SM 136a - Tachyarrhythmias Flashcards
Pictures and ECGs are taken from Dr. Kim's SM 135a slides
What is the typical history of a patient with Torsades de Pointes?
Young, multiple episodes of syncope due to stress, fright, anger, and/or exercise
What is the most common supraventricular tachycardia?
AVNRT
[Thank you Sasha Becker!]
What causes AVNRT?
Reentry around the AV node, perfect timing of the fast and slow pathways
Which arrhythmia does this ECG show?
Polymorphic Ventricular Tachycardia
Wide QRS complex, beat-to-beat changes, >100 BPM
What are the common causes of Torsades de Pointes?
Things that lengthen the QT interval
- Drug therapy (most common cause)
- Type IA, IC, III anti-arrhythmic drugs
- Phenothiazines
- Tricyclic antidepressants
- Some antibiotics
- Electrolyte disturbance
- Low K+
- Low Mg2+
- Congential long QT syndrome
What are the 3 principle mechanims by which arrhythmias are initiated?
- Automaticity (initiation)
- Enhanced (increased phase 4 slope)
- Abnormal (myocytes do not have phase 4 activity)
- Triggered activity (initiation)
- Increased intracellular Ca2+
- Reentry (propagation)
What are the 3 requirements for generating reentrant arrhythmias?
- Potential for a circuit around an anatomic or functional obstacle
- An area of slow conduction
- A unidirectional block
The result of these 3 factors is premature heartbeats
Which picture represents an AV nodal echo?
C
An initial premature atrial beat conducts through the slow pathway, because the fast pathway is in refractory from the previous beat.
The fast pathway is not in refractory when it is re-joined by the slow pathway. Retrograde conduction occurs up the fast pathway, depolarizing the atrium and causing another premature beat. The slow pathway is still in refractory from the first premature beat, and the fast pathway is in refractory from retrograde conduction, so conduction ends.
Torsades de Pointes is a subest of which arrhythima?
Polymorphic Ventricular Tachycardia
How is Non-Sustained Ventricular Tachycardia defined?
- 3 or more consecutive beats of ventricular origin
- >100 BPM
- Lasts <30 seconds
- Not associated with hemodynamic collapse
What is the typical heart rate of people in AVNRT?
150-180 BPM
Which arrhythmia is shown in this ECG?
Atrial flutter
Regular QRS complexes, sawtooth pattern in between
What are the precipitating factors for atrial fibrillation and atrial flutter?
Any process that dilates the atria
- Valvular disease
- Heart failure
- LV hypertrophy and/or hypertension
- Atrial infartion
- Pericarditis
- Thyroid disease
- Acute pulmonary disease
If no atrial dilation, it is called “lone atrial fibrillation”
What 3 general factors cause the initiation of an arrhythmia?
Substrate: cardic structural abnormality
+
Initiator: Premature atrial or ventricular complexes
+
Other modulating factors: Electrolyte imbalance, metabolic abnormality, sympathetic tone (exercise, emotional stress)
Which picture represents a premature atrial beat?
B, C, D
In B: The fast pathway is in refractory from the previous beat when an initial premature beat comes, so conduction proceeds through the slow pathway. The fast pathway is still in refractory when the signal re-joins the fast pathway, so there is no echo
In C: The premature atrial beat causes an AV nodal Echo. The fast pathway is not in refractory when it is re-joined by the slow pathway. Retrograde conduction occurs up the fast pathway, depolarizing the atrium and causing another premature beat. The slow pathway is still in refractory from the first premature beat, and the fast pathway is in refractory from retrograde conduction, so conduction ends.
In D: The slow pathway is not in refractory when the retrograde fast pathway caues atrial depolarization. The signal propagates through the slow pathway, and triggers another retrograde impulse through the fast pathway when they rejoin. This is AVNRT.
In all cases, there will be a long PR interval after the premature beat due to conduction through the slow pathway
What causes AVRT?
Accessory atrioventricular connection (pathway)
+
AV node
+
Ventricular muscle
Which arrhythmia does this ECG show?
Torsades de Pointes
(Polymorphic Ventricular Tachycardia with a prolonged QT interval)
- Wide QRS complex
- Beat-to-beat changes in QRS morphology
- Prolonged QT interval (>440 ms males, >460 ms females)
(by definition, honestly I can’t tell in this ECG)
Describe antidromic AVRT
Anterograde conduction occurs through the accessory pathway
Retrograde conduction occurs through the AV node
- Less common than orthodromic AVRT
- QRS complex is wide (delta waves present)
- Antegrade conduction is slower because it is cell-to-cell, resulting in slurred QRS compelexes
How is monomorphic ventricular tachycardia treated?
-
Implantable cardioverter defibrillator
- First line
- Antiarrhythmic drugs can be adjunctive
- Do not prevent sudden death
- Can be pro-arrhythmic
- Ablation if VT is recurrent
- Adjunctive to defibrillator
Suppose an ECG shows a patient with a supraventricular tachycardia (SVT).
You notice delta waves. What kind of SVT is this likely to be?
AVRT; delta waves are cauesd by antidromic reentry
What causes Atrial Tachycardia (AT)?
Many potential mechanisms;
May be triggered, automatic, or due to micro-reentry (a small circuit that appears focal
Which picture represents normal sinus rhythm?
A
What is the mechanistic basis behind ventricular tachycardia in patients with structural heart disease?
VT is usually due to reentry in the border zone between infarction and adjacent surviving tissue
Surviving muscle bundles are intermingled with fibrosis, creating a slow conduction pathway. (slower than healthy tissue only)
This sets up a potential circuit and a unidirectional block
What is the “substrate” for initiation of AV re-entry?
Accessory pathways of conducting fibers
Which arrhythmia does this ECG show?
Monomorphic Ventricular Tachycardia
Wide QRS complex, no beat to beat changes, >100 BPM
Define Torsades de Pointes
Polymorphic Ventricular Tacycardia with a long QT interval
- >440 ms in males
- >460 ms in females
What causes atrial fibrillation?
Rapid, focal source that conducts throughtout the atria in a disorganized manner
Either caused by…
- A “Mother Rotor”
- One large functionally reentrant circuit that can wander or give off smaller wavelets
- Multiple wavelets
- Many small reentrant circuits throughout the atria
- Often arising from pulomnary veins: “myocardial sleeve” in the pulmonary vein
What are the common causes of monomorphic Ventricular Tachycardia?
Idiopathic
Structural heart disesae
Describe orthodromic AVRT
Anterograde conduction occurs through the AV node
Retrograde conduction occurs through the accessory pathway
- More common than antidromic AVRT
- QRS complex is narrow (because conduction is through the fast pathway)
Which picture represents AVNRT?
D
- An initial premature atrial beat causes conduction through the slow pathway, because the fast pathway is in refractory from the previous beat
- When the pathways rejoin, the fast pathway is ready (no longer in refractory)
- Depolarization from the slow pathway causes retrograde conduction, depolarizing the atrium and causing another premature atrial depolarization
- The slow pathway is not in refractory when the retrograde fast pathway caues atrial depolarization. The signal propagates through the slow pathway, and triggers another retrograde impulse through the fast pathway when they rejoin.
What are the differences between monomorphic and polymorphic ventricular tachycardia?
-
Monomorphic
- Ventricular tachycardia with a consistent beat-to-beat morphology on ECG
- Same magnitude, shape
- Associated with structural heart disease, or may be idiopathic
- Ventricular tachycardia with a consistent beat-to-beat morphology on ECG
-
Polymorphic
- Ventricular tachycardia with beat-to-beat changes in morphology on ECG
- Different magnitudes, shapes
- May have a long QT (Torsades de Pointes) or normal QT interval
- Ventricular tachycardia with beat-to-beat changes in morphology on ECG
Both will have wide QRS complexes (due to cell to cell conduction after reentrant rhythm)
How is Ventricular Tachycardia (VT) defined?
- Consecutive ventricular beats of a single electrocardiographic morphoogy
- Discrete QRS complexes
- Lasts >30 seconds
- >100 BPM or associated with hemodynamic collapse
- Can be monomorphic (idiopathic or structural heart disease) or polymorphic (Normal or long QT interval)
Which principle mechanisms of reentry are considered “focal sources” of arrhythmia?
These focal sources of arrhythmia both cause problems relating to initiation of action potentials
- Automaticity
- Enhanced or abnormals automaticity
- Triggered activity
- Due to increased intracellular Ca2+
What structural heart diseases are associated with monomorphic ventricular tachycardia?
Cardiomyopathy of any etiology that causes scar deposition. The scar is the substrate for reentrant ventricular tachycardia
(Chronic myocardial infarction, dilated cardiomyopathy, hypertrophic cardiomyopathy, sarcoidosis)
What is the “substrate” for initiation of ventricular tachycardia?
What is the “trigger?”
Substrate: Previous MI, myocyte disarray, or dispersion of refractory times
Trigger: Premature Ventricular Tachycardia
How is Ventricular Fibrillation (VF) defined?
- Chaotic ventricular activation
- No discrete QRS complexes
- >100 BPM
- Does not usually self-terminate
- Associated with hemodynamic collapse and death
- Usually a reentrant tachyarrhythima
What are the 3 major supraventricular tachycardias?
- AV Nodal Reentrant Tachycardia (AVNRT)
- Atrioventricular Reentrant Tachycardia (AVRT)
- Atrial Tachycardia (AT)
Polymorphic VT with a normal QT interval is usually due to _____________
Polymorphic VT with a normal QT interval is usually due to Cardiac Ischemia
What causes atrial flutter?
A macro-reentrant circuit in the right atrium around teh tricuspid valve
-
Typical: Involves the cavotricuspid isthmus
- A band of myocardium between the tricuspid and inferior vena cava
-
Atypical: Does not involve the cavotricuspid isthmus
- Can be anywhere else
- Usually involves scarring from a prior surgery or heart disease
What is the “substrate” for initiation of atrial fibrilation?
Dilated left atrium
What are the possible symptoms of paraoxysmal supraventricular tachycardia (PSVT or SVT)?
None
Heart racing
Chest discomfort
Dyspnea
Syncope
Heart failure
Aborted sudden death
What is the mechanistic basis behind idiopathic ventricular tachycardia?
Structurally normal heart
Usually a triggered rhythm
- Focal
- Usually in a right ventricular outflow tract
- Reentry using purkinje system (usually posterior fascicle)
Describe the ECG manifestations of Atrial Flutter
Atrial rate of 240-350 BPM (slower than fibrillation)
Sawtooth patern between regularly spaced QRS complexes
How can increased intracellular Ca2+ initiate an arrhythmia?
Increased Ca2+ can cause…
- Premature depolarization
- Early in phase 3
- Afterdepolarization
- In phase 4
This can be due to genetic mutations, or some drugs (digitalis)
What is Wolff-Parkinson-White syndrome?
Wolff-Parkinson-White syndrome is a condition in which an individual has an extra atrioventricular pathway
WPW predisposes people to developing AVRT, which can be orthodromic or antidromic
Describe the ECG manifestations of Atrial Fibrillation
Atrial rate >350 BPM
Irregularly irregular: Disorganized and chaotic rhythm
No P-waves
Which arrhythmia does this ECG show?
Ventricular Fibrillation
Wide QRS complex, very irregular
