Is this ACS? Look at the previous ECG!!

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Is this ACS?  Look at the previous ECG!!

A male in his 40's complained of 4 hours of chest pain.

Here is his initial ECG:

There is ST elevation in II, III, and aVF, with a minimal amount of reciprocal ST depression in aVL.  There is also minimal ST elevation in V2-V4, with a QTc of 375 and STE at 60 ms after the J-point is 2 mm. R-wave is 14.5 mm.  So the equation value is only 19.75.  Not an LAD occlusion.  However, the Q-wave in V4 is unusual.  The equation study excluded ECGs with Q-waves in V2-V4, so this must be evaluated with that in mind.

There was a previous ECG on file:

This one has no ST elevation anywhere, and no ST depression in aVL, and smaller Q-waves in V4-V6.

Here are all the leads side-by-side for easier comparison.  For each lead, the presentation ECG complex is on the left and the old ECG complex on the right:

Now the difference is more apparent.  One can also see now that the T-waves in V1-V6 are larger, and in V2-V4 are really hyperacute.

While you may not want to activate the cath lab based on this, you should certainly order serial ECGs every 15 minutes if the pain is ongoing.

80 minutes after the initial ECG, the troponin returned elevated.  At this point, it would be again important to obtain a repeat ECG.  This was not done.  It is now clear that the chest pain and ECG findings are due to ACS, and it is high risk ACS.

If there is any increase in ST elevation, the patient should go to the cath lab emergently.

In any case, given that the pain is ongoing, and there is no doubt that it is ACS, aggressive antiplatelet, antithrombotic, and anti-ischemic therapy is indicated.  The patient should be started on aspirin, high dose clopidogrel (600 mg), a GP IIb-IIIa inhibitor like eptifibatide (Integrilin), and Heparin (LMWH or unfractionated, depending on the institution), and a nitroglycerine drip if the pain is still ongoing. 

If these do not relieve the symptoms, or at least resolve the ECG findings, consult the interventionalist for possible emergent angiography.

The management above was undertaken and the patient's pain resolved.  The STE also resolved:

Most STE is resolved.  ST depression in aVL is resolved.  Q-waves persist.

Outcome:

Troponin I peaked at 23 ng/ml.  Echo showed an apical and distal inferior wall motion abnormality.  Angiogram showed a wraparound LAD supplying the apex and inferior wall.  There was a proximal LAD culprit with thrombus, but open with TIMI III flow.  It had embolized to the distal LAD (which supplies the inferior wall) resulting in 100% occlusion there,and hence inferior infarction with ST elevation.


Here is the ECG Immediately after angiogram:

There is terminal T-wave inversion identical to Wellens' type A

Day after angiogram:

Further evolution of T-wave inversion.

 The patient did well.

Man in his 70's with presyncope. Some interesting data on troponins included.

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Case:

A man in his 70's presented with presyncope.  He denied CP or SOB.  He had no medical problems and had not seen a doctor in a long time.

Here is his initial ECG:

Sinus rhythm.  There is high voltage, possible LVH.  There is abnormal ST segment depression (STD) in leads II and aVF and V3-V6, with minimal ST elevation in aVR.  This is very suggestive of ischemia.

The patient remained asymptomatic in the ED.

At 26 minutes, another ECG was recorded:

There is slightly less STD here

Another ECG was recorded at 2 hours:

The ST depression is almost completely resolved.

So there is subtle, but real, and dynamic ST depression.  ST depression can be either secondary to an abnormal QRS (such as in LVH or LBBB).  Or it can be "primary", that is, not due to the abnormal QRS.  In this case it appears to be primary.

Such primary ST depression can be due to a baseline finding, in which case it is not dynamic.  It can be due to hypokalemia, but this patient was not hypokalemic.  Or it can be due digoxin, but this patient was not on digoxin.  Therefore, one must presume it is due to ischemia.  And, in such a patient, ischemia is probably due to ACS.

The patient was given aspirin and clopidogrel.  He was admitted.  His every 3 hour troponins [Ortho Clinical Diagnostics (OCD), level of detection = 0.012 ng/ml, manufacturer's 99% reference = 0.034 ng/ml] were: 0.014, then 0.020, then 0.017, then 0.012.  One last one measured a couple days later was less than 0.012 (undetectable).

So the troponins do not reach the level for diagnosis of NonSTEMI (which would require the troponin to reach 0.035 ng/ml).  But there is a rise and fall.  This, especially along with the EKG findings, is diagnostic of unstable angina.

Some data on troponins:

The manufacturer's 99% reference level is determined by testing a heterogeneous population of people, some with chronic diseases, and in the case of this OCD assay, 99% have a level less than or equal to 0.034.  Recently, Apple et al. (Clinical Chemistry 58(11): xxx-xxx; 2012; http://hwmaint.clinchem.org/cgi/doi/10.1373/clinchem.2012.192716) studied troponin levels in over 500 truly normal individuals and found that the 99% reference for the OCD assay is 0.019 ng/ml.  So if the definition of MI were based on this, rather than the manufacturer's level, one could call this an MI.

Here are 3 articles suggesting that, with high sensitivity troponin, many cases of angina are detectable, and that they have a rise and fall beneath the 99% reference for MI:

1.            Januzzi JL, Jr., Bamberg F, Lee H, et al. High-sensitivity troponin T concentrations in acute chest pain patients evaluated with cardiac computed tomography. Circulation 2010;121(10):1227-34.

2.            Sabatine MS, Morrow DA, de Lemos JA, Jarolim P, Braunwald E. Detection of acute changes in circulating troponin in the setting of transient stress test-induced myocardial ischaemia using an ultrasensitive assay: results from TIMI 35. Eur Heart J 2009;30(2):162-9.

3.            Venge P, Johnston N, Lindahl B, James S. Normal plasma levels of cardiac troponin I measured by the high-sensitivity cardiac troponin I access prototype assay and the impact on the diagnosis of myocardial ischemia. J Am Coll Cardiol 2009;54(13):1165-72.

In any case, the rise and fall of  troponin, whether above or below the 99% reference, repesents ACS.  It is important to note, however, that in ACS, the lower the troponin level, the lower the risk.  Nevertheless, a rise and fall like this, even if below the level for diagnosis of MI, indicates ACS and puts the patient at risk of a larger MI and even death.

Outcome

The patient was in the hospital for several days.  He had some episodes of what is described as variously as bundle branch block and as ventricular tachycardia.  He had a normal echocardiogram, and a normal stress test EXCEPT that he had runs of V Tach during the test.

An angiogram showed a 90% RCA stensosis.  He received a stent.

Conclusion:

1. The patient had unstable angina, but without pain.
2. Dynamic ST depression is nearly diagnostic of ischemia
3. Rise and fall of troponins, even if too low to diagnose MI, indicates ischemia and, in the this clinical context, unstable angina.

Looks like a Posterior STEMI. Is it?

An elderly woman was found down near her bed, confused but awake.  She was on coumadin for atrial fibrillation.   Other medications were uncertain.  She was somewhat shocky and hypotensive.  The following ECG was recorded:

The viewer is drawn to marked ST depression in leads V2 and V3, with tall R-waves, suggestive of posterior STEMI.  But there is another finding that you should focus on.  What is it?

A posterior ECG was recorded:

V4-V6 are really V7-V9, on the posterior chest at the level of the tip of the scapula.  There is no ST elevation here, which makes posterior STEMI significantly less likely.  The finding that leads to the diagnosis is still here.

The diagnostic finding is accelerated junctional rhythm. This is most commonly caused by Digoxin toxicity, and is the most common manifestation of digoxin toxicity.  In addition, digoxin leads to a short QT interval.  In these 2 ECGs, the QTc is 380 and 375 ms, respectively.  The patient has known atrial fibrillation at baseline, and therefore should have an irregular rhythm, and it should be at a faster rate.  This fact should lead you to suspect that she is on Digoxin for rate control.  The digoxin toxicity blocks the AV node completely so that there is no ventricular response to the atrial fib.  It also leads to an accelerated junctional escape.

A previous ECG was found to confirm that she has atrial fib:

This shows atrial fib with a controlled irregularly irregular ventricular rate, with a QTc of 309 by the computer, and the classic "Dig effect" of scooped ST depression.

The patient's creatinine returned elevated at 2.6 mg/dL.  Further review of charts confirmed she was on Digoxin.  The postassium was 6.1 mEq/L.  Digoxin level returned at 10 ng/ml (therapeutic range is 0.5 - 2.0 ng/mL).

Along with other resuscitative measures, Digibind was given and this was the ECG thereafter:

There is still a junctional rhythm, but slower.  There is less ST elevation.  Interestingly, the QTc has gone back down to 320 ms, where it was on therapeutic levels of digoxin.

An echocardiogram showed no wall motion abnormality.  Troponins were low grade positive, consistent with demand ischemia due to shock.

Learning point:

Accelerated junctional rhythm should be thought to be Digoxin toxicity until proven otherwise.

A Man in his 20's with Syncope. What is diagnosis? And what does the old ECG show?

A young man presented after a syncopal episode.  He felt fine in the ED.  He had no previous cardiac history, but stated that he does have an abnormal baseline ECG.

Here is his ED ECG:

There is a hyperacute T-wave in lead III which is far larger than a small QRS.  There is reciprocal ST depression and and inverted reciprocally hyperacute T-wave in lead aVL and I.  Precordial leads support the diagnosis of STEMI, showing posterior STEMI.

So this young person with syncope and no other symptoms is having a STEMI?

Could it be that this is his abnormal baseline ECG?

NO.

There is no baseline abnormality which looks like this.

There is a condition of baseline inferior ST elevation ("early repolarization" in the limb leads).  We have shown that this never has reciprocal ST depression.  Here is the reference:

Bischof J.  Thompson RP.  Tikkanen J.  Porthan K.  Huikuri H.  Salomaa V.  Smith SW.  ST-segment depression in lead aVL differentiates benign ST elevation from inferior Acute STEMI.  ACEP Research Forum 2012.  Annals of Emergency Medicine 60(4 Suppl):S8-S9; October 2012.

The patient was taken for PCI of 100% thrombotically occluded RCA.  The etiology of the syncope is uncertain, but probably some dysrhythmia related to the inferior STEMI.

Later, his baseline abnormal ECG was obtained.  Here it is.

This is classic "Benign T-wave Inversion"

To learn all about Benign T-wave Inversion, read this.

Transient Inferior OMI, with RV OMI, missed. It became obvious on a near fatal stress test.

A middle-aged woman with a history of hypertension presented with typical chest pain.  Her BP was 160/80.  Here was her presenting ECG, with chest pain:

Inferior leads show hyperacute T-waves and reciprocal STD in aVL, with a reciprocally hyperacute T-wave in aVL.  This is all but diagnostic of inferior OMI. 
 
There is also subtle STE in V1-V3.  In the context of the inferior OMI, this is diagnostic of right ventricular OMI (RVMI).

The pain improved with Nitroglycerine.  Creatinine was 4.3.  She underwent another ECG at 6 hours (when she was pain free):

The T-waves in leads II, III, and aVF are now significantly smaller, and there is terminal T-wave inversion in III, with reciprocal down-up T-wave in aVL.  These are signs of reperfusion.   The T-wave in I has also changed.
Now these reperfusion findings make the first ECG absolutely diagnostic of OMI

The troponin peaked at 16 ng/mL (also retrospectively diagnostic of OMI) and there was a "probable" inferior wall motion abnormality.

Because the patient had advanced renal insufficiency and because there was "no evidence for a current of injury on her presenting EKG's", a non-invasive approach was undertaken.  While undergoing a stress test as a part of the non-invasive approach, she developed chest pain and hypotension and had this ECG:

There is sinus bradycardia with massive inferior ST elevation, as well as ST elevation in V1-V3, diagnostic of inferior and right ventricular (RV) STEMI.  When there is ST elevation due to RVMI in V1-V3 in a left sided ECG, it is also called a "Pseudoanteroseptal MI".

She went immediately to angiogram and had occlusion of the RCA at the ostium.

Looking back, one can see ST elevation in V1-V3 on the initial ECG that is nonspecific, but, in retrospect, is probably due to RV Injury.

Hyperkalemia in the setting of Left Bundle Branch Block

I'm sorry, but there was an error in the previous post and I had to remove it.  Depending on information received, I may be able to repost it.



A dialysis patient presented with vomiting.  He has  known baseline left bundle branch block.  Here is his initial ECG:

There is left bundle branch block, with a QRS duration of 220 ms according to the computer analysis.

Here is his previous ECG, recorded with normal postassium:

Here, the QRS duration was 160 ms.  So the previous one is widened by 60 ms.

A widened QRS should always make you suspicious of hyperkalemia.  Indeed, the potassium was 7.3 mEq/L.  After therapy, the widening resolved.

Here is a similar case involving right bundle branch block.

What is the normal QRS duration in LBBB?

In this study of consecutive patients with LBBB who were hospitalized and had an echocardiogram, a QRS duration less than 170 ms (n = 262), vs. greater than 170 ms (n = 38), was associated with a significantly better ejection fraction (36% vs. 24%).  Only 13% had a QRS duration greater than 170 ms, and only 1% had a duration greater than 190 ms.

Obviously, if you have a previous ECG for comparison, you can diagnose prolonged QRS in the setting of LBBB easily.  But it is clear that if your patient with LBBB has a QRS duration greater than 190, then there is more going on.

Chronic Right Ventricular Hypertrophy, or Acute Right Heart Strain? The ECG Helps Make the Diagnosis.

A middle-aged, obese, non English speaking man presented as a walk-in with SOB and leg swelling. His O2 saturations were 59% on room air.  Systolic BP was in the 170's.  He appeared to be mildly dyspneic, in no great distress, and was speaking in almost full sentences.  Breath sounds were slightly distant but seemed to be clear.  Pulses were full and extremities warm, but with bilateral leg edema.  The patient was put on Bilevel Positive Airway Pressure [BiPAP (R)] and an immediate ED cardiac ultrasound was performed (there are 2 clips here; the RV is on the left and LV on the right of the screen):








These ultrasounds were interpreted to show a very large right ventricle (RV) and also left ventricular hypertrophy.  The differential included acute right heart strain (such as pulmonary embolism) and chronic right ventricular hypertrophy (RVH).  A high quality ultrasound could tell the difference between these two, but in the ED at that moment, only a bedside ultrasound without Definity contrast was available.

However, an ECG was immediately recorded:

There is a large S-wave in lead I and a very large R-wave in V1.  This is diagnostic of RV hypertrophy, not of acute right heart strain.

Now the suspicion was that this patient has chronic hypoxia, such that he is not in great distress from a saturation of 59%.  He likely has any one of a number of problems that cause chronic hypoxia, pulmonary hypertension, and RV hypertrophy.  The possibility of a septal defect, or other defect, with right to left shunting (Eisenmenger's syndrome) was entertained.

On BiPAP with 100% O2, the O2 saturation came up to 97%, suggesting that if a right to left shunt were present, it could not be very large.  Obstructive sleep apnea, with chronic hypoventilation, with hypoxia and hypercarbia and resulting RV hypertrophy, was also high on the differential diagnosis.

Finally a BP of 170/100 was obtained by manual blood pressure.  The hemoglobin returned at 20g/dl, confirming chronic hypoxia.  The total CO2 returned at 33, suggesting chronic hypercapnia.  A venous blood gas returned with pCO2 of 66, confirming present hypercapnia.

Further history thru an interpreter was obtained: the patient had been SOB for months, worse recently, and much worse in the last day.  He had no medical history and was on no medications.

Bedside ED Ultrasound of the lower legs was done and confirmed no DVT.

The patient was much better after the nitroglycerine dose reached 200 mcg/min and the BP was down to 130 systolic.  Furosemide was also given.

A rapid d dimer was obtained which was only minimally elevated, effectively ruling out pulmonary embolism.

Subsequent testing revealed a previously undiagnosed congenital heart defect, with right to left shunting and Eisenmenger's syndrome, complicated by acute heart failure.

The ECG was instrumental in differentiating chronic RV hypertrophy from acute right heart strain, and helped guide therapy towards left heart failure (nitroglycerine) which could be dangerous in pulmonary embolism.