Arrhythmia Flashcards
Reverse use dependence
Increased effect at slow heart rates All class III drugs including dofetilide
III: block outward potassium channel activity (IKs) and prolong refractoriness
Dofetilide side effects
Hypomagnesemia, hypokalemia, QT prolongation
Pacemaker cardiomyopathy
12% of patients who are paced >20% of the time-> change or upgrade to biventricular
Ventricular pacing alone (without atrial pacing) increases
Afib
Management of LQTS
Genetic testing of index patient Beta blockers ICDs if strong personal risk factors for SCD QTC > 480ms more definitive Polymorphic VT
Persistent afib
Paroxysmal
Long-standing persistent
Permanent
> 7 days
<7 days
12 months
We have stopped attempts to control and accepted it
Primary prevention ICD (MADIT-II trial)
Just EF and GDMT?
CRT (biventricular ICD) indication
EF <35%, QRS> 150, LBBB, sinus rhythm, class II-IV despite GDMT
Palpitations work up
24 hour holter vs event monitor
If risk factors for cardiac disease, attempt to correlate with monitor
Event monitor generally shown to be better
Palpitations and lightheaded ness with exercise and emotion in young person, positive family history
CPVT
Ryanodine receptor mutation more common
Transforming growth factor-beta (TGF-β) mutations
Familial thoracic aortic aneurysms
Fibrillin mutation
Marfan
Myosin heavy chain mutation
HCOM and dilated cardiomyopathy
Plakophilin mutation
ARVC
Monomorphiv VT that originates in RVOT
Differential
LBBB morphology (down in V1) with inferior axis, can ablate / BB/ CCB/ class 1C
idiopathic VT and arrhythmogenic right ventricular cardiomyopathy (ARVC)
RVOT VT is usually not ischemia driven
ARVC
Epsilon wave after QRS and TWIs in V1-V3
Get CT/MRI
Arrhythmias in Brugada
Beta blockers CI- increase ST elevation
Amiodarone is pro arrhythmic
Treat fever, avoid drugs and alcohol
Quinidine for
ICD w/ multiple shocks for VT
ICD is CI
LVOT VT
LBBB, inferior axis, early R wave progression
VT in structurally normal heart
VT in abnormal heart
Meds or ablate
ICD
Most common cause of VT (wise complex, positive concordance, monophasic R in V1) in CAD
Scar-mediated, re-entrant
Torsades in LQTS mechanism
Early afterdepolarizations
Mobitz type II vs complete heart block
Fixed PR interval
Brugada
Sodium channel blockers (flecainide, propafenone) can exacerbate the transient ECG abnormalities that occur in patients with Brugada syndrome who commonly have normal ECGs.
AF with aberrancy, WPW
Do not give
Beta blocker, adenosine, dig.
Use ibitulide and procainamide
AF with WPW vs plain AF
Wide complex vs narrow complex
2:1 block, differentiate between Mobitz I and II
I may be due to increased vagal tone in athletes- improves with exercise
II is due to His disease- worsens with exercise
atrial tachycardia, atrial flutter, or atrial fibrillation in adult congenital heart disease patients
progressive hemodynamic deterioration of the underlying disease
Obtain TTE and address arrhythmia
Marked first degree AV block can cause fatigue
> 300, cannon a waves
Due to AV dyssynchrony- atrium contracts before complete filling-> decreased ventricular filling
May benefit from pacing
Cardio inhibitory syncope
Vagally mediated
Sotalol side effect
Non sustained torsades
Sotalol
Class III
Blocks inward potassium channel, prolongs QT
Risk is higher in bradycardia, female sex, pre-existing QT prolongation, history of heart failure, history of ventricular tachycardia/ventricular fibrillation, or hypokalemia.
Sustained torsades treatment
If unstable- shock
If stable- IV mag
IV isoproterenol (increases HR, decreases QT) No beta blockers or amiodarone
Underlying causes of afib
hypertension, obstructive sleep apnea, and obesity
AV block (complete heart block) vs AV dissociation (AIVR)
Atrial rate is faster
Ventricular rate is faster
Tachy Brady syndrome
Post AF conversion pause - sinus node dysfunction + afib
Avoid sodium channel blockers like flecainide
ARVC lifestyle
high risk of ventricular arrhythmias and sudden death
avoid competitive sports and endurance training
Can do billiards, bowling, cricket, curling, golf, and riflery
Consider family screening, may need ICD
Polymorphic (multiple QRS morphology) tachy risk factors
Drugs
Ischemia is a common cause
baseline QT prolongation, bradycardia, and electrolyte disturbances (especially hypokalemia and hypomagnesemia, and less often hypocalcemia).
Levo and albuterol
Non–isthmus-dependent (atypical) atrial flutter mechanism
Underlying etiology
Treatment
macro–re-entrant circuits elsewhere in the RA or LA
congenital heart disease, after cardiac surgery, and after catheter ablation of AF.
Rate control-> EPS
Afib mechanism
AVNRT mechanism
Rapid focal ectopic activity (pulmonary veins)
Re-entry within triangle of Koch
Type 1 Brugada, sudden death in family member
ICD is not indicated
Indicated in personal history of cardiac arrest or syncope (at rest, not vasovagal)
Typical atrial flutter vs atypical
Sawtooth in inferior leads, positive in V1: cavotricuspid, can be ablated
Fossa ovalis or SVC
Acute renal failure, stop
Atenolol, accumulates
ARVC VT
Idiopathic RVOT VT
Beta blocker -> ablation
Ablation
Afib underlying causes
hyperthyroidism, pericarditis, pulmonary embolism, and electrolyte abnormalities (r/o)
AVNRT
Most frequent SVT, Cannon a waves (neck discomfort)
AVRT
Atrial tachycardia
Narrow complex regular tachycardia
SVT: AVNRT (dual pathway) AVRT (accessory pathway) AT (ectopic Ps, organized atrial activity with adenosine) Sinus tachycardia Junctional tachycardia
Narrow complex irregularly irregular tachycardia
AF
MAT
Sinus arrhythmia
Any pattern= regularly irregular
Flutter or fib for less than 48 hours
Can be DC cardioverted without TEE
- Rate control is difficult in flutter, aim for rhythm control if possible* (cardioversion preferred)
Brugada type 2 (saddle back)/ 3
ECG with superior placement of V1 and V2/ block sodium channels with flecainide to unmask
Provocative testing such as drug challenge with procainamide or flecainide or programmed electrical stimulation during electrophysiology testing
Prolonged QT-> PMVT-> vfib mechanism
Early after depolarizations
Hydroxychloroquine
PMVT due to acute ischemia mechanism
causes re-entry due to loss of the epicardial action-potential dome in phase II.
Treatment of recurrent symptomatic SVT
Ablation
Fever, alcohol and cocaine unmask Brugada
Gene mutation
SCN5A
PVC ablation
Work up
> 25%
Holter monitor-> implantable loop recorder
Inappropriate sinus tachy treatment
Ivabradine (if current in SA node, drives sinus rate)
Beta blockers not effective
Sinus node dysfunction
persistent sinus bradycardia , chronotropic incompetence, paroxysmal or persistent sinus arrest with replacement by subsidiary escape rhythms in the atrium, atrioventricular (AV) junction, or ventricular myocardium
Chronotropic incompetence
Deconditioning
peak heart rate <100 bpm and <70% age-predicted maximum heart rate.
Exaggerated HR response during exercise
First degree vs Mobitz I vs Mobitz II
No dropped ps vs increased PR, narrow complex vs normal PR, sometimes wide qrs
Mobitz I vs Mobitz II
AV nodal block vs His
Carotid sinus massage worsens AV block, improve His conduction
Exercise improves AV conduction, worsens His
Flecainide/ propafenone
Sotalol
Class Ic, Na blocker
Dissociate slowly during diastole-> use dependence
Effective for pill in pocket SVT
can exacerbate underlying conduction system disease, unmasking sinus node dysfunction (post conversion pause), atrioventricular block, or infrahisian block, and increases in the P-R and QRS intervals of ≤25%
Class III, potassium channel blocker
Reverse use dependence, effective at slower heart rates, use daily
Afib > 48 hours
Post cardioversion anticoagulation (there is risk with cardioversion)
Anticoagulate and TEE before cardioversion 4 weeks (Long term AC is determined by CV score)
VT/ NSVT/ PVCs:
Negative in V1( left bundle morphology)
Positive in V1( right bundle morphology)
Differentiate normal heart from structural heart disease
RVOT (idiopathic vs ARVC) Left ventricle (different morphologies= cardiomyopathy)
ICD if there is structural heart disease
Bidirectional VT
Digoxin toxicity (dronaderone increases, so does amiodarone)
Amiodarone and warfarin also = drug interaction
WPW EKG
EKG+ symptoms
If uninterested in ablation
Noninvasive exercise testing to risk stratify
Disappearance of delta wave = low risk
Persistent, gradual shortening= high risk
Straight to ablation, no need for stress test
If no SHD, beta blocker / CCB, flecainide or propafenone
Afib+ asymptomatic, normal EF
Target HR
Rate control and AC
Can consider ablation if symptomatic or decreases EF
<110 (RACE-II)
Rate control = rhythm control
Factors to consider
age (rate in older), symptoms (rhythm?), duration of AF (>48 hrs- rate) evidence of tachycardia-mediated cardiomyopathy (rhythm), or difficulty in achieving adequate rate control.???
Permanent AF
Can prevent effective pacing
Can not restore sinus, so no need for antiarrhythmic drugs
Can ablate AV junction for rate control
Pacing + LBBB
No response to CRT causes
RV pacing only
atrial fibrillation with rapid conduction, inappropriate device programming, and frequent ventricular ectopy, loss of LV lead capture or poor LV lead position
Response depends on >90% biv pacing
CV risk of stroke
Corresponds till 4, then sequential increase 5_->7, 6-> 9, 7-> 10, 9-> 15
SCD during swimming
LQTS syndrome treatment
Long QTS
Loss of function in potassium channel-> delay in membrane repolarization
Beta blocker -> ICD
AF/flutter + HCOM
AC regardless of CV score
1st / 2nd degree Brugada relative with normal ECG
Genetic testing
PMVT-> acute ischemia
ongoing chest pain with a normal ECG canbe seen with an acute circumflex artery occlusio
Monomorphic VT mechanism
Re-entry around a scar
Or
Single focus in structural heart disease
BRUISE CONTROL
peridevice surgery anticoagulation
Warfarin better than lovenox
Sinus node dysfunction types
symptomatic bradycardia, sinus pauses due to sinus arrest or sinoatrial exit block, and chronotropic incompetence.
RVOT PVCs
LBBB with inferior axis and late R-wave progression, beyond V3
Ablate
Irreversible symptomatic Brady due to SND or AV block (both types of second degree )
Pacemaker
HCOM ICD
prior cardiac arrest/ sustained VT/ first degree SCD/ wall thickness >30 mm/ unexplained syncope
- do not do dobutamine stress= increase LVOT gradient-dangerous*
Unexplained syncope
Investigate with monitoring for arrhythmia and echo for LV dysfunction
LQTS genetic testing
Strong clinical suspicion for LQTS and qt prolongation
Asymptomatic, idiopathic qtc >500/480 /460
Prolonged qtc underlying causes
Bundle branch block, meds
WPW treatment
Procainamide, ibutilide, cardioversion
No amiodarone or lidocaine
Predicted max HR
Goal max HR
Chronotropic incompetence
220-Age
(220-Age)* 0.85
Inability to reach 80%
Atrial tachycardia treatment
Ablate
If resistant, beta blockers, nondihydro
MNVT mechanism
RVOT VT mechanism
Torsades mechanism
Scar mediated re-entry
Delayed and early afterdepolarization
Early afterdepolarization
Timolol eye drops can cause
Brady arrhythmia in drug interactions with paroxetine for example
Rule out drugs before diagnosing SND
VT
SHD
No SHD
ICD
Drugs or ablation
Left ventricle fascicular VT
Re entrant tachy
Sensitive to verapamil
Can ablate
Characteristic of wenckebach
Short PR after dropped P
Hyperkalemia
Peaked T, wide QRS, prolonged PR
Hypokalemia ECG
U wave
bradycardia treatment
hemodynamically unstable, third-degree AV block with escape rates <40 bpm: transcutaneous pacing Infra nodal (wide qrs, Mobitz II onwards): isoproterenol, will need pacemaker eventually AV nodal (narrow qrs, first degree, Mobitz I): atropine dopamine?
advanced degree AV block
2 or more consecutive ps are blocked
1 second on ecg strip
infranodal block
5 large boxes
wide qrs, mobitz II onwards (can be mobitz I)
posterior fascicular VT
anterior fascicular VT
RBBB+ LAD
RBBB+ RAD
2:1 block
Differentiate b/w Mobitz I vs II with carotid sinus massage or ETT
Regularization of QRS in afib
Complete heart block
Indeterminate axis differential
LAFB+ RVH
Regularization of QRS in afib
Complete heart block
Indeterminate axis differential
LAFB+ RVH
Electrical storm treatment
Propanol
