Incomplete LBBB, posterior STEMI, posterior leads, in a snowstorm

A 76 yo male had Chest Pain followed by a cardiac arrest. He was resuscitated in the field, and had hypotension annd electrical storm in the ED.


There is a QRS duration of 120 ms, with a wide R-wave in lateral leads (but also a Q-wave). This is either an incomplete LBBB or a very wide left anterior fascicular block. There is concordant ST depression in precordial leads.
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Posterior leads were applied (V4=V7, V5=V8, V6=V9) for the following ECG:

There is now clearly concordant ST elevation. Whether LBBB or not, ST elevation of 0.5 mm or more in just one lead is enough for the diagnosis of posterior STEMI.

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Electrical storm continued, with 8 defibrillations.

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Unfortunately, there was a storm outside, too. A huge snowstorm, and the cath lab personnel could not get to the ED fast enough.

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Tissue plasminogen activator was given and 30 minutes later the patient stabilized with a BP of 130/70. Echo showed a posterolateral wall motion abnormality. Later cath showed 3-vessel disease but the exact culprit could not be established. The troponin I peaked at 40 ng/ml.

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Unfortunately, in spite of therapeutic hypothermia, the patient died of cerebral anoxia.

LAD occlusion in the setting of paced rhythm

An 80 yo male presented with chest pain.


There is clearly a ventricular paced rhythm. Normally in a paced rhythm, the QRS is all negative from V1-V6 because the pacing wire is in the apex of the RV and thus all depolarization goes away from the apex.
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In the above ECG, the QRS in V2 is positive and all others are negative, as in the patient's previous ECG below. This implies some problem with lead placement. Nevertheless, leads V1, V3, and V4 have excessively discordant ST segments.
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Though there is not a lot of data to support it, the ratio used for left bundle branch block seem to be applicable to paced rhythm. An ST/S ratio in V1-V4 > 0.20 is, I believe, quite specific for LAD occlusion. V2, though suspect because of the positive QRS, has a concordant ST segment, which is diagnostic of STEMI.

Previous ECG 2 months prior:


The emergency physician needed to do some persuasion with the interventionalist, but succeeded and the patient was taken for angiography and PCI of a 100% LAD occlusion.

This is the ECG 2 days later:



This is a much more difficult ECG because only complexes 4 and 5 are paced now. The precordial leads have an RBBB morpholoyg, with some minimal persistent ST elevation in v2 and V3 with T-wave inversion, suggestive of reperfusion.

Ischemic symptoms and a paced ECG with excessive discordance in V1-V4, with ST/S ratio > 0.20, is anterior STEMI until proven otherwise.

Weakness due to Bradycardia 2nd Degree Sinoatrial block, with Ashmann's phenomenon

A 68 yo female with a history of HTN on metoprolol and of paroxysmal atrial fib presented with weakness. This is her ECG.

There is sinus bradycardia at a rate of about 55, with a p-wave every 1.05 seconds. There are 2 dropped p-waves. The succeeding p-wave in each case is exactly 2.1 seconds later. This means that the sinus node continues to depolarize and do its pacemaking job every 1.05 seconds, but that occasionally that signal fails to leave the sinus node and get to the atrium where it would depolarize the atrium resulting in a p-wave.

Notice that the p-wave that comes directly after the 8th QRS conducts, but the one that comes after the 4th QRS does not.  This is Ashmann's phenomenon: the refractory period of a beat is longer when the preceding R-R interval is longer.  In this tracing, it is not obvious (you must measure it), but the R-R inverval between R-waves 3 and 4 is longer than the R-R between R-waves 7 and 8.

She was also found to be hypothyroid.

This is sino-atrial exit block. The sinus node fires but it does not escape. The combination of bradycardia (exacerbated by metoprolol), with paroxysmal atrial fib and sino-atrial block are typical of sick sinus syndrome. It will inevitably progress to the point where a pacemaker will be necessary.

Cardiac Arrest, hypotension, tachycardia

A 65 yo woman had felt ill for 36 hours, had seen her MD but without undergoing a cardiac evaluation. She collapsed and 911 was called; she was found pulseless. After epinephrine, atropine, and defibrillation x 2, there was a return of pulses. Exact rhythm during arrest is uncertain. The patient presented with a bp of 90/60 and heart rate of 140. Here is the initial ECG:
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There is sinus tach with PACs. The axis is vertical and down, and is suggestive of left posterior fascicular block (small r in aVL followed by deep S-wave). There is ST depression in II, III, and aVF that is concerning for reciprocal depression from high lateral STEMI in aVL, where there is some ST elevation. There is also ST depression in precordial leads, greatest in V3 and V4, concerning for posterior STEMI. However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia.
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Arguing for posterior STEMI are two things: 1) precordial ST depression is not pronounced in V5 and V6; 2) T waves are inverted away from the ST segment deviation in aVL (down) and in II, III, aVF (up) and in V3 and V4. This is all highly suggestive of posterolateral STEMI that is either subacute or reperfused, but not very acute (in the acute phase, T-waves are upright with the ST elevation).
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Everything is complicated by the arrest and hypotension: Is the ischemia caused by the instability, or the instability caused by the ischemia? What was the inciting factor?
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The diagnosis is in doubt.
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Thus, a bedside echo was performed by the emergency physician and is shown 30 seconds into this video:

65 yo F witnessed arrest from hqmeded.com on Vimeo.
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For those who haven't watched the video, it shows pericardial clot, consistent with myocardial rupture. The patient was taken to the OR by cardiovascular surgery and found to have a necrotic lateral wall with a ventricular leak. The patient died is spite of resuscitative efforts.
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Myocardial rupture is not uncommon. It is found on 1% to 3.5% of autopsies of patients who died of MI. It is associated with transmural MI; since most STEMI are aborted with reperfusion therapy, it is not as common as it once was. It is more common in women, and in patients who have a first MI and have a good EF, as it requires a pump force from the healthy myocardium to produce high pressure which ruptures the infarcted myocardium. The "rupture" is not an explosion, rather a small tract through the myocardium which leaks blood into the pericardium, and kills by tamponade.
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Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP). PIRP is indicated on the ECG by 2 findings: 1) persistenly positive (upright) T-waves at 48 hours, or 2) premature reversal of inverted T-waves to positive deflection by 48 to 72 hours after STEMI. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual. There should be QS-waves indicative of completed transmural MI.
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Patients who present with chest pain or cardiac arrest and have an ECG diagnostic of STEMI could have myocardial rupture. Obviously, administration of heparin and/or lytics is hazardous. These patients may survive. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. 5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound.
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Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.
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For more information, see chapter 28 of Smith's "The ECG in Acute MI."

Two more Cases of Takotsubo Stress Cardiomyopathy

Case 1.

This is the ECG of a 50 yo old woman who collapsed, was found to have a pulse, but then found to be in ventricular tachycardia. She was shocked into sinus rhythm. She presented to the ED comatose.

There is marked ST elevation especially in leads V3 to V6, as will as limb leads I and II, with no reciprocal ST depression. The cath lab was activated for STEMI, but the patient had clean coronaries. Before initiating therapeutic hypothermia, a head CT was done and showed fatal subarachnoid hemorrhage.

Case 2.

This 81 yo was found comatose.
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There is ST elevation in V1-V3 with hyperacute T-waves and Q-waves in V2 and V3. This is highly suspicious for acute anterior STEMI. However, she was found to have a fatal pontine hemorrhage and had a maximum troponin I, at 12 hours after presentation, of 2.0 ng/ml. Echocardiogram showed an anteroapical wall motion abnormality. In this case, since no angiogram was done, it is not proven that she did not have a simultaneous anterior STEMI, but with a low maximum troponin and alternative explanation, it is highly unlikely.
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These cases demonstrate that SCM can present with STEMI pseudoinfarction patterns.

Takotsubo Stress Cardiomyopathy

Unfortunately, the ultrasound images of this case were lost.

Briefly, this woman without significant cardiac history went into pulmonary edema with respiratory failure. Her ED echo (not shown) is diagnostic of apical ballooning, also known as "stress cardiomyopathy" (SCM) or "takostubo cardiomyopathy" (because the heart, with its apical ballooning, resembles the Japanese octopus trap called a "takostubo"). The contraction at the base of the heart remains intact, while contraction of the distal or apex is very poor.

Here is the first ECG after the patient became ill.

There is sinus tach with some anterior ST elevation, however not an alarming amount.

Several hours later, she had this ECG recorded:

There is anterior T-wave inversion and very long QTc (680 ms). These are classic SCM findings after the hyperacute phase.


This ECG was recorded the following day:

The QTc is even longer now, at > 700 ms. T-waves are bizarre.

The coronaries were clean, the troponin had a small bump, and the patient recovered. The apparent trigger was stress from losing custody of children.

SCM may happen from a wide variety of psychological or physiological stresses, including respiratory failure (although in this case a psychological stress led to poor myocardial function and then pulmonary edema, then respiratory failure) and intracranial bleeding.

In this case, the ECG never mimicked a STEMI. I will proceed to post a couple cases in which SCM does mimic STEMI.

Computer misses again -- two cases: one very obvious, one very subtle

Case 1.

A 63 year old male had chest pain and syncope after playing hockey (this is Minnesota). A prehospital ECG showed inferior ST elevation and the cath lab was activated by paramedics from the field. Initial BP was 96/60 with a pulse of 65. While waiting for the cath team, an ED ECG was recorded.



This is an obvious inferior STEMI. However, the computer algorithm read "ST elevation with normally inflected T-waves, probably early repolarization. Marked ST depression, probable subendocardial ischemia."

Just remember: if it can be so wrong in this case, then it can also be wrong in the cases you may miss.

There was no right sided ECG available, but a bedside ED echo showed good LV fct, a very large and poorly functioning RV, and a full IVC, all indicative of an RV MI. Volume loading improved blood pressure.

Immediate cath confirmed a very proximal RCA occlusion.


Case 2.

A 67 yo male with h/o mechanical aortic valve and h/o MI stopped taking his coumadin months ago due to depression. In the last couple weeks he has had some CP with exertion. On the day of presentation he had the onset of CP 5 hours previous.

3:01 PM. Read by computer as "nonspecific ST and T wave abnormality"



There is ST elevation of 1 mm in at least 2 inferior leads, and reciprocal ST depression and T-wave inversion in aVL. There is also some ST depression in V2 and V3; any ST depression in these leads is abnormal. This is diagnostic of inferior posterior STEMI.

There was some disagreement about intervention, partly because of the possibility of an emoblism from the valve, and after aspirin and heparin, the patient had some resolution of symptoms, so he underwent a second ECG 1.5 hours later.


4:30 PM

There is now resolution of ST elevation.

The next day, cath revealed an embolism in OM-1, 100% occluded. Peak troponin I was 22 ng/ml. The ECG showed increased T-wave amplitude in V2 and V3, which I have noticed frequently in reperfused posterior STEMI and call "posterior reperfusion T-waves."

ST depression V2-V4: Posterior leads, resolution of pain, and absence of posterior wall motion abnormality ruled out posterior STEMI

I saw this 59 year old male 3 weeks ago. He had no previous history of CAD, and presented with very typical waxing and waning chest pain, much worse with exertion but also present at rest and on presentation, though his pain was minimal at the time of the ECG. Blood pressure was 150/80.

There is sinus rhythm with a normal QRS, except for some increase in R-wave amplitude in V2 and V3, with ST depression in V2-V4. This is all suggestive of posterior STEMI, but not definitely diagnostic.
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A posterior ECG was done and showed no ST elevation, not even 0.5 mm (0.5 mm in only one posterior lead is highly sensitive and specific for posterior STEMI). Aspirin, nitroglycerine sublingual were given and the next ECG showed no change.
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I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. IV nitroglycerine was started and titrated up to 60 mcg/min until the pain resolved and a repeat ECG showed near complete resolution of ST depression.
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Heparin and eptifibatide were started for probable NSTEMI, though spontaneous reperfusion (of either the infarct-related artery, or through collateral circulation) of posterior STEMI was not entirely ruled out.
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The ECG normalized overnight. Maximum troponin was 2.1 ng/ml. The patient was taken for angiography which showed severe proximal and mid LAD disease as the culprit. Two stents were placed. The RCA was also severely diseased. There was a new anterior, septal, and apical wall motion abnormality.
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ST depression in V1-V4, isolated, may be either posterior STEMI or NSTEMI. When there is ST depression in precordial leads associated with LAD NSTEMI, it usually stretches out to V5 and V6 (it usually is not maximal in right precordial leads).
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Absence of posterior ST elevation was critical in my decisions on this, as were resolution of symptoms and of ST depression with maximal medical therapy, along with ultrasound showing absence of posterior wall motion abnormality.

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Cardiogenic Shock and Pulmonary Edema due to Subacute Anterior STEMI

This is a 72 yo male whose symptoms began with a cough 12 hours prior to presentation, at which time he had CP, SOB, and resp distress. On evaluation, he had pulmonary edema and progressive hypotension. His first ECG at 0714 is shown here:

There are QS-waves in V1 and V2, and ST elevation in V1-V3. This morphology is suggestive of either old anterior MI with persistent ST elevation or subacute anterior STEMI. There was a previous ECG on file from one year previous:

This ECG is comparatively normal, without QS-waves or ST elevation. So, at some time between one year ago and the time of presentation, the patient suffered a large anterior MI. That he felt fine until 12 hours ago strongly suggests that the MI began at that time.

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The patient was aggressively supported with mechanical ventilation and pressors. A bedside echo confirmed antero-apical wall motion abnormality. His first troponin returned at 10 ng/ml, confirming subacute anterior STEMI. He went to the cath lab and was found to have a "chronic total LAD occlusion" that received flow from collaterals from the RCA. There was severe 3-vessel disease and also left main disease. A balloon pump was placed and he went for CABG. Here is his post cath ECG.

The ST elevation is resolved. He remains very tachycardic. He is still intubated now. The troponin peaked at 177 ng/ml.

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There was clearly a very significant coronary event. Formal echo confirmed new anterior wall motion abnormality. ST elevation resolved after flow was restored. This was a very large anterior transmural STEMI. One must wonder whether the occlusion was definitely chronic. Clearly, the interventionalist could not cross it with the wire. The exact culprit lesion was not found.