Sunday, December 3, 2017

A 50-something with h/o coronary bypass has chest pain and a ventricular paced rhythm

A 50-something male with h/o CAD and CABG, and dual chamber pacemaker due to sick sinus syndrome, called 911 for onset of acute chest pain 2 hours prior.

Here was the prehospital ECG:

There is sinus rhythm with very long PR interval (about 300 ms).

There is a wide QRS [(nonspecific intraventricular conduction delay (IVCD)]

Neither RBBB nor LBBB

There is some ST elevation discordant to deep wide S-waves in III and aVF, and V3 and V4, appears baseline.

There is some reciprocal ST depression in aVL, but this is normal when there is ST elevation in III that is likely to be due to LBBB, LVH, IVCD, or WPW (in this case, it appears to be due to IVCD)

V1 has some ST elevation, and V2 has absence of expected discordant ST elevation, with a very flat ST segment.

This is all non-diagnostic.

The medics brought the patient to the critical care area, as they were suspicious of acute MI.

The pain started at rest, was constant, sharp in the sternum and radiating to the jaw and left arm and into the upper back, associated with diaphoresis but no SOB. No history of venous thromboembolism.  It was not relieved with nitroglycerin at home, but decreases from 9/10 to 7/10 after EMS gave NTG.  He stated it felt like a prior MI. 

Here is the first ED ECG, at time zero:
There is a wandering baseline in the limb leads.
Nevertheless, there is a suggestion of proportionally excessively discordant ST elevation in inferior leads, with proportionally excessively discordant reciprocal ST depression in aVL.

There is also almost excessively discordant ST elevation in precordial leads, but due to wandering baseline, it is hard to say whether it reaches 25% of the preceding S-wave.

Lots of change since the prehospital ECG! 

The prehospital ECG has normal conduction without ischemic ST elevation.
The ED ECG now has a ventricular paced rhythm (VPR).
The ED ECG now has new ST Elevation.
Is all this new ST elevation only due to VPR.

Smith modified Sgarbossa criteria (for use in LBBB and in VPR):

Rule 1 (80-90% sensitive, 95% specific)
Any one of:
1. 1 mm concordant STE in any one lead.
2. 1 mm concordant STD in any one of leads V1-V3
3. At least 1 mm discordant STE that is greater than or equal to 25% of preceding S-wave in at least one lead.

Rule 2 (Only 64% sensitive, but 98% specific, for occlusion):

Any single lead with proportionally excessively discordant STE or STD of at least 30% of preceding S- or R-wave.

Lead aVL seems to have STD that is at least 30% of preceding R-wave.

Smith modified Sgarbossa criteria are being studied now in the PERFECT  study (Paced ECG Requiring Fast Emergent Coronary Therapy).  Preliminary Results are encouraging that they work in ventricular paced rhythm as well (not surprisingly).  See abstract and references below.

Case continued

The physicians were worried about this, and 16 minutes later recorded this ECG:
Now there is clearly excessively discordant STE in III and aVF, with excessive STD in aVL.
Notice there is also quite a bit of ST elevation in V1; is this due to RV MI?

The cath lab was activated.

It was a very interesting angiogram.

There was a known chronically occluded proximal RCA, proximal to the RV marginal branch supplying the RV.
The RCA distal to this was known to be supplied by a CABG graft to the posterolateral branch of the RCA (on the posterior wall!), such that flow to the RCA was retrograde.
This posterolateral branch (not the graft itself) was occluded such that that branch could no longer supply the inferior wall and the RV.
Therefore, it caused inferior and RV STEMI.

It was opened and stented with good results.

Full angiogram report:
1. Left main: patent stent.
2. LAD: 70% stenosis in the mid segment at the take-off of a diminutive D1 (angiographically unchanged from previous angiography in 9/2017), then >90% stenosis after D2 (D2 has a 2.0-2.5 mm caliber). The distal LAD is supplied by a patent LIMA.
3. LCX: chronically occluded. The OM is supplied by a patent vein graft.

4. RCA: known chronic occlusion, therefore not studied. The RPLA is supplied by a patent vein graft. Antegrade flow into the RPLA is good, however, retrogradely the RPLA is occluded with contrast hang-up indicative of a thrombotic occlusion. Hence the flow to the RPDA is compromised.

Here is the post intervention ECG:
Atrial, but not ventricular, pacing.
STE resolved
T-wave inversion (reperfusion T-waves) in inferior leads.
Reciprocally upright T-wave in aVL

Lateral T-wave inversion.
Was there indeed ischemia in the myocardial territory under V3-V6?

The patient went into a paced rhythm, and so had a paced ECG recorded about the same time post cath as the above ECG:
Post cath with some ventricular paced beats and some native beats with atrial pacing.
V1-V3 and the first complexes of V4-V6 have ventricular paced beats.
In the paced beats:
There is new STE in V2 with a large upright T-wave, suggesting that the first paced ECG, with isoelectric ST segment in V2, was due to posterior MI.
There is less STE in V3-V6, and some T-wave inversion, suggesting that there was ischemia in this territory as well, that is now resolved.
I'm not sure exactly how to correlate the angiogram with the findings in V3-V6.

Learning Point:

Modified Sgarbossa Criteria are very useful in Ventricular Paced Rhythm

Smith modified Sgarbossa criteria:

Validation in LBBB: 

Meyers HP.  Limkakeng AT.  Jaffa EJ.  Patel A. Theiling BJ. Rezaie SR. Stewart T. Zhuang C.  Pera VK. Smith SW.  Validation of the Modified Sgarbossa Rule for Diagnosis of STEMI in the Presence of Left Bundle Branch Block. American Heart Journal 170(6):1255-1264; December 2015.

Derivation in LBBB:

--> Smith SW.  Dodd KW.  Dvorak D.  Henry TD.  Pearce LA.  Diagnosis of Acute Myocardial Infarction in the Presence of Left Bundle Branch Block using the ST Elevation to S-Wave Ratio in a Modified Sgarbossa Rule.  Annals of Emergency Medicine 2012; 60(12):766-776.

STEMI in Ventricular Paced Rhythm

We have some preliminary results of the PERFECT study, presented today at the Society for Academic Emergency Medicine.

The short version: They work!!

Here is the long version

Paced Electrocardiogram Requiring Fast Emergent Coronary Therapy (PERFECT) Study Identifier:

Dodd KW.  Zvosec DL.  Elm K.  Hart M.  Karim R.  Lurie K.  Smith SW.  Performance Characteristics of the Modified Sgarbossa Criteria for Diagnosis of Acute Coronary Occlusion in Emergency Department Patients with Ventricular Paced Rhythm and Symptoms of Acute Coronary Syndrome.  Academic Emergency Medicine 2017; 24(S1):S36. Abstract 82.

Background: The ECG diagnosis of acute coronary occlusion (ACO) in the setting of ventricular paced rhythm (VPR) is purported to be impossible. However, VPR has a similar ECG morphology to LBBB. The validated Smith-modified Sgarbossa criteria (MSC) have high sensitivity (Sens) and specificity (Spec) for ACO in LBBB. MSC consist of ≥ 1 of the following in ≥ 1 lead: concordant ST Elevation (STE) ≥ 1 mm, concordant ST depression ≥ 1 mm in V1-V3, or ST/S ratio < -0.25 (in leads with ≥ 1 mm STE). We hypothesized that the MSC will have higher Sens for diagnosis of ACO in VPR when compared to the original Sgarbossa criteria. We report preliminary findings of the Paced Electrocardiogram Requiring Fast Emergency Coronary Therapy (PERFECT) study (#NCT02765477).

Methods: The PERFECT study is a retrospective, multicenter, international investigation of ED patients from 1/2008 - 12/2016 with VPR on the ECG and symptoms suggestive of acute coronary syndrome (e.g. chest pain or shortness of breath). Data from four sites are presented. Acute myocardial infarction (AMI) was defined by the Third Universal Definition of AMI. A blinded cardiologist adjudicated ACO, defined as thrombolysis in myocardial infarction score 0 or 1 on coronary angiography; a pre-defined subgroup of ACO patients with peak cardiac troponin (cTn) >100 times the 99% upper reference limit (URL) of the cTn assay was also analyzed. Another blinded physician measured all ECGs. Statistics were by Mann Whitney U, Chi-square, and McNemar’s test.
Results: The ACO and No-AMI groups consisted of 15 and 79 encounters, respectively. For the ACO and No-AMI groups, median age was 78 [IQR 72-82] vs. 70 [61-75] and 13 (86%) vs. 48 (61%) patients were male. The median peak cTn ratio (cTn/URL) was 260 [33-663] and 0.5 [0-1.3] for ACO vs. no-AMI. The Sens and Spec for the MSC and the original Sgarbossa criteria were 67% (95%CI 39-87) vs. 46% (22-72; p = 0.25) and 99% (92-100) vs. 99% (92-100; p = 0.5). In pre-defined subgroup analysis of ACO patients with peak cTn >100 times the URL (n = 10), the Sens was 90% (54-100) for the MSC vs. 60% (27-86) for original Sgarbossa criteria (p = 0.25).
Conclusions: ACO in VPR is an uncommon condition. The MSC showed good Sens for diagnosis of ACO in the presence of VPR, especially among patients with high peak cTn, and Spec was excellent. These methods and results are consistent with studies that have used the MSC to diagnose ACO in LBBB.


Friday, December 1, 2017

What is the cause of this patient's inferior ST depressions?

Written by Pendell Meyers, edits by Steve Smith

A nurse brought this ECG to me, stating that she had recorded it because she was just notified by the lab of an elevated troponin result. She asked me if I was worried about the ST depressions in the inferior leads. I did not know who the patient was, and I had no other clinical context.

I took a look and asked in return: "Is the patient on any unusual cardiac medications?"

The physician taking care of her overheard the conversation and told me that the patient was on mexiletine.

What do you think?

The rhythm is atrial flutter with 2:1 block. Flutter waves are clearly visible in leads II, III, and aVF, which create the illusion of ST depression in the inferior leads. Typical 2:1 atrial flutter has an atrial rate of ~300 bpm with a resulting ventricular rate of ~150 bpm. This patient interestingly has an atrial rate of slightly over 200 bpm with resulting ventricular rate of 106. This is very unusual, and I have only seen this in the setting of sodium channel blockade (decreased slope of phase zero, Na-dependent depolarization leading to decreased speed of action potential propagation) and/or extreme atrial dilation (the bigger the reentry loop, the longer it takes to do a lap).

I was able to recognize this simply because I have seen it several times before on this blog!

I later found out that the patient had been transferred from another institution after suffering a large stroke, and there was no clinical concern for ACS. Her elevated troponin was most likely due to a type II MI in the setting of significant stroke.

One more point
If this atrial rate were to slow even more, then the AV node might conduct every beat and the ventricular rate could go up, dangerously so.  See this post:

Wide complex tachycardia at a rate of 270

For this reason, do not try to convert the flutter with more sodium channel blockade unless you first block the AV node!  It can result in slower flutter and a faster ventricular rate.

Learning Points:

Atrial flutter frequently causes the illusion of ST segment changes.

Atrial flutter usually has an atrial rate of ~300 bpm, which results in a ventricular rate of ~150 bpm when there is regular 2:1 AV block. These rates can be affected by various pathologies or medications including sodium channel blockers.

Be careful of slowing atrial flutter without first blocking the AV node.

Here are some other similar posts:

What is the Diagnosis?

Is this inferor STEMI?

Thursday, November 30, 2017

"Steve, what do you think of this ECG in this Cardiac Arrest Patient?"

I was shown this ECG.  The resident asked: "Steve, what do you think of this ECG in this Cardiac Arrest Patient?"
What do you think?

Here is more history:

An elderly woman with h/o CAD and CABG presented after out of hospital cardiac arrest with subsequent resuscitation and return of spontaneous circulation.  It was an unwitnessed arrest and down time was unknown.  The initial prehospital rhythm was asystole.

Here is the initial ED ECG:
Rhythm is regular, but no definite P-waves are visible.
There is a Brugada-like morphology in V1.
There is profound ST elevation in lead III and aVF, with ST depression in aVL
There is profound ST depression in V2.
What else?

Here was my response:

"What was the potassium?"

Answer: 7.6 mEq/L

The QRS is very wide.

Case continued:

The physicians thought this was STEMI and activated the cath lab.

Cardiology opined that this was a metabolic ECG.

Later, the K returned and they treated the hyperkalemia aggressively.

There was a complex resuscitation which included, among other medications, administration of calcium and insuline.

1 hour later, this ECG was recorded:

See these other hyperK cases also:

Case 1.  A Tragic Case

This patient presented with weakness.

45 minutes later:

Case 3 
PseudoSTEMI due to Hyperkalemia

Case 4
PseudoSTEMI due to hyperkalemia

Also, see this collaborative post on critical hyperkalemia written by Pendell Meyers with edits by Steve Smith and Scott Weingart:

EMCrit - Critical Hyperkalemia by Pendell Meyers

Monday, November 27, 2017

A 54 yo male with sudden chest pain. Computer says normal. Paramedic disagrees.


There is now an Android app for the 3- and 4-variable formulas. It is of course free (#FOAMed).  It was written by Yannick Schäfer (a medical student in France):

Remember there is also an iPhone app called "SubtleSTEMI"


This was sent by a very astute paramedic.

A 54 year old male came to the door of the fire department because of sudden chest pain while working.  It was squeezing and substernal.

The medic recorded an immediate ECG:
What do you think?
There is ST elevation, but it looks exactly like normal ST elevation ("Early Repolarization"), right?
By the way, "Unconfirmed" means a human needs to overread it.

This medic wanted to be certain that this ST elevation with large T-waves was normal ST Elevation, and not a subtle LAD occlusion that only appears to be normal.

He recorded another 1 minute later:
Not much change.
The medic applied the LAD occlusion vs. early repol formula immediately.

1st ECG:
STE60V3 = 3.5
QTc = 390
QRSV2 = 19
RAV4 = 11

3-variable formula value = 23.61 (most accurate, but not most sensitive, cutpoint is 23.4)
4-variable formula value = 18.18 (most accurate, but not most sensitive, cutpoint is 18.2)

2nd ECG
STE60V3 = 3.5
QTc = 383
QRSV2 = 20.5
RAV4 = 10.5

3-variable formula value = 23.36 (lower)
4-variable formula value = 17.72 (lower)

The medic used the 3-variable formula and obtained values of 23.4 and 23.5 (positive)

He activated the cath lab from the field.

The cath team was ready when he arrived less than 5 minutes later.

Before going to cath, the patient had this ECG in the ED:
Not much change.
STE60V3 = 3.5
QTc = 450
QRSV2 = 19.5
RAV4 = 10
3-variable formula = 27.46 (very high)
4-variable formula = 21.49 (very high)
This last ECG obtains a much higher value because the computerized QTc measurement, at 450 ms, is much longer.  Even if we doubt the last QT measurement by the computer, and assume that it is much shorter, with a QTc a value of 400, both formula values remain very high.

The MDs in the department did not think it was an MI.

The patient went to cath within 5 minutes and had a 100% LAD thrombotic occlusion.

This was his ECG after stenting:
Now the EKG is normal (and the computer would agree!)
The ST elevation and tall T-waves are all resolved.
This would be how the patient's baseline ECG would have looked, if one had been available.
This reperfusion was so fast that the peak troponin was only 0.3 ng/mL.  There was no residual wall motion abnormality.  Symptom onset to balloon time was less than 30 minutes.

Learning Points
1. This shows how any individual patient's normal ST segments may have zero ST elevation.
2. Other individuals may have quite a bit of normal ST elevation.

Therefore, if there is any ST elevation, it is up to you (not the computer!) to determine if it is normal or ischemic.

The formulas are very helpful in this regard.

Again, the computer called the ECG "normal."  

I have argued that physicians should view these ECGs even if the computer interprets it as completely normal.  This is because the computer is so bad at finding subtle occlusions.  Physicians have argued that they don't have the time and that they will be no better at identifying these subtle cases than the computer will be.  

Well, a doctor might not see it, but a paramedic did.  Kudos!!

That is because the paramedic learned.  

I am sure that MDs can learn too!

Recommended Resources