Regular, steady, and fast at 170 (wide or narrow?), hypoxic, crackles in lungs, B-lines, unconscious

A 60-something who lives in a nursing home was found unconscious and hypoxic.

EMS was called and their monitor showed an "SVT" at a rate of 170.  The complexes appeared wide on the EMS monitor.

He arrived in the ED and we saw this on the monitor:

It is an apparently regular tachycardia.  There is an initial wave, analogous to a Q-wave, which makes it appear to be wide complex.  Or is it narrow?

As it was extremely difficult, we could not get any echo views of his heart or even of the IVC.  There were B-lines.

What do you want to do?














There was a suggestion that he be empirically cardioverted.

But what if the patient is in sinus tachycardia?  That would probably not be dangerous, but would certainly not be helpful.

Though clearly critically ill, he was not crashing, and there was time for a 12-lead ECG.

As I was assisting on the case, I considered applying the monitor leads in the Lewis lead configuration, as I had done here:

Wide Complex Tachycardia. What is the Diagnosis?

But I thought that we would have a hard time seeing the P-waves on the monitor as the rate is so fast.

The rate was exactly 170 and never wavered, a feature typical of a re-entrant rhythm.

We could not see his heart or IVC on ultrasound, so could not readily assess volume (why is this important to identify the rhythm?)

Comment:
--If hemodynamic instability is caused by tachydysrhythmia, then it is due to poor cardiac output which will result in backup with high pulmonary pressures, possible pulmonary edema, and consequently high right sided pressures (full IVC).  The LV will generally have a large end diastolic volume but poor stroke volume because of inadequate filling time.
--If volume depletion can be established by ultrasound, then it is likely that the rhythm is sinus and the treatment is volume.  A small hyperdynamic LV, small RV, and flat IVC support sinus tachycardia.
--Of course sinus tachycardia alone could be due to multiple other shock etiologies which can be suspected from POCUS: for instance, large RV with small LV is suggestive of PE, and pericardial tamponade.

Case continued

But we had time for a 12-lead ECG:

What do you think?

This has definite P-waves.  Look at lead V1: there is an up-down biphasic wave that is typical of the P-wave in V1, but distorted by the tachycardia.  Always look for this on ECGs with sinus tachycardia and you will get used the seeing the second part of the P-wave (negative part of the biphasic wave) being very far below the first part because it is superimposed on the downward slope of the preceding T-wave.

Here I have annotated the ECG:

The blue arrow points to the upright part of the P-wave in V1 (the right atrial component) and the red arrow points to the inverted part (the left atrial component).
The left blue line is at the beginning of that P-wave, and the right blue line at the end, and I have extended them down to lead II across the bottom to show that it corresponds to a wave which is consistent with the P-wave in lead II.

This establishes sinus tachycardia.
Do not shock (cardiovert).

(There is also a left anterior fascicular block, with a QRS duration of around 110 ms, with some ST depression)

If this is sinus tachycardia, then the patient is probably very dry.  Why the B-lines?  B-lines may be seen in pneumonia.  The inferior vena cava and heart could not be assessed for volume, but hypovolemia was assumed and fluids were given.

The patient was intubated, and then we placed a transesophageal echo (TEE):


Normally, one sees the left atrium directly apposed to the transducer.  Here we only see the LV, and it is a very small LV cavity, and hyperdynamic.  This confirms volume depletion.

In cases of atrial flutter, a good TEE view of the atrium will show 2 atrial beats for every ventricular beat.  We did not see this.

Fluids were given, Chest X-ray showed a vague infiltrate, and the patient was treated for sepsis and pneumonia. The heart rate gradually fell but only down to 150.

An ECG was recorded some time later:

Here the P-wave in lead II appears quite bizarre.

They do not look like the previous P-waves.

In V1, P-waves are completely negative, but as they are also completely negative in V2, they could be sinus beats with leads placed too high.
This ECG may represent atrial tachycardia 
(not a macro-reentrant tachycardia such as atrial flutter)
There is also an incomplete RBBB and some ST depression.

Atrial tachycardia would explain why the heart rate did not continue to fall with resuscitation.

Later, this ECG was recorded:

Sinus rhythm

Learning Points:

1. You usually have time to obtain a 12-lead ECG before cardioverting.
2. You will be surprised how often a tachycardia is sinus, not a shockable rhythm.
3. Lewis leads may help in identifying P-waves
4. B-lines do not necessarily mean fluid overload; they may also be present in pneumonia, or a false positive.
5. Sometimes sinus tachycardia has a constant unwavering rate
6. Establishing whether filling pressures are high or low helps to determine whether a tachycardia is sinus tachycardia or a tachydysrhythmia
7. Transesophageal echo (TEE) is extremely helpful in resuscitation.


See this case:

A Relatively Narrow Complex Tachycardia at a Rate of 180.

I received a text message with this image: "Cardioversion didn't work.  Any thoughts?" 

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Comment by KEN GRAUER, MD (5/4/2019):

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Excellent post by Dr. Smith. I will simply expand on the 1st and 5th Learning Points. There are many reasons to get a 12-lead ECG during a tachycardia when the patient is hemodynamically stable enough to do so.

• In my experience — there will often be uncertainty from the monitor recording about the fundamental question of whether the QRS complex is wide or narrow. This most important point can be instantly resolved by a hard copy 12-lead recording. I have seen monitor rhythms that look wide but are narrow (as occurred in this case) — as well as monitor rhythms that look narrow but are really wide. IF your patient in tachycardia is hemodynamically stable — Get a 12-lead during tachycardia!
• If you are not certain what the tachyarrhythmia is, but the patient is hemodynamically stable — then doing a 12-lead will allow you to “stall” while looking intelligent as you do so. Practically speaking, by the time you get a 12-lead ECG — the patient will have often spontaneously converted out of the rhythm (making you look good, without having to do anything… ).
• Many clues to the etiology of a tachyarrhythmia may be provided by a hard-copy 12-lead ECG (ie, QRS morphology; frontal plane axis; P wave appearance in other leads) — so it will often become a lot easier to deduce what the rhythm is with the benefit of 11 additional leads.
• That said, sometimes even after conversion to sinus rhythm — you may still not be sure of the etiology of the rhythm. Having a hard copy of the 12-lead during the tachycardia may allow retrospective determination of what the tachyarrhythmia was (ie, ease of comparison between pre- and post-conversion morphology).

Regarding the rate of sinus tachycardia:

• While true that sometimes the rate of sinus tachycardia will temporarily remain constant — often the rate will change as the patient’s condition improves or gets worse. Sometimes the change in rate will be subtle — such that you’ll only notice it if you print out periodic rhythm strips.
• In contrast — the rate of reentry SVT rhythms and atrial flutter are less likely to change unless antiarrhythmic medication is being administered.
• Slight slowing of the rate of sinus tachycardia may sometimes be all that is needed to allow separation of P waves from T waves that were initially hiding them. And sometimes you won't be able to notice these newly emerging P waves — unless you have "hard copy" from 12 different lead pespectives ...