Tachyarrhythmias Flashcards
non-sustained ventricular tachycardias
≥ 3 consecutive beats of ventricular origin at a rate > 100 beats per minute lasting less than 30 seconds and not associated with hemodynamic collapse
sustained monomorphic ventricular tachycardia
consecutive ventricular beats of a single electrocardiographic morphology lasting greater than 30 seconds with a rate > 100 beats per minute or associated with hemodynamic collapse
ventricular fibrillation
chaotic ventricular activation associated with hemodynamic collapse and death. Most likely a reentrant (functional) tachyarrhythmia
polymorphic ventricular tachycardia
ventricular tachycardia with beat-to-beat changes in morphology on the surface electrocardiographic recordings
drugs that cause torsades de pointes
Type IA, IC, and III antiarrhythmic agents
phenothiazines
tricyclic antidepressants
Certain antibiotics (i.e. pentamidine)
drug combinations (erythromycin or ketoconazole with Seldane)
idiopathic ventricular tachycardia
patients have normal hearts, rarely associated with sudden death
usually a triggered rhythm
can be a reentrant rhythm utilizing the purkinje system
isthmus
a channel that is critical for formation of reentrant rhythms
long QT syndrome
congenital or drug-induced
patients at risk of sudden cardiac death due to polymorphic ventricular tachycardia such as Torsades
mostly due to defects in potassium channels
sodium and calcium have also been implicated
Brugada Syndrome
patients have ST elevation and T wave inversion in leads V1-V3 and an incomplete right bundle branch block pattern
due to sodium channel mutation in the epicardium in the right ventricular outflow tract, allowing for reentry
patients are susceptible to dying from ventricular fibrillation
treatment for ventricular fibrillation and tachycardia
treat underlying condition if reversible
antiarrhythmic drugs
implantable cardioverter defibrillator
tachyarrhythmia mechanisms
abnormality in impulse formation due to abnormal automaticity or triggered activity
abnormality in impulse formation due to reentry
triggered activity
increased calcium leads to afterdepolarizations
if these are large enough, these can cause an action potential to form
focal source arrhythmia
early afterdepolarization (EAD)
occurs in phase 3
delayed afterdepolarization (DAD)
occurs in phase 4
reentry
requires two pathways:
one with slow conduction and rapid recovery
another with fast conduction and prolonged recovery
atrioventricular nodal reentrant tachycardia (AVNRT)
slow pathway and fast pathway in and around the AV node
paroxysmal supraventricular tachycardia
regular, narrow-QRS tachycardia
includes AVNRT, AVRT, and ectopic atrial tachycardia (AT)
**AVNRT is the most common
possible symptoms of SVT
none
heart racing
chest discomfort
dyspnea
syncope
heart failure
aborted sudden death
atrioventricular reentrant tachycardia (AVRT)
uses atrioventricular accessory pathways
muscle bundles that connect the atrium and ventricle across the valves
known as bypass tracts or Kent bundles
congenital but may lose conduction with age
can sometimes be seen as a delta wave
orthodromic vs antidromic tachycardia
orthodromic goes through accessory pathway last
antidromic goes through accessory pathway first
othrodromic is more common
atrial tachycardia
focal tachycardia confined to the atrium
does not require the AV node
can be sustained, paroxysmal, or incessant
mechanisms of atrial tachycardia
triggered, automatic, or micro-reentry (small circuit that appears focal)
atrial fibrillation
most common arrhythmia
appears as disorganized atrial activity usually with an irregularly irregular ventricular response
350-450 depolarizations/min in the atrium
atrial flutter
fixed reentrant circuite around the tricuspid annulus
organized, rapid, and regular atrial rate
often regular ventricular rate
categories of ventricular tachycardia
monomorphic and polymorphic
monomorphic VT
a single consistent QRS morphology
polymorphic VT
morphology changes beat-to-beat between 100 and 300 bpm
setting of a normal QT interval
setting of a long QT interval - Torsade de Pointes
substrates, triggers, and modulating factors of VT
substrate - MI, myofiber disarray, dispersion of refractoriness
triggers - PVCs
modulating factors - electrolyte imbalance, ischemia, autonomic tone
idiopathic ventricular tachycardia
structurally normal hearts
not associated with sudden death
most commonly triggered by focal rhytms
right ventricular outflow tract is an important pathway
reentry using the Purkinje system - usually the posterior fascicle
cardiomyopathies that can cause VT
chronic MI
dilated cardiomyopathy
sarcoid
hypertrophic cardiomyopathy
treatments for VT
implantable cardioverter defibrillator
antiarrhythmics
ablation for reccurent VT
What defines a long QT?
a normal QT is about 1/2 the length of the RR interval
long QT syndrome
can be due to congenital causes because of LQT gene mutations
drugs, electrolyte imbalances, and idiotpathic reasons can also cause long QT syndrome
ventricular fibrillation
primary - non-reversible causes such as cardiomyopathies
secondary - acute MI, ischemia, electrocution, severe electrolyte disturbances, drugs
symptoms and treatments of ventricular fibrillation
symptoms - syncope and sudden death
treatment - treat cause if any, ICD, agents to control recurrences
usually does not self-terminate
mechanism of ventricular fibrillation
depends on substrate
cardiomyopathy - scarring causes reentry
primary electrical abnormalities - functional reentry
