Paroxysmal SVT (PSVT) that repeatedly recurs in spite of successful conversion with adenosine

An elderly male complained of dyspnea.  His pulse was regular at just under 150.  BP was 110/70.  There was no evidence of shock or pulmonary edema.  Here is his ED ECG:

There is a very rapid, wide complex tachycardia (QRS = 150 ms).  There are no P-waves before the QRS's.  There is a definite Right Bundle Branch Block and Left Anterior Fascicular Block pattern, so this is not VT.  
The bifascicular block was new.  It could be a new block, or a rate-related BBB
 If you look closely, you can see the inverted (retrograde) P-waves.
(See annotated ECG below, with arrows pointing to inverted P-waves) 
It is clearly SVT with aberrancy.

See arrows pointing to retrograde P-waves

He was given 6 mg of adenosine, and converted to sinus rhythm for about 20 seconds, then reverted back to PSVT.

This was repeated with the same results.

What would you do?











Farther below is what we did (skip the rationale for now, if you already know the pathophysiology of PSVT).  The rationale for management cannot be fully understood without the following.  Here is a good review article in the New England Journal (free full text).

Anatomy of PSVT: Most PSVT is AVNRT (AV nodal re-entrant tachycardia), with the re-entrant circuit in the AV node ("dual AV nodal pathways).  (The remainder is due to an accessory pathway such as WPW and to atrial tachycardia).    In AVNRT, there are two pathways within the node which have different conduction speeds.  In addition, the fast pathway has a long refractory period and the slow pathway has a short refractory period.

Sinus Rhythm: Normally, a sinus beat gets to the dual pathways and travels down both: it gets down the fast pathway quickly and then proceeds both down the HIS bundle and up the slow pathway.  As it travels up the slow pathway, it meets the impulse coming down the slow pathway from above and they both stop each other.

Initiation and propagation of PSVT: 

The common form of the arrhythmia is known as "slow-fast AVNRT".  It is initiated by a premature beat, usually a premature atrial beat (PAB, or more commonly known as PAC), and much less often due to a premature junctional or ventricular beat.

If that premature beat arrives at the AV node when the fast pathway is still refractory, it terminates there. And if it arrives at just the right time, when the slow pathway is no longer refractory (the refractory period is shorter than that of the fast pathway), then it can proceed down that slow pathway.  It then will travel to the bundle of HIS and activate the ventricles.  But it will also go retrograde up the fast pathway.  (The fact that it made its way down the slow pathway gave the fast pathway time to recover from its refractory period).

If you happen to witness the PAB, you will notice that it has a longer PR interval than the sinus beats because it is conducting through the slow pathway.

Now the beat goes back up the fast pathway and when it gets to the top, it proceeds BOTH up to the atrium (resulting in a retrograde P-wave that is usually buried in the QRS), and down the slow pathway (which is no longer refractory because it has a short refractory period).  Every time it gets to the inferior junction it conducts to the ventricles, an every time it gets to the superior junction it conducts to the atria.  It goes around and around the two limbs.

To terminate this re-entrant rhythm, all you need to do is stop conduction in the pathways until the sinus node can take over again.  This can of course be done with vagal maneuvers, adenosine, verapamil, or electrical cardioversion.

However, if the SVT recurs, then brief interruption of conduction in the AV node, such as with adenosine, will only be a temporary solution.  Same with electricity.

Thus, in this case, we need to prevent initiation of the SVT, or use a drug that maintains prolonged AV blockade.  To do so, one can try to prevent the formation of PABs.  Beta blockers are pretty good at preventing PABs, and also at slowing AV conduction.



Further management

The plan was to load with a beta blocker, then convert again with adenosine if necessary, with the expectation that the beta blockade would prevent another PAB and the rhythm would remain sinus.  Additionally, it is also possible for beta blockade to convert the rhythm (in addition to preventing PABs) because it slows AV node conduction. 

Therefore, we started esmolol (500 mcg/kg) by bolus and drip (50 mcg/kg/min).  We chose esmolol because it is short acting and can be turned off if there are hypotensive complications.  There were no adverse effects (and no response either), so another 500 mcg/kg bolus was given, with increase in the drip to 100mcg/kg/min.  No response, so another bolus and drip was increased to 150mcg/kg/min.  There was still no response.

At this point I was sure that if we gave adenosine, the patient would convert and remain in sinus.

So we gave adenosine 6 mg.  He converted.  10 seconds later there was a PAB and her reverted to PSVT again.

What would you do now?

Now the patient needs either:

1) a drug that will block AV nodal conduction for longer than adenosine, and better than esmolol did at the given dose.  A calcium channel blocker such as verapamil or diltiazem would be good (In the era prior to adenosine, we used to give verapamil  regularly for PSVT, with good results).  There is some potential for significant negative inotropic events with these medications.  A word of caution: avoid use of both beta blockade and calcium channel blockade simultaneously.


OR

2) a drug other than a beta blocker to prevent a PAB


After reading the New England journal article above (while managing the patient), I was considering  either verapamil or ibutilide.  I called our consulting cardiologist and he suggested amiodarone, followed by adenosine to convert again.  Like beta blockers, amiodarone prevents the initiating beat.

We gave 150 mg of amiodarone over 10 minutes, then started an infusion.  The rhythm stayed  in SVT but slowed gradually to 130 then 120 beats per minutes, then converted spontaneously to sinus.

Here is the post conversion ECG:

There is now sinus rhythm.  The BBB is still present, so this was not rate related.

Outcome:

The patient did well.  He had an episode of atrial fibrillation, but spontaneously converted.   Ultimately, the SVT was controlled with metoprolol.


Lesson

1. SVT that recurs needs therapy to either block the AV node for a prolonged period (adenosine's effect is for seconds only), or therapy to prevent the PABs that initiate any recurrent SVT.

K. Wang Video: Simple Electrophysiologic Characteristics of the Conduction System

45 year old with chest pain

A 45-year-old male was in his usual state of health until three hours prior to arrival, when he developed left-sided chest pressure with radiation to the neck while walking. His pre-hospital ECG is identical to the first emergency department ECG shown in Figure 1. Based on this, the paramedics activated the cath lab, administered nitroglycerin, and the pain resolved.

There is at least 2-mm ST-elevation at the J-point in leads V2 and V3, but the morphology of the T-wave is typical of early repolarization (slow upstroke, fast downstroke). There is minimal ST elevation in leads I, aVL, V5, and V6. There is no inferior ST-depression, no upward convexity, no precordial T-wave inversion, no Q-waves, and no terminal QRS distortion.  There is some lateral ST elevation also: V5, V6, I, aVL, although none of it unambiguously diagnostic.

This is when the Early Repolarization vs LAD Occlusion Equation can be applied – STE60V3 is 4 mm, QTc is 416ms, and RA-V4 is 15mm. Plugging these values in yields 23.753. Being > 23.4, the equation points to STEMI. The specificity of the rule is not perfect, but a value above 23.4 should at least prompt you to aggressively evaluate the patient.


As for the patient’s clinical course, his chest pressure resolved. A bedside emergency department echocardiogram (not a formal echo) reportedly showed no wall motion abnormality. The equation was not used. The cath lab was de-activated. A repeat ECG showed less ST-elevation:

In the second ECG, V2-V5 have less ST-elevation and the T-waves are smaller. It appears normal, different from the presenting ECG.  This apparently was not noticed, or its diagnostic significance was not appreciated.

An application of the Early Repolarization vs LAD Occlusion Equation has equivocal results, depending on whether the STE60V3 is measured at 1.5 or 2.0 mm. Nevertheless, the change shows that the previous ECG was indeed due to acute coronary syndrome (ACS).


Remember – not all ACS has a positive troponin! When negative, it is – of course – called “unstable angina.” It usually presents with a normal or nonspecific ECG, with ST-depression, or T-wave inversion – but unstable angina may also present with transient ST-segment elevation. Perhaps more disgruntling, transient ST-elevation does not always result in a positive troponin. The ischemia may resolve so quickly that there is both no wall motion abnormality and the troponin is negative!

With the advent of high-sensitivity troponin in the future, perhaps such cases will become more rare. But this increased sensitivity may come at the expense of worse specificity, or more false positive troponins.

The patient ruled out for acute MI with serial troponins remaining < 0.04 ng/ml (using a sensitive troponin assay). And so the patient was discharged. Yet 13 days later, he again presented with chest pain that again resolved. Another ECG was done after resolution of pain, as seen in Figure 3.

There is new T-wave inversion in I, aVL, V4-V6. There is terminal T-wave inversion (biphasic) in V2 and V3, but complicated by the U-waves seen in these leads. This T-wave inversion represents a form of Wellens’ syndrome, indicating spontaneous reperfusion of a brief left anterior descending coronary occlusion.

This time troponin was positive, and the patient underwent coronary angiography, which showed severe subtotal left anterior descending artery disease and 70% left main disease. He underwent coronary artery bypass surgery.

Lessons

1. This case illustrates the importance of paying close attention to the ECG and its evolution. The initial ECG is extremely difficult to differentiate from early repol, though the formula did so handily.  But the diagnosis is much easier if one pays attention to the change on the subsequent ECG. With the formula applied, this patient’s ACS could’ve have been diagnosed earlier.  He could easily have died in spite of a negative troponin.

2. Serial negative troponins do not rule out ACS.  One still must pay attention to the ECG.

3. If a formal echo had been done the next day, it most likely would have been normal as well: stunning in such cases resolves quickly.  See this case.  And this case.

5 hours of chest pain. How acute is the STEMI?

A male is his 30's with h/o HTN presented after 6 hours of chest pain.  The pain was crushing and substernal, associated with nausea, vomiting, and diaphoresis, radiating to his back, 10 out of 10 in intensity, the "worst pains ever experienced". He described the sensation as "an elephant sitting on chest".  Here is his EKG by EMS:

Obvious anterior STEMI with very large T-waves.  Is this consistent with 5 hours of injury?

The cath lab was activated prehospital.  Patient received 324 aspirin and 3 nitroglycerin tablets sublingually prior to arrival to the ED with mild improvement of pain.

Here is the ED ECG:

Very hyperacute T-waves and ST elevation.  Somewhat diminished after Nitroglycerine.

Suppose you were at a small hospital that only has thrombolytics.  You have the option of giving thrombolytics or of transferring to a PCI capable hospital.  The Door (small hospital) to Balloon (PCI hospital) time will be 90 minutes.

Should you give thrombolytics?

It is well known that thrombolytics work best with fresh thrombus, within 2 hours of onset of occlusion (Steg et al., see reference 8 below).  But this patient has had 5 hours of chest pain.

However, the ECG shows a very high level of "Acuteness," as demonstrated by 1) the size of the T-wave 2) the amount of ST elevation and 3) the absence of Q-waves.   Hyperacute T-waves are present when there is a large amount of viable, salvageable, myocardium.  As the myocardium infarcts (Q-waves), rather than being "injured," (as manifested by ST elevation and hyperacute T-waves), the size of the T-wave diminishes, and also the ST elevation diminishes and Q-waves begin to form (although in anterior STEMI Q-waves may form very early due to ischemia of the conducting system, not infarct!). 

The most specific sign of a very early MI are hyperacute T-waves.

We know that ACS is a very dynamic process, with opening and closing of the vessel.  The time of onset of chest pain is not a good determinant of the time of onset of irreversible ischemia (infarct).  We also know that pain is not a very reliable indicator of reperfusion/reocclusion.  Studies of patients on 12-lead ST segment monitors shows rise and fall of ST segments while patients are asymptomatic.

So, this ECG is very hyperacute.  Almost all the myocardium at risk is viable and can be salvaged.  The thrombus has been forming and lysing spontaneously, which means that it is fresh thrombus, and very amenable to lysing with tPA or TNK-tPA.

If I saw this patient, assuming there are no contraindications, I would give thrombolytics (fibrinolytics) and transfer. 

When the patient arrives at the PCI-capabel hospital, if there is no reperfusion, as measured by less than 50% ST-segment resolution in the single lead with maximum elevation, or clinical evidence of failed reperfusion within 90 minutes after fibrinolysis, then rescue coronary intervention can be performed.  See this article in the New England Journal.

Outcome

The patient went for angiogram/PCI, and a 100% mid-LAD occlusion was found and opened.

The peak troponin I was 0.9 ng/mL (very low).  The ECG the next day is here:

There is subtle Wellens' waves in V2 and V3. These waves are signs of infarction.  (It is my theory that Wellens' is simply spontaneously reperfused anterior STEMI in which the ST elevation is never recorded.  This demonstrates this phenomenon well).

Echocardiogram next day: There was a mild antero-apical wall motion abnormality.  The convalescent echo, which is done after recovery of "stunned" myocardium at 4-6 weeks, will almost certainly be normal.

Of the significant myocardium at risk in the anterior wall, almost all of was salvaged because of the hyperacute nature of the injury, as manifested by huge T-waves, and the rapid reperfusion.


Lesson:

1. The ECG is a better indicator of acuteness than the time since onset of chest pain.
2. When the ECG is very acute, thrombolytics are beneficial, and waiting for PCI has much less benefit, and probably relative harm.



Relevant references, in addition to the New England Journal article above

1.            Engblom H, Strauss DG, Heden B, et al. The evaluation of an electrocardiographic myocardial ischemia acuteness score to predict the amount of myocardial salvage achieved by early percutaneous coronary intervention Clinical validation with myocardial perfusion single photon emission computed tomography and cardiac magnetic resonance. J Electrocardiol 2011;44(5):525-32.

2.            Armstrong PW, Fu Y, Westerhout CM, et al. Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention. J Am Coll Cardiol 2009;53(17):1503-9.

3.            Sejersten M, Ripa RS, Maynard C, et al. Timing of ischemic onset estimated from the electrocardiogram is better than historical timing for predicting outcome after reperfusion therapy for acute anterior myocardial infarction: a DANish trial in Acute Myocardial Infarction 2 (DANAMI-2) substudy. Am Heart J 2007;154(1):61 e1-8.

4.            Engblom H, Heden B, Hedstrom E, Wagner G, Arheden H. ECG Estimate Of Ischemic Acuteness and Time from Pain Onset for Predicting Myocardial Salvage in Patients Undergoing Primary Percutaneous Coronary Intervention. AHA Abstract 2404. Circulation 2007;116(Suppl II):II_528.

5.            Wong CK, Gao W, Raffel OC, et al. Initial Q waves accompanying ST-segment elevation at presentation of acute myocardial infarction and 30-day mortality in patients given streptokinase therapy: an analysis from HERO-2. Lancet 2006;367:2061-7.

6.            Gersh BJ, Stone GW, White HD, Holmes DR, Jr. Pharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future? JAMA 2005;293(8):979-86.

7.            Taher T, et al. Aborted myocardial infarction in patient with ST segment elevation: Insights from the Assessment of the Safety and Efficacy of a New Thrombolytic Regimen-3 Trial Electrocardiographic Substudy. J Am Coll Card 2004;44:38-43.

8.            Steg PG, Bonnefoy E, Chabaud S, et al. Impact of time to treatment on mortality after prehospital fibrinolysis or primary angioplasty: data from the CAPTIM randomized clinical trial. Circulation 2003;108(23):2851-6.

9.            Heden B, Ripa R, Persson E, et al. A modified Anderson-Wilkins electrocardiographic acuteness score for anterior or inferior myocardial infarction. Am Heart J 2003;146(5):797-803.

10.         Corey KE, Maynard C, Pahlm O, et al. Combined historical and electrocardiographic timing of acute anterior and inferior myocardial infarcts for prediction of reperfusion achievable size limitation. Am J Cardiol 1999;83(6):826-31.

11.         Hochrein J, Sun F, Pieper KS, et al. Higher T-wave amplitude associated with better prognosis in patients receiving thrombolytic therapy for acute myocardial infarction (a GUSTO-1 substudy).  Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded Coronary Arteries. Am J Cardiol 1998;81(9):1078-84.

12.         Wilkins ML, Pryor AD, Maynard C, et al. An electrocardiographic acuteness score for quantifying the timing of a myocardial infarction to guide decisions regarding reperfusion therapy. Am J Cardiol 1995;75(8):617-20.

13.         Anderson ST, Wilkins M, Weaver WD, Selvester RH, Wagner GS. Electrocardiographic phasing of acute myocardial infarction. J Electrocardiol 1992;25 Suppl:3-5.

Outstanding General Lecture on the ECG in Acute MI: 34 minutes by Dr. K. Wang.

ECG Manifestations of Myocardial Infarction from HQMedEd on Vimeo.
cited previous videos:
Ta Wave (Atrial Repolarization Wave), how it affects the ECG interpretation
http://hqmeded.com/ta-wave-atrial-repolarization-wave-2/

Usefulness of PVCs
http://hqmeded.com/usefulness-of-pvcs-2/

ST Elevation in Conditions other than Acute MI
http://hqmeded.com/st-elevation-in-conditions-other-than-acute-mi-2/

K. Wang, MD
Clinical Professor of Medicine
Cardiology Division
University of Minnesota

med.umn.edu/cardiology/faculty/wang/home.html

P2Y12 Inhbitors in the ED for NonSTEMI. Criticisms of the ACCOAST-ed trial of Upstream vs. Delayed Prasugrel

Rick Body had a nice piece in St. Emlyn's about the ACCOAST-ed trial, a study recently published in the NEJM on the use of Prasugrel in NonSTEMI: should it be given "upstream" in the ED, or should it be delayed until the anatomy is defined by angiography?  The study found no difference between upstream and waiting.

Here is Rick's piece.

I have these criticisms of the trial, and am still using Clopidogrel 600 mg for NonSTEMI:

1. Patients planned for intervention within 2-48 hours, but they do not break down the data on whether their was efficacy for those whose intervention was closer to 48 hours.  Sitting on these patients for a long time may be bad, but this study does not tell us.
2. One of the major benefits of the P2Y12 inhibitor is it would theoretically prevent further platelet aggregation during the waiting time for PCI.  The longer the time to PCI, the more likely it is to have a beneficial effect. 
3. Mean time from symptom onset to admin of Prasugrel was 15 hours in both groups.  Strange.  Patients should be receiving their P2Y12 treatment very shortly after arrival and immediately upon diagnosis of NonSTEMI.  These medicines take time to work.   Something is amiss here.
4. First loading dose to start of angiography was 4.4 hours.  So they waited a long time to give the medicine, then did angiography immediately.  Of course there is no difference if "upstream"  and "at the time of angiography" only have a 4 hour difference.
5. GRACE score > 140 vs. < 140 (the level at which Mehta et al. (NEJM 360:2165; 2009) found benefit for immediate angiography vs. delayed): they did not analyze and compare these groups even though they collected GRACE scores on all patients.  Why not?
6. The bleeding was significantly greater in the Prasugrel group, but this was only statistically, not clinically significant: rates were about 1%!!
7. Heparin is much less evidence-based than P2Y12 inhibitors.  There is ZERO evidence for its efficacy in the PCI era.  All weak evidence in its favor comes in the era of no intervention at all!

Look at the PVCs!!

An elderly woman presented with chest pain.  She was hemodynamically stable.  Here is her initial ECG:

There is bigeminy.  There is high voltage.  There is ST elevation in the normal beats.  Is this STE baseline, due to the high voltage??  How about the PVCs?  
The computer read: "ST elevation: MI vs. pericarditis vs. early repol."  
What do you think?  See below.

There are a few findings which are all but diagnostic of anterior STEMI:

1. The PVCs, which normally have discordant ST segments (just like Left Bundle Branch Block), have proportionally excessively discordant ST elevation.  The ST elevation in the PVC in V4 is 5.5-6 mm at the J-point.  The preceding S-wave is 21 mm.  The proportion is thus 25% or more (the normal is much less than 20%).  Furthermore, the T-wave is enormous (hyperacute!)  While there is no proof that the rule applies to PVCs, as it does to LBBB, in my experience it is very similar but slightly less specific.

2. Perhaps more importantly, the T-waves in the PVCs from V3-V6 are enormous (hyperacute).  They are far more massive than any typical PVC.

3. There is a fragmented QRS in the PVC in lead V2, similar to Cabrera's sign, which is fairly specific for MI (either new or old) in the presence of LBBB, and probably also in a PVC. 

4. Finally, there is also ST elevation in the beats with a normal QRS.  There are 1.5 mm of STE at the J-point in V2 and 2 mm in V3.  These meet the 2013 guidelines for STE in women (at least 1 mm in 2 consecutive leads, but at least 1.5 mm in V2 and V3).  "Criteria," as I have stated before, are not very sensitive or specific, but in an elderly woman, this much ST elevation is rarely normal.  On the other hand, the high voltage could lead to a false positive.

The findings in the PVCs are the most convincing findings for STEMI.


How would the formula for differentiating "normal variant" ST elevation from STEMI perform on this ECG (see sidebar excel applet or "SubtleSTEMI" iPhone app)?  For those who want to see its performance, here goes:  The computerized QT was 462 ms and QTc was 515 ms.   Into the formula, enter 3 mm for ST elevation at 60 ms after the J-point in lead V3, 515 for the QTc, and 27 mm for the R-wave amplitude in V4.  The result is 25.17, which would indicate STEMI.  This QT, however, is obviously both a misread (of the QT, which is really only 420 ms) and of the QTc [which is the QT divided by the square root of the PRECEDING R-R interval.  In this ECG, the R-R interval preceding the normal beats (not preceding the PVCs) is 1100 ms, so the QTc MUST be less than the QT).  I calculate the QTc as 400 ms.  So, using my manually derived numbers, the formula comes to 18.38, which would not be STEMI. 

The physician who saw the patient was alarmed by these PVCs, and so ordered a serial ECG just 12 minutes later:

Now there is a clear increase in the ST elevation of BOTH the normal QRS beats and the PVCs.  The ST/S ratio in the PVC in lead V4 is now 9/15 = 0.60, clearly diagnostic of STEMI.  

How about the formula now?  The Computerized QT was 440ms, and QTc = 511.  It seems to be misread again: I get 400ms for the QT, and QTc of 460ms.  Now the STE is 5 mm and R-wave in V4 is 23 mm.  If I use the formula with the computer's QTc, the value is 28.6 (very high). If I use my QTc, the value = 25.6 (still a STEMI).  Now, no matter which numbers are used for the formula, it indicates STEMI

The cath lab was activated and a 100% mid LAD occlusion was found and opened.


The physician who saw this patient had been to several of my lectures on anterior STEMI, and sent this with the quote, "Probably not the first time, but your lecture helped in saving another life."  I quote this only to demonstrate that these morphologies can be studied and learned, and ECG interpretation can improve with learning and practice.

Lesson:

Use the PVCs to diagnose STEMI.   

Here are some other cases, including a video lecture by Dr. Wang of the "Usefulness of PVCs".




The cover of Dr. Wang's new book shows a STEMI that is seen best in the PVC:

 

55 year old woman with chest pain and precordial T-wave Inversions

This 55 year old woman presented with chest pain:

There is sinus rhythm.  There is ST depression and there are negative T-waves in V1-V4. There is also STE in aVL, with reciprocal ST depression in II, III, and aVF.  Looks like acute posterolateral MI, no?  See below.

No, it is not acute MI.  Notice that there is a prominent S-wave in lead I (right axis deviation) and a large R-wave in V1.  This is diagnostic of right ventricular hypertrophy, which is an abnormality of depolarization (abnormal QRS) that results in secondary abnormal repolarziation (ST-T wave).  These negative T-waves and abnormal ST segments are entirely due to RV hypertrophy. 

The physician recognized the abnormal QRS and the appropriate ST-T changes and did not activate the cath lab or initiate anti-ischemic or antiplatelet therapy other than aspirin. 

The patient ruled out for MI.  Echocardiogram showed RV hypertrophy and pulmonary hyptertension.

EMS 12-lead has a great discussion of pulmonary pressures and ECG patterns, and they show another example of this.

Syncope and ST Segment Elevation. And another finding. How well does the computer interpretation perform?

A woman of approximately 50 years of age had been feeling weak and febrile, then had syncope.  EMS recorded this ECG:

Sinus Rhythm. 
The ECG computer read "ST Elevation, Anterior Injury, *****ACUTE MI*****"
The medics activated the cath lab prehospital.
Is the computer accurate?

No.  This is not the morphology of anterior STEMI, nor even of right ventricular STEMI, though there are similarities. 

There is right ventricular conduction delay (R' wave), with downsloping ST elevation and T-wave inversion (TW inversion is slight in this case).  This morphology is Brugada pattern, or at least very similar to Brugada pattern, and could actually be Brugada, though not necessarily, but it is not completely classic, as this one is. 

On arrival, she was febrile (39.4 degrees C), and this ECG was recorded:

The ST elevation is not as pronounced now.
What else is present?

If you look closely, it appears that the QT interval is very long in lead II (about 400 ms, with QTc of 500ms).  However, if you look at leads V2-V5 (especially V4 and V5), you see prominent U-waves.  A U-wave then probably accounts for the apparently long QT in lead II (in other words, what appears to be a QT interval is a QU interval).

The patient had a K of 3.8 mEq/L, but the Magnesium level was 1.2 mEq/L, which is slightly low.  It is well known that hypoMg causes hypoK, which of course leads to U-waves, but there is also some evidence that hypoMg alone, even in the absence of HypoK, produces prominent U-waves.  There may or may not be a causal relationship here.

Lesson:

1. The computer is very unreliable in diagnosing acute STEMI.  The literature would indicate that this shortcoming is usually in poor sensitivity (around 60%) but with reasonably good specificity (not many false positives).  In my experience, the computer has many false positives.  Because of the limited accuracy of the computer aided diagnosis, our protocol requires not only that the computer reads ***Acute MI***, but that the patient also have active chest pain.  Although this protocol will miss many STEMIs, it limits the false positives. 
2. The computer is very unreliable at measuring the QT interval when it appears long to the naked eye
3. The computer is very unreliable at finding U-waves. I do not ever remember a computer diagnosis mentioning U-waves.  I am not even sure if they are part of the algorithm.
4. Brugada pattern ECG is a common PseudoSTEMI pattern.  Although there is ST elevation, its morphology is completely different from ischemic ST elevation.  The T-wave inversion morphology is also completely different from ischemic T-wave inversion.


Outcome

The emergency physicians immediately recognized this as Brugada pattern and de-activated the cath lab.  Closer history also revealed that she had only had pre-syncope; she remember the entire event.  There was no family history of sudden death or syncope.

She was admitted and ruled out for MI and will get cardiology follow up.  She had influenza.

Here is her ECG when not febrile:

Findings have mostly resolved.  Perhaps the prehospital ECG had some fever-induced Brugada pattern.

ST Elevation and Positive Troponin. Is it STEMI? No. And it is not even ACS.

A male in his 60s complained of constant chest pain for 12 hours.  He has a h/o DM and HTN and has been off his meds, including clonidine, for 3 days.  His first two BP measurements were 176/108 and 191/126, with a pulse of 100-112.  Here is his initial ECG:


ED ECG with pain:

There is sinus tach at a rate just above 100.  There is profound LVH, with deep S-waves in V1-V3 and a large R-wave in V6.  There is left atrial enlargement, with a very large negative deflection of the P-wave in V1, also supporting LVH.  There is 3-4 mm of ST elevation in V1-V3: this is classic for the pseudoSTEMI pattern of LVH: 1) location: V1-V3 and 2) preceded by a deep, high voltage S-wave.  Armstrong et al., concluded that an ST/S ratio of less than 0.25 in the presence of LVH is very unlikely to be due to STEMI.  There are small Q-waves in III and aVF that suggest, but are not diagnostic of, old inferior MI.

Although this ECG is abnormal, I see no evidence of ischemia on this ECG.  It is nondiagnostic.  There certainly could be ischemia hidden in this ECG.  But there is nothing specific for ischemia.   And it is not an ECG that should result in cath lab activation.

Just to prove the point, I will show his previous ECG when he was symptom free:

It is very similar but at a higher heart rate.  But there are also clearly inferior Q-waves, strongly suggesting that he had a pre-existing inferior MI.  This proves that the baseline ECG has high ST elevation in V1-V3.  But you did not need to see this previous ECG to know that the ST elevation on the presenting ECG was due to LVH!  This amount of ST elevation is APPROPRIATE for an ECG with such deep S-waves.  In LVH, as in LBBB, the ST elevation in precordial leads is appropriately discordant, but if it is baseline, it should be proportionally discordant.  As indicated before, Armstrong's research suggests that an ST/S ratio of 0.25 is an appropriate amount of proportional discordant ST elevation.

The hypertension and tachycardia could be due to, among other things, clonidine withdrawal: the abrupt withdrawal of clonidine can result in rebound central sympathetic outflow, with increase in both blood pressure and heart rate.  The patient was administered clonidine which resulted in a modest improvement in his vital signs.

The initial troponin I returned at 0.155 ng/mL, all but diagnostic of Acute MI (I say "all but" because, strictly speaking, there must be a rise and/or fall of troponin to confirm Acute MI).  It was confirmed with a rise to 0.222 ng/mL on the next).  But acute MI does not necessarily mean ACS (plaque disruption, thrombus, need for anti-platelet and antithrombotic therapy).  Is this patient having a type I or type II MI?  That is to say, is there demand ischemia due to the increased O2 demand of hypertension and tachycardia?  Or is there ACS?  There is no way to tell for certain without an angiogram showing a culprit or not.   In either case, as long as there is good cardiac function and no contraindications, beta blockers are indicated.  (For explanation, see this case posted this week on the use of anti-ischemic therapy, including metoprolol, in ACS)

The patient was not started on metoprolol in the ED, but was (appropriately) given Nitroglycerin.  Nitro may lower the BP, but won't lower the heart rate, and both cause increased oxygen demand with ischemia.  His pain continued.

An echocardiogram was ordered and done in the ED just before the patient was transported upstairs.  The report returned as a large inferior wall motion abnormality (WMA) with extension to the lateral wall.  (There was also "Abnormal left ventricular diastolic performance grade 3, Severe restrictive pattern)"  This is consistent with the LVH on the ECG.

It was unknown for certain if the WMA was new or old.  He was started on carvedilol 25 mg po bid at admission.  His pain abated and he was taken to cath the next morning, at which time a 100% occlusion of a small dominant distal circumflex was found (to the inferior wall).  It could not be crossed with a wire.  It appeared to be a chronic total occlusion.   There was good collateral circulation and it was a very small vessel.  The peak troponin was only 0.270 ng/mL.

This was recorded 24 hours after presentation:

Now the heart rate is slower and there is only 2-3 mm of ST elevation in lead V2.  It is very common for tachycardia (ECG above) to result in more ST elevation than is present at baseline.  There is still no sign of an infarct.

Interpretation:

1. Type II MI (demand ischemia) from hypertension and tachycardia due to clonidine withdrawal
2. Right Precordial ST Elevation from LVH
3. Inferior Q-waves due to old inferior MI
3. Dense inferior wall motion abnormality due to old MI

Follow Up:

He was taken off clonidine and started on lisinopril and carvedilol.

Lessons:

1.  MI is not necessarily due to a coronary event.  It may be due to increased demand (Type II MI)
2.  MI and ischemia due to a coronary event is usually subendocardial ischemia and the ECG is usually nondiagnostic, or has ST depression of subendocardial ischemia.  ST elevation is possible, but very unusual.
3.  A large amount of ST elevation may be due to pseudoSTEMI patterns such as LVH.  A positive troponin may have nothing to do with the ST elevation
4.  When there is Hypertension, don't forget beta blockade such as metoprolol.  Again, see here for details.  An alternative is esmolol: if you are worried about the potential adverse effects of beta blockade, esmolol is very short acting.  It is given as a bolus and drip, and its effect wears off very quickly after discontinuation of the drip