Another Guest post from K. Wang: What is the rhythm/conduction problem?

What does this rhythm strip of lead V1 show?

How about choosing from multiple choice?

a) Acceleration AV junctional rhythm with occasional premature atrial beats

b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats

c) Extreme sinus bradycardia (34/m) and AV junctional acceleration and occasional capture beats

d) Extreme sinus bradycardia and complete AV block with AV junctional escape rhythm



Here is a ladder diagram of the rhythm:

Answer: b) NSR and AV junctional acceleration with AV dissociation and occasional capture beats.

Discussion. As diagrammed, P waves from the sinus impulse occur regularly at a rate of 65/m (P1,2,3...etc). The blips pointed by the arrows are not r' of rSr', but sinus P waves, judging from the timing.  If it were an r', then all QRSs would have it.   The primary problem in this patient is AV junctional acceleration. P1 is conducted to R1. P2 was going to be conducted but accelerated junctional beat (R2) occurred sooner than that. P2 and R2 are dissociated because they occur close together during the physiologic refractory periods of each other. R3 is the accelerated junctional beat which failed to conduct to the atria and next sinus P wave is uninterrupted and occurs on time and conducts to the ventricle (R4). And the cycle repeats. 

Thus, there is AV dissociation without any AV block.

The primary problem is junctional acceleration. What is the clinical significance of junctional acceleration? One has to consider digitalis intoxication, myocardial ischemia or infarction, or excess amount of catecholamines circulating which means any stressful condition. Again, a given ECG tracing can be dissected into primary disorder and secondary manifestations and ask what is causing the primary disorder, so that the patient can be treated appropriately, promoting quality patient care.

Widespread ST Elevation. Activate the Cath Lab?

A 40 year old male with several chronic illnesses presented to the ED with decreased level of consciousness and hypotension.  He had an ECG recorded quite early and it was alarming:


When I was shown this ECG a day later, it took me about 1 second to say, "Cool case of Early Repol!"  A cardiologist who had been consulted had the same reaction.  How do we know that this is early repol in all 3 regions (inferior, anterior, lateral)?  That is hard to explain, but you can always use the early repol equation for anterior ST elevation (see sidebar, or the iPhone App "subtleSTEMI").  QRS duration 85 ms and Computerized QTc is 394 ms, STE at 60 ms after the J-point is 4mm, and R-wave amplitude in V4 is at least 22 mm.  Result = 20.85 (less than 23.4 is very unlikely to be an anterior STEMI).

But what about inferior and lateral STEMI?  Is it one or all of the above?   There appears to be ST depression in aVL, but, if you look closely, that is due to wandering baseline.  Without reciprocal ST depression in aVL, it is highly unlikely to be an inferior STEMI.

Certainly a widespread STEMI (anterior, inferior, lateral, from a large wraparound LAD) is consistent with hypotension, so we should not be quick to dismiss this possibility.

How about looking for a previous ECG?  There was an ECG available for comparison from 6 weeks earlier:


Computerized QTc = 359 ms.  This is quite different, and may make you more worried that the findings today are new, especially those that are inferior and lateral.

And another ECG from 4 months earlier was available, which I'm not sure that they saw:


Computerized QTc = 373 ms.  QRS 85 ms.  In this one, the anterior leads have some STE, but not as much as there is today.  And there is none in the inferior or lateral leads.

Not inappropriately, they activated the cath lab.  Then they did a bedside echocardiogram (this is a parasternal short axis view:
 

 (Right Ventricle is on the left, next to the septum, anterior wall is on the top of the image, inferior/posterior wall is at the bottom, and lateral on the right side of the image):

This shows a hyperdynamic heart with all walls functioning perfectly, and is not consistent with infarct.

Many of you are probably thinking "Widespread ST elevation! It must be pericarditis!"  And that is certainly high on the differential.  In my opinion, due to much researching for true pericarditis cases (with objective evidence such as effusion or rub or typical evolution of the ECG), I believe that pericarditis is a very unusual cause of ST elevation, and that benign (normal variant) ST elevation is much more common.

In any case, there is no PR depression anywhere on this ECG.  There was no rub or effusion.

The patient had sepsis and hypovolemia.

1) I do not think hyperkalemia was the etiology of the change.  I might be wrong.  It looks like early repolarization to me
2) Contrary to widespread belief, early repol may come and go; it is not always present in any given individual.  See article by Kambara below.
3) Tachycardia, or stress testing, may diminish the ST elevation of early repol.

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation. Elevations in inferior leads were less than 0.5mm in 18 of 20 cases. Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs.
 

Dr. Smith gives a lecture/workshop live online Sunday April 28 1030-1230 Central Time

Dr. Smith gives a lecture/workshop on subtle ECG findings of patients with "NonSTEMI" who have coronary occlusion. The lecture will be broadcast live online on Sunday April 28, 10:30-12:30 central daylight time, free of charge. Here is the link to watch: http://www.ustream.tv/channel/best-of-hennepin-2013.

This will be lecture format with audience participation (both live and moderated online). These lectures have been very well received. Scott Weingart invited me to give one at Sinai last year. Here is his note from after the lecture:

"The feedback was OUTSTANDING. Aside from some terror induced in the faculty audience members that they had been practicing for years and not knowing these subtle signs.”
Comments include: "best ekg lecture I have ever heard" (this one was repeated countless times)

Dr. Smith Lectures Free Online on Sunday April 28, 1030-1230 Central Time

#FOAMed Dr. Smith gives a lecture/workshop on subtle ECG findings of patients with "NonSTEMI" who have coronary occlusion. The lecture will be broadcast live online on Sunday April 28, 10:30-12:30 central daylight time, free of charge. Here is the link to watch: http://www.ustream.tv/channel/best-of-hennepin-2013

This will be lecture format with audience participation (both live and moderated online).  These lectures have been very well received.  Scott Weingart invited me to give one at Sinai last year.  Here is his note from after the lecture:

"The feedback was OUTSTANDING. Aside from some terror induced in the faculty audience members that they had been practicing for years and not knowing these subtle signs.”

Comments include: "best ekg lecture I have ever heard" (this one was repeated countless times)

What Kind of AV Block is This? Guest Post by Dr. K. Wang (The Rhythm Master), Using a Ladder Diagram

In my residency training and beyond, I learned much from Dr. Kyuhyun Wang (here is his bio) and from his Atlas of Electrocardiography.  It has finally been published for all to obtain.

He is especially talented with rhythms, and a wizard with ladder diagrams.  This is his first guest post.  I will ask him for more in the future.

What kind of AV block is this?

Explanation, with ladder diagram, is below

Question:

            The ECG tracing in Figure 1 shows (choose one from the list below).

a)               Complete AV block with AV junctional escape beats

b)               2:1 AV block with AV junctional escape beats.

Answer:

c)               2:1 AV block with AV junctional escape beats.

Discussion:  Narrow QRS occurs slowly at 37/min.  P-waves occur regularly at 74/min with no fixed relationship to the QRS, suggesting 3° AV block with AV junctional escape rhythm.  However, R3 has a P-wave in front of it (P4) which appears to be conducted from that P-wave.  This question, which is important, can be settled by measuring the R-R intervals, realizing that an A-V junctional rhythm is a very regular rhythm.  R3 occurs 1.4 s after R2 while all other R-R intervals are 1.6 s.  200 ms difference in R-R interval is sufficient and conclusive evidence that R3 is not a junctional beat but conducted from P4, proving that this patient does not have 3° AV block.  What this patient has is 2:1 AV block. 

In a patient with 2:1 AV block, if two P-P intervals are longer than junctional escape interval, the latter will escape just as an electronic demand pacemaker would if programmed to pace at 1.6 s interval.  (We were all born with a demand pacemaker!)   

That is what is happening in this tracing as diagrammed in Figure 2.  R3 is conducted from P4.  The next P-wave (P5) is blocked because this patient cannot conduct at that R-P interval.  The next P-wave (P6) was going to be conducted.  How do I know that?  This patient’s AV junction can conduct at 1.4 s as demonstrated by R3.  R3-P6 interval is certainly longer than that assuring that P6 would have conducted to the ventricles if it weren’t for the junctional escape beat (R4); thus, the diagnosis of 2:1 AV block is securely established.  This repeats again and again.  If, later, a P-wave occurs with a conductible R-P interval which is shorter than AV junctional escape interval (1.6 s in this patient), that P-wave would conduct to the ventricles as P4 did.  These junctional escape beats occur close to sinus P-waves during each other’s refractory period and AV dissociation (not necessarily AV block) results with those beats. 

A given ECG tracing can be dissected into the primary disorder and secondary responses.  AV junctional escape and AV dissociation are all obligatory secondary responses.  Sometimes these secondary manifestations make the tracing look more complicated and eye-catching.

A good example of the same situation was posted at “theheart.org” arrhythmia/EP section “ECG of the month” program in 2/2012.  It generated a lot of heated debate even though it was easier to visualize than this case because a tracing was available when that patient actually was in 2:1 AV block with a faster sinus rate. 

Dr. Smith's Comment:

These two cases (this one and the one on theheart.org is another demonstration of how not every complex that has AV dissociation is demonstrating AV block.  Here is another case posted in June 2011.

Pulmonary Edema, Hypertension, and ST Elevation 2 Days After Stenting for Inferior STEMI

A male in his 40's who had been discharged 6 hours prior after stenting of an inferoposterior STEMI had sudden severe SOB at home 2 hours prior to calling 911.  He had no chest pain.  Medications were aspirin, clopidogrel, metoprolol, and simvastatin.  He was in acute distress from pulmonary edema, with a BP of 180/110, pulse 110.  Here is his prehosptial ECG:

There are inferior Q-waves with ST elevation T-wave inversion.  There is reciprocal ST depression in aVL and I.  There is ST depression in V2 and V3, with biphasic T-waves (down-up).  The computer read is:  *****Acute MI*****

The protocol for prehospital activation in the EMS system that this patient presented to requires 2 elements:

1) Chest pain
2) A computer read of *****Acute MI*****

Only 1 of 2 was present, so there was no prehospital activation.



The patient was transported to the ED.  On arrival, he was hypoxic, with saturations of 92% on room air.  He was in distress, diaphoretic, with signficant work of breathing.  He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema.   Blood pressure was 215/124 and HR 115 (on metoprolol).   Here is his ED ECG:

There is sinus tachycardia.  There are Q-waves in inferior leads, with ST elevation in II, III, and aVF, and reciprocal ST depression in aVL.  There is also ST depression in V2 and V3, now with fully upright T-waves.  Is this acute STEMI?

Of course, papillary muscle rupture and mitral regurgitation should be on the differential here, as in this case, but it is not very likely when the BP is so high.














Is this an acute STEMI?  -- Unlikely!

The prehospital ECG is indeed alarming, and activating the cath lab is certainly not wrong.  The ED ECG is less alarming: acute STEMI generally has an upright T-wave, unless reperfused or reperfusing (analogous to Wellens'), if not through the infarct artery, then through collaterals.  Thus, the absence of an upright T-wave in the leads with ST elevation (or an upright T-wave in leads reciprocal to ST elevation, such as V2 and V3 here) is a strong indicator of an open artery.  In this case, the inferior T-waves are down, and the T-waves that are reciprocal to the posterior leads (recorded in anterior leads) are upright, which suggest reperfusion of both inferior and posterior walls. See this explanation of posterior reperfusion T-waves.

The presence of the Q-waves, and the history of previous MI, are also strong clues that re-occlusion of the infarct-related artery is not the etiology of the symptoms.  Furthermore, the patient has no chest pain (certainly many STEMI do not have chest pain, but it should always make you especially scrutinize the ECG and the clinical situation) and there was severe hypertension.  The hypertension alone is the likely etiology of the pulmonary edema.

So it would be wise to look at the pre-discharge ECG, which was available:

There are Q-waves and ST elevation on this pre-discharge (post-stent) ECG.  The amount of ST elevation and depression is slightly less than on the ECG above, but there is also no tachycardia, which tends to exaggerate ST deviation.

The patient was treated with bilevel positive end expiratory noninvasive ventilation, given 3 sublingual nitroglycerine and started on a nitro drip titrating quickly to 80 mcg/min.  There was immediate relief of dyspnea, and the BP fell to 138 systolic with a pulse of 95 and saturations of 96%.

Before activating the cath lab, it would be useful to obtain another ECG at this point in time, and it is likely to appear very similar to this last one above, in which case the entire clinical presentation could be attributed to to the hypertension/pulmonary edema vicious cycle.

The cath lab was activated.  At angiogram, there was no change in the coronary arteries.  All symptoms were due to a combination of hypertension and fluid overload, and then the vicious cycle of pulmonary edema and SOB causing catecholamine burst, then more HTN and more pulmonary edema, etc.

Inferior LV "aneurysm" morphology


Electrocardiographic "LV Aneurysm" morphology simply means "persistent ST elevation after previous MI."  Not all such ECGs represent anatomic aneurysms (on echo this is "diastolic dyskinesis"), but do generally represent an area of dense akinesis on echocardiogram.  (This patient's previous and repeat echo had dense inferoposterior wall akinesis.)  I have discussed anterior LV aneurysm morphology at length in previous posts (for example, this post), but have not discussed inferior "aneurysm" nearly as much.

First, to be called "aneurysm," the MI must be at least a couple weeks old, so this case does not strictly apply.  Nevertheless, persistent ST elevation immediately after reperfusion is a sign of poor microvascular reperfusion and associated with worse function and higher mortality (and is a more accurate predictor of all kinds of outcomes than is TIMI flow), and also is associated with later persistent ST elevation (but not always).  This patient had had rapid reperfusion of his STEMI 2 days prior (TIMI-3 flow); nevertheless, his troponins rose very high and he had a dense wall motion abnormality.  This is typical of patients whose ST elevation is persistent.

Whereas in anterior "aneurysm," there is virtually always a QS-wave (or only a vestigial r-wave left), in inferior "aneurysm", a QS-wave is relatively less common and a QR-wave is very common.  For this reason, distinguishing acute inferior STEMI from inferior "aneurysm" is significantly more difficult than for anterior "aneurysm."

Nevertheless, in both instances, there are well-formed Q-waves, which is not very common in acute inferior STEMI (though very common in subacute STEMI, which also requires reperfusion therapy).

The patient did very well, and this time was discharged on lisinopril in addition to other medications.