Epigastric pain, Syncope, and Saddleback ST Elevation

A male in his 30's who is an elite athlete with no risk factors for coronary disease had brief epigastric pain followed by brief syncope.  He presented to the ED never having had any chest pain or SOB, and with mild epigastric pain.

Here is his prehospital ECG:

There is sinus rhythm with a large peaked P-wave in lead II, and there is some minimal right axis deviation with S > R is lead I.  ST Elevation is minimal in V2, and more pronounced in V3 and V4.   There is also some supsicious ST elevation in aVL and I, with large T-waves and reciprocal ST depression in lead III.  Application of the STEMI vs. Early Repol formula, with values for QTc (computer) = 408 ms, STE60V3= 4 mm, and R-wave Amplitude V4 = 14.5 mm gives a value of 24.13, which is greater than 23.4 and thus indicates anterior STEMI, but not by much.  The closer the number is to the cutpoint of 23.4, the more uncertain the result.

The ST segment in V2 has a saddleback morphology.  In my experience, a saddleback in V2 has always been a STEMI mimic, not STEMI.  So I approach these with great skepticism.

There is an rSR' in V1 and V2, possibly due to right ventricular hypertrophy (given the right axis deviation), but without right bundle branch block (QRS duration is only 102 ms).   There is right ventricular conduction delay.  The large P-wave in lead II supports right atrial enlargement and possible right ventricular hypertrophy, which may all be affecting the ST segments.

The absence of chest pain in a young healthy male should make you more skeptical of STEMI and suggest a false positive.  However, we all know that chest pain is far from universal in STEMI.  In a recent study, 14% of men under age 55 do not complain of chest pain with their ACS.

On arrival in the ED, he underwent another ECG:

The saddleback is even more pronounced.  But so is the ST elevation.  Admittedly, this looks scary.  And the formula here, given STE60V3 of 5mm, QTc of 414 ms, and R amplitude V4 of 18.5 mm, gives a value of 24.38, still high.

The cath lab was activated and the patient was taken for angiogram, which was normal.  There was a small first diagonal and the angiographer noted that "a ruptured plaque that may have caused a temporary D1 occlusion is not inconceivable." 

An echocardiogram the next day was completely normal.  Initial Troponin I was 0.058 (99% reference 0.025) and succeeding ones were 0.073, 0.044, and 0.069.  This rather random rise and fall suggests false positives, which we have had many of since changing to our new Abbott assay.

Here is his ECG at 24 hours:

Sinus bradycardia.  The ST elevation remains, there is a less pronounced T-wave in precordial leads, but this could be due to the slow heart rate.  There is little evidence that there was any infarct.  This confirms that all the findings on the initial ECGs were baseline.

Conclusion:

This is a tough case and the safe thing to do was done: an angiogram, in order to be certain this was not a STEMI. 

Because of some reasonable doubt, it would also have been reasonable, if it could be obtained quickly, to get a stat echocardiogram with high resolution (using contrast (Definity).  I think it would have shown normal wall motion all around and saved the patient an angiogram. 

Nevertheless, it is good to remember:

1. Saddleback in V2 should make you doubt the diagnosis of anterior STEMI
2. Absence of Chest pain or SOB in a young, healthy male should make you skeptical and lead you to think about seeking confirmation of your ECG diagnosis.
3. The early repolarization/anterior STEMI formula does have false positives and negatives.  Accuracy was about 90% (which was far better than ST elevation)

K. Wang Video: The Genesis of Aberrant Conduction (13 minutes)

Right Bundle Branch Block with ST elevation in V2, V3. Why?

This young male patient had a very atypical presentation for STEMI (near syncope and abdominal pain after smoking an unknown drug), but we can pretend that it was not atypical and think about how we would interpret the ECG:

There is right bundle branch block with an rSR' in V1 and wide S-wave in lateral leads.  The ST segment is elevated in V2-V4.  Usually, in RBBB, the only secondary repolarization abnormalities are some minimal ST depression in V2 and V3 and there should not be ST elevation (see image of normal RBBB at bottom, and image of RBBB with anterior STEMI still further down).       In the right context, might this be STEMI?  Interpretation below.

My Interpretation:

Normally, in RBBB, the transition from rSR' to RS or to qRS is between leads V3 and V4.  On this ECG, the transition is between V1 and V2.  There is no R' wave in V2 or V3, thus there is no discordant ST depression and discordant negative T-wave, as one would normally see in these leads in RBBB.   Instead, there is a wide S-wave, which in RBBB is usually followed by an upright T-wave, but not by ST elevation (in uncomplicated RBBB).   

But this case is probably an exception: in a young male, when the S-wave is in leads V2 and V3 (which is very uncommon in RBBB), it may be normal to have some ST elevation, as young males usually have ST elevation in V2 and V3 (early repolarization) and in this case of RBBB, that ST elevation would not be hidden by the repolarization abnormalities (ST depression and T-wave inversion) which normally come with RBBB.

My admittedly invented diagnosis: RBBB with early transition, and with ST elevation due to early repolarization that is not obscured by RBBB because of the early transition.

In any case, when I was showed this ECG by a worried resident, I was quite sure it was not STEMI even before hearing the clinical history, and much moreso after.  And he ruled out for MI.


Normal RBBB:

                          There are secondary repolarization abnormalities: ST depression and T-wave                   inversion in leads with an R' (V1-V3)

RBBB with anterior STEMI (LAD occlusion):

There is STE in V2 and V3 concordant with the R' wave.  This was an acute LAD occlusion.

K. Wang video: "Glossary of Cardiac Rhythms" (11 minutes)

Two interrupted sinus beats. What is the etiology?

Thanks to our electrophysiologist, Rehan Karim, and to Dr. Wang for their assistance in this case.

This is from a young person with palpitations, on no medications, and with no known heart disease.  There was no syncope or history of cardiac disease.

There is sinus rhythm, but with two pauses of about 1.6 seconds, which are almost exactly double the shorter P-P intervals. The P-wave of the second complex is different.  Is this sinus arrest? Sinus pause?  Sinoatrial exit block?  Or just simple sinus "arrhythmia" (benign, vagally induced)?

Sinus arrhythmia is unlikely because, in sinus arrhythmia, the rate usually gradually slows and then gradually speeds up.  Here, the long R-R intervals are nearly exactly the same as each other, and nearly exactly double the short R-R intervals, which are, in turn, nearly exactly identical to each other.   It can't be sinus pause or arrest because the pause is less than 2 seconds.  Also, sinus pause would not start up again at a multiple of the other P-P intervals.

Thus, it is almost certainly sinoatrial exit block.  This means that the underlying sinus node depolarizes at a constant rate, but occasionally does not "exit" the sinus node and depolarize the atrium; hence, no P-wave.

The fact that the long intervals are not EXACTLY double the short ones argues only weakly against this because the sinus rate is not always exactly the same.

Why is the P-wave after the first long interval different from the others?  Dr. Karim explained:

"The sinus node is a very long structure, extending from SVC/RA junction coming down on the RA wall.

Of course, without the actual SA recordings, no one can say for sure, but we essentially rely on the P-wave morphology and axis to make a determination about the origin of those p-waves.

"The exit site of the Sinus node activity is usually high up and therefore P-waves are usually positive. Sometimes, the exit site from sinus node can vary in the same person and can potentially result in slightly different morphology.

"The P-wave in question is different, but still appears like sinus to me, with a slightly lower exit and therefore the positivity is not as pronounced. The pause that occurs afterwards shows the p-wave that’s similar to other sinus p-waves."

Furthermore, the fact that the sinus node impulse is exiting at different parts of the long sinus node suggests that it is being blocked from its normal exit, and supports sinoatrial exit block.


Final explanation of this case, which I believe is SA exit block second degree type II (with an interesting twist):

SA block in this case: Suppose the impulse cannot exit using the normal transitional (T) cells (SA block), but does succeed in travelling down the SA node and exiting elsewhere.  Then you get a different P-wave morphology, as we have in this case.  In this case: the first PQRS is normal.  The second sinus impulse is completely blocked and there is no p-wave or QRS.  The third is partly blocked, but exits the SA node in a different area and you get a PQRS but with a different P-wave morphology.  Then there are 7 normal beats, but the 11th sinus impulse is completely blocked but the 12th exits normally and the P-wave morphology is normal.

Management: The patient was admitted, had an uneventful overnight stay except was diagnosed with hyperthyroidism, and discharged.  He will get follow up for the sinus abnormality.  Patients with asymptomatic SA block do not need treatment (palpitations would not be a significant symptom).  Patients with syncope or near syncope must be evaluated further.

Sinus Node Dysfunction (SND):

Partly adapted from the AHA/ACC guidelines for pacemaker insertion (JACC 2008; 51(21):e1-e62) and from online textbook UpToDate:

"SND refers to a broad array of abnormalities in sinus node and atrial impulse formation and propagation. These include persistent sinus bradycardia and chronotropic incompetence without identifiable causes, paroxysmal or persistent sinus arrest with replacement by subsidiary escape rhythms in the atrium, AV junction, or ventricular myocardium." (ACC/AHA)

Anatomy and Pathology of SND

The sinoatrial (SA) node has pacemaker, or "P" cells and transitional, or "T" cells which transmit the impulse from the P cells to the atrium.   It may be diseased due to ischemic, infiltrative, inflammatory, or fibrotic changes, or to excessive vagal tone, beta blockers, calcium channel blockers, or hyperkalemia.

1. Sinus pause:  At least 2 seconds of pause

2. Sinus arrest: I could not find a definition, except that there is a complete absence of P-waves.  If an escape beat comes within 3 seconds, is that sinus arrest or sinus pause?  Lower pacemakers (AV node, bundle of HIS, right or left bundle, ventricle)  which produce "escape" rhythms do not always function, so asystole is a possible outcome of sinus arrest.


Etiology of sinus pauses and arrest: alteration in the impulse rate of the P cells.  Therefore, the pause length is variable and not necessarily a multiple of the basic sinus rate. Pauses up to 3 seconds during carotic sinus massage (vagal stimulation) are within normal limits.  But symptomatic carotid sinus hypersensitivity may be an indication for a pacer.

3. Sinoatrial nodal exit block (SA exit block): SA pacemaker, or P cells, are working but the impulse is not transmitted by the T cells to the surrounding atrial tissue.  So there is no P-wave.  The sinus impulse is invisible on the surface ECG if there is no P-wave (the P-wave comes from atrial activity).

3a. First Degree SA Block: slowing of impulse exit only.  This cannot be seen on the surface ECG 
3b. Second Degree SA Block:
          Type I: (Wenckenbach): progressivley decreasing P-P intervals prior to a pause; the pause has a dduration less than 2 P-P cycles.
          Type II: P-P interval is a multiple of the normal P-P intervals
3c. Third Degree SA Block: the impulse does not reach the atrium at all and thus cannot be differentiated from sinus arrest on the surface ECG.


Sick Sinus Syndrome findings include:

1. chronic, inappropriate, sinus bradycardia, which may be symptomatic if there is failure of "escape" rhythms
2. Sinus pauses, sinus arrest, and sinoatrial exit block
3. Alternating bradycardia and atrial tachyarrhythmias, including atrial fib (tachy-brady syndrome)

Not all patients with sick sinus syndrome need a pacemaker immediately, but if you encounter a patient who has symptomatic sinus pauses in the ED (syncope or near syncope) and you are not sure that it is sinus arrhythmia, as I see it, you cannot safely send the patient home without further evaluation, usually by a cardiologist.  Although the serious outcomes may take some time to manifest (see paper below), I don't know of any way to predict that they won't happen immediately in your symptomatic ED patient, unless you can find and reverse an identifiable cause such as hyperkalemia or drug effect.  Anyone with any better information on this, please comment and I will edit this.



Natural History of Sick Sinus Syndrome

In this study of 35 patients with sick sinus syndrome, as diagnosed by (1) age at least 45 years; (2) mean sinus rate at rest less than 45 beats/min, and/or intermittent sinoatrial block in at least 1 standard electrocardiogram recorded during diurnal hours on different days; (3) symptoms attributable to sinus node dysfunction, such as syncope or dizziness, and/or easy fatigue or effort dyspnea, the patients were followed up for up to 4 years (mean 17 ± 15 months). During follow-up, 20 patients (57%) had cardiovascular events that required treatment: 8 had syncope (23%); 6 had overt heart failure (17%); 4 patients had chronic atrial fibrillation (11%); and 2 patients had poorly tolerated episodes of paroxysmal tachyarrhythmias (6%). Actuarial rates of occurrence of all events were 35%, 49%, and 63%, respectively, after 1, 2, and 4 years. At univariate analysis, age at least 65 years, end-systolic left ventricular diameter at least 30 mm, end-diastolic left ventricular diameter at least 52 mm, and ejection fraction less than 55.

New K. Wang Video: Chamber Enlargement or Hypertrophy (9 minutes)

Male in his 50's with chest discomfort

A male in his 50's with a history of type I DM was riding his bike to work when he developed squeezing chest pressure and a sensation that "something wasn't right."   He rode his bike directly to the ED.  Here was his initial ECG:

There is very subtle, nondiagnostic (but suspicious) ST elevation in II, III, and aVF.  aVL is particularly worrisome as it has a biphasic T-wave (down-up) which is almost always ischemia. Down-up is usually reciprocal to reperfusing inferior MI, though there is no evidence of reperfusion in inferior leads.  V2 has a suspiciously flat/downsloping ST segment as well.

He was given one sublingual NTG and became pain free.  

There was, at this moment, no absolute indication for immediate angiography, as the patient was pain free and the ECG was not diagnostic of STEMI.  However, it is nearly diagnostic of ischemia, there is minimal ST elevation, and we know that a high percentage of NonSTEMI, when they do get their angiograms at 24 hours, have an occluded infarct-related artery even though the patient has remained asymptomatic.  These patients have larger infarct size, higher incidence of heart failure, lower EF, and higher mortality. 

Also, it was daytime, and the cath lab was free, so why not go immediately to the cath lab?

He went for immediate cath and had a 95% thrombotically occluded mid-RCA that was opened and stented, with thrombectomy.

Here is the post-cath ECG:

The inferior ST elevation is entirely resolved.  The T-wave in III is fully inverted (reperfusion), now with a fully upright T-wave in aVL (reciprocal to inferior reperfusion).  The T-wave in V2 is now larger and more upright (reperfusion).

The last troponin I measured was 1.0 ng/mL.  The echo showed a possible mid to basal inferior wall motion abnormality.  (Remember, wall motion abnormalities frequently disappear if ischemia is mild or brief)

The physician made a great call on this ECG; I like to think that, having seen so many similar cases here (as he had), made a difference.

See the very important question below in the comments section, and my answer.

Chest pain and Bradycardia

An elderly male complained of chest pain.  He had no previous cardiac history and was only on aspirin, a statin, and a proton pump inhibitor. He was hypotensive but in no distress and well perfused.  Here is the prehospital ECG:

The heart rate is 38.  There are no p-waves and the baseline appears to fibrillate.  Thus, there is new atrial fibrillation with a slow response.  The ventricular rate is regular.  The QRS is narrow.  There is inferior ST elevation and ST depression in V1-V4.  Diagnosis: Atrial Fibrillation with complete (3rd degree) AV block and inferoposterior STEMI.

The medics activated the cath lab.

In the 1980's, it was believed that the right precordial ST depression that frequently accompanies inferior STEMI was due to "anterior subendocardial ischemia."  Then numerous angiographic studies refuted this and showed that it is almost always due to posterior STEMI.   [There are exceptions to this and in most cases the patient has reason for demand ischemia - hypotension and/or tachycardia - AND the ST depression is diffuse, including the precordium].

Atrial fibrillation in STEMI: Atrial fibrillation is uncommonly an acute and immediate result of STEMI, but is a common pre-existing condition in elderly patients with STEMI.  When new onset, it is usually accompanied by a rapid ventricular response because the patient is not already on AV nodal blockers.

When initiated in acute STEMI, atrial fibrillation may be due to sympathetic output, atrial stretch due to LV or RV dysfunction, or atrial infarction.  It occurs much more often in large infarcts or anterior infarcts, especially during the hospital course in those who develop CHF, ventricular dysrhythmias, advanced AV block, or pericarditis.   It may also occur in inferior STEMI because the RCA supplies the sinoatrial nodal artery.

Had this patient had atrial fibrillation with rapid ventricular response, cardioversion would have been indicated (hypotension and very recent onset).  Obviously, in the setting of heart block, cardioversion will have no benefit.


On arrival, here is the ED ECG:

No significant change.

Heart block in inferior STEMI is due to ischemia of the AV node.  In anterior MI, heart block is much more dangerous, as it is due to ischemia of the Bundle of HIS and Purkinje fibers.  Thus, in inferior MI, there is usually a high (junctional or HIS) escape which is narrow.  In anterior STEMI, if there is block, the escape is usually low and is slower and a wide complex (ventricular, or perhaps involves escape of the left or right bundle, which will result is RBBB or LBBB pattern, respectively). 

There was consideration for pacing for this heart block with hypotension, but the patient was not in shock (in spite of hypotension) and the best management for him is to get to the cath lab.

As this may be a nodal escape, and the AV node is responsive to atropine, atropine was given with a temporary increase in heart rate to 50.

A right sided ECG was performed.  Inferior STEMI is often associated with right ventricular MI, especially when the patient is hypotensive.  This is usually accompanied by ST elevation in V1.  However, such ST elevation can be attenuated or cancelled by the (reciprocal) ST depression of posterior STEMI.  So it is not unreasonable to record a right sided ECG.  If (+), the patient is more likely to respond well to fluids without pulmonary edema.

V1-V6 are really V1R (V1 right) to V6R (V6 right), where V1R = V2 and V2R = V1.  As you can see, the R=wave amplitude is low on the right side.  There is no ST elevation.  0.5 mm of STE is the standard criterion for right ventricular MI.  There is none here. 

While waiting for the cath team, posterior leads V7-V9 were recorded.  V7 is at the posterior axillary line, V9 at the paraspinal border, and V8 between them, all at the level of the tip of the scapula:

These are a mirror image of V1-V3, EXCEPT they are lower voltage, as the impulse must travel through an air-filled chest.  There is greater than 1 mm of ST in all 3 leads.  The standard "criterion" for posterior MI, with about 80% sensitivity andd specificity, is 0.5 mm (presumably in 2 consecutive leads, but this important study by Wung et al in 2001 is vague on that). So this easily meets criteria for posterior STEMI.

In the cath lab, a temporary transvenous pacer was quickly placed.  Then the artery was opened with some difficulty and a large thrombus burden was suctioned out. 

Here is the post cath ECG:

There is now sinus rhythm (restored with restoration of perfusion) and there is persistent ST elevation (and precordial depression).

When microvascular reperfusion is incomplete, there may be persistent ST elevation after PCI.  This is more likely to result in long term persistent ST elevation and even diastolic dyskinesis of the inferior and posterior walls ("aneurysm").

A couple days later, the patient was tachycardic and had this ECG recorded:

There is sinus tachycardia and now there is much more ST elevation and depression.  ST elevation and depression can be exaggerated by tachycardia, and this is the probably mechanism here.  Because I don't know the exact clinical situation at this moment, I am not certain.

The patient did well and was sent home.   His last troponin I was 152 ng/ml.   His EF was 40% with a hypokinetic inferior wall.  Posterior wall was not commented on.