What is the rhythm? And is there new left bundle branch block (LBBB)?

A 90 yo with a history of orthostatic hypotension had a near syncopal event followed by chest pain. Chest pain was resolved upon arrival in the ED.

His previous ECG was normal.

Here is his initial ECG:

There is a wide complex regular rhythm at a rate of about 80. What is it? Answer below.

There are no p-waves before each QRS, but there are inverted p-waves aftert the QRS (see arrow).   This is either a junctional rhythm with left bundle branch block, or it is accelerated idioventricular rhythm (AIVR, an automatic rhythm -- not a reentrant one -- initiated in the ventricles and which propagates retrograde and results in retrograde p-waves).  If it initiates in the right ventricle, it will have the appearance of LBBB.  Is there ischemia?  Whether it is AIVR or LBBB, the rule of appropriate discordance applies, so there should be discordant ST elevation in leads V2 and V3, but there is not.  In fact, there may be less than 1 mm of concordant ST depression in lead V3.  But it is not conclusive.  

Idioventricular rhythm is a common "reperfusion arrhythmia."  In other words, after reperfusion therapy for STEMI, the appearance of AIVR is usually a good sign, meaning that the artery is reperfused.

Some would argue that it cannot be "idio" if it conducts to the atria.  But by usage, even these are called AIVR.  It is very important to not try to treat AIVR.  In fact, especially if there is no conduction to the atria, suppression of AIVR may result it asystole.  This is a safe rhythm and usually has reasonable cardiac output, as the ventricles have time to fill.

ECG Diagnosis is either:
1) junctional rhythm with new LBBB, and possibly ischemia
2) accelerated idoventricular rhythm with possible ischemia, and possibly related to restoration of normal perfusion.
3) AV nodal re-entry???? with rate-related LBBB.  Our electrophysiologist, Rehan Karim, states he has ablated AVNR"T" ("T" because it is not tachycardia) in a 90 year old, and that he has seen rate-related BBB at very slow rates.

A repeat ECG had sinus rhythm at a rate of 54 and normal conduction (no LBBB), and was completely  normal with no ischemia.  The second explanation (AIVR), whether as a reperfusion dysrhythmia or not, seems most likely.  The slow sinus rate supports the notion that this could be rate-related BBB. 

The patient had a transient rise in troponin I from 2 values less than 0.012 ng/ml (undetectable) to 0.020 ng/ml (detectable but still below the 99% reference threshold).

Chest pain and possible ischemia were attributed not to ACS, but to transient hypoperfusion from orthostatic hypotension.

So there may have been 1) transient AIVR, or 2) junctional rhythm with transient or rate-related LBBB, or even 3) AVNRT with rate-related LBBB.  Exactly how they relate to ischemia, chest pain, and reperfusion can only be speculated about.

Wide Complex Tachycardia: what is it?

I'm going to show you this one without history.



Rate is 133.  There are no definite p-waves.  The QRS is only 126 ms.  See answer below







When the QRS duration is less than 140 ms, it is more likely SVT. Furthermore, there is a left bundle branch block morphology, supporting SVT.   A rate of 130 - 170 should make you think of atrial flutter with 2:1 block and prompt a search for flutter waves, best seen of course in leads II and V1.   Of course PSVT is also possible.

In this case, the flutter waves are best seen in lead aVR (usually leads II and V1 are easiest.  I have annotated this with lines below.  I found the waves in aVR and drew red lines down to the lead II rhythm strip across the bottom.  Then I can find the same bumps on lead II across the entire ECG and draw black lines up. 

Wide complex?  Left bundle branch block (LBBB), possibly rate related

Here is the obvious atrial flutter rhythm after AV nodal blocking with Diltiazem.

Atrial flutter with variable (3, 4, and 5) to 1 block.  LBBB persists, so it is NOT rate related

Prolonged Chest Pain. Is this LV aneurysm or acute anterior STEMI? Acuteness of STEMI and viable myocardium.

This patient had no significant past medical history.  He presented with chest pain of 48 hours duration which became worse in the previous several hours.  The pain was stabbing and 10/10 and associated with SOB.  The pain was partly relieved with sublingual nitroglycerin.   Here is the initial ECG:

There are QS-waves in leads V1-V3, and a QR in lead V4.  It looks like anterior LV aneurysm.  Is it? Answer below.

In acute STEMI, the T-wave is large, whereas in LV aneurysm, the T-wave is not so large.  How large?  We have made two pretty accurate formulas: (Here is another more detailed post on this)

Rule 1: TV1 + TV2 + TV3 + TV4 divided by QRS V1 + QRS V2+ QRS V3 + QRS V4
If the value is less than 0.22, then it is usually LV aneurysm.  If greater than or equal to 0.22, then acute anterior STEMI.
Applied to this ECG: 4.5 +4 + 3.5 + 4 divided by 20 + 22 + 8.5 + 4 = 16/54.5 = 0.29 (> 0.22 correlates with anterior STEMI)

Rule 2. If there is any one lead of V1-V4 with a T/QRS ratio greater than 0.36, then it is likely to be anterior STEMI.  Applied to this ECG: Lead V4 is 4/4 = 1 (>0.36 correlates with anterior STEMI).

The problem with this method: Almost all of our false negatives (in both the derivation and validation groups) were in patients who had at least 6 hours of pain.  In other words, in a subacute anterior MI there may be well formed QS-waves and the T-wave amplitude diminishes as the infarct progresses.   Therefore, in this patient with 48 hours of symptoms you would be particularly suspicious of a negative result.


He had a previous normal ECG and had no history of MI, so new Q-waves are that much more suspicious for subacute STEMI.
 
Is there benefit to PCI in patients with prolonged symptoms and persistent ST elevation?

Schomig et al. (JAMA 2005;293:2865-72) showed in a randomized trial that such patients who underwent PCI had a smaller left ventricular infarct size than those show did not.

How accurate is time from symptom onset in determining the amount of viable myocardium remaining?  Not very.  In this study of "aborted" STEMI, 11% of patients with a 5 hours symptom onset to PCI time had no significant biomarker elevation.  These patients had a lower mortality than those with more elevated biomarkers, and much lower if they had > 70% ST resolution after artery opening (This ECG marker is the best sign of restored microvascular reperfusion, even better than TIMI flow in the artery).

The ECG may be much better than time since symptom onset at determining viable myocardium and benefit from reperfusion.  There are several papers on the Anderson Wilkins Acuteness score, which uses a complex equation involving measurements of T-waves and Q-waves.  In one such study, the ECG was better than time since symptom onset at measuring the "acuteness" of the infarct.   High T-wave amplitude is associated with higher acuteness (more viable myocardium at risk and more benefit to reperfusion); in contrast, well-formed Q-waves are associated with lower acuteness and with less benefit.  A recent study by Engblom et al. that used pre- and post-reperfusion myocardial imaging to compare ischemic myocardium at risk to final infarct size did not substantiate this, but there are problems with the study, including prolonged time from ECG to tracer injection and with the equation itself, which does not use proportions: T-wave amplitude is absolute and not relative to the QRS.


The cath lab was activated.  His initial troponin I returned at 13 ng/ml, confirming prolonged duration of STEMI.  Angiogram revealed a 100% mid LAD occlusion which was stented.

Diagnosis: Subacute STEMI from LAD occlusion

New LBBB after Cardiac Arrest

An elderly man with a history of DM and renal failure had a complaint of back pain, and called 911.  En route, he had a seizure, then lost pulses.  No rhythm was recorded, but he was resuscitated with chest compressions, epi and atropine. Here is his first ECG:

An old ECG had LVH; a different one had IVCD, but there was no LBBB.

First ECG at 1507:

There is sinus with new LBBB.  There is no concordant ST elevation.  There is proportionally excessively discordant ST elevation, or nearly so, in lead V2 (see enlargement below), with a ratio of 4.5/20 = 0.225.  Depending on whether the cutoff is 0.20 or 0.25 (and this does vary in my research), this might represent LAD occlusion.

Excessively discordant ST elevation?  Very suspicious in lead V2.  

The T-wave in V5 is concordant, but this is nonspecific.  

There is a fragmented or notched QRS on the upstroke of the QRS in lead V3, which may be a sign of old infarction.  
This is to be distinguished from Cabrera's sign, which is a notch on the upstroke of the QRS in leads V3-V5.  
There is absence of an r-wave in V4, with fragmentation of the downstroke of the QS-wave.

 

There are often ST abnormalities after cardiac arrest, usually ST depression.   In the setting of post cardiac arrest, when an ECG is not clearly diagnostic, I always recommend waiting 10-15 minutes for a repeat ECG to see if the findings resolve.

Also, the K was 6.0, and one must entertain the possibility that hyperkalemia is causing this apparent new LBBB, possibly with ST changes. 

At 1502, this was recorded.  There had been no therapy for hyperkalemia:

There is less ST elevation, and more of a normal LBBB, though still with a fragmented QRS.

This ECG was recorded at 1922:

There is yet more resolution

There was no wall motion abnormality.  The peak troponin was only 0.064 ng/ml (99% reference = 0.034), so this was barely elevated, consistent with cardiac arrest but it would be highly unusual to be this low even in a transient STEMI.  But not impossible.

Also, there was no wall motion abnormality the next day.  Of course, with transient STEMI, there might not be any WMA.

I can't prove there was not a transient LAD occlusion.  There might have been.  No cause of the arrest was found.  No cath was done.

Learning point:

1) Post cardiac arrest, the ECG may have transient ST abnormalities.

Peer Reviewed Lecture: ECG Diagnosis of STEMI-equivalent in Left Bundle Branch Block (20 minutes)

This is a lecture for the journal Academic Emergency Medicine, which now publishes lectures that have been peer-reviewed. This is the second one they have published. Thanks to the publisher Wiley Blackwell for making this free to the public. It will also be on the front page of the journal at www.aemj.org

ECG Diagnosis of Acute STEMI-Equivalent in the Presence of Left Bundle Branch Block from Academic Emergency Medicine on Vimeo.

What is the Diagnosis?

A 60 yo woman presented with CP and troponin I of 0.85 ng/ml.

There is RBBB, but without the usual rSR' in right precordial leads.  [There is some left axis deviation as well, probably a left anterior fascicular (hemi-) block.]  The initial r-wave is gone, so that there are QR-waves (diagnostic of myocardial infarction, whether old or acute).  There is ST elevation (which is never normal in RBBB).  The negative T-wave makes it very unlikely that this acute MI, but it could be either subacute or old. 






My interpretation was RBBB with old anterior MI and LV aneurysm.  We admitted her treated her for NonSTEMI.

Subsequent course:

There was no ECG evolution.  Echo showed decreased left ventricular systolic performance, at least moderate, with an estimated EF = 35 - 40%.  There was a regional wall motion abnormality in the LAD distribution: distal septum, anterior and apex, large and the wall was "akinetic or possibly dyskinetic," confirming LV aneurysm.  There was also a left ventricular apical thrombus, which is a frequent complication of aneurysms. 

She was treated medically for her NonSTEMI and LV thrombus.

Here is a very detailed discussion of RBBB with LV aneurysm, with several ECGs.

Lecture: Acid Base Disorders (Sorry, no ECGs!) -- 50 minutes

Inferior Dynamic T-waves

A 51 yo healthy male had been lifting 5 lb. weights, then went to shower when, at 0800, he developed severe crushing 10/10 left sided chest pain radiating to his left arm that lasted 3 minutes and then mostly, but not completely, subsided.  He had SOB and diaphoresis. He went to his clinic and they sent him to the ED.  Exam and vital signs were normal.  Here is his baseline ECG from 2 years prior:

Normal.  Small normal Q-wave in lead III.

He had this ECG recorded at 0819:

The QRS and T-wave in III are now upright and the T-wave in aVL is flattened

His initial troponin was normal.  He continued to have some chest discomfort, and underwent this ECG at 1024. 

There is now a prominent Q-wave in lead III with a biphasic T-wave

This was not appreciated, and the patient was set up for a CT coronary angiogram.


The CT results returned hours later showing severe stenosis of both the RCA and LAD.  After this, a repeat troponin I returned at 0.51 ng/ml.

The T-wave in lead III is fully inverted now.

 Here is a right-sided ECG at 1728.  V1(R) = normal V2.  V2(R) = normal V1

There are further dynamic changes in leads III and aVL.  The T-wave in V1(R) [V2] is very large, with ST elevation, suggesting RV MI.

Subsequently, the patient was treated maximally for NonSTEMI, but developed several episodes of bradycardia, hypotension, and chest pain that was not controlled medically.  No ECG ever showed ST elevation or hyperacute T-waves.

Here is the succession of ECGs, side by side, with recording times.  aVL is on top, lead III on the bottom:

Ever changing T-waves

The patient was taken to the cath lab and had a 99% mid-RCA with enough flow to prevent large infarct.  [The STE and large T-wave in V1(R) is not explained by this.]  It was opened and stented.  The LAD would be fixed later.

Peak cTnI was 15 ng/ml.  There was an inferior wall motion abnormality.  The patient did well.

Learning points:

1. Serial ECGs are very important
2. New biphasic T-waves are quite specific for ischemia.  These are Wellens' waves of the inferior wall.
3. Hemodynamic instability in due to ACS is an indication for immediate angiography and PCI if indicated.