20 year old woman with dizziness and hypotension

This is posted courtesy of Jaber Ibrahim Almajbri.  He posted it on Facebook EKG club and gave me permission to post it here.

This 20 year old has hypotension, 70/40.

What is it?

 It is irregularly irregular, so it is atrial fibrillation.  The QRS complexes are not all the same, so it is not just atrial fib with aberrancy (RBBB, LBBB, other IVCD).   Some R-R intervals are less than 160 ms, corresponding to a possible heart rate of almost 400.   The AV node cannot conduct this fast. These are conducting down an accessory pathway.

Thus, it is atrial fibrillation with WPW.

I doubt that one could really get a diastolic BP at this rate.  This case shows how fast the heart rate can be in this condition.

This can easily degenerate into ventricular fibrillation, especially if any AV nodal blocker is given.  This must be cardioverted immediately.

Then the patient will need ablation by an electrophysiologist.

An elderly man with severe chest pressure......

This was sent to me by a medical student:

The patient is an elderly man with no significant past medical history who developed what he describes as chest tightness throughout his anterior precordium, 9/10 in severity, associated with nausea, vomiting, diaphoresis and shortness of breath, lasting for greater than 2 hours, that started while he was lifting firewood. His symptoms did not go away with rest. He presented to his primary care physician's office. An EKG was recorded at 135 minutes after pain onset:

There is no old ECG for comparison.  What do you think?

He was treated with sublingual nitroglycerin and aspirin, which improved his chest discomfort. He was transported by ambulance to the hospital. On initial evaluation in the emergency department he still had pain and had this ECG recorded at 150 minutes (2.5 hours) after pain onset: 

What do you think?  See below.

The med student asked what I thought, and I wrote: "hyperacute T-waves in V4-V6."  Here is the normal relationship between the T-waves and the QRS in V4-V6:

Knowing this is the normal proportion, what do you NOW think about the above 2 ECGs?

It is clear that the T-waves in V4-V6 on the first two ECG are hyperacute.  They are far too large for the QRS.  In addition, if you look closely, you will see that there is more ST elevation on the second ECG.  In fact, on the 1st ECG, V5 had zero ST elevation but has almost 2 mm on the 2nd ECG.

These findings, along with the pretest probability (a 77 year old with persistent substernal chest pressure and diaphoresis!!) mandate at least a stat formal echo, but preferably emergent coronary angiography

Initial cardiac markers were negative. The patient became chest pain-free.  

He was admitted for a "rule out."

A cardiologist evaluated his ECGs:

"In the emergency room an EKG was obtained which showed Q-waves throughout the precordial leads and some reciprocal mild ST elevations but with a distinct J-point and less than 1 mm STE.  I was asked to see the patient and review the ECGs and I felt this represented old anterior MI which had been completed at some point in the remote past."  

I do not fully understand this explanation.

He underwent more ECGs: 200 minutes (2 hours 40 min) after pain onset: 

Complexes 8 and 12 are PVCs. R-waves in leads V4-V6 are much diminished and T-waves are not nearly as tall as they were.

At 270 minutes (4.5 hours) after pain onset, the patient reported a slight increase in pain, and another ECG was recorded:

Now there is ST elevation in V4-V6, the T-waves are still large, and there is poor R-wave progression

The cardiologist wrote this note:

“Pt reported a slight increase in pain. Repeat EKG showed no clear ischemic changes. Old Q waves.”  

At 10.75 hours after the pain onset, the pain was increasing.  Troponin I returned at 7.42 ng/mL.  This ECG was recorded:

Well developed infarction with QS-waves, diminishing T-waves and some terminal T-wave inversion

Another ECG was recorded at 13 hours after pain onset: 

Deepening T-wave Inversion

At 15 hours after the first ECG, the patient was taken for angiogram and had a 100% distal LAD occlusion.  It was opened and stented.

Here is the post cath ECG:

There is deepening T-wave inversion.

Peak troponin I = 29 ng/mL.  Formal echo shortly after the stent placement showed a dyskinetic anterior wall and an EF of 35-40%.


Learning Points

1. T-waves should be proportional to the QRS.  If they are too large, you must suspect hyperacute T-waves and aggressively evaluate the patient with at least a high quality emergent echocardiogram

2. When the ECG is diagnostic, as here, do not wait for troponins to be positive before acting.  Most coronary occlusion has initially negative biomarkers.  Once the troponins are positive, much damage is done.

Male in early 40's with 1.5 hours of chest pain

A third year medical student sent me this ECG and asked for my interpretation:

Recorded 0625

Here is what I wrote back: 
"Tough one.  Probably is acute LAD occlusion, needs serial ECGs/echo."

Standard ST elevation criteria

Note there is not enough ST elevation to meet the standard criteria, which require at least 2 mm ST elevation at the J-point, relative to the PQ jct., in leads V2 and V3 for a male over 40 years old.  In this case, there is 1 mm in V2 and 2 mm in V3.

1. Standardization and Interpretation of the Electrocardiogram, full text
2. MacFarlane 2004 (47% sensitive and 98% specific for MI as diagnosed by biomarkers.)


I had used my formula:

STEV350 = 2.5 mm (but it might be 3 mm)
QTc = 410
R amplitude in V4 = 14 mm

The value I obtained was 22.6 (23.2 if 3.0 mm is used for STE V3).

At a cutoff of 23.4 (my typically recommended cutoff), the sensitivity for LAD occlusion among subtle cases is 86% (much higher if all LAD occlusions are used as the denominator), with a specificity of 91%.

At a cutoff of 22.0, the sensitivity was 96% but with decreased specificity of 81%.

To me, the T-waves looked too fat to be normal.  And even though the formula was not greater than 23.4, at 22.6 or 23.2, it is close enough to be worried.

Outcome:

The pain had started at 5 AM, so that initial ECG above was at 1.5 hours after pain onset.

It was not recognized as possible LAD occlusion.  Initial troponin T was negative at less than 0.01 ng/mL (99% is less than 0.10 ng/mL).

2.5 hours later, the patient was seen by a cardiologist and the ECG interpretation was: "ECG - NSR without any ST-T changes.  No STEMI.  Will cycle markers and admit to Observation unit for rule out and stress test."

Comment: this is a patient who needs intensive evaluation in order to rule in, not rule out, MI

At 11:14, almost 5 hours after presentation and first ECG, the troponin T returned at 0.37 (this is pretty high for Trop T).   CK was 368.

A 2nd ECG was recorded:

All ST elevation has resolved, proving that the first ECG was indeed STEMI.  Fortunately for the patient, the LAD appears to have spontaneously reperfused.  There are persistent R-waves, suggesting that not too much damage was done.  But these can be misleading.

At 12:21 another ECG was recorded:

Now there is recurrent ST elevation.  The LAD is re-occluding.

The patient was taken for Cath at 1414 and was found to have a 100% proximal LAD occlusion after a large D1 (the D1 had a 90% stenosis).  So, mid-LAD occlusion.

Trop T at 1752 was 2.11 ng/mL (this is really quite high and indicates a large infarct and significant myocardial loss).

Learning points:

1.  Beware large fat T-waves.  Use the formula for differentiating normal variant ST elevation from subtle LAD occlusion.  A value less than 22.0 will only miss 4% of subtle LAD occlusion.  If the value is higher than 22.0, serial ECGs are essential.

2.  Cardiologists are not generally trained to find these subtle signs of coronary occlusion.

3.  This is a NonSTEMI due to coronary occlusion.  Many NonSTEMI are due to occlusion and do not get rapid reperfusion,  They are not diagnosed until late, when biomarkers return,  They usually do not go to the cath lab until the next day (because they are "NonSTEMI") and they thus have worse outcomes, higher biomarkers, and higher mortality than NonSTEMI who have an open artery at cath.

Chest Pain and Right Bundle Branch Block

A male in late middle age with a history of RCA stent 8 years prior complained of chest pain.  EMS recorded the following ECG:

What do you see?  The computer read "Right Bundle Branch Block"

There is RBBB and LAFB, which can make it difficult to see the end of the QRS.  I have annotated it here:

The lines mark the end of the QRS and beginning of the ST segment.  In RBBB, there should be no ST elevation, or minimal.  In fact, V1-V3 should have some ST depression and T-wave inversion.  In other words, the ST segment and T-wave should be discordant to (in the opposite direction of) the positive R' wave [see the 2nd ECG of this post].  Here you can see abnormal (diagnostic) ST elevation and an upright T-wave in V2-V3, with diagnostic ST elevation in V4-V6 and in I and aVL, and with reciprocal ST depression in III and aVF.  So this is diagnostic of proximal LAD occlusion.

New RBBB + LAFB is a very bad sign.  It is highly associated with proximal LAD occlusion and bad outcomes.

See this paper by Widimsky et al, which shows the high association of RBBB, especially with LAFB, with LAD occlusion.  Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAH) on the admission ECG.

Here are three more dramatic cases that illustrate RBBB + LAFB

Case 1 of cardiac arrest with unrecognized STEMI, died.

Case 2 with 68 minutes of CPR and good outcome

Case 3 with LAD occlusion, cardiac arrest, could not be resuscitated


Case Progression

In order to keep patient confidentiality, I will only give the barest of follow up:

As the emergency physician was immediately assessing the patient, he had a v fib arrest.  He could not be resuscitated in the ED but was taken to the cath lab while on LUCAS (mechanical) CPR, underwent successful PCI of a proximal LAD occlusion during chest compression, and after opening the artery, achieved ROSC (return of spontaneous circulation).  

See this article by Widimsky:

Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy

 https://academic.oup.com/eurheartj/article/33/1/86/2398223

Is this acute STEMI? LV Aneurysm? Would you give Thrombolytics?

Recently I posted a case describing "Acuteness" on the ECG and how to assess whether it is too late for reperfusion, especially thrombolytics.

This case was recently posted by Tyron Maartens on Facebook EKG club (he agreed to let me post it here), with the following clinical information:

"42 year old male with two weeks of intermittent chest discomfort, awoke 4 hours prior to this ECG with a more severe, heavy chest pain (5/10). Self-medicated with 600 mg Ibuprofen and 750 mg Paracetamol (no change) prior to driving to the ED. BP 112/80, SpO2 100%. Patient appears only slightly anxious. No risk factors, leads a healthy lifestyle. Unremarkable physical examination.

Not a difficult ECG per se, but what's your management plan? PCI is not an option."

Would you give thrombolytics?
We all know that some other information would be helpful, but he did not offer it.
So let's just go with what we have.
See my answer below.

There were many comments that it was too late for thrombolytics or that this signified an LV aneurysm, not acute MI.

This is my response:

"This is definitely acute or subacute. It is not chronic. See my formula for differentiating anterior LV aneurysm (that is to say, persistent ST elevation after old MI) from acute anterior STEMI. There is no question that this benefits from immediate PCI. See this full text link to an article from JAMA on PCI in patients who present at 12 to 48 hours. As for thrombolytics, that is a bit riskier. I think the ECG supports an occlusion time of less than 12 hours and I would risk it."  

Here is a link to a blog post with the formula, which we have recently validated and will publish.  The single highest T/QRS ratio is V4 at 1.5/3.0 = 0.50 and then V3 at 4/9 = 0.44, both greater than 0.36 and the sum of T amplitudes divided by the sum of QRS = 11/38.5 = 0.28, which is greater than 0.22.  Both support acute anterior STEMI.

Tyron's response was: "he received lytics and did well."

Then he sent some more information which helps in the decision:

2 weeks of intermittent chest discomfort, then at 8 PM the pain increased and he went to sleep.  He awoke 4 hours prior to this ECG (~1 AM) with a more severe, heavy chest pain (5/10).  BP was 112/80, SpO2 100%.  Patient appears only slightly anxious.  No risk factors, leads healthy lifestyle.  Unremarkable physical exam.  There was no dyspnea and lungs were clear.  Troponin I taken 10 minutes after presentation returned at 0.67 ng/mL.

This last bit of information on the troponin would have been very helpful in interpreting this ECG.  Why?  Because the main question is not whether this is acute STEMI or not (it is - see discussion of formula for differentiating acute anterior STEMI from anterior LV aneurysm), but whether it has been going on too long to give thrombolytics.  A very elevated troponin would support that latter; this very low troponin supports high acuteness.

Standard teaching is that if pain lasts more than 12 hours, as in this case, thrombolytics are contraindicated.  [PCI, being much safer, is OK.]  This is clearly an oversimplification, as many patients have pain for very long periods that is not irreversible infarction but rather ongoing angina.  The ECG is the best way of telling how late the infarct is presenting.  Read all this information on acuteness for details, but in summary, there are several factors that differentiate between prolonged occlusion and acute occlusion:

1. The height and size of the T-wave.  Hyperacute T-waves are present when the myocardium is still viable and their size diminishes as the infarct progresses and becomes irreversible.
2. The height of the ST segments.  After the hyperacute phase, the ST segments rise and only fall with either 1) reperfusion or 2) prolonged ischemia leading to irreversible infarction.
3.  Presence and depth of Q-waves, preservation of R-waves.

The other consideration is that this is an old anterior MI with persistent ST elevation (LV aneurysm).  That is reasonable possibility as there are very well formed QS-waves in V2 and V3, typical of LV aneurysm.  My formula to help differentiate the two depends on the height of the T-wave relative to the QRS.  The higher that ratio, the more likely that it is acute.  In fact, in our studies, the false negative cases for acute STEMI were due to prolonged occlusion (at least 6 hours).  See the formula here.  We have validated this formula and will publish it soon.

Of course, if you have bedside echo and are good at it, it is helpful to differentiate aneurysm from acute MI, but not subacute MI from acute MI!  A formal echo was not available to this team.


Outcome:

Aspirin and Clopidogrel were administered, along with sublingual nitrates and morphine, which did not relieve his pain. After ECG interpretation and screening the patient was thrombolysed with Streptokinase and received heparin. At 30 minutes and 35 minutes after strep there were 30 second runs of AIVR. Reperfusion T-waves developed, ST-elevation subsided and the patient's pain dissipated. Formal echo three days later showed good left ventricular function (LVEF >40%) and a cath at 5 days showed good coronary flow (TIMI 3) in all arteries. At four months there was no morbidity.

This was a highly skilled interpretation by Dr. Maartens that resulted in a very good outcome. Well done!

Inspiratory Threshold Device Works if CPR is Adequate: New Evidence from ROC-PRIMED Trial

Re-Analysis of Data from the ROC-PRIMED Trial, presented at the AHA meeting in Chicago, shows that if CPR is done at the correct rate and depth, that the Inspiratory Threshold Device (ITD) improves survival from 4.1% to 7.2%. 

The ITD inhibits entry of air down the endotracheal tube for a fraction of a second, so that increased NEGATIVE pressure is created in the chest during recoil from chest compressions.  This negative pressure increases venous return, cardiac output, and coronary blood flow.

There are numerous laboratory experiments that prove this, and many studies in patients with hypotension from various causes (here is one study I conducted myself on spontaneously breathing hypotensive patients)

And don't forget the Landmark ResQTrial, in which the use of BOTH compression-decompression CPR and ITD increased survival by 50%.

More detail here:

New University of Minnesota analysis shows strong partnership between CPR and a common assist device may result in better outcomes for patients.

Research was presented at the annual meeting for the American Heart Association in Chicago

MINNEAPOLIS/ST. PAUL (November 17, 2014) – New analysis shows the use of an impedance threshold device (ITD) in partnership with quality CPR may lead to better outcomes for patients experiencing cardiac events. The analysis was being presented at the American Heart Association (AHA) Scientific Sessions in Chicago on November 15, 2014.

The analysis is a second look from the Resuscitation Outcomes Consortium (ROC) PRIMED Trial, which was published in the New England Journal of Medicine in 2011. This new analysis was led by Demetris Yannopoulos, M.D., research director for interventional cardiology at the University of Minnesota Medical School and the medical director of the Minnesota Resuscitation Consortium. He is also the Robert K Eddy Endowed Chair for Cardiovascular Resuscitation at the University of Minnesota.

The initial study sought to determine if an ITD, designed to cover the mouth during CPR and increase circulation, can help provide better CPR practice and, consequently, better outcomes for patients experiencing respiratory failure. Researchers employed a blinded model in which some patients were administered the working ITD and others were treated with a device that looked identical to the ITD but did not perform the intended function. Researchers reported no difference in outcomes based on the active or sham device.

“The ROC PRIMED Trial was a landmark study in helping to better understand CPR and the ITD,” said Yannopoulos. “Still, the PRIMED study did not account for the quality of the CPR being performed in partnership with the ITD. We suspected the quality of CPR may make a difference when employing the ITD to help revive a patient.”

Analysis of the ROC PRIMED data by Yannopoulos and his team shows there is indeed an interaction between CPR quality the ITD and the primary endpoint of survival to hospital discharge with good neurological function, in contradiction with the results of the initial trial. The new analysis also showed that use of an active ITD, combined with high quality CPR, increased survival to hospital discharge for cardiac arrest patients by a relative 75%. High quality CPR was defined as a compression rate of 80-120 compressions per minute, with a depth of 4-6 centimeters and a compression fraction of >50%, all consistent with AHA guidelines at the time of the study.
“Our analysis showed when high quality CPR was performed, neurologically-intact survival in the active ITD group was actually 75% higher than when the sham device was used,” said Yannopoulos.

About the ITD

The impedance threshold device (ITD) was conceived at the University of Minnesota by professor Keith G Lurie MD and is used widely by hospitals and EMS systems to improve blood pressure and perfusion during CPR. An ITD regulates pressure in the chest to reduce intrathoracic and intracranial pressure and maximize the blood drawn into and pushed out of the heart with each
chest compression. These new data further validate that Intrathoracic Pressure Regulation (IPR) Therapy provided by the ITD improves hemodynamics and survival when used with high quality CPR.

Acute Severe Pulmonary Edema and New LBBB, with Bedside Echo

A middle-aged woman had sudden pulmonary edema in the middle of the night.  There was no known history of left bundle branch block.  There was no chest pain.

Her blood pressure was 200/110.  Here was her initial ED ECG:

Sinus Tachycardia with Left Bundle Branch Block.  There is no concordant ST elevation.  There is no proportionally excessively discordant ST elevation.  The highest ST/S ratio is in V1 at 2.5/27 = 0.093 (normal).
There is no evidence of ischemia on this ECG, and certainly no evidence of STEMI

In our study of occlusion in STEMI, we excluded patients with tachycardia or pulmonary edema because they often have false positive ST elevation (tachycardia exaggerates the discordant ST elevation and depression of LBBB).  They do not commonly have false negative ST elevation.  I would be very surprised if a patient with this ECG had active persistent LAD occlusion, though as with any ECG, circumflex occlusion can easily be missed.


A bedside echo was done by a highly skilled ED Echo expert.  Here is the parasternal long axis view:

He then performed a parasternal short axis view:


This appears to show an anteroseptal wall motion abnormality.

Images were done with speckle tracking, but unfortunately could not be uploaded. Here are some images of ultrasound speckle tracking from another case of LBBB.

However, LBBB affects the sequence of activation  of the ventricle (dyssynchrony) which appears to the interpreter as a wall motion abnormality.  Is this just dyssynchrony, or is there a wall motion abnormality? 

Chest X-ray and sonographic B-lines confirmed pulmonary edema.

The patient was put on BiPAP and high dose nitroglycerine.

The cardiologist was consulted for possible cath lab activation and was certain this was not acute coronary occlusion.  The cath lab was not activated.

The patient was able to be weaned from BiPAP in the ED.  A repeat ECG was obtained:

Slower rate, even less ST elevation (expected, as discordant STE in LBBB is exaggerated by tachycardia)

Was this a brief occlusion of the LAD that was invisible on the ECG, and only showed up as a wall motion abnormality?

A Formal Echocardiogram was done:

Decreased left ventricular systolic performance severe .
Left ventricular hypertrophy concentric borderline.
Regional wall motion abnormality-mid anterior wall with sparing of apex.

(Our ED echo expert was correct).  But the ECG was even more correct.

Troponin I Peaked at 0.054 (0.030 is 99%).

Thus, a non-emergent angiogram was done:

Angiogram: Normal coronary arteries.  (No plaque at all.)

Final diagnosis: Idiopathic cardiomyopathy.  Etiology of WMA unknown.  No MRI done for assessment of other etiologies.


Learning points:

1.  In acute pulmonary edema, if the ECG does not show ischemia, and there is another etiology (severe hypertension), and the pulmonary edema resolves with supportive care and NTG, then it is unlikely to require emergent angiogram for severe ACS.

2.  New LBBB by itself, without any concordance or excessive discordance, is of little value in diagnosing acute STEMI or severe ischemia.

What is the infarct artery? (Complex analysis, in this case)

This case was put on Twitter by Elisha Targonsky, who has a nice EM blog (http://thechartreview.org).  He provided it for posting here.  On Twitter, he asked for an analysis of the infarct artery.

Analysis of the infarct artery is mostly an academic exercise.  The patient clearly needs cath lab activation.  However, it is of some clinical value: interventionalists like to know what artery is affected because it often determines which artery they will investigate first with angiography.

So it does have some value, but is not critical.

But moreover, it is an exercise which helps one understand all the ST vectors at play in an ECG.

What is your analysis?  See mine below.

Notice this is a 15 lead ECG, with posterior leads V8 and V9 and also Right sided lead V4R.

Here was my Twitter response without any other information:
Tweet 1: Prox large RCA, also to lateral and posterior walls. Ant MI is RV, not LV. V2 less STE b/o posterior MI.
Tweet 2: In other words: pseudo anterior MI (RV: V1-V4) from large RCA, to post & lat also. V2 STE attenuated by post

One must explain several findings:
1. Inferior ST elevation
2. Anterior ST elevation (V1 and V3), but very little in V2
3. ST elevation in V4-V6 (but also ST depression in aVL)
4. Posterior ST elevation
5. ST elevation in V4R


--One is tempted to call this LAD occlusion with anterior MI and wraparound LAD to the inferior wall.  But then how do you get a posterior STEMI also?

--One might say: OK, it is left main, and that is why there is BOTH anterior (LAD) and Posterior (Circ) STEMI.

Why the inferior STE?  Maybe it is a left dominant system, so the circ also goes to the inferior wall.

But then one must still explain 2 findings: the patient is still alive AND there is ST elevation in V4R.

ST elevation in V4R can conceivably be caused by LAD occlusion, as some individuals have the RV supplied by rightward branches of the LAD.  This is a possibility, but you would expect such a patient to be in shock.

What was the clinical scenario?

A middle-aged male with h/o CAD, HTN, DM, hyperlipidemia.
Previous LAD stent, then 2 years later had bare metal stent to RCA.
Presented without shock, with 10/10 substernal CP.  Diaphoretic and nauseated.

--So left main is very unlikely.

--What then?   The ST elevation in V4R is the big clue.  This is almost always due to Right Ventricular MI.  RV MI also may cause anterior ST elevation mimicking anterior MI ("Pseudoanteroseptal MI").  In these cases, the maximum ST elevation is in V1 or V2, and becomes less as one goes out to V3, V4, etc.

So the IRA is the RCA.

--What does this RCA supply besides the RV?  It supplies the inferior wall, the posterior wall, the inferolateral wall (STE in V4-V6 without high lateral STE in aVL)

--Why is there less STE in V2 than in V1 or V3?
1. The posterior ST elevation is exactly reciprocal to V2 and is attenuating the STE in V2.
2. That downward pull is not as opposite V3 as it is opposite to V2.
3. The RV ST elevation is greater in V1 than in V2
4. The lateral ST elevation has more "upward" pull on V3 than there is downward pull from posterior.

--Why is there ST depression in aVL but ST elevation in precordial lateral leads V5 and V6?
V5 and V6 are situated more inferior than aVL.  Many inferior MI have ST elevation in V5 and V6.  And all inferior STEMI have ST depression in aVL.  In our series of 150 inferior STEMI, 27 had ST elevation in V5 and V6.  All had ST depression in aVL.

What direction is the ST vector?
There is diffuse ST elevation, except towards leads I, aVL and V2:
To the right
Inferior
Posterior
Left inferolateral
Left anterior
Right anterior



Angiography Results:

No disease in LAD or circ
RCA dominant with acute thrombosis
Thrombectomy and stent.

Good outcome.

Is this inferor STEMI?

I received this ECG from a reader:

This is a very elderly female with chest discomfort and SOB.  Our interpretation was STEMI or demand ischemia.

Is there inferior STEMI?
Answer Below

The apparent ST elevation in II, III, and aVF is all due to the atrial flutter baseline causing PseudoSTEMI pattern.

There is no evidence of ischemia.

Read this ECG

What is the diagnosis here?

The computer read was ****Acute STEMI****What is really going on?
See Answer Below

This is a trauma patient (motor vehicle collision) who arrived with a temperature of 27 degrees Celsius.  Among many injuries was a traumatic diaphragmatic hernia, which may also affect the ECG.

The prominent features are: relative bradycardia (one would expect in this ill trauma patient) and Osborn Waves in V3-V6.  The most common finding in hypothermia is atrial fibrillation with a slow ventricular response (not seen here).  The computerized QTc was 489 ms (accurate).

After warming, another ECG was recorded:

The ECG in hypothermia 

Rhythm: The most common rhythms in hypothermia are sinus bradycardia, junctional bradycardia, and atrial fibrillation.  Shivering artifact is common.  Atrial flutter may also be seen.  At temperatures below 30 C, the patient is at risk for ventricular fibrillation.   In this study of 29 humans cooled to 28-30 C for cardiac surgery, 19 developed atrial fibrillation and 2 ventricular fibrillation.

QRS: Osborn waves are thought to be pathognomonic of hypothermia, but can also be seen in normothermic patients.  "J-waves" or "J-point notching" is very common in early repolarization.   Very narrow Osborn waves were reported in severe hypercalcemia (level 16.3).  Sometimes a short ST segment of hyperCa can be misinterpreted as an Osborn wave; that is not the case in the aforementioned case report.   J-wave syndromes are proposed to give a unifying pathophysiology to Osborn waves of hypothermia and early repolarization, as well as Brugada syndrome.

See other examples and more discussion here.

Cold symptoms and bradycardia. What is this pre-excitation?

A young man presented to the ED for cough and runny nose and was bradycardic, so an ECG was recorded:

There is sinus rhythm with complete AV dissociation due to complete (third degree) AV block.  The escape has a slurred upstroke.  Is this a delta wave?

The patient stated that he knows he has this and that whenever he feels weak he just takes some methamphetamine and he feels fine!  He refused any treatment or evaluation.


The rhythm is interesting, though, and we have some disagreement about whether it is an nodal escape with a fasciculo-ventricular accessory pathway, or a ventricular escape with "Pseudo" Delta waves.  In any case, there must be some pre-excitation.

If it is fasculo-ventricular, as our EP expert says (and I defer to him), then this is a potential ladder diagram, as drawn by Christopher Watford:

K. Wang has graciously offered to let me insert pages 212 and 213 on Pseudo Delta waves from his great Atlas of Electrocardiography:

It seems to me that Pseudo Delta waves are only "Pseudo" in that the do not necessarily represent an accessory pathway, the way we normally associate delta waves with WPW.

However, it also seems that any delta wave implies some pre-excitation.  Ventricular beats often take some time to reach the conducting fibers and will thus often have pre-excitation of some sort.

A Young Woman with Chest Pressure and Subtle, Focal ST Elevation/Depression

A very healthy woman in her 20's (who, however, is a heavy smoker) presented with 4 days of waxing and waning substernal chest pressure radiating to the throat and both shoulders.  It was not sharp, not pleuritic.  There were no myalgias, no viral symptoms, no F/C/S.

Looking at her, she was the picture of health, and I thought to myself: "Is there any possible way she could have an MI?".  My answer, of course was yes.  

I've seen it too often before in young women, as for instance:
in this case, and 
in this case, and others.

So we ordered an ECG, of course:

I found this very interesting and worrisome.

--The most obvious is ST elevation is in V3-V6. This could be normal, myopericarditis, or MI.

--However, there is another finding which had me very worried: ST depression in lead III and opposing ST elevation in I and aVL.

--There is PR depression that is within normal limits

--The ST elevation in aVL is only 0.5 mm, but the QRS has even less amplitude.

Let's look at III and aVL enlarged:

Notice the QRS voltage is less than 0.2 mV (less than 2 mm) in aVL, and the ST segment is nearly 1 mm.  So the proportional ST elevation is quite high.
This is only partly due to the difference in axis between the QRS and ST segment.  QRS axis is 60 degrees, towards lead II, and the ST axis is 0, towards lead I.

Pericarditis only manifests ST depression in lead III if it is focal to the high lateral wall. Focal pericarditis is unusual, but focal myocarditis is not.  Most pericarditis is electrocardiographically diffuse, with an ST vector towards leads II and V5 and no reciprocal ST depression except in aVR.

A bedside echo was normal.  Troponin I was sent.  Chest X-ray was normal.  She was given aspirin and sublingual nitroglycerine, and her pain subsided slightly.  Another ECG was recorded:

The ST deviation is less.  Thus it is dymamic, which is not usually associated with myo-pericarditis, but probably because serial ECGs are not frequently obtained for this condition. 

Here is the enlargement:

The troponin I returned at 18.9 ng/mL. 

Is it MI or myocarditis?

See this excellent study of patients with suspected MI and normal angiograms (from 2001, it is still the best study I can find).

Of 45 patients, 35 had myocarditis by Indium scintigraphy (unfortunately, I don't know how accurate this test is, and it seems that no diagnostic test is terribly accurate for myocarditis. Even the reference standard, endomyocardial biopsy, often misses the involved myocardium).
--Half of them had focal myocarditis and half diffuse.
--28% had reciprocal ST depression.
--62% had regional wall motion abnormalities.
-- In the U.S. Myocarditis treatment trial, 89% of these highly selected patients (not ED patients) had a syndrome consistent with a viral prodrome.

Thus, unfortunately, if there is a wall motion abnormality, one is really unable to differentiate acute MI from myocarditis in the emergency department. 

Case Progression 

I consulted our cardiologist, who sent his echo tech, and we obtained a high quality, Definity contrast echo.  This was done and showed a lateral wall motion abnormality.

So we activated the cath lab.  The interventionalist was very pleased to come evaluate this young woman's coronary arteries, agreeing wholeheartedly that you can't "sit on" someone all night who has chest pain and a positive EKG and troponin.

The angiogram was completely normal.

The left ventriculogram showed a dense lateral regional wall motion abnormality, very highly suggestive of focal myocarditis.

Serial troponin I went from 18.9 ng/mL, to 19.7 at 6 hours, to 16.8 at 9 hours, to 16.1 at 24 hours to 11.5 at 42 hours.

An ECG was recorded the following morning:

Now there is much more widespread ST elevation, with no reciprocal ST depression. This is classic myopericarditis.

An MRI of the heart confirmed inflammation of the lateral wall, all but diagnostic of myocarditis.

She was treated with colchicine and ibuprofen.

A final ECG at 42 hours was resolving:

Learning Points:

When the differential diagnosis is myocarditis vs. acute MI, it is difficult to make any conclusions without an angiogram.  In half of myocarditis, there will be a wall motion abnormality (focal myocarditis) and it will be impossible to distinguish from MI.  If there is no wall motion abnormality, one can be reasonably confident that it is diffuse myocarditis and avoid the emergent angiogram.

I am not at all troubled by activating the cath lab to be certain that she was not having a coronary thrombus.  It put everyone's mind to rest.