Supraventricular and Ventricular Arrhthmias Flashcards
What are the mechanisms of arrhythmias?
Automaticity due to changes in phase 4 depolarization
Single focus - drug toxicity
Triggered beats - rapid firing at single focus, triggered by beat before = early or late afterdepolarizations during phases 3 or 4, often single focus due to drug toxicity
What are escape beats?
Arise from ectopic focus and occur after pause in heart rhythm
What are the alpha and beta re entry pathways?
Alpha - typically slow conduction, short refractory period
Beta - typically fast conduction, long refractory period
What is the mechanism of symptoms of SVTs?
Degree of symptoms often correlates with HR and underlying cardiac abnormality
Decreased BP due to poor LV filling secondary to rapid rate –> weakness and light headedness
Pounding sensation due to cannon a waves - suggests AV nodal reentry
What is WPW?
EKG has delta wave, short PR interval and prolonged but narrow QRS
accessory pathway connecting atrium and ventricle - an AVRT
Orthodromic - ventricles activated down normal conduction system during tachycardia, no delta wave during tachycardia just at rest
How can you get a normal PR and QRS in WPW without a delta wave?
Premature atrial contraction may result in block in accessory pathway
What is antidromic?
Direction of AV reentry circuit that travels through AV node in opposite direction
AP in WPW activates first
Wide complex even though it is SUPRAventricular - less common
What is the mechanism of AV nodal reentrant tachycardia (AVNRT)?
Both reentrant circuits in AV node - EKG normal at sinus rhythm - looks like just fast pathway, only hints of p waves during tach
Slow and fast AV pathway
Premature atrial beat - fast pathway blocks resulting in prolonged PR from slow pathway
Rhythm continues until conduction block in one of pathways
What does atrial tachycardia result from?
Reentry, automaticity, or triggered activity at distinct atrial focus Paroxysmal or show a warm up in rate Tends to turn on and off Usually 1:1 conduction to ventricles Different p wave from distant site
How can you use the p wave to differentiate between AVRT, AVNRT, and atrial tach?
P after QRS in AVRT
P in QRS in AVNRT (more common)
P before QRS in atrial tach
What is the most frequent type of atrial arrhythmia?
A fib
What is an important target for ablation in a fib?
Triggered activity and reentry originating in or around pulmonary veins
What are the different types of a fib?
Paroxysmal - self initiating and self terminating 7 days and requiring intervention to terminate
Chronic or permanent - accepted as final rhythm
When can atrial fibrillation be dangerous?
Occurring during WPW
In a fib, the accessory pathway causes rapid conduction to ventricles, resulting in low BP, syncope, or death
QRS complex is wide since ventricles activated via AP
= af with RVR (rapid ventricular response)
What are the possible complications of a fib?
Risk of atrial thrombus formation - most commons place for embolism is the brain –> ischemic stroke
When should you treat a fib with aspirin and when with warfarin or neither?
If CHADS score is 0 - treat with aspirin
If CHADS score is 1 - treat with aspirin or warfarin
If CHADS score is at least 2 - treat with warfarin
What are the CHADS score criteria?
CHF - 1 HT - 1 Age at least 75 - 1 Diabetes - 1 Stroke or TIA in past - 2
How are treatment decisions of rate vs rhythm control made in a fib?
Similar outcomes
Depends on symptoms
What can drive a fib?
Hyperthyroidism
Drug or alcohol use
After cardiac surgery
Where does the reentry happen in most a flutter?
Encircling tricuspid annulus
Impulse conducts up septum and down lateral right atrium
What is the main complication and treatment for a flutter?
Atrial thrombus formation
Same treatment as a fib
Which supraventricular tachycardias can be cured with ablation?
Ablate slow pathway in AVNRT or in a flutter has high success
A fib possible but less success
When is a PVC more likely to precipitate a more serious ventricular arrhythmia?
Occurs during ventricular repolarization on a t wave
Particularly in setting of ischemia, MI, with prolonged QT interval
How many PVCs constitute v tach?
3 or more
What can sustained VT lead to?
Hemodynamic collapse, particularly in those with LV dysfunction
What two manifestations of VT allow its identification and diagnosis?
AV dissociation
Fusion beats or capture beats - sometimes SA node can still conduct through to capture some or all of myocardium and you get fused or normal QRS complex
What is outflow tract VT?
Repetitive monomorphic VT due to triggered activity
Originates from right or left outflow tract regions
Inferior axis - positive in leads II, III, and aVF
Typically occurs in setting of structurally normal heart
What different morphologies does RVOT vs LVOT have?
RVOT - right ventricle depolarized firsts looks like LBBB
LVOT - left ventricle depolarized first looks like RBBB
What is outflow tract vt sensitive to?
Adenosine and beta blockers
Treatable with ablation
What is idiopathic left VT?
In normal ventricle due to macro reentrant circuit in LV septum that utilizes part of left fascicle
EKG has right bundle, superior axis morphology
Sensitive to verapamil but give with caution because can cause hemodynamic collapse in other VTs
Doesn’t occur in short bursts and not necessarily with exercise
What is hereditary long QT syndrome?
AD disorder caused by mutations in genes encoding prominent ion channel complexes that control cardiac action potential
Usually in otherwise normal heart
10 gene abnormalities known - prolong phase III repolarization which increases likelihood of triggered activity that can lead to torsades de pointes
Negative genetic test doesn’t rule it out
Typical patient is 15-20 yrs old
What is the EKG appearance of hereditary long QT syndrome?
Different depending on specific gene defect
Broad t wave in lqt1 - events due to exercise, esp swimming
Notching of t wave in lqt2 - events due to changes in arousal level, like waking up suddenly
Peaked t waves in lqt3 - events during rest or sleep
Torsades de pointes look like spiraling around azis
What does therapy for hereditary long QT syndrome include?
Beta blockers in carrier or ICDs in patients with recurrent syncope or resuscitated cardiac arrest
Genotype specific therapy with mexilitine being explored for patients with sodium channel abnormalities
What is brugada syndrome and how is it treated?
Genetic disorder due to premature repolarization - opposite than LQT Abnormality in cardiac sodium channel increased risk for VF usually at night Therapy involves ICD implant Beta blockers may be harmful
What does the EKG of brugada syndrome look like?
St elevation and t wave inversion in v1 and v2 often in setting of RBBB
What drugs are particularly offending agents in development of drug induced LQTS and torsades de pointes?
Class Ia and III antiarrhythmics
Selected antipsychotic and antidepressants
When is VF more common than VT due to abnormal LV function?
In absence of acute ischemic episode when altered channel function due to myocardial ischemia can change cellular refractoriness or automaticity
When is VT more common than VF in LV dysfunction?
Absence of acute ischemia, reentrant VT more common due to reentry within scar due to prior MI
What is the single greatest risk factor for SCD and what are other risk factors?
LV dysfunction with EF<30% is most robust marker
Presence of PVCs and nonsustained VTs increases risk
Survivors have increased risk
What is the SCD paradox?
Individuals with fewer risk factors make up larger position of victims even though risk is low
Makes identifying populations that will benefit from ICD difficult
What is the preferred preventative strategy for SCD in almost all situations?
Implantation of ICD
