Arrhythmias Flashcards
Sotalol QT prolongation (torsades)
Class III, blocks inward potassium channel
reverse use dependence: QT lengthens as HR slows
Also dofetilide.
stable torsades
unstable torsades
IV mag-> IV isoproterenol-> pacing
defib
Causes of polymorphic VT
preceded by a pause or transient slowing of the heart rate with prolonged QT= prolonged QT
myocardial ischemia
sinus pauses, tachy brady in afib due to
sinus node disease
flecainide (class 1C)-> blocks sodium channels-> bradycardia
Azithromycin
Prolongs QT-> Triggers early afterdepolarizations-> PMVT
Class 1a, III drugs also do this.
Acute ischemia VT mechanism
re-entry due to loss of the epicardial action-potential dome in phase II
Typical atrial flutter
Atypical
Atrial arrhythmias origin
positive in V1, from CTI
fossa ovalis or superior vena cava
crista terminalis
Brugada ECG
Brugada ICD
use high precordial leads in the second intercostal space or after administration of sodium channel blocking drugs (flecainide or ajmaline). Do in type 2 or type 3.
Type 1+ syncope+ fam SCD. If asymptomatic, no ICD.
ARVC arrhythmia diagnosis
isoproterenol challenge
Marked first degree AV block can cause near syncope and confusion through
AV dyssynchrony (atrial contraction before complete atrial filling-> ventricular filling is compromised)= cannon A waves, >300 ms
Cardio inhibitory syncope
vagally mediated
WPW afib treatment, stable
unstable
Ibutilide or IV procainamide
cardioversion
Acute onset AF, >48 hours AC:
CV 0
CV 1
4 weeks after cardioversion, then nothing
AC forever
Monomorphic VT in CAD mechanism
Electrolyte abnormalities VT mechanism
Reentry
Enhanced automaticity
probability of positive genetic screen for LQTS.
QT>480 + recurrent syncope
QT >480 ms
LQTS. No need for genetics
Unstable VT
Cardiovert
Palpitations with exercise and emotional stress+ fam SCD
CPVT (ryanodine receptor or calsequestrin receptor
AF with RVR in patient with CRT
Can decrease pacing percentage and efficacy -> AV nodal ablation
(TGF-β) mutations
fibrillin
plakophilin
familial thoracic aortic aneurysm diseases
Marfan
ARVC
Antiarrhythmics in AF
Do not use in permanent AF
Periprocedure AC
Don’t stop AC in moderate-to-severe mitral stenosis, a mechanical heart valve, or hypertrophic cardiomyopathy. If CV is super high, also continue.
Chronotropic incompetence due to sinus node dysfunction
Deconditioning
Must reach 80% maximum predicted HR
Exaggerated HR response
Normal HV interval
35-55 ms. If prolonged-> PPM
Univentricular pacing > 40%
upgrade to CRT
CV stroke rate
Corresponds to number until
5-> 7%
6->10%
7->10%
8->7%
9->15%
Afib w/u
r/o hyperthyroidism, pericarditis, pulmonary embolism, and electrolyte abnormalities, echo
flecainide class, mechanism
1c, slow conduction by blocking open sodium channels, effective at rapid heart rates= use dependent.
Propafenone also. Can unmask sinus node dysfunction, prolong PR, prolong QRS. Get 30 day monitor.
mexilitine class, mechanism
1b, increase the rate of membrane depolarization, increase delayed afterdepolarizations, and shorten the refractory period
sotalol class, mechanism
III, blocks potassium channels, resulting in prolongation of repolarization, action potential duration, and the refractory period. Reverse use dependence. Also dofetilide.
QT prolongation drugs
lytes
hydroxychloroquine, fluroquinolones, albuterol
hypomag, hypokalemia
unexplained syncope
get echo. do not get eeg/carotid u/s
When SCN5A variant is identified in primary Brugada patient
asymptomatic first and second degree family members should get genetic screening
symptomatic RVOT VT
may be seen in normal hearts.
left bundle branch block with inferior axis and late R-wave progression beyond V3.
In normal hearts=Ablate. If ARVC: beta blockers-> ablate.
ICD for every EF <30%
regardless of functional status
CRT if NYHA class II, III, or ambulatory IV HF+ LBBB+ QRSd ≥150 msec
Atrial flutter or AT after ablation for AF due to
macroreentry in the atria due to atrial scarring
RVOT VT mechanism
CPVT mechanism
Triggered activity encompasses both delayed and early afterdepolarization.
Delayed afterdepolarizations
Ischemic VT mechanism
Fascicular VT mechanism
enhanced normal automaticity and abnormal automaticity
Enhanced automaticity within the fasicular system
LBBB PVC+ up in inferior leads
LBBB + inferior axis+ early R wave transition (by V3)=
LBBB+ inferior axis+ late R wave transition
inferior axis
LVOT VT
RVOT
2:1 block
exercise (improves AV conduction and worsens His conduction) to differentiate b/w Mobitz 1 (AV nodal) and 2 (His).
Carotid massage does the opposite.
different p wave morphology in sinus vs tachycardia=
atrial tachycardia, atrial activity during period of block after adenosine. Ablate.
Tachycardic pacing due to
PMT or tracking SVT
treatment of inappropriate sinus tach
ivabradine, blocks iF current (located in SA node)
WPW first line therapy for symptomatic patients.
asymptomatic WPW.
any recurrent symptomatic paroxysmal supraventricular tachycardia
ablation
risk stratify first with exercise, procainamide challenge is alternative.
ablate
ARVC (RVH, epsilon wave) lifestyle changes
avoid competitive sports and endurance training. Physical activity may accelerate structural progression.
Can play billiards, bowling, cricket, curling, golf, and riflery.
Stable AF+ normal EF+ asymptomatic
rate control is adequate
Brugada unmaskers
Brugada drug treatment
Febrile illnesses, alcohol or cocaine use, procainamide, flecainide, amio
Quinidine for ICD+multiple appropriate shocks or if ICD is not possible
Atrial flutter management
Do not try to rate control. Go to rhythm control. If atypical (h/o atrial surgery, concordant ps)-> cardiovert.
Persistent afib
Longstanding persistent
> 7 days
12 months
Ventricular arrhythmia management
Evaluate for SHD.
If SHD-> ICD
If no SHD-> drug therapy or catheter ablation
WPW Exercise
WPW BB/ valsalva (vagal maneuver)
less apparent because exercise improves AV conduction
More apparent because they worsen AV conduction
most common mechanism of a regular narrow complex tachycardia
AVNRT, then AVRT, then AT
Verap+ dofetilide
Amio+ warfarin
Increased toxicity of dofetilide
Amio increases AC effect of warfarin
ARVC EKG
anterior TWIs, epsilon wave, RVH, RBBB. Even if echo is normal, get MRI if there’s h/o VT.
ARVC VT: beta blockers-> ablation
Torsades mechanism
Early afterdepolarizations
Afib lifestyle changes
Weight loss of ≥10%, treat OSA, treat htn
AVNRT ablation target
posterior slow pathway in Koch’s triangle
Vasovagal syncope
treatment
while standing, positive tilt test.
conservatively: avoid triggers, hydration, salt, and compression stockings-> midodrine if no HTN, HF or urinary retention
LQTS first line
nadolol
ICD only if they fail nadolol even if there’s already syncope
CRT response
Causes of nonresponse
> 90% pacing
AF with RVR, inappropriate device programming, frequent ectopy, loss of LV lead capture or poor LV lead position.
LQTS meds
Avoid all QT prolongers and treat electrolyte abnormalities immediately.
Timolol brady
worsened by paroxetine
Digoxin+ amio
have to decrease digoxin dose, otherwise can cause bidirectional VT. Give digifab.
fascicular VT treatment
verap, cure with ablation
sustained VT in normal heart treatment
beta-blockers, CCB, and catheter ablation are considered first-line therapies
Mixelitine VT
reentry or scar treatment
No ablation for asymptomatic arrhythmias
AC arrhythmia
CV is irrelevant in
AF and AFL
valvular afib, HCM, mechanical valve
When is it only warfarin for AC?
Mechanical valve, HCM, moderate to severe MS
Symptomatic (syncope) 2:1 block=
pacemaker
