complete heart block
  • PPM indicated if symptomatic or asymptomatic but very bradycardic
26
Q

SVT treatment

A
  • Vagal
  • Adenosine
  • Verapamil - don’t’ give for VT as it can cause hypotension and cause a MI
27
Q

Catecholaminergic polymorphic VT

A
  • Induced by physical or emotional stress
  • No structural heart changes
  • Genetics - autosomal dominant
    Ryanodine receptor (RyR2), CAS!
  • Key is exercise stress test - brings on VEBs, NSVT with continued exercise VT
  • Classic feature is BIDRECTIONAL VT
28
Q

What are capture and fusion beats?

A
  • Capture Beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration

Fusion Beats — occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.

• AV dissociation (capture and fusion beats) – hallmark of VT
	○ P and QRS complexes at different rates
	○ P waves are often superimposed on QRS complexes and may be difficult to discern The presence of AV dissociation is characteristically marked by the presence of sinus capture or fusion beats.

Cardiology (8 decks)

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