Would you activate the cath lab prehospital?

 A 54 yo with history of hypertension awoke in the AM with substernal chest pain.  It did not abate, so at 0930, he called 911.

Medics arrived and recorded this ECG:

There is sinus tachycardia at 105 bpm.  Leads II, III, and aVF have very minimal r-waves and rather large T-waves, with straightening of the ST segments.  Leads V4-V6 have greater than 1 mm of ST elevation at the J-point (abnormal), as well as large T-waves.  V1-V3 are unremarkable except for low voltage in V1 and V2.  There is upward concavity in all leads.  There is only very subtle reciprocal ST depression in aVL, with T-wave inversion.  This helps to make the diagnosis of inferior MI.

This is highly suggestive of acute inferolateral STEMI, though not classic.  By any millimeter criteria, one would have to call it STEMI.  I would call it STEMI but it is not obvious.  [Also, tachycardia should always alert you to impending cardiogenic shock, or to possibly another diagnosis such as pulmonary embolism; however, this has none of the other classic findings of PE.]


Our prehospital protocol is:
--If a patient has chest pain and the computer algorithm reads ***Acute MI***, then they are to activate the cath lab from the field.
--If only one of these is present, they are not to do so.

The computer algorithm made no comment on any of it.

Fortunately, our medics sometimes go outside the rules.  That is what they did here: activate the cath lab.

The patient arrived in the ED at 1022 and had this ECG recorded at 1028:

Now there is new ST elevation in V2 and V3, with Q-waves forming.  Diagnostic of anterior STEMI.  Inferior leads now have much more ST elevation.  Again, all leads have upward concavity and there is only very subtle reciprocal ST depression in aVL.

The patient was taken to the cath lab at 1039.  As he was being transferred to the cath table he had a v fib arrest.  He was defibrillated.  Angiogram showed a type III (wraparound) LAD, occluded distally (but also with an 80% diagonal stenosis), such that he was having an infero-antero-apical STEMI.  The thrombosis was opened, thrombus suctioned, and the lesion stented, with a door to balloon time of 45 minutes (thanks to prehospital activation by the medics).

Medics are getting very good at reading the ECG; maybe it is time to let them overrule the computer? --This requires a formal study.  


General methods:

Take one or more EMS service(s) in which medics are well trained in reading the 12-lead. Search for all patients who had a prehospital ECG.  Find the cath outcome, or troponin outcome if no MI.  Find the computer read on the ECG.  Have 2-4 medics read the ECG blinded to the computer and the outcome.  Compare.

Chest pain, SOB, and tachycardia. What is the rhythm? Is it MI?

This was sent to me by a reader from India (Thank you, Rama Krishna).  The patient presented recently (age unknown).  He had a history of DM, HTN, COPD, and previous anterior wall MI.

Here is his presenting ECG:

 The answer is below:









It is ventricular tachycardia with 1:1 retrograde conduction to the atria and also with electrical alternans.  The small drawn circles, which appear to be p-waves, are not actually the p-waves.  Rather, the small negative deflection following these circles (narrow black arrows along the lead II rhythm strip at the bottom), are retrograde p-waves.  They are negative because of the retrograde conduction.  The alternate QRS has a negative p-wave that is buried in the negative T-wave (green arrow).  These p-waves are upright in aVR (see the blue arrows, and red arrow for the alternate QRS)  Also, the retrograde p-wave can be seen in V1 (purple arrow).

As for repolarization, there is ST elevation in V2-V4 (thick black arrow) diagnostic of MI.  It looks like it is old MI, not acute (see discussions of LV aneurysm on other posts).  Of course, these discussions apply to normal conduction, not normally to ventricular tachycardia.  But in this case it is fair to say that the ST segments are a result of MI [almost certainly old MI (which also fits the patient's history), possibly acute] rather than being due to the abnormal QRS.

Without reciprocal ST depression or hyperacute T's, inferolateral MI and myo- or pericarditis are impossible to distinguish

A 63 y.o. female with a past medical history of lupus and MS presents with chest pain and SOB she has never had before, starting approximately 1615.  The pain gradually diminished since onset.  It was described as pressure, with SOB, and no radiation.  There is some reproducibility with palpation, but the pain is not positional or pleuritic.   She has no h/o CAD, HTN, or DM.  There is no pericardial friction rub.  NTG by EMS improved pain.   The pain resolved after 1 hour in ED.

Here is her initial ECG at 1954 (3.5 hours after onset of CP):

There is sinus rhythm with minimal inferior ST elevation (and no reciprocal depression in aVL).  There is moderate ST elevation in V3-V6, not quite 1 mm. V3 and V4 have almost 1 mm of STE.  STE is greater in II than III.  There are no hyperacute T-waves.  There is no ST depression anywhere.  (For comparison, her previous ECG had no ST elevation anywhere.)

Inferior MI virtually always has reciprocal ST depression of some amount, or at least T-wave inversion, in aVL. 

See this case and this case for patients who were erroneously thought to have pericarditis, whose ECGs had subtle reciprocal ST depression in aVL.

When there is inferior and lateral STEMI or inferior and anteroapical STEMI, the reciprocal ST depression can be attenuated or completely abolished by the lateral ST elevation.  Thus, the ECG can look identical to myo- or pericarditis.

The reading by the cardiologist was: "diffuse ST elevation, consider pericarditis."  Subsequent ECGs are of little interest, only showing some resolution of ST elevation, but no T-wave inversions or other diagnostic findings.

Clinically, the patient has pain more typical of ischemia.  Her initial troponin I was 8.56 ng/ml.   Therefore, whatever the process is, it must have been going on longer than 3.5 hours.   Subsequently, every 4 hours, the levels were 9.96, 8.96, 8.40, 7.48, 6.62, so there is some rise and fall, though not dramatic.  A steady state is typical of myocarditis, whereas a rise and fall is more typical of MI.

The differential diagnosis, then, is myocarditis vs. inferolateral STEMI (most likely).

Echocardiogram showed wall motion abnormalities of the distal anterior wall, apex, and septum as well as the inferior wall.  This could be seen in either MI or myocarditis, but favors MI, as myocarditis less frequently has focal myocardial dysfunction.

Her angiogram showed a Type III LAD ("wraparound LAD, that supplies the inferior wall).  It had moderate diffuse disease in the distal segment of the vessel, which would be the supply to the inferior wall.  There was no definite culprit or thrombus, so no definite explanation of the findings.

Therefore, an MRI was done with gadolinium, to assess for myocarditis.

MRI report
1) Mild to moderately reduced LV function with large apical wall motion
abnormality. Calculated ejection fraction is 45%.
2) Small, discrete focus of transmural enhancement, consistent with
myocardial scarring, in the mid inferior wall of the left ventricle. This
pattern of enhancement is unlikely to be from myocarditis, and is more
suggestive of a small infarct.

Thus, the diagnosis is myocardial infarction of the distal wraparound LAD, with STE in II, aVF, V3-V6.

As I've had more and more experience, I've noticed that most of what is thought to be myo- or pericarditis on the ECG turns out to be MI.  As we have better and better tools to make the ultimate diagnosis, we find that cases that should have been diagnosed as MI were diagnosed with pericarditis.  That was not the case here, but it did happen here.

Prehospital ST Elevation and pain resolve with NTG. ECG and Echo normal in ED.

The resolution of symptoms and the ECG in this case is similar to the last post, but the ST and T-wave morphology of the ECGs are quite different, and the outcome is remarkable.


65 yo male with h/o HTN, DM, and hyperlipidemia had onset of intermittent chest pressure and SOB at 2 AM.  He has never had anything like this and has no h/o CAD.  The pain is substernal and radiates to the left arm.  It is not reproducible, pleuritic, or positional.  It became much worse at approximately 1230 and he called 911.  Medics recorded this ECG with pain 10/10:

The computer calls this normal. The medics were worried about the ST elevation.  The ST elevation could be MI or early repol, though one should be skeptical of early repol in patients of more advanced age as it becomes much less common.  Additionally, there is straightening of the ST segments.  The early repol vs. MI "score," based on STE 60 ms after the J-point of 3.0 mm, QTc of 425 ms, and R-wave V4 of 17 mm, is 23.773 (greater then 23.4 is the best cutoff for MI).

He was given sublingual NTG, and his pain improved to 7/10 at 1303, to 3/10 at 1309, and to  1/10 at 1313 after a second NTG.

At each of these times, he had another ECG recorded by the medics, and the resulting decrease in ST elevation and T-wave amplitude is demonstrated here, with all of them side by side, including the 5th ECG recorded in the ED.  (I have also posted the entire 1st ED ECG, recorded at 1334, below this figure).

Here is the full 12-lead from the ED at 1334:

T-waves and ST elevation are subtly but significantly less pronounced.  ER vs. MI score is now 20.324 (STE V360 = 1.5 mm, QTc = 408, R-wave amplitude = 17)

A formal echo was done at 1349 which was entirely normal.  There was no anterior wall motion abnormality.  It was read by one of the most experienced echocardiographers anywhere.  Then his first troponin I returned at 0.18 ng/ml (0.10 is positive).


He was treated for NSTEMI.   Subsequent troponins every 4 hours were: 0.41, 0.90, 1.14, 1.18, 1.01, then 0.98.    Next day had angiography, which showed a 90% LAD stenosis (culprit) as well as severe 3-vessel disease.

He went for CABG on day 5, and this ECG was recorded after the operation:

There is new anterior infarction that has happened some time within the last few days.

A troponin I was measured at over 80 ng/ml, indicating that the infarct had occurred some time between admission and operation, probably before the operation.

1. Transient ST elevation is hazardous
2. Pay attention to ECG changes
3. After the ECG has normalized, the echo may normalize as well.
4. While in the hospital, such a patient should have continuous 12-lead ST segment monitoring.  It is likely that a repeat STEMI was completely missed while he was waiting for CABG.

The last post: why is it not pericarditis? (hint: previous ECG has LV aneurysm morphology)

Yesterday, I posted this interesting transient STEMI.

I was asked why it is not pericarditis.  I have edited the post (see red text) to add the following:

Added to description of presenting ECG:
The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology).  The new ECG has relative reciprocal ST depression in lead III, with ST elevation in aVL.  This rules out pericarditis, which essentially never has reciprocal ST depression.

Added to description of old ECG:
Notice the ST elevation in lead III that follows a deep Q-wave. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology".  LV aneurysm is very different for inferior vs. anterior MI.

And have added the following to the conclusions:

4. This is not pericarditis because:

            a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)

            b. There is relative reciprocal ST depression in lead III.

                      Pericarditis does not have reciprocal depression.

            c. ST elevation of pericarditis  is maximal in leads II and V5, V6. 

                      Here the ST elevation is maximal in V2-V4.

            d. Pericarditis does not have hyperacute T-waves.

            e. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

  

Transient STEMI, serial ECGs prehospital to hospital, all troponins negative (less than 0.04 ng/ml)

This is a 45 yo male who had an inferior STEMI 6 months prior, was found to have severe LAD and left main disease, and was supposed to be set up for CABG a few weeks later, but did not follow up. 

3 hours prior to calling 911 he developed typical chest pain. 

The medics recorded this prehospital ECG at 1535:

There is ST elevation and tall T-waves in precordial leads, with reasonably good R-wave progression.  He is a 45 year old male, so this could be male pattern benign early repolarization (BER, or ER).  But it could be anterior STEMI.  40% of anterior STEMI has upward concavity in all of leads V2-V6.

How can one decide whether this is ER or MI?  First, if an old ECG is available, then compare.  Only rarely does early repolarization change from date to date, though it is possible.

Second, I have developed a score that helps to differentiate the two.  His BER score, based on ST elevation at 60 ms after the J-point in lead V3, QTc (400), and R-wave amplitude in V4 is 23.9 (greater than 23.4 is likely anterior STEMI).

(1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm)

Third, one can do an immediate cardiac ultrasound.

Medics gave him nitroglycerine sublingual and his pain resolved.  He arrived in the ED and had this ECG recorded at 1544

It is essentially the same as the previous, and the score is again about 24 (MI more likely than early repol).  Also, compare with the patient's previous ECG below; concentrate on reciprocal leads III and aVL.  The old ECG has a Q-wave with persistent ST elevation in lead III, and some reciprocal ST depression (typical for aneurysm morphology).  The new ECG has relative reciprocal ST depression in lead III, with ST elevation in aVL.  This rules out pericarditis, which essentially never has reciprocal ST depression.

A previous ECG was found:

This has no ST elevation, and T-waves are not tall.  Notice the ST elevation in lead III that follows a deep Q-wave. This is "Persistent ST elevation after previous MI" or "LV aneurysm morphology".  LV aneurysm is very different for inferior vs. anterior MI.

The patient remained pain free, and this ECG was recorded at 1606:

He remained pain free.  A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist.  They could see no anterior wall motion abnormality.  Diagnosis of ACS was in doubt.

His old angiogram was reviewed and it was known that his disease was not amenable to PCI.  He needed CABG.  He was therefore treated with eptifibatide, heparin, and aspirin, and referred for CABG, but not immediately.

The next AM, this ECG was recorded:

There is some residual ST segment elevation.  The T-waves are far less tall. 

8 days later.  All ST elevation resolved.

It is often difficult to see changes unless they are directly side-by-side.  Here are V1-V3 from start to finish.  I did not include the prehospital because it is identical to the first ED ECG:

Self explanatory, no?

All troponins were undetectable (less than 0.04 ng/ml). 

The patient had a critical LAD stenosis.  Flow had spontaneously been restored, perhaps aided by nitroglycerin.  He underwent CABG. 

Conclusions:
1.  Anterior STEMI can look very much like early repolarization.  There are means to distinguish the two.
2. Transient ST elevation is very hazardous.  Even when the serial troponins are negative, the ECG is critical to the diagnosis of ACS. 
3. When flow is restored, wall motion may completely recover so that echocardiogram does not detect the previous ischemia.

4. This is not pericarditis because:

            a. Pain was typical for MI (substernal, not postional or sharp, resolved with NTG)

            b. There is relative reciprocal ST depression in lead III.

                      Pericarditis does not have reciprocal depression.

            c. ST elevation of pericarditis  is maximal in leads II and V5, V6. 

                      Here the ST elevation is maximal in V2-V4.

            d. Pericarditis does not have hyperacute T-waves.

            e. Tight proximal LAD stenosis explains STE in precordial leads and I and aVL.

The development of an inferior-posterior STEMI, from prehospital to hospital

For other cases of inferior hyperacute T-wave click here and here.
For more on lead aVL, click here and here.  Also use labels on the right sidebar.

Case
A 65 yo woman called 911 for pain in her upper back (between the shoulder blades) and in the left shoulder and left biceps, and some "mild chest pressure" elicited by the medics.  Exam was normal. All but the back pain resolved with nitroglycerine

Medics recorded 6 prehospital ECGs.  Below are 3 of them:

1430

There are hyperacute T-waves in II, III, and aVF.  Note T-wave inversion in aVL, which is the earliest finding in acute inferior STEMI, as well as in V2, suggesting posterior wall involvement

 1432

No significant change

 1445

Now there is clear ST elevation in inferior leads.  T-wave inversions in aVL and V2 have evolved to ST depression.  

They arrived in the ED at 1503.  BP was 116/70.  CXR and cardiac and aortic ultrasound were done to look for any evidence of aortic dissection.  All were normal except for a possible inferior wall motion abnormality.

In the ED, the following ECGs were recorded. 

1512

ST segments have almost normalized. Hyperacute Ts are less prominent, as is T inversion.  There is probably some spontaneous reperfusion of the infarct-related artery.  The computer noticed only some "minimal" ST depression.

1532

Inferior ST elevation is more obvious, with 1 mm in II and III, but T-waves have normalized.  ST depression in V2 is clearly abnormal.  Computer did not read MI.

1542

Now the most obvious findings are ST depression in aVL and V2

Cardiology was consulted.  Again, a cardiology fellow opined that this was not a STEMI, and went to talk with the interventionalist. 

A posterior ECG was recorded:

Only aVL was of great concern.  There is no posterior ST elevation.

The interventionalist was very concerned and activated the cath lab.  The patient was taken to the cath lab.  The proximal RCA was 100% occluded.  It was stented.  Door to balloon time was 62 minutes.  Peak troponin I was 5.15 ng/ml.

Post PCI ECG

T-waves and ST segments are back to normal

Chest pain and LBBB. LBBB resolves and there is V1-V3 T-wave inversion.

A 59 year old man with no cardiac history was at work when he developed very typical substernal chest pressure.  He went to a clinic across the street and had this ECG recorded:

There is sinus tach with LBBB with appropriate discordance and no excessive discordance.  

To learn about appropriate and excessive discordance, please see this post:
http://hqmeded-ecg.blogspot.com/2011/05/lbbb-is-there-stemi.html


911 was called, the medics arrived, and recorded this ECG:

Again, there is sinus tach and no concordant ST elevation, all ST segments are appropriately discordant.  There is lead misplacement: the axis is different and all of I, aVL, V5, V6 should have upright R-waves; the fact that they are negative in I and aVL confirms lead misplacement.  The S-waves are not very deep, but that is because they are cut off.  If projected, they are indeed very deep.

The patient arrived in the ED and had this ECG:

No difference.  Sinus tach with appropriate ST segments.

The following ECG was recorded later:

Now the heart rate is 72 and LBBB is gone.  There is, however, T-wave inversion in leads V1-V3, suggestive of Wellens' syndrome.

Is this an anterior STEMI with LBBB?  Did the occlusion reperfuse, resolving the LBBB and leaving the patient with reperfusion T-waves (Wellens' syndrome)?

He was taken to the cath lab.  All coronaries were completely normal.  All troponins were undetectable.

Explanation:
The patient had a worrisome history: 59 yo with significant substernal chest pressure, so his pretest probability of MI (and even of STEMI) is reasonably high.  However, he had a left bundle brach block with normal appropriate discordance on 3 EKGs.  Only 5-13% of patients with chest pain and LBBB have MI; many fewer have coronary occlusion.  Additionally, appropriate discordance is common in NonSTEMI, but very unusual in coronary occlusion (STEMI).   

Moreover, and importantly, there was sinus tach.  Whenever you see tachycardia with bundle branch block, you should suspect that it is rate related BBB.  Indeed, once the heart rate came down, the BBB resolved.

After resolution, there was T-wave inversion in V1-V3, highly suggestive of ischemia.  There are features of the T-wave inversion, however, which argue against ischemia.  First, as I have pointed out in posts on pulmonary embolism (see links), T-wave inversion of anterior infarction (Wellens' syndrome) almost always has an upright T-wave in lead III.  Also, anterior ischemia is unlikely to spare lead V4 as in this case.
http://hqmeded-ecg.blogspot.com/2011/03/chest-pain-sob-anterior-t-wave.html
http://hqmeded-ecg.blogspot.com/2010/03/anterior-t-wave-inversion-due-to.html

Cardiac Memory
There is another more likely explanation of this T-wave inversion: "Cardiac Memory."  Cardiac Memory (CM) has been described for a couple decades.  It is most common after termination of pacing and other etiologies of abnormal depolarization such as Left Bundle Branch Block.  After resolution of the abnormal depolarization, there may be transiently inverted T-waves that last for hours to days (these T-waves are the heart's "memory" of the previous abnormal conduction).  This phenomenon is poorly understood, but involves "transient electrical remodeling." 
http://www.heartrhythmjournal.com/article/S1547-5271%2807%2900801-6/abstract

Shvilkin et al. described the way to differentiate CM from ischemia:
http://circ.ahajournals.org/cgi/content/full/111/8/969
In short, the combination of:
(1) positive T_aVL (as in this case) and
(2) positive or isoelectric T-wave in lead I (as in this case) and
(3) maximal precordial T-wave inversion greater than the T-wave inversion in lead III (as here: maximal precordial T inversion is in lead V2, at 4.5 mm, and T-wave inversion in lead III is only 2.5 mm) was

92% sensitive and 100% specific for CM, discriminating it from ischemic precordial T-Wave Inversion.

Thus, the very well informed physician could differentiate these ECGs from those of an LBBB patient with MI:
1) no concordance
2) no excessive discordance
3) LBBB with tachycardia, probably rate related
4) subsequent T wave inversion that, according to Shvilkin et al., is diagnostic of cardiac memory.  It is NOT Wellens' syndrome.

AV Dissociation. Is there AV block?

This patient had a drug overdose with oxcarbazepine and this ECG was recorded.

What is the rhythm?  Is there AV block?

See the comments on the annotated ECG below

Answer

There are p-waves and there are QRS complexes and many seem to have no relation to each other.  It is easy to believe there is complete AV block.  

But there is not AV block.  There is accelerated junctional rhythm and a sinus rate that is very near the junctional rate.  See the annotated ECG below: 

Black arrows show p-waves that do not conduct either because the sinus beat came after the AV node, or, if the p-wave is before QRS, because the rapid junctional rhythm initiated a beat before the sinus node was able to conduct through the AV node.  In these beats, the p-wave is upright because it is sinus.  It is sinus because the sinus node fired before the ascending impulse from the AV node could affect it.  Had the AV node conducted up to the atrium first, there would be an inverted p-wave.  The green arrows show normal sinus beats that are conducted before the AV node can initiate a beat on its own.  The thick blue arrow shows a capture or fusion beat: in this case the p-wave occurred late enough that, by the time it conducted through the AV node, the QRS was no longer completely refractory; however, it was slightly refractory and therefore the QRS is slightly abnormal (wider). The narrow blue arrow is also a fusion beat; the p-wave is buried in the previous T-wave (that's why the previous T-wave looks larger than all the other.  The right bundle branch is still refractory, but the left bundle is not, so it has an Right Bundle Branch Block morphology.   

Dr. K. Wang, the rhythm master, had this to say: "The 8th QRS holds the key. It occurs with a shorter R-R interval with a reasonable PR interval, indicating that it is conducted from the P-wave.  Thus, there is no complete AV block, just accelerated AV junctional rhythm with interference AV dissociation.  Accelerated Junctional Rhythm is a very regular rhythm, and any QRS that occurs with a shorter R-R interval is not from the junction, but is a beat conducted from above."

Thus, there is no AV block and the danger to the patient from the drug overdose is not nearly what it would be had there actually been AV block.

AV Dissociation does not necessarily mean AV block!!

Take a look at this prehospital ECG:

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A 49 year old woman with chest pain arrived.  The medics had recorded this ECG.  What is the diagnosis?

See explanation below

Let's go back in time 13 days:

A 49 yo woman with a h/o LAD stent, on aspirin and clopidogrel, complained of brief episodes of substernal pressure-like chest pain relieved by nitroglycerine.  She was seen in the ED on day 0 and was pain free in the ED.   She had had a previous anterior MI and had some baseline minimal wall motion abnormality.

Here is her ECG from 2 years prior:

It is normal except for some poor R-wave progression consistent with previous MI.  

Here is her ECG on the first day of presentation (day 0):

The T-wave in V1 is more upright and prominent, and there is subtle nonspecific ST segment depression in V5 and V6 (new).

Initial troponin I was less than 0.010 ng/ml (undetectable).  She was started on heparin, and was admitted to the hospital.  Her second troponin was 0.025 ng/ml (less than the 99th percentile of 0.030 ng/ml).  The third was again less than 0.010 ng/ml.  These troponins are below the diagnostic threshold for MI, but with such a rise and fall, even though below the diagnostic cutoff for MI, they suggest unstable angina, especially in the context of typical pain and h/o CAD.

The cardiologist decided to do an sestamibi stress test.  The first part of the test was done as an inpatient, but the patient was sent home with instructions to follow up for the second part of the scan.

Apparently she did not show up.


On day 13, this woman presented with chest pain.

And this brings us back to the ECG at the top.  It was recorded at t=0 on day 13 by EMS, 15 minutes prior to ED arrival.

This is the same as the one at the top: There are hyperacute T-waves in V1-V4, ST elevation in V1 and V2, and ST depression in II, III, aVF, V5 and V6.  This is diagnostic of LAD occlusion. 

The physician did not know at the time that she had a previous ECG and a visit 13 days prior, but since the ECG is diagnostic, the cath lab was activated.

The cardiology fellow looked at the ECG and did not recognize MI, and wanted to deactivate the cath lab, but reconsidered after the following initial ED ECG was recorded.

This is obviously diagnostic of anterior STEMI

The patient had a 100% in stent thrombotic re-occlusion.  It was opened and stented.  Her initial troponin I was 0.07 ng/ml, and it peaked at 18 ng/ml because of a very fast door to balloon and symptom onset to balloon time.

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Here is a rhythm strip.  What is the rhythm?

This (above and below) also is from Dr. Wang's Atlas of Electrocardiography, with permission.

It is same as the last post.  AV nodal rhythm with reverse Wenckebach, this time the R-P is normal, then prolonged, then drops, as outlined in the graphic below: