Why VTs have wide QRS complex?
Brief answer: VT usually presents with wide QRS tachycardia because it originates in ventricular myocardium, travels muscle to muscle instead of the normal conduction system. However, VTs need not be wide always, if it captures the conduction system early and more proximally it can be as narrow as SVT.
Further reading: Only for cardiology fellows
Two empirical statements are made here. (The scientific chances of both being reasonably correct are fair)
- 80 % of wide QRS tachycardia by default is VT. That means 20 % of wide QRS is not VT. We all accept that.
- 80 % of narrow QRS tachycardia is SVT. It may also mean, up to 20 % of VT can be narrow QRS.
It’s obvious, not all VTs are dramatically wide. When it is not wide, they test our knowledge and patience. Let us be clear about the factors that determine the QRS width during VT. Once we know this we can have our own inference.
What determines the width of QRS in VT?
1.Origin of VT
The focus of origin is extremely important. Pure myocardial focus distal to the conduction system is invariably very wide. We know VTs originating right over the fascicles are narrow.
2.His Purkinje breakthrough
The time taken to capture the normal septal conduction system is a critical determinant of QRS width during VT.This makes the VT from septal origin narrower.VT arising from the free walls obviously takes a longer time to engage the HIS Purkinje system. Imagine , If VT originates from the lateral mitral annulus, how much time it may take to reach RV free wall and lastly RVOT. Here the VT will become bizarrely wide.
3.The structural integrity of His Purkinje
It is important to emphasize a fact , even if the VT captures HIS Purkinje early, if they are diseased , still the VT will be wider.(Example bundle branch reentry in DCM in which VT keeps going around the conduction system still, it’s wider)
4.Course
Length of the re-entrant circuit. Macro reentry is expected to be wider. Focal or micro reentry will often be narrow, provided the distal circuit is not diseased.
5. Scars as barriers and boulders
If the VT circuit is interrupted by random scars en-route (from origin to exit) the VT width prolongs. (Evidence for scars is often visible in sinus rhythm ECG as notches /slurs or fragmentations in QRS )
6.Exit point of VT
This is a poorly understood term (at least for me) It is believed, VT can exit only epicardially. The line joining the focus of origin and the exit point is expected to decide the QRS axis. The problem comes when VT breaks out multiple paths and possibly sub-endocardial as well.
7.LV dysfunction
A severely dysfunctional ventricle can stretch the QRS irrespective of conduction system integrity.
8.The Ionic milieu of cells Interstitial resistance
We know, biological current is nothing but Ions in motion. So, no surprise it can alter the QRS morphology. The classical example is hyperkalemia , that can make ECG a wide and blunt sine wave. Local acidosis, hypoxia also influence the QRS duration.
9.Drugs
Any drug which has class 1C or 3 properties can slow the VT circuit velocity. Typically flecainide is well known to make QRS wider. Amiodarone may reduce the ventricular rate. in VT instead of reverting it. Apart from this these drugs depress the ventricular myocardium severely and prolong the QRS width independent to its action on the conduction system.
10.Mechanism of changing width
VTs can have varying QRS width as reentrant circuits change or experience slow conduction due to autonomic influences. VT with downstream aberrancy is also possible as the VT rate by itself influences the conduction property distally.(Just lie SVT with aberrancy)
A paradox about the width of QRS in VT
A curious phenomenon is often seen, when VT occurs in patients with baseline ECG which is already wide (As in an ischemic dilated cardiomyopathy with LBBB/RBBB). Here, the VT prematurely stimulates viable muscles distal to the diseased HIS Purkinje system (Which they are deprived of early activation of till then) .They seem to relish the early arrival of electrical impulse by brisk activation that converts wide QRS complex to narrow one. (This behavior is one of the principles of cardiac resynchronization therapy where we attempt to rewire the heart with multiple leads and shrink the QRS.)
*One more mechanism of wide QRS sinus rhythm becoming narrow during VT is due to a concept called source -sink relationship. The VT delivers enough energy overcoming His Purkinje resistance downstream. (This property is used in HIS bundle pacing )
Postamble
*Forget about wide vs narrow QRS debate. A significant chunk of VTs falls within intermediate width QRS(100-120ms) . Whether to label these as wide or narrow QRS squarely lies on whims of the reader. (Should we take the widest QRS in 12 lead ECG? Pre-cardial vs limb lead etc are not clear) Unfortunately, we don’t have a separate algorithm for this category. This issue demands a separate discussion.
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