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
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
Which arrhythmia does this ECG show?
Monomorphic Ventricular Tachycardia
Wide QRS complex, no beat to beat changes, >100 BPM
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.
Which arrhythmia does this ECG show?
Ventricular Fibrillation
Wide QRS complex, very irregular
