Showing posts with label SVT with aberrancy. Show all posts
Showing posts with label SVT with aberrancy. Show all posts

Sunday, March 18, 2012

Weak, SOB, "DKA", Chest Pain, and Wide Complex Tachycardia: Is there STEMI?

This case was sent by a reader:

A 60 year old man presented with "DKA," Weakness, Dyspnea, and Chest pain with vomiting.  He denied fever or abdominal pain.

Heart rate was  in 150's, systolic BP in 90's, RR 30's, and pulse oximetry in the 90's.

He "looked gray".  His K was 5.2 and glucose 740 mg/dL.

He was acidotic: pH = 7.00, pCO2 = 25, pO2 of 78.

Here is his initial ECG:

There is a wide complex tachycardia.  If you look at V1, there is a narrow r-wave followed by a deep S-wave, typical of LBBB.  However, there are 4 narrow complex beats interspersed (see black arrows in image below).  Are these capture beats in the midst of VT?  If they were, they should come early, but they do not.  So is it VT or SVT with aberrancy?  That is a tough question.  If it is SVT with aberrancy or sinus with aberrancy, all I can surmise is that most of the time the left bundle is refractory at this fast rate, but in 4 instances it recovered in time to avoid LBBB.  The QRS duration is best seen in V1, where it appears to be only 120 ms. 
There have been a lot of interesting comments  on this ECG.  One is how V2 does not seem to fit between V1 and V3 and may be a misplaced lead.  Another points out the notch in descending limb of V1, which is one of Brugada's criteria for VT of the LBBB morhology type (see Brugada types below).  I am not 100% convinced of VT because of the apparently short QRS at 120 ms and I initially favored sinus with aberrancy and obscured p-waves, but have received some contrary feedback which you can read below in the comments section.  The bottom line is I am not certain if it is VT or not.

Brugada criteria for regular wide complex rhythm:
In Brugada's derivation sample, the sensitivity and specificity were 99% and 97%, but subsequent validation studies have not confirmed this. As an example, Vereckei et al. compared Brugada to his two algorithms and found Brugada's to be 86% accurate compared to 91% accuracy for the two Vereckei algorithms.


1. Is there absence of RS complex in all leads V1-V6? (concordance)
--If yes, then VT
2. Is interval from onset of R-wave to nadir of the S > 100 msec in any precordial leads?
--If yes, then rhythn is VT. If no, step 3
3. Is there AV dissociation?
--If yes, then VT, If no, step 4
4. Are morphology criteria foor VT present (see image below)?
--if yes, then VT.


Here are the Brugada morphologies of VT:



Next you need to determine whether there is ST segment elevation or depression

I have annotated the same ECG here:
The black arrows are the interspersed narrow complex beats.  It is easy to find the onset of the QRS in V1.  From V1, I draw black lines up to demonstrate the onset of the QRS in the other leads.  The red lines are the end of the QRS.  As you can see, there is concordant ST elevation or excessively discordant ST elevation in several leads.  II, III, and aVF have massive excessively discordant STE, diagnosing inferior STEMI.  There is excessively discordant reciprocal ST depression in leads I and aVL, confirming this.  V2 has concordant ST depression, diagnosing posterior STEMI.  V3 through V6 have excessively discordant STE or concordant STE, diagnosing anterior STEMI as well.

How could there be both inferoposterior and anterior STEMI?  There are three possibilities:

1) this is an LAD with a "wraparound" Type III LAD that feeds the inferior wall
2) there is either an LAD or RCA occlusion, but shock is so severe that the other wall has severe demand ischemia with ST elevation.
3) there is no acute thrombotic occlusion, rather there is only severe demand ischemia from shock, extreme tachycardia, and fixed coronary stenoses.

The second ECG was similar but without the few narrow complexes:



Then the patient rolled over, vomited, and became unresponsive.  He was cardioverted, intubated, had a bradycardic arrest, chest compressions, and epinephrine, and was resuscitated.

Some time during this, this ECG was obtained:

The rate is 220 and it is very wide.  This is clearly ventricular tachycardia.

After resuscitation, this ECG was obtained:

Now there is a narrow complex. There is only inferoposterior STEMI now, with additional ST elevation in V4 and ST depression in V5 and V6.  The rate is 164.  It is hard to say whether this is sinus.  The upright p-wave in V1 suggests atrial flutter with 2:1 block and the second flutter wave hidden in the QRS, but it is difficult to correlate that in lead II.


The cath showed a proxima RCA occlusion and severe 3 vessel  disease.  Unfortunately, he expired the next day.


Here is the VT discussion:

Vince D, Mar 18, 2012 02:26 PM


While I'm very tempted to take opinion of Dr. K. Wang as inherently correct, I still get the sense that those are fusion beats of some sort in tracing #1. Here's what's spinning around in my head at the moment:

1)The initial deflection of each narrow complex matches that of its wide brethren, common for fusion.

2) Although it is an extremely regular tachycardia, and it's true that the narrow beats don't arrive early, the complex immediately following a narrow beat is consistently just a little ahead of schedule, with the following beats shifting forward in time accordingly. This suggests that the entire mechanism of the tachycardia is affected by each fusion.

3) There seems to be a relationship between the narrowness of the complexes and how early the next beat arrives. I'm far from an expert at such things, but points 2 and 3 have me leaning towards some sort of re-entry for the underlying mechanism. It's not just a single early beat following the "event" as in enhanced conductivity. I've only looked at a couple of cases of V-Tach with fusion beats, but this pattern seems to match. I haven't taken the time to compare it to other automatic or re-entrant arrhythmias.

4) Although the morphology is a bit different, the QRS axis of the apparent V-Tach in tracing #3 very closely matches tracings 1 and 2 in both the frontal and precordial planes.

5) In most leads with clear R or S waves, they are slow to reach their peak or nadir.

At the beginning of this comment I was very skeptical of the initial tracings being V-Tach and just meant to bring up my a point of dissonance for me. At this point, however, I have a pretty strong suspicion that V-Tach is actually the diagnosis. Thoughts, or am I off-base?


I will note that my initial suspicions revolved around the idea of the narrow beats being the fusion of LV PVCs in the face of a supra-ventricular rhythm with LBBB, but I just couldn't rectify that with the other findings. I especially wanted it to be a parasystolic LV rhythm, but the irregularity of their appearance nixed that idea early.



Reply
Steve Smith, Mar 18, 2012 04:09 PM

Vince, you're not at all off base.

Your arguments are sound and it very well could be VT. I don't think it's a slam dunk either way.

One argument against a rate-related LBBB is that the rate is yet faster in the last ECG, but there is no BBB.

One argument against VT is that you would have to say there are two different VT morphologies in this patient (the first and third EKGs). You thought they are similar morphologies? To me they look very different.

If these are fusion beats, and I understand your arguments in favor, then on all 4 the supraventricualar beat arrives at exactly the same time as the ventricular beat. This is possible but very unusual. It is unusual to see even one fusion beat in VT, much less 4, but then this is in any case an unusual ECG.

I tried applying some of the rules, for instance, Sasaki (not validated, and none of the rules are really excellent):

Step 1: Initial R in aVR?

This means is there a large single (upright) R-wave (not a small r-wave) in aVR. This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.

--If yes, then rhythm is VT. If no, step 2.

Here the answer is NO.

Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?
--If yes, then rhythm is VT. If no, step 3.

Here I get a maximum of 80 ms. So NO.

Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)

--If yes, then it is VT. If no, then it is SVT. "No" here, therefore it is SVT

I see only one lead where there is an initial r- or q-wave of about 40 ms, and that is aVR. So the answer here is also NO.

Then you have to figure in the low pH, which can alter conduction.

In any case, whether VT or not, the STEMI is evident. And when in doubt, shock a fast rhythm in an unstable patient.

Steve Smith



Saturday, October 22, 2011

Wide complex tachycardia in a 36 year old

A 36 year old male presented with palpitations.  He has had these many times for many years, episodes lasting 30-60 minutes, without syncope or pre-syncope.  He has a bit of chest pressure, but is otherwise comfortable.  He has no other medical history and is on no significant medications.
There is a wide complex tachycardia at a rate of 179 bpm.  The QRS duration is 139 ms.  The frontal axis is 180 degrees.



What action do you want to take?  Answer below.


But first:
If this is ventricular tachycardia (VT), is it likely to be a dangerous type?  No.  With no history of any structural heart disease, no syncope or pre-syncope in spite of many prolonged episodes, and no other medical problems, this is unlikely to be a life-threatening dysrhythmia.  This does not mean that it cannot be VT.  Some VT is not life threatening, and most of these are called "idiopathic."   The most well known of these are: 1) posterior fascicular, verapamil sensitive, "idiopathic" VT or 2) right ventricular outflow tract (RVOT, adenosine sensitive) idiopathic VT.  Both of these entities occur in a structurally mostly normal heart with fairly normal ejection fraction.  In terms of danger, they act more like SVT.  Two other more rare types are: idiopathic propranolol-sensitive (automatic) VT (IPVT), catecholaminergic polymorphic VT (CPVT).  See this excellent full text online review.

There are ECG instructors who warn against using adenosine for wide complex tachycardia.  They warn that, if it converts, it might be the adenosine-sensitive VT, and you might discharge to home a patient with a diagnosis of SVT when in reality it is VT.  I do not subscribe to this for three reasons: first, these are comparatively rare; second, these are not dangerous and it is ok to send the patient home; third, because it is wide complex, you will have the patient follow up with a cardiologist. 


Why would any physician give adenosine rather than just sedate and cardiovert?  While most recently trained emergency physicians routinely give propofol for sedation, there are many other physicians who are not so comfortable with it.  For them, cardioversion may not be so safe.

FYI: I posted this case of SVT with aberrancy last month and many readers thought it was RV outflow tract VT.  The reason that RVOT VT was very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive.  In this case, there was an initial Q-wave in inferior leads. I'm sorry I do not have a case (yet) of RVOT VT.

--Best answer: sedate and cardiovert
--Acceptable answer: give adenosine (but it would not work)
--You are brilliant and very sure of yourself: verapamil
               --If you have the diagnosis right (idiopathic VT), this will work.
               --If it is non-idiopathic VT, verapamil is dangerous.


Let's take a close look at this one using Sasaki's system to diagnose wide complex tachycardia:

Step 1: Initial R in aVR?
--This means is there a large single (upright) R-wave (not a small r-wave) in aVR, indicating that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.
--If yes, then rhythm is VT. If no, step 2.  Not here.
 
Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?  See image below.  
--If yes, then rhythm is VT. If no, step 3.  Not here.
 
Step 3: Initial r or q ≥ 40 ms in any lead?
--If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)
--If yes, then it is VT.   If no, then it is SVT.  "No" here, therefore it is SVT

However, this is one of the exceptions.  This is VT that looks like SVT.  Why?  Because this is VT that originates in conducting fibers of the ventricle; therefore, the initial impulse is conducted quickly through conducting fibers, just as in SVT.  So the initial part of the QRS is narrow, and the entire QRS is less than 140 ms (normal VT is usually greater than 140 ms).  Andrade FR et al. [J Cardiovasc Electrophysiol January 1996; 7(1):2-8] found in all their 11 cases of fascicular VT that the QRS duration was 105 to 140 ms, and the RS interval, which in normal VT is more than 100ms, was always less than 80 ms.

In this case, there is a fast depolarization at the initial part of the QRS, just as you would see in SVT with aberrancy.  However, there is also an RBBB morphology and a rapid narrow depolarization towards leads II and aVL, and a subsequent wide depolarization towards inferior lead III, with aVF relatively isoelectric.  The axis is directly to the right.  This is typical of an idiopathic fascicular VT.  The most common form of fascicular VT originates in the left apical inferior septum, corresponding to the posterior fascicle, and therefore has an RBBB morphology with a leftward axis, as in RBBB + left anterior fascicular block.  Less commonly, it originates in the anterior fascicle and has a rightward axis.  So this would appear to be due to the less common variety.  Fascicular VT is apparently due to "false tendons" which are conducting and which can be seen on transesophageal echo.  See this excellent full text article (Thakur RK et al.  Anatomic substrate for idiopathic left ventricular tachycardia. Circulation 1996;93:497-501.)


Further historical information: this patient had been to EDs many times, and received adenosine several times without success.  He had been electrically cardioverted successfully several times.  On this occasion, he was cardioverted, with this subsequent ECG:

Notice T-wave inversions in II, III, aVF and V3-V6.  It is typical for the baseline ECG of patients with idiopathic VT to have some shallow abnormal T-wave inversions like this in inferior and lateral leads.

The patient was diagnosed with verapamil sensitive idiopathic fascicular VT.   He was put on verapamil SR 240 mg per day, and this only partly controlled his symptoms.

Therefore, he underwent an EP study.  This did not show the typical abnormalities one finds in posterior fascicular type (near the septum), but rather possible "false tendons" on the lateral wall.  These were ablated and the patient has had relief from the frequency and severity of palpitations, but not complete.

Here is his baseline ECG after ablation:

Normal ECG, T-wave inversions are gone.



Monday, October 3, 2011

Fusion Beat During Supraventricular Tachycardia: No criterion is absolutely accurate in differentiating wide complex tachycardia

Yesterday, I posted this case of wide complex tachycardia, and some steps to help in differentiating VT from SVT with aberrancy.

One step was this:  
"Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT."  It is generally thought that fusion beats are diagnostic of VT.

This prompted our excellent electrophysiologist, Dr. Rehan Karim, to make the point that no criterion or algorithm can make a certain diagnosis of wide complex tachycardia.  And so he provided me with the interesting tracing below (sorry, no 12-lead because this just happened to occur in the EP lab while they were recording):


There is a wide complex tachycardia; rate was 171.   It was proven at EP study to be SVT.  You can see the RBBB morphology, with rSR' in V1 (green arrow) and a wide S-wave in lateral leads (see lead I, red arrow).   There is a fusion beat (black arrow) which was proven in the EP lab to be due to a PVC occurring in the midst of the SVT!!

Learning point: whatever system or rule you are applying, it is not perfect.  Dr. Karim also wanted to make the point that Brugada's algorithm had very good sensitivity and specificity in the derivation group, but attempts to validate it were not nearly as successful.  This may be just as true for Sasaki's rule. 

Nevertheless, while appreciating the limitations of all algorithms, I like Sasaki's rule because it depends on many of same principles as the other algorithms (principles which, though fallible, are pretty reliable), but is quite a bit simpler to apply.

Saturday, October 1, 2011

Wide Complex Tachycardia: Ventricular Tachycardia or Supraventricular Tachycardia with Aberrancy?

Before we start, here is another popular post on wide complex tachycardia.
What is the ECG rhythm diagnosis?
Wide complex regular tachycardia at a rate of 209, so it is not atrial fibrillation. 

First, in regular wide complex tachycardia: when in doubt, just use electricity, even in stable patients!  Electricity is safer than medications and will work no matter the diagnosis.   A small dose of propofol is adequate for the patient to be amnestic to the cardioversion.

But even if you can manage it, it may be useful to determine the diagnosis:

Which is it?
1) VT 
2) SVT with aberrancy (usually AV nodal reentry tachycardia with aberrancy)
3) AV reciprocating tachycardia [antidromic, up through AV node and down through bypass tract, (AVRT)]4) What can you do if you don't know? (Does it matter?)

4) I should briefly mention idiopathic VT, which occurs in structurally normal (or nearly normal) hearts, and is therefore not as dangerous as standard VT; this includes adenosine-sensitive VT (RV outflow tract, with LBBB morphology, monomorphic R-wave in inferior leads) and verapamil-sensitive VT (posterior fascicle, RBBB morphology).  I will discuss this in a future post.



Here is the clinical data
26 yo male with chest pain and SOB and no history of structural heart disease.  He was not hypotensive or in shock.

A young person with no cardiac history is likely to have SVT, not VT, but let's consider the ECG alone:

When assessing for the rhythm in wide complex regular tachycardia, these are the assessments I make, though no method is foolproof:

1) Look for hidden p-waves before each QRS.  Don't miss sinus rhythm! Not here.
2) If there is a transition from narrow to wide, is the rate the same?  Then it must be SVT.  Not here.
3) QRS duration: VT usually (but not always) has a QRS duration of at least 140 ms.  A prominent exception is fascicular VT.  The longer the QRS, the more likely it is to be VT.  Here it is 155 ms, so it is plenty long for VT.
4) Is there RBBB or LBBB morphology and is the initial part of that BBB narrow?  Then it is very likely to be SVT.  This one has LBBB morphology with a narrow initial R-wave.
5) Do a quick look for obvious fusion beats and AV dissociation.  If found, then VT.   None here.
6) Do a quick look for concordance (all QRS's in the same direction in precordial leads, not the same as concordance when evaluating ST segments in LBBB).  Concordance means there is no RS.  No concordance here: this is easy to see comparing V4 to V6.
7) Finally, because it is easy to apply, I like a new rule better than Brugada's or Vereckei #1 or Vereckei #2 (aVR).  It is Sasaki's rule (Sasaki K.  Circulation 2009; 120:S671), and it had 86% sensitivity and 97% specificity among 107 cases of wide complex tachycardia.  It has not been validated; this is important: remember that Brugada's rule was much better in the initial study than in subsequent validation studies.
 
Step 1: Initial R in aVR?

This means is there a large single (upright) R-wave (not a small r-wave) in aVR.  This indicates that the beats originate and propagate from the apex to the base, so that it must be coming from the ventricle, hence VT.
--If yes, then rhythm is VT. If no, step 2.  Not here.
 
Step 2: In any precordial lead, is the interval from onset of R-wave to the nadir of the S ≥ 100 msec (0.10 sec)?  See image below.  
--If yes, then rhythm is VT. If no, step 3.  Not here.
 
Step 3: Initial r or q ≥ 40 ms in any lead?

If there is, this means that, for the first 40 or more milliseconds, conduction is slow as would occur through myocardium (left ventricle, VT), not through conducting fibers, as would occur in SVT)
--If yes, then it is VT.   If no, then it is SVT.  "No" here, therefore it is SVT


Treat without a diagnosing
If you don't know what to do, you can always use electricity, but you can also give adenosine.  As long as the rhythm is regular, not irregularly irregular (atrial fibrillation), adenosine is safe.   It will usually (safely) convert SVT with aberrancy and AVRT (antidromic reciprocating tachycardia) without harming a patient in VT, and may convert a patient with fascicular VT.

Obviously, synchronized cardioversion should be undertaken if the patient is unstable.

If it is irregular with a wide QRS, it could be WPW, in which case an AV nodal blocker could be life threatening (see this post).

Diagnosis: SVT with aberrancy; it resolved with adenosine.

Added Oct 22, 2011: many readers thought this was RV outflow tract VT.  The reason that RVOT VT is very unlikely is that RVOT starts in the outflow tract and propagates inferiorly; therefore, inferior leads are all positive.  In this case, there is an initial Q-wave in inferior leads.

Here is the post-conversion ECG:
There is slight slurring at the beginning of each QRS, suggestive of delta waves, and the QRS is thus 109 ms (borderline wide).  The PR interval is 138 ms, so WPW is very unlikely.  There is also some ST depression which appears to be secondary to this slightly abnormal QRS, and lends some further credibility to some sort of pre-excitation.

There is no further follow-up at this point.