Acute Respiratory Distress, Hypoxia, and a Large Right Ventricle on Bedside Ultrasound

A 50-something presented in acute hypoxic respiratory failure, alert and in respiratory distress.  She required Bilevel positive pressure ventilation.

Pulse was 139 and BP 99/75.  She was diaphoretic.

A bedside ultrasound was done immediately:

Notice the very large RV and very small, but well functioning, left ventricle.

What do you think?
















There were also B-lines (not shown).

Here is here initial ECG:

What do you think?

There is sinus tach.  There is a large S-wave in lead I.  There is a Q-wave in III.  Do these indicate acute right heart strain, typical of pulmonary embolism?











No!

First, there is no full S1Q3T3 (no T-wave inversion in lead III; for significance of S1Q3T3, see notes at the bottom).

More importantly, there is also a large R-wave in lead V1.  This combined with the right axis deviation (S greater than R in lead I) is all but diagnostic of RV hypertrophy (in contrast to acute right heart strain) which is a chronic condition.  Notice there are also large upright P-waves in right precordial leads (though not in lead II).  These are also suggestive of right atrial hypertrophy, which often accompanies right ventricular hypertrophy.

Seeing this, the probability of PE was greatly diminished.  The B-lines on lung ultrasound was also very strong evidence against PE.

She turned out to have chronic pulmonary fibrosis and acute pulmonary edema.  The RV enlargement was chronic.

A previous formal echo was found:

Pulmonary hypertension. The estimated peak systolic PA pressure is 60 mmHg

plus RA pressure and diastolic pressure 13 mmHg plus RA pressure.   Right ventricular enlargement with distortion of the position of the interventricular septum consistent with right ventricular pressure

overload.  Decreased right ventricular systolic performance. The left ventricular is relatively small with decreased systolic performance. The estimated left ventricular ejection fraction is 39 %.

There are no convincing regional wall motion abnormalities.

After therapy for pulmonary edema, she improved.

Learning Points:

In the context of hypoxic respiratory failure and a large RV on echo, the ECG can help to differentiate acute right heart strain (which can be due to acute hypoxia, especially from pulmonary embolism) from chronic RV hypertrophy.

The presence of a large R-wave in lead V1 well differentiates acute right heart strain from chronic RV hypertrophy.



S1Q3T3

This is a paper worth reading: Marchik et al. studied ECG findings of PE in 6049 patients who had clinical findings suspicous of PE, 354 of whom had PE.  They found that S1Q3T3 had a Positive Likelihood Ratio of 3.7, inverted T-waves in V1 and V2, 1.8; inverted T-waves in V1-V3, 2.6; inverted T-waves in V1-V4, 3.7; incomplete RBBB 1.7 and tachycardia, 1.8. Finally, they found that S1Q3T3, precordial T-wave inversions V1-V4, and tachycardia were independent predictors of PE. 

What is an S1Q3T3?  Very few studies define S1Q3T3.  It was described way back in 1935 and both S1 and Q3 were defined as 1.5 mm (0.15 mV).  In the Marchik article, (assuming they defined it the same way, and the methods do not specify this), among patients with suspicion for PE, S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Syncope During Exercise in a 12-Year Old

This was sent by a paramedic who wishes to remain anonymous.

911 was called because a 12 year-old female had a "seizure" at the gym. 

On arrival, medics found the patient supine on gym mats, conscious but lethargic. Her skin was very pale, cold, and diaphoretic, and there was no radial pulse but only a palpable brachial.  Her lips were cyanotic and firefighters had already begun oxygen therapy. She complained of nausea and bilateral rib pain not worsened by palpation or inspiration. She did not have any obvious injuries on exam, but we noticed bladder incontinence. She was still cyanotic 15 minutes after the "seizure."

The patient's coaches stated that she was "warming up" for practice when she suddenly lost consciousness, fell, and had brief seizure-like activity. They denied seeing her sustain any other injuries aside from a ground-level fall onto a soft surface. She regained consciousness within a few minutes, but remained altered. 

Later on during transport, the patient was able to recall what happened: she was running when she became very dizzy and lost consciousness. The patient's family stated that she had no medical history, no previous seizures or similar episodes with exercise, and no family history of cardiac problems or sudden death. 

A monitor strip showed frequent PACs.

After a quick exam and history we took her out to the ambulance, where her first set of vitals were: BP 100/63, HR 72, SpO2 99%, RR 22. Her lungs were clear and she never complained of dyspnea.

A prehospital 12-lead was recorded:

Sinus rhythm.  There are clear ischemic (down-up) T-waves in II, III, aVF and V4-V6.
There is an rSr' in V1, but this is not abnormal.  It can especially be due to high lead placement.
The QRS duration is 98 msec (normal)
The computerized QTc is 461 ms (slightly long, but not dangerously so).

Case Continued:

After about 6 or 7 minutes on oxygen, the patient's cyanosis resolved and so did the premature beats. Her mental status and skin greatly improved. However, for the remainder of transport her systolic blood pressure remained in the 80s (86/56) despite improvement otherwise (I wondered later if the first BP was an incorrect reading). We started a fluid bolus and by the time we reached the ED, her only complaint was fatigue.

She was admitted to a children's hospital.

The followup was somewhat sketchy, as it did not come from medical records but from family via a third party:

She  was found to have an anomolous left main coronary artery which reportedly became "pinched" during exercise, causing severe ischemia with drop in cardiac output and syncope.  

She had surgery to move the artery and is reportedly doing well.  They are just having difficulty keeping her inactive. 

Learning Points:

1.  It may help to record an ECG in cases of "seizure"

2. Syncope in children can be due to ischemia, as well as due to pure rhythm disturbances such as long QT, WPW, Catecholaminergic polymorphic VT (CPVT), Brugada, AV block, etc.

3. Syncope during activity is particularly worrisome.

Check out this case:

A 16 year old girl has syncope while playing basketball.....

Here is my article on ED Syncope Workup:

Emergency Department Syncope Workup: After H and P, ECG is the Only Test Required for Every Patient.....

My Very Smart Colleagues are Getting Very Good at Diagnosing Subtle Occlusion

My very smart colleagues are getting very good at this!

A male in his 40's with a significant history of coronary disease and stents called 911 for sudden onset "terrible" left sided chest pain radiating to the jaw, with diaphoresis and vomiting.  He appeared very uncomfortable.

Here is his prehospital ECG, recorded approximately 15 minutes after onset of pain:

Normal

On arrival, another ECG was recorded 16 minutes after the prehospital ECG, approximately 30 minutes after the onset of pain:

There is a normal amount of ST elevation in V2-V4.
However, it is greater than in the prehospital ECG.
Upward concavity in all of V2-V6, no reciprocal ST depression, no Q-waves, no T-wave inversion.
The computerized QTc is 387 ms.
The LAD occlusion formula value, using:
ST Elevation at 60 ms after the J-point = 3 mm
Computerized QTc = 387 ms
R-wave amplitude in V4 =  9.5 mm
Formula = 23.32
This is just below the cutoff of 23.4, which would make LAD occlusion very likely.
I consider any value above 22.0 as suspicious, and needing serious evaluation.

_____________________________
Dr. Ken Grauer added the following nice points:

I would make the following points regarding serial ECGs in this case. ECG #1 is normal. One needs to compare serial tracings by going lead-to-lead. Even without use of the formula — there ARE changes that should be readily apparent from lead-to-lead comparison between ECGs #1 and 2. That is in V1 — the T wave is now positive in ECG #2; in V2 — the T wave is now disproportionately tall with respect to the QRS in this lead, and the J-point is now elevated; in V3 — both QRS complexes now show clear ST elevation with what looks like broadening of the T wave base, compared to relatively normal appearing ST-T waves in ECG #1. Given the history in this case — this lead-to-lead comparison should be more than enough to prompt immediate cath. That the formula has now become positive supports this clinical decision.
____________________________________



There was an old ECG for comparison from 8 months prior:

This has less than 0.5 mm STE in V2 and V3.  This is a significant change.

So there is a change in the ST elevation.

Kambara (see below) showed that early repolarization is dynamic; see this case and discussion: 

Increasing ST elevation. STEMI vs. dynamic early repolarization vs. pericarditis.

However, in this case:
1. The formula is nearly diagnostic
2. There is definite increase in ST elevation
3. The patient has a classic clinical presentation for anterior MI

Possible Management Strategies:

1. It is very early in the patient presentation, and there has not yet been time for much ECG evolution.  Therefore, serial ECGs may be particularly useful
2. Do bedside cardiac ultrasound.  If there is clear wall motion abnormality, then activate cath lab.  If none, then do formal contrast echo or, if unavailable, then speckle tracking echo cardiography.
3. The ACC/AHA does recommend emergent angiogram for patients with ongoing, refractory chest pain and high suspicion of coronary syndrome, even in the absence of ECG or biomarker evidence of ischemia.  In this case, there is even very good ECG evidence.

As with 50% of STEMI, the initial troponin was negative (Initial cTnI = 0.028 ng/mL, 99% upper reference level = 0.030 ng/mL).

My very astute colleagues simply activated the cath lab after giving aspirin, heparin and ticagrelor.  The interventionalist was skeptical but gladly took the patient to the cath lab.

Here is the cath report:

--Culprit Lesion (s): 90% ruptured plaque in mid LAD proximal to the previously placed stent; initial flow in distal LAD TIMI III 

--The right coronary is occluded - in-stent - at the aortic ostium in the presence of L to R collaterals

The interventionalist remained skeptical even after the angiogram:

"Unstable angina/ACS with putative mid-LAD culprit (90% stenosis with TIMI III flow on initial angiography) - recommend continued troponin levels to define whether the current event represented an acute myocardial infarction.  Suspect chronic total occlusion of the ostial RCA (instent)"

Post PCI ECG:

All the previously noted increase in ST Elevation has resolved.QTc = 379 ms
This proves that the ST elevation was indeed due to ACS.
At the time of the ECG, there would have been TIMI 0 or 1 flow, but spontaneous reperfusion occurred, aided by adjunctive pharmacotherapy (ASA, heparin, ticagrelor)

What is the post-angiogram formula value?
STE = 1
QTc = 379
RAV4 = 11
Formula now = 19.971 (clearly normal)More evidence that the presenting ECG represents LAD occlusion.

Here is the subsequent formal echo:

The estimated left ventricular ejection fraction is 67 %.

Normal estimated left ventricular ejection fraction .

Left ventricular hypertrophy concentric .

Regional wall motion abnormality-anterior hypokinetic.


Here is the next day ECG:

There was such rapid and complete reperfusion that no reperfusion T-waves (Wellen's waves) did not evolve. This is somewhat unusual in patients who have a significantly elevated troponin.
Troponin I peaked at 4.44 ng/mL

Learning Points:

1. Pre-test probability is critical (here there is history of CAD and very typical presentation, with sudden onset, vomiting, and diaphoresis)
2. Use the Subtle LAD occlusion formula
3. Compare with previous ECG
4. Record serial ECGs
5. Compare with the prehospital ECG
6. Interventionalists' opinions are important, but not the gold standard (see reference below).


References

1. McCabe JM.  Physician Accuracy in Interpreting Potential ST-Segment Elevation Myocardial Infarction Electrocardiograms.  J Am Heart Assoc. 2013;2: e000268 doi: 10.1161/JAHA.113.000268
http://jaha.ahajournals.org/content/2/5/e000268.full.pdf+html

Although interventionalists performed the best among physician groups, there sensitivity for coronary occlusion in this study was 70% (specificity 89%).

All EKGs are at the end of this article and you can test yourself.  I had 93% sensitivity and 100% specificity. 

2. Kambara H, Phillips J. Long-term evaluation of early repolarization syndrome (normal variant RS-T segment elevation). Am J Cardiol 1976;38(2):157-61.  

Kambara, in his longitudinal study of 65 patients with early repolarization, found that 20 patients had inferior ST elevation and none of these were without simultaneous anterior ST elevation.  Elevations in inferior leads were less than 0.5mm in 18 of 20 cases.  Kambara also found that, in 26% of patients, the ST elevation disappeared on follow up ECG, and that in 74% the degree of ST elevation varied on followup ECGs. 

ST Elevation: Inferior MI or Early Repol? Ultrasound Speckle Tracking Can Help.

Rob Reardon, our ultrasound director, showed me this ECG of a 50 yo with chest pain he had seen a few days prior:

I said "Early Repolarization in Limb Leads".
He had thought there might be some reciprocal ST depression in aVL and was worried about inferior MI.
I can see what he means, but I don't think it qualifies.

 

But these ECGs can be difficult.

As our ultrasound fellowship director, his solution was to do bedside ultrasound with Speckle Tracking Strain Echocardiography on our sophisticated Toshiba ultrasound machine.


We reported on Speckle Tracking recently in the American Journal of Emergency Medicine, where you can read about it in detail:

Diagnosis of acute coronary occlusion in patients with non–ST-elevation myocardial infarction by point-of-care echocardiography with speckle tracking: a case report

With Speckle Tracking, you mark the endocardium visually on a still picture, and then the computer follows that endocardium through the cardiac cycle, both showing and plotting its wall motion.

It is the next best thing to a contrast echocardiogram.

Here is the video he obtained:

The three segments at lower left are the inferior wall (AI = inferior apical, MI = mid apical, BI = basal inferior)

Speckle Tracking makes it so you can see that all of them contract (shorten and thicken) very well.

The graph on the right shows that your visual diagnosis is correct: the deep waves to (-30) confirm perfect function of all segments of the inferior wall.

Here is a still image:

On the left, the 2 arrows point to the mid inferior and basal inferior segments.
On the left, the one arrow points to the Purple-blue line corresponding to the purple-blue basal inferior segment, confirming that it has full contractility.

This allayed his concerns of inferior MI, but only because he is a real expert at doing this.

The patient ruled out for MI by biomarkers and the ECG did not evolve.

Speckle Tracking can also be falsely re-assuring if not done right and improperly interpreted" see this very instructive example:
Low HEART score. Acute LAD occlusion. Detected only by analysis of subtle ECG.

Learning Points:

1. Speckle Tracking can be done by an experienced emergency physician.

2. Speckle Tracking can help you to recognize a STEMI mimic if there is perfect wall motion in the echocardiographic segment in question.

3.  However, you can have false negatives, especially if you are not expert in this.

4.  Fuly trust negative results only when your clinical and ECG suspicion are already low.

5.  Do not use it to definitively "rule out" coronary occlusion.  Rather, continue to evaluate with serial ECGs and possibly emergent formal contrast echo.

60-something with Chest Pain, resolved upon arrival to the ED

A 60-something male called 911 for chest pain of less than one hour duration.  He arrived in the ED pain free and had this ECG recorded:

What to you think?

There are hyperacute T-waves in V2-V4, but the patient was pain free.  I did wonder if he had had a prehospital ECG recorded, and what it showed.  

This was 10 years ago, just when we had started doing prehospital 12-lead ECGs.  I was not even certain that one had been recorded, but if it was, I wanted to see it.

I had to look around for it, and here is what I found:

Pretty amazing, huh?

Here I have circled the computer algorithm interpretation, just so you don't miss it:

Early Repolarization???
Notice STE is both precordial and in I/aVL.

He was taken to the cath lab and there was a fresh thrombus in the proximal LAD with 80% stenosis.  

Serial troponins were all undetectable (these are less sensitive than today, but as I pointed out in my last post, the initial troponin in STEMI, even with high sensitivity troponin, can be below the level of detection.

Here is another case where the physicians did not seek out the prehospital ECG and it led to loss of myocardium, but in this case for missing the evolution.  The initial troponin was below the level of detection.

Learning Points:

1.  In spontaneously reperfused "Transient STEMI," hyperacute T-waves may still be present after resolution of pain and resolution of ST segments.

I say: "you get hyperacute T-waves on the way up (as ST segments are on the way up, shortly after occlusion) and on the way down (after ST segments have normalized, shortly after reperfusion)

2.  The Initial troponin is often undetectable in STEMI

3.  Serial troponins may be all negative in transient STEMI

4.  Always look for and examine the prehospital ECG.

Abnormal ST-T in V1-V3. What is it? Many interesting and informative twists to this case.

A middle-aged woman with a history of CAD and stents, but also a history of several subsequent visits for non-cardiac chest pain, called 911 for chest pain of 5+ hours duration.

The medics recorded this ECG at time zero:

Note the downsloping ST depression in V1-V3, with down-up T-waves in V2 and V3.

Down-up T-waves in right precordial leads during chest pain is likely posterior MI.

When I showed this to a resident, she asked if these are Wellens' waves.  I pointed out that Wellens waves are 1) up-down and 2) after resolution of pain.  And they indicated, of course, LAD thrombus with a reperfused artery (good flow), whereas this is indicative of no or low flow to the posterior wall.  I did add that subendocardial ischemia is also possible.

The medics gave NTG, and the chest pain resolved. This was recorded at time 12 minutes:

Now V2 and V3 have a long flat ST segment with a tiny upright T-wave.  This is also highly suspicious for posterior MI, probably resolving.
V5 and V6 appear to have smaller T-waves now as well.

The patient was brought to the ED, at which time she had pain again, and this ECG was recorded at time 30 minutes (nearly 6 hours after onset of pain):

New but subtle downsloping ST depression with down-up T-waves in V2 and V3.
Interestingly, limb leads are not very helpful here.

The patient's chest was quite tender, and the initial contemporary troponin was below the level of detection (0.010 ng/mL).

I activated our "Pathway B."  Pathway B is intermediate between "admit for serial troponins" and "activate the cath lab (Pathway A)".  That means I call the cardiologist on call, and he/she gets further evaluation going immediately.

The interventionalist came down immediately and talked to the patient, looked at the ECG, and decided to take her to the cath lab.

Angiogram:

100% In-stent Occlusion of a large circumflex, easy to cross with wire.  There was no collateral filling.  A stent was placed.

However, it is very puzzling:

All serial troponins remained below the LoD!

But to the angiographer the lesion was not a chronic total occlusion.

The echocardiogram showed a new inferolateral wall motion abnormality, but it was only hypokinesis, not akinesis, and the EF was 60%.  One cardiologist did not initially see the WMA.  This suggests either ischemia with stunning (unstable angina) or small infarct.

Here is the post procedure ECG, 5 hours after PCI:

ST segments and T-waves are mostly normalized, supporting acute ischemia on the previous ECGs

The patient had no more of what she describes as her "heart attack" type chest pain.


This was recorded the next day:

Fairly normal

Coronary thrombosis is a Dynamic process!

The artery opens and closes spontaneously.  Thrombus propagates and lyses (remember there is endogenous tPA).  If the occlusion is brief, then there is no infarct and troponins are negative.  There might still be stunning from ischemia with a WMA.  Then if it occludes again just prior to the angiogram, the angiogram shows 100% occlusion, even if it has only been brief.

This appears to be a case of unstable angina due to coronary occlusion that was complete at the time of the angiogram, though opening and closing prior to the angiogram.

Alternatively (and I think less likely), it could be that she had her MI more than 2 weeks prior and all troponins are now negative.  The lesion might still be easy to cross with the wire.  She would have a wall motion abnormality.  However, with no collateral circulation and a total occlusion, there should be a dense wall motion abnormality (but it was not dense).  If this hypothesis is correct, then she was having post-infarct angina (but that begs the question of why?  Where was the new angina/ischemia originating from?)

Unstable angina still exists.  And it may have an occluded artery at angiogram.

My next post will show another example of unstable angina due to occlusion, with all negative troponins.

In our UTropIA study (see here at clinicaltrials.gov) of about 2000 consecutive ED patients who had troponin ordered, we measured both contemporary and high sensitivity troponins (Abbott Architect Troponin I) and found that one of 9 STEMI patients (there were quite a few more patients who had ECGs diagnostic of occlusion but that did not meet STEMI criteria) had an initially undetectable high sensitivity troponin.  About half had an initial hs trop below the 99% reference value.

Resuscitated from ventricular fibrillation: what is the ECG Diagnosis?

A reader (someone in training) sent me this ECG, and asked for my interpretation.

Clinical info:  "The patient was found down in cardiac arrest, defibrillated with ROSC in the field, was unconscious on arrival. Attached is the initial ED ECG."

"I will provide details and outcome to come after your impression." 

Here is the EKG: 

Here is my interpretation: Sinus at a rate of about 80, RBBB, LAFB, ST Elevation in aVL, reciprocal ST Depression in II, III, aVF.  No precordial ST Elevation, but STE often does not show in precordial leads when there is LAD occlusion with RBBB and LAFB.  Proximal LAD occlusion.


When confronted with RBBB and LAFB in a patient with cardiac arrest or typical chest pain or cardiogenic shock, one should assume acute LAD occlusion.  Any occlusion can fail to show in ECGs with normal conduction, with LBBB, and with RBBB.  But in my experience, huge myocardial infarctions are particularly difficult to discern in the presence of RBBB and LAFB.  This is not well described, but I have seen it very often.

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 LAFB) on the admission ECG.

How do you assess ST elevation on these ECGs?  First, find the lead which you believe most clearly manifests the end of the QRS.  I believe that in this ECG it is lead V4.  Then draw a line down to the lead II rhythm strip at the bottom.  Then, using the same point on the complex under leads (I, II, III), (aVR, aVL, aVF), (V1, V2, V3), you can draw a line up and see the end of the QRS in all leads.  In this way, one can see the subtle, downsloping ST elevation in aVL, with reciprocal ST depression in II, III, and aVF.

Here it is:

His response:

Yes.

This was an interesting case, especially when you red the providers' interpretations of the ECGs.  After the 2nd ECG the diagnosis should be clear, but for some reason they call it "NSTEMI".   No cath done initially, and on day 3 they decided to avoid cath because they thought she was neurologically unrecoverable.

On autopsy on day seven, "99% LAD stenosis".

Here is more detail:

Old ECG on file:

Sinus.  Normal conduction (no BBB).  Baseline Q-waves in V2, V3. Nonspecific ST-T abnormalities.

ECG #2 at 19 minutes:

Smith: RBBB/LAFB persist, but the STEMI is quite obvious here

ECG #3 at 63 minutes

The right bundle branch block has resolved, suggesting that perhaps the artery has opened, but the ST elevation persists, especially in aVL.  [aVL II, III, aVF are diagnostic of high lateral STEMI with reciprocal ST depression. Note that there is NOT 1 mm STE in 2 consecutive leads, but in one lead only (aVL)]
There is some STE in V1-V3 and STD in V6 also.

ED Physician Assessment:

“Initially wide complex PEA. Responded best to bicarb and calcium. Had VT and VF and torsade in field as well…ECG shows wide complex rhythm in 80s. Suspected hyperK given wide complex and response to calcium and bicarb…On repeat ECG rate 77, sinus, now more of an incomplete LBBB pattern with STD in inferior leads and 2mm STE in aVL only. Concerning but technically does not meet STEMI criteria. Resident discussed with CCU fellow and cath lab. Not STEMI criteria.”

Initial potassium: 5.8 mmol/L

Smith comment: Although it is possible that such an ECG represents hyperkalemia, it is a very atypical ECG for hyperkalemia.  

More importantly, such an ECG would only be seen with a potassium greater than 7.0 mEq/L.

____________________________________

Here are some typical pseudoSTEMI patterns for hyperkalemia (multiple examples at this post):

Cardiac Arrest and ST Elevation: You Should Learn to Recognize This!

Here are some cases of RBBB and LAFB

Wide Complex Tachycardia; It's really sinus, RBBB + LAFB, and massive ST elevation

don't miss this one!

What, besides large anterior STEMI, is so ominous about this ECG?

Chest Pain and Right Bundle Branch Block

____________________________

Clinical Course

Pt was admitted to MICU with cardiology following.

Troponin T (normal is less than 0.10 ng/mL): 1.19 ng/mL → 7.67 ng/mL → 19.53 ng/mL <0 .10="" 1.19="" 19.53.="" 7.67="" b="" nbsp="">(Smith comment: remember that, as far as one can correlate troponin levels with infarct size, troponin T levels are only 1/10th as high as troponin I levels.  So this may correspond to a troponin I level of about 200 ng/mL.)

ECG #4, next morning

There is some persistent STE in V1-V3 and aVL (and reciprocal STD), different from patient's baseline ECG.

Cardiology consult note on day 2:

“Inciting cause is unknown although there is evidence supporting coronary ischemia and metabolic derangements including hyperkalemia and acidosis.  Prognosis is tenuous and neurologic function cannot be assessed while the patient is sedated. The incremental benefits of an early invasive approach in management of this ACS may outweigh the risks as long as cognition improves and metabolic derangements are corrected. The clinical approach for ACS in ESRD is usually individualized; effectiveness data is limited and treatment related morbidity is not uncommon.”

“Assessment: “Cardiac arrest…..Non-ST elevation acute coronary syndrome”

“ECG 1: Sinus rhythm, rate 90, QRS duration ~190ms, left axis deviation with late terminal forces moving rightwards and anterior.

ECG 2: SR, rate 80; QRS 120ms with late terminal left/anterior, left axis deviation, ST elevation (~1mm in I, 1-1.5mm aVL)

ECG3: SR, rate ~75. ST elevation (1-2mm aVL, 1mm V2/3), ST depression (II, III, aVF, V4-6).”

Cardiology consult day 3:

“59 yo patient with ESRD on HD, DMII, who is currently in cardiogenic shock in the wake of cardiac arrest after NSTEMI. The pressing issue is whether this patient should undergo left heart catheterization today. I think this hinges on neurologic status, which at this time is largely unknown. Pt was reported to have 1 hour down time prior to being resuscitated. She has been without sedation for several hours and has no corneal or gag reflexes per the primary team. There is enough evidence to call into question her neurological viability at this time, thus a left heart catheterization would be of questionable utility.”

Autopsy, day 7:

Anoxic brain injury with total cerebral necrosis 99% stenosis of the proximal LAD, with acute transmural infarct of the anterior and anterolateral walls of the LV 75% stenosis LCx, 50% RCA, 25% LM

10 Cases of Inferior Hyperacute T-waves

In the last post, I showed: 

Ten (10) Examples of Hyperacute T-waves in Lead V2 (a few in V3), due to acute LAD occlusion

Today, 10 examples of inferior hyperacute T-waves.

Details in every case make it even better, so click on the link!!

Case 1.  

Chest Pain in a 61 year old male. Inferior STEMI without inferior ST elevation.

In this case, the followup ECG is diagnostic because of lead V1

Case 2.

Inferior Hyperacute T-waves

Case 3.

Chest Pain in a Male in his 20's; Inferior ST elevation: Inferior lead "early repol" diagnosed. Is it?

This case was missed.  Read about it.

Case 4.

Series of Prehospital ECGs Showing Reperfusion

This has an incredible sequence of ECGs!

Case 5.

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

Case 6. 

Friday's post produced skeptics.....

This case made a lot of readers angry, denying that these are hyperacute Ts

Case 7.

A Case of Clinical Unstable Angina in the ED

This case shows how hyperacute is only relative to the baseline T-waves.  Also, the critical role of reciprocal ST depression and T-wave inversion in aVL.

Case 8.

Is this STEMI? Pattern Recognition is Key 

Go to the link, and this case shows an inferior pseudoSTEMI for contrast

Case 9.

Inferior hyperacute T-waves. The clue is T-wave inversion in aVL. Serial ECGs evolve to ST Elevation.

Case 10.

Subtle Inferoposterolateral STEMI