Broad Complex Tachycardias Flashcards
What is the definition of a BCT?
a heart rate >100 bpm and a QRS longer than 120ms
Can be self-terminating <30 seconds, or sustained >30 seconds
BCTs can be ventricular occurring in the myocytes or can be supraventricular occurring in the SAN or AVN
What causes a BCT?
BCTs occur when the ventricular system is not working properly e.g bundle branch block, or the electrical circuit does not involve the AV node properly.
This can happen because of:
1. direct myocardial/conduction tissue damage e.g ischaemia or cardiomyopathy
2. Myocarditis
3. Drugs e.g class 1 antiarrhythmics e.g Fleccanide
4. Ventricular excitation syndromes e.g Wolff Parkinson White syndrome
5. Hyperkalaemia/Hypermagnesaemia
6. Pacemaker-generated
7. Hypothermia
8. Drug toxicities
Why are BCTs dangerous?
They can become ventricular fibrillation and cause sudden cardiac death.
What are the two mechanisms of BCT generation?
- Re-entry circuits
2. Myocardial Automaticity
BCT caused by Re-entry circuits:
Occurs when there are 2 pathways with differing electrical properties-generally in an area of ischaemia or fibrosis where impulses are not conducted properly so are very slow, refraction allows the other faster impulse to travel in a retrograde fashion and sets up a re-entry circuit.
Usually initiated by an extra-systole (ectopic)
Can be micro or macro in scale (can be isolated or involve the whole or a large part of the heart)
*patients with chronic ischaemic heart disease suffering VT are likely to be caused by re-entry circuits set up in scar tissue
BCT caused by Automaticity:
A group of cells from congenital e.g cardiomyopathy or acquired from heart disease e.g ischaemic/fibrosed, that generate their own potentials at a much faster rate than sinus rhythm-generally accelerate but then slow markedly before stopping
What are the two classes of regular BCT?
- Ventricular Tachycardia
2. Supraventricular Tachycardia with Abberrancy
Regular Ventricular Tachycardia:
A ventricular rhythm faster than >100 bpm
Can be sustained >30 seconds, or non-sustained <30 seconds
Originates in the ventricles (re-entry or automaticity) generally in an area of ischaemia or fibrosis
ECG waves are monomorphic and show identical concordant QRS complexes
Regular Supraventricular Tachycardia with Aberrancy:
An abnormally fast heart rhythm >100 bpm originating in the atria that is transmitted to the ventricles
*aberrancy = the intermittent abnormal intraventricular conduction of a supraventricular impulse
What are the two types of SVT with abberrancy that cause BCT?
- Re-entrant mechanism e.g Wolff Parkinson White
2. Bundle branch block causing prolonged QRS
How does Wolff-Parkinson White produce an SVT with Aberrancy BCT?
An abnormal connection (an accessory pathway) exists between the atria and the ventricles.
Can be antegrade (Orthodromic) and retrograde (Antidromic)
IT IS THE ANTIDROMIC TYPE THAT CAUSES BCT
An impulse from the SAN is propagated down the accessory pathway into the ventricles faster than it is propagated through the atria and AVN, so the impulse comes back up the bundle of his and through the AVN in the opposite direction to normal. This is then propagated through the atria and back to the accessory pathway and the whole cycle keeps going.
*This is generally initiated by an extra systole that disturbs refraction patterns e.g by automaticity or re-entry
On ECG shows a wide QRS complex delta wave and P-waves aren’t visible
How does Bundle Branch Block create an SVT with Aberrancy?
An atrial tachycardia e.g AF by automaticity or re-entry, propagates impulses to the ventricles intermittently but wide QRS complexes are created because a bundle branch block SLOWS conduction so contraction of the ventricles is delayed = wide QRS
ECG features of a VT:
Very broad QRS >160ms
AV dissocation (no P-wave preceding every QRS)
Capture beats (SAN transiently captures the QRS in AV dissociation making it look normal when it isn’t)
Fusion Beats (QRS complexes appear to look normal because a normal impulse from the SAN is propagated through the AVN and fuses with an impulse generated by automaticity/re-entry in the ventricles making the QRS complex look normal)
Brugada’s Sign (R to S interval >0.1 secs)
Josephson’s Sign (Small notch at bottom of s wave)
RSR complex with taller LEFT
Concordance of QRS
Absence of BBB morphology
Axis deviation
Risk factors e.g Previous MI
*If an emergency situation it is likely to be VT
ECG features of an SVT with Aberrancy:
QRS complex 120-160ms No AV dissociation No capture beats No fusion beats No brugada's sign No josephson's sign RSR complexes with taller RIGHT No QRS concordance BBB morphology (william and marrow) No axis deviation *Basically the opposite of VT!
Algorithms for Identifying VT or SVT:
Brugada, 1990 (other simpler versions since produced)
But meta analysis of all algorithms showed low specificities and sensitivities so not very useful
Lack of usefulness thought to be due to lack of algorithm proficiency and differing types of BCT compared to original studies
*The use of these algorithms relies on being able to interpret an ECG so requires teaching
