Monday, June 6, 2016

Dyspnea, Right Bundle Branch block, and ST elevation

An elderly male called 911 for acute onset of shortness of breath and vomiting.  EMS found him with a heart rate as high as 180 and hypoxic with O2 saturations in the 80's.

A prehospital 12-lead was obtained:
There is atrial fibrillation (irregularly irregular, no P-waves) with a rapid ventricular response.
There is right bundle branch block (RBBB).
There is ST elevation in V2-V5.
Is this acute STEMI??

On arrival in the ED, the patient had this ECG recorded:
Atrial fibrillation with RVR.
ST Elevation in V2-V5.
Is this acute STEMI?

Note the well-formed Q-waves in the leads with ST elevation!  This suggests old MI.

Comment: Old MI with persistent ST elevation, otherwise known as "LV aneurysm" morphology, usually has QS-waves (deep S-wave without a subsequent R-wave).  But RBBB alters the sequence of ventricular activation such that the wave of depolarization ends by going to the right.  Thus, an R-wave which would otherwise be absent is present in right precordial leads.

Normally, RBBB has rSR'.  But with old infarction, the initial r-wave is obliterated and one is left with a QR.  This can occur in acute STEMI with RBBB, but should raise the suspicion for LV aneurysm.

Let's look at a second instructive case in which the patient alternated between RBBB and normal conduction:
Note classic anterior LV aneurysm morphology (QS-waves in V1-V3 with ST elevation).  There is ST elevation, but the T/QRS ratio is less than 0.36 in all of leads V1-V4, indicating that it is not acute STEMI.
I derived and validated this rule.

The patient with the above ECG presented twice with chest pain and RBBB, with this ECG:
There is ST elevation in V1-V4 without the deep QS-waves.
But there is RBBB.  The patient has an intermittent, possibly rate-related, RBBB.
This fools you into thinking that there is no ECG aneurysm morphology.
However, the typical aneurysm morphology is transformed by the RBBB!!
This patient received inadvertant thrombolytic therapy twice because this morphology was not understood. Neither time was it an acute MI.  

Back to the first case:

The patient's record was available.  It revealed that the patient had a known LV aneurysm with this ECG 4 months prior:
Same, except there is a slower ventricular response.

The Previous Echo
--Left ventricular ejection fraction is 29%
--Decreased left ventricular systolic performance, severe.
--Regional wall motion abnormality-distal septum anterior and apex diastolic
distortion with dyskinesis (aneurysm) large.
--Regional wall motion abnormality-distal inferior wall akinetic (part of LV
--No evidence for left ventricular thrombus

Further history revealed that he had nausea and vomiting earlier in the day and that he might be dehydrated. His inferior vena cava was "collapsing" on ultrasound (this is not always reliable).  On the other hand, there were B-lines and reported pulmonary edema on CXR.  The ejection fraction on bedside ultrasound was consistent with the previous echo.

On history, he claimed to have been taking his chronic AV nodal blockers for atrial fib.

Exam revealed lower extremity cellulitis, but there was no fever.

Thus, the clinical picture was confusing.  A Diltiazem drip was started, with some improvement but a fall in blood pressure.

The ultimate interpretation of the data was that some dehydration and sepsis had led to high adrenergic state and rapid ventricular response, which led to decreased ventricular filling and, paradoxically, pulmonary edema.

He improved greatly with both fluids and diltiazem.

There was no acute coronary syndrome.

Troponin I peaked at 0.829 ng/mL (consistent with demand ischemia and type 2 MI).

Learning Points:

1. LV Aneurysm can mimic acute STEMI
2. RBBB distorts the ECG of LV aneurysm morphology, further mimicking acute STEMI.
3. Most Atrial Fib with RVR is due to acute disease superimposed upon chronic atrial fib
4. Management of fluid status and rate control in chronic atrial fib can be very complex.\


  1. As usual,... a Great case!

    Week after Week i learn a lot with your cases and share them with my students and collegues!

    Thank you again!

    Viva la #FOAMed!

  2. PART 1 — Highly illustrative case for showing distinction between ECG changes of acute vs old infarction with likely LV aneurysm.

    One key for appreciating ECG changes that may or may not be seen in association with BBB (Bundle Branch Block) — is to remember that under normal circumstances, after the impulse arrives at the AV node, it first travels down the LEFT side of the septum. As a result — septal depolarization normally travels from left-to-right. Left sided leads (ie, leads I,aVL; V4,5,6) therefore often see the initial vector of ventricular depolarization as moving away (as the septum is depolarized from left-to-right). This is the reason it is so common to normally see small and narrow “septal” q waves in one or more of the lateral leads.

    Since the RBB (right bundle branch) travels down the RIGHT side of the septum — this initial vector of ventricular depolarization is not altered with RBBB. As a result, small lateral q waves not indicative of infarction may still be seen with RBBB. And, since Q waves are written during the 1st part of writing the QRS complex — you CAN (and generally do) see infarction Q waves when there is RBBB.

    In contrast, with LBBB — the initial vector of ventricular depolarization IS altered — because the LBB (left bundle branch) travels down the left side of the septum where initial depolarization of the ventricles normally begins. As a result — when there is LBBB, septal depolarization will have to occur from right-to-left. This means that you should no longer see “normal septal q waves”. In fact, seeing a Q wave in any lateral lead in association with LBBB strongly suggests septal infarction has occurred at some point in time. In addition, since LBBB alters the direction of initial ventricular depolarization (and that is the time when Q waves are written) — inferior Q waves are generally not seen with LBBB, and anterior Q waves (or QS complexes) may be misinterpreted, since LBBB itself may produce anterior QS complexes.

  3. PART 2: With that as a background — it becomes much easier to interpret the insightful tracings presented in this Blog post. Commenting on the 2nd tracing from the ED (since this high quality red background ECG is far easier to interpret than the 1st B&W ECG) — there are exceedingly wide and deep Q waves in leads V2-thru-V6 in association with complete RBBB. This is diagnostic of extensive prior infarction. Q waves this deep and wide and diffuse do not develop over minutes or hours. More than just Q waves — there is LOSS of r wave as one progresses from lead V1 (which shows an rSR’ complex) to V2 (which shows a QR complex, but no longer the characteristic small initial r wave of RBBB). Loss of anterior r wave (when not due to lead misplacement) is a specific sign for prior infarction. Finally, there should be no doubt that the wide and deep lateral chest lead Q waves are not “normal septal q waves”, but definite infarction Q waves. Even without use of Dr. Smith’s clinically derived formula — it should be obvious that the relatively minimal amount of anterior ST elevation pales compared to the size of precordial lead Q waves (especially in the absence of reciprocal ST depression in inferior leads). This 2nd ECG is not the picture of acute anterior STEMI.

    The 3rd and 4th ECGs are fascinating. As per Dr. Smith — the faster ventricular rate in the 4th ECG supports this being a rate-related RBBB. Remembering the concepts I derived above — the initial vector of ventricular depolarization with RBBB is IDENTICAL to the normal initial vector. RBBB is a “terminal delay” — in which the QRS abnormality of tall R’ in lead V1 and wide terminal S waves in lateral leads develops AFTER a normal initial depolarization vector. Compare the 3rd and 4th ECGs, going lead-by-lead. In each of the 12 leads — the initial part of the QRS in the 3rd ECG is IDENTICAL to the initial part of the QRS after RBBB develops in the 4th ECG. So the anterior QS complexes we see in V1,2,3 in the 3rd ECG remain as Q waves after RBBB develops. The fascinating part is how much the ST-T waves in precordial leads changes once RBBB develops, mimicking a stemi. That said — once again, the exceedingly wide precordial Q wave in association with RBBB should make one suspicious that all that is seen may simply reflect old injury with LV aneurysm in the setting of rate-related RBBB.

    THANKS to Dr. Smith for presenting this highly insightful case!

  4. Great case and ECG again, Dr Smith.

    My point would be this time more around the choice of diltiazem for treatment of acute HF in the context of low EF in this patient.

    In one of our courses ( we had a big discussion around the issue of using CCB for those patients. In one Quebec's city, it seems that the general teaching suggests CCB at first place for HF with low EF (< 40%). Which is not my practice and not what I teach. I must also confess I use more BB, considering that most of our patients also have CAD or HF. But I would be very reluctant to us CCB in such a patient.

    We then reviewed actual literature around this specific point and consulted HF specialists, to convince ourselves that the choice NIT to use CCB is supported, as we thought. We then gave back our references to the people who came to our course. But then, you published your case (and we already told our crowd that you never fail :-).

    So I would be very interested to have you comment on this specific aspect. Here's our references.

    Canadian cardiovascular society, in his 2010 ED AF guidelines, in the section about IV meds for rate control, said, « CCB should not be used in patients with HF or LV dysfunction. »

    AHA Afib 2014 is less clear, but said that « either a BB or nondihydropyridine CCB is recommended for patients with persistent or permanent AF and compensated HF with preserved EF »

    And finally, HF EsCardio 2016 said in its guidelines that « CCB are not indicated for the treatment of patients with HF and low EF. » In the acute section table, CCB isn't mentioned as a choice for acute HF, BB is 1A for patients in class I-III and Digox / IV Amio is Iia.

    So, I would be very pleased to hear you more on this question.


    Alain Vadeboncoeur MD

    1. Alain,
      The data and recommendations are all based on literature on chronic rate control, not acute ED rate control. What little literature there is, and I have reviewed it, is inconclusive about BB vs. CCB.
      Some of our faculty like dilt, some esmolol. We cannot detect a difference is adverse events between the two.
      I still use digoxin if neither BB nor CCB seem safe, or if either leads to adverse events.
      Most important is that the vast majority of these patients need no chemical rate control at all; they need treatment of the underlyihng illness which led to excessive catecholamines and excessive rate: dehydration hemorrhage, hypoxia, sepsis, etc.

  5. Smith sir,
    Your cases are very fascinating, sir can u elaborate more about t/qrs significance in st elevation mi

    1. T/QRS ratio is higher the more acute is the STEMI. Large upright (hyperacute) T-waves correlate with size of myocardium at risk and with viability. So a large, early STEMI with lots of viable myocardium (reperfusion is particularly beneficial!) has, on average, proportionally larger T-waves and higher T/QRS ratio.
      Steve Smith


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