Monday, June 17, 2024

Another deadly triage ECG missed, and the waiting patient leaves before being seen. What is this nearly pathognomonic ECG?

Written by Bobby Nicholson, MD

67 year old male with history of hypertension and hyperlipidemia presented to the Emergency Department via ambulance with midsternal nonradiating chest pain and dyspnea on exertion. Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage.

What do you think?





If this EKG were handed to you to screen from triage without any clinical information, what would you think?  (for those of you who do not do Emergency Medicine, ECGs are handed to us without any clinical context)

The ECG was read simply as "No STEMI." Unfortunately, there was a long wait and the patient left before being seen by a provider. However his EKG was overread as "abnormal" the following day and he was asked to return to the Emergency Department for evaluation.

Upon presenting to the Emergency Department the next day, the patient reported chest pain for approximately 10 days with associated shortness of breath and diaphoresis. He also reported an episode of syncope which occurred earlier in the morning.

VS on arrival: HR 95, BP 131/83, RR 14, SpO2 98%, Temp 36.7 C

Examination notable for diaphoresis, 1+ bilateral lower extremity edema, regular heart rate and rhythm, and no signs of respiratory distress with normal breath sounds.

EKG obtained on arrival to the Emergency Department:



Has your differential diagnosis changed since the original presentation?

Labs obtained and notable for an elevated troponin I to 0.10 ng/mL, BNP 2790, and lactate 3.7. Repeat troponin I obtained ~5h after the first results as 0.14 ng/mL.

While waiting in the Emergency Department, the patient attempted to ambulate to the restroom and developed recurrence of his chest tightness which was associated with shortness of breath and diaphoresis after walking approximately 10-15 feet.


Do you appreciate any dynamic changes compared to the patient’s prior EKG?

Given his exertional chest pain and elevated troponin, the patient was admitted to the hospital for "NSTEMI" with a plan for left heart catheterization the next day. He was started on a heparin drip and CTA of the chest was ordered to rule out pulmonary embolism.

Upon admission, CTA of the chest revealed pulmonary emboli with large clot burden extending from the main pulmonary artery to the lobar, segmental, and subsegmental arteries affecting all 5 lobes with infrahepatic contrast reflux and evidence of heart strain.

Echocardiogram showed severe RV dilation with McConnell’s sign and an elevated RVSP. The patient was upgraded to the ICU for closer monitoring.

This is a case like many others posted (see list below) and the EKG from the patient’s original presentation can be quickly recognized as diagnostic for pulmonary embolism. In fact, Kosuge et al. showed that among patients with either acute coronary syndrome or acute pulmonary embolism and negative T waves in the precordial leads (V1-V4), that inverted T waves in leads III and V1 were present in only 1% of patients with acute coronary syndrome and 88% of patients with pulmonary embolism. “The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of APE were 88%, 99%, 97%, and 95%, respectively.”

1. Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves - ScienceDirect. Accessed May 28, 2024. https://www.sciencedirect.com/science/article/pii/S0002914906023745


Smith comments

The ECG at the top was texted to me and, without clinical info, I said "It looks like PE."  It is nearly pathognomonic for PE.  Why?  There is T-wave inversion in V1-V4 AND T-wave inversion in lead III (see above).  Moreover, the T-wave inversion morphology in V1-V3 is typical of PE.  One characteristic of that morphology is this, in V1-V3: a small R-wave and relatively deep S-wave.   

See this very instructive post:

A crashing patient with an abnormal ECG that you must recognize


More PE ECGs with that typical morphology from the above post:
Contrast with Wellens' T-wave inversions below [Both Pattern A, biphasic terminal T-wave inversion in panels A and B, and Pattern B, deep symmetric in panel C).  There are well preserved R-waves in Wellens waves.


Pendell: See our other acute right heart strain / pulmonary embolism cases:


A man in his 50s with shortness of breath


A man in his 40s with RUQ abdominal pain

A woman in her 50s with shortness of breath

A crashing patient with an abnormal ECG that you must recognize

A man in his 40s with a highly specific ECG

Chest pain, ST Elevation, and tachycardia in a 40-something woman

Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

A 30-something with 8 hours of chest pain and an elevated troponin

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

What do you suspect from this ECG in this 40-something with SOB and Chest pain?




Reproduced from a prior post:

Primer on the ECG in Pulmonary Embolism:
These are findings of acute right heart strain, and could be seen in any condition which results in a rapid rise in pulmonary artery pressure. This includes hypoxia because of "pulmonary hypoxic vasoconstriction" 

The ECG is not sensitive for PE, but when there are findings such as S1Q3T3 or anterior T-wave inversions, or new RBBB, then they have a (+) likelihood ratio and the S1Q3T3, or even just the T3, may help to differentiate Wellens' from PE. 

Stein et al. found normal ECGs in only 3 of 50 patients with massive PE, and 9 of 40 with submassive PE.  Today, however, that number would be higher because we diagnose more of the submassive PEs that have minimal symptoms.

This is a paper worth readingMarchik et al. studied ECG findings of PE in 6049 patients, 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), S1Q3T3 was found in 8.5% of patients with PE and 3.3% of patients without PE.

Kosuge et al. showed that, when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS.  In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads."

Witting et al. looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls.  This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common.  In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrari found that anterior T-wave inversions were the most common ECG finding in massive PE. 





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MY Comment, by KEN GRAUER, MD (6/17/2024):

===================================
Today's case by Drs. Nicholson and Meyers provides an important reminder of a potentially life-threatening entity that still gets overlooked — namely, acute PE (Pulmonary Embolism).
  • We've come a long way since the days of my residency training — in which hypoxemia on ABGs (Arterial Blood Gases) served as a KEY test for initial suggestion of acute PE (albeit pain-induced hyperventilation induced by this bedside procedure often obscured results).
  • In 2024 — once the diagnosis of acute is contemplated, point of care Echo and/or CTPA (Computed Tomography Pulmonary Angiography) enable expedited confirmation. 

  • That said — as shown again by today's case, the diagnosis must be thought of. And, as is also shown again by today's case — recognition of the ECG signs of acute PE often provide a KEY clue to massive (and often submassive) acute PE — IF we are listening ...

An Often Forgotten Clinical NOTE:
 
Initial assessment of the patient for possible acute PE begins by counting the respiratory rate. During my decades of working with residents when hospital Attending — by far, the most commonly overlooked vital sign was respiratory rate. 
  • KEY Point: The respiratory rate that is written on the chart does not count! I cannot tell you how many times such "written" documentation was off, due to the tendency to inscribe a normal number instead of counting for 30 seconds because "the patient looked like they were breathing normally".
  • Patients may "look" like they are breathing normally — when in fact they are tachypneic if you simply take the time to watch them and count. All it takes is a few seconds of concentration for you to determine how fast the patient is breathing. And IF the patient's respiratory rate is increased and their initial ECG looks like the initial ECG in today's case — You have made the diagnosis of acute PE until proven otherwise!
  • The RR (Respiratory Rate) in today's case is recorded as 14/minute at the time the patient presented to the ED on the day after their initial presentation. I maintain that this written RR may or may not be accurate. The only way to know for certain would be for YOU to count.
  • No RR was noted on the 1st day that the patient was seen at triage. Given the appearance of the initial ECG in today's case (which was recorded at that first triage visit) — this represents an opportunity lost ...

Today's Initial ECG:
As per Drs. Nicholson and Meyers — Given the history of this 67-year old man with chest pain and shortness of breath over the days prior to presenting to the ED — this patient's initial ECG (that I've reproduced and labeled in Figure-1) — is diagnostic of acute PE until proven otherwise.
  • Drs. Nicholson and Meyers provide numerous links at the end of their discussion to insightful related cases of acute PE that we've presented in Dr. Smith's ECG Blog. I refer to My Comment in the March 4, 2023 post — in which I included a Table with ECG Findings of Acute PE. I have amended this Table to the one that I show below in Figure-2 — with a note that emphasizes the key clinical point highlighted in their Primer on the ECG in PE.
  • As per their Primer — When T waves are inverted in precordial leads — IF they are also inverted in leads III and V1 — then acute PE is far more likely than ACS.

Figure-1: I've labeled the initial ECG in today's case.


Today's initial ECG shows the following:
  • Sinus rhythm at ~85/minute.
  • Normal intervals and axis — although the S wave in lead I is deeper than is usually seen in this left-sided lead. I thought this was a subtle harbinger of the increasing right axis deviation that evolved over the next 2 tracings in today's case.
  • No chamber enlargement.
  • Slightly delayed transition — with the R wave becoming taller than the S wave is deep between leads V4-to-V5 (with the taller, then shorter R wave in lead V2 compared to V3 probably the result of slight chest electrode lead misplacement).
  • Another subtle sign of PE is persistence of precordial S waves that are seen through to lead V6 (YELLOW arrows in Figure-1 — with there typically not being S waves this far over in lateral chest leads).

  • KEY ECG Findings in Figure-1 that suggest acute PE until proven other are: i) S1Q3T3; — ii) Deep, symmetric T wave inversion in leads V1-thru-V4 (BLUE arrows in these leads = RV "strain"); — iii) In the presence of chest lead T wave inversion — there is prominent T wave inversion in both lead V1 and in lead III; — andiv) Not only do we see RV "strain" in the chest leads — but the T wave inversion in leads III and aVF suggest RV "strain" also in the limb leads.

  • To Emphasize: We do not see all of the ECG signs of acute PE in today's case. Most of the time — we will not see all of these ECG indicators that I list in Figure-2 (and which I discussed in My Comment in the March 4, 2023 post). That said — the pattern of T wave inversion in ECG #1 that is absolutely diagnostic of acute RV "strain", in association with the clinical history — makes the diagnosis in today's case until proven otherwise.

Figure-2: ECG Findings associated with acute PE.









Saturday, June 15, 2024

Palpitations while awaiting CABG

Written by Willy Frick

A 57 year old man with was admitted to the hospital with chest pain. He underwent coronary angiography which showed severe multivessel disease, and he agreed to proceed with workup for CABG. Overnight, his cardiac telemetry showed the following:

Telemetry Sample 1
What do you think?

The rhythm terminated before it could be captured on 12-lead. Upon questioning, the patient reported palpitations. The team immediately paged cardiology, concerned for polymorphic ventricular tachycardia. Further review of telemetry showed the following just a few seconds before the above.

Telemetry Sample 2
Does this change how you feel?




Close inspection of telemetry sample 2 shows regularly spaced QRS complexes marching through the entire strip.


Since sinus conducted QRS complexes cannot co-exist together with ventricular tachycardia, this must all be artifact. Returning to telemetry sample 1, we can use the same calipers to identify the underlying QRS amid all the artifact.


Here is another example which also prompted cardiology consultation. The red coloring is because the telemetry software incorrectly identified the artifact as VT. See if you can identify the underlying QRS complexes.


Answer shown below:






What about when the underlying rhythm is not regular? Such as atrial fibrillation or sinus rhythm with extrasystoles. Here is an example of that. Again, see if you can find the underlying QRS complexes, including the extrasystoles.


Answer shown below:





This can be even more challenging with atrial fibrillation where the only thing you can rely on is careful morphologic inspection.

Learning points:
  • Artifact can be challenging to tell apart from VT, especially on telemetry. If you've ever inspected the application of telemetry electrodes, you can see they often end up in totally bizarre configurations (for example multiple electrodes all closely spaced in one area of the thorax.
  • VT cannot co-exist with sinus conducted QRS complexes. If you can identify the latter, the "VT" is artifact.
  • Sometimes this type of artifact happens in atrial fibrillation and it can be very challenging. Your only clue might be that the VT just seems a little "off."
  • Take advantage of all the telemetry leads. The native QRS may be more obvious in one lead or another.




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MY Comment, by KEN GRAUER, MD (6/15/2024):

===================================
I was not taught about artifact in medical school. Like most clinicians — I learned about artifact "the hard way" = by seeing clinical cases that initially fooled me. But artifact is "alive and well" — and learning to recognize it will amaze many of your colleagues (and may serve to avoid an unnecessary defibrillation or two).

In today's case — I fully acknowledge that I was not certain about the etiology of Tele Sample #1 when I first saw this tracing.
  • I immediately thought this tracing looked bizarre!
  • The deflections were clearly irregularly irregular — but very fast — yet seemingly "geometric" (straight) and not nearly as wide as I would expect for PMVT (PolyMorphic VT). 
  • Obvious artifact was present in the last part of the tracing for the 2 lower leads — yet not so much in the upper lead.
  • There seemed to be no ST-T wave.
  • AND — This rhythm occurred on overnight telemetry, yet the patient was not dead the next morning.

  • BOTTOM Line: Although I was not certain — the above impressions strongly suggested to me that this rhythm was not "real". I suspected the answer might be found in additional monitor tracings — and sure enough (as per Dr. Frick) — Tele Sample #2 confirmed the artifact.

KEY Point: As per Dr. Frick: i) Artifact is "alive and well" in 2024. We need to maintain a high index of suspicion when "something doesn't look right"; andii) The BEST clue to artifact is being able to find the underlying rhythm undisturbed by the unusual deflections (as is masterfully demonstrated by Dr. Frick in today's case!).


================================  
Links to Examples of ARTIFACT:
What follows below is an expanding list of technical "misadventures" — most from Dr. Smith's ECG Blog — some from other sources (NOTE: As I did not previously keep track of these — there are additional examples of artifact sprinkled through Dr. Smith's ECG Blog that I have not yet included here ... ).






Thursday, June 13, 2024

The Expert Witness re-visits a chest pain Malpractice case using the Queen of Hearts

This case was posted by Eric Funk (https://twitter.com/medmalreviewer), editor of the Expert Witness Newsletter, on his site.

Here is the case on his site.   He has graciously allowed me to repost it here. It is a case he presented several years ago, but then want to re-visit in light of the Queen of Hearts AI system.

Don't miss his analysis and assessment of the Queen of Hearts AI OMI ECG bot 

       -- that assessment is at the very bottom of the post.

Click here to sign up for Queen of Hearts Access

Case

A 58-year-old woman presented to the ED with burning chest pain that started 2-3 hours earlier while sitting on a porch swing.

Her first set of vitals were documented:

  • BP 116/57

  • Pulse 94bpm

  • Respiratory rate 24/min

  • O2 sat 90% on room air

  • Temp 97F

She had been cleaning a Jeep in the sun, and was sunburned.

Past medical history included Crohn’s disease, hyperlipidemia, hypothyroidism, and she smoked 1ppd.

Here is her ED EKG:

What do you think?
Since it is in the Expert Witness Newsletter, there must be something that was missed, right?









I would have very high suspicion for OMI on this ECG.  But which artery?  There is STE and a large T-wave in V1, with reciprocal ST depression in V5 and V6.  This is typical of LAD occlusion proximal to the first septal perforator, an ECG for which we have coined the term "Swirl".  

However, the pattern is also seen in inferior OMI with right ventricular OMI. (V1 sits over both the RV and the septum, so transmural ischemia of either one with give OMI pattern in V1 and reciprocal STD in V5 and V6.  

See this post: 

Septal STEMI with ST elevation in V1 and V4R, and reciprocal ST depression in V5, V6.  (Also seen in inferior + RV OMI.)

There appear to be hyperacute T-waves in inferior leads.  There is also STD in V2.  This suggests inferior-posterior OMI and makes me lean to a proximal RCA occlusion.  But there is also perhaps some STD in inferior leads -- this would support LAD.

In any case, it is diagnostic of OMI in a chest pain patient.

The Queen of Hearts agrees:

It is interesting to see what the Queen of Hearts highlights on this explainability map: ST depression in V5 is the most important finding for her.


Case progression:

The automated EKG interpretation was “sinus rhythm with sinus arrhythmia, right atrial enlargement, rightward axis, possible anterior infarct, age undetermined, abnormal ECG”.

The physician documented “normal sinus rhythm”.


The patient was given 0.4mg nitroglycerin SL, which did not change her pain.

She was given 500mL of normal saline and IV Toradol 30mg.


CBC and CMP were unremarkable.

A troponin was normal at 0.06 (normal range 0.00 - 0.10).

CK MB was 1.9 (normal range 0.0 - 3.6).

A chest x-ray was unremarkable.


The physician documented that she was “improved” and the patient was discharged.


The following morning, the patient collapsed in the kitchen in front of her family.

EMS arrived to a pulseless patient in V fib.

She was successfully defibrillated and taken back to the ED.

After being transferred to an academic center, she was taken to the cath lab:

Proximal RCA occlusion (causing inferior and RV OMI)


Unfortunately, she continued to decline despite aggressive measures.

The family elected to switch to comfort care and she died.


The family filed a lawsuit against the physician and the hospital.

They sued the the county-operated EMS service for allegedly not dispatching the call fast enough.

They also sued both EMTs for allegedly not starting chest compressions and defibrillating quickly enough.

The family sued.  

You can read the defense EM expert report on Dr. Funk's site: 

https://expertwitness.substack.com/p/occlusion-myocardial-infarction-queen


Case Outcome

The EMTs were found to have personal immunity as part of their employment with the local government. They were dismissed.

The 911 call center and EMS service were also dismissed.

The hospital and doctor reached confidential settlements.


MedMalReviewer Analysis:

After originally working on this case several years ago, I became interested in re-analyzing it in light of The OMI Manifesto. In short, the OMI paradigm offers an improved method of EKG interpretation that seeks to replace the STEMI/NSTEMI dichotomy that currently dictates emergency cath lab activation (but is rife with false positives and false negatives). While initially promising, I grew frustrated with the OMI model due to the extreme nuance it mandates in EKG interpretation, and my own inability to identify findings that the OMI experts claimed were obvious. I remain skeptical that the average physician should be expected to unilaterally interpret EKGs to the level of the OMI experts.


However, my frustration quickly reversed with the release of the Queen of Hearts algorithm, which was trained by Dr. Stephen Smith using AI to detect occlusion myocardial infarction that is often missed using standard STEMI criteria. It allows users to take a picture of an EKG, which is digitized and then analyzed for OMI.

Naturally, I ran the EKG from this case through the Queen of Hearts algorithm. Sure enough, it detected OMI with high probability:

I was initially skeptical that the algorithm was just flagging everything as OMI. I repeatedly tested the algorithm with multiple other EKGs, and my anecdotal report is that I found it to be highly reliable.




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MY Comment, by KEN GRAUER, MD (6/13/2024):
===================================
Interpretation of the subtle ECG changes seen in a significant percentage of acute OMIs can be difficult. This task is made even more challenging when technical issues such as erroneous lead placement or excessive artifact — call into question our ability to accurately interpret a number of leads on the tracing in front of us. 
  • To illustrate this point — I've labeled the initial ECG in today's case.
 
QUESTIONS:
Before looking at my labeled Figure-1 — Take Another LOOK at the unlabeled initial tracing shown above at the beginning of today’s case.
  • Is there ST depression in the inferior leads in Figure-1?
  • Is there ST elevation in lead aVL?
  • Are there any leads with definite abnormal findings?


MY Thoughts on Today’s Initial ECG:
The history in today’s case is concerning (ie, = a 58-year old woman with longterm tobacco use, who presented with new-onset CP [Chest Pain]).
  • As we frequently emphasize — this type of history automatically places today’s patient in a higher-prevalence group at risk of an ongoing cardiac event. As a result — our threshold for interpreting ECG changes as “abnormal” should be lowered. Given this history — the onus falls on us is to rule out ACS (Acute Coronary Syndrome) — rather than ruling it in.

  • That said — technical issues with today’s initial ECG (in the form of an extremely wavy baseline in 4 of the limb leads) — make it difficult to know IF we truly are seeing ST depression in the inferior leads? — and, if there is truly ST elevation in lead aVL?
  • KEY Point: I think it important to appreciate how we are handicapped in our interpretation of today’s initial ECG by the technical issue of a wavy baseline that calls into question the ECG information conveyed from 4 of the 12 leads. While I thought it likely that there is inferior lead ST depression — and Q waves with subtle-but-real ST elevation in lead aVL — I was less than certain about this given the excessively wavy baseline in these 4 limb leads.

       Figure-1: I've labeled the initial ECG in today's case. 

 
My Continuing Assessment of ECG #1:
Despite uncertainty about the ECG information provided by leads II,III,avF and aVL — there are other leads in this initial tracing that are definitely abnormal.
  • In a patient such as the woman in today’s case (ie, who presents with new CP)there is no way the ST-T wave appearance of the 2 leads within the RED rectangle in Figure-1 can be normal.
  • In lead V1 — The ST segment straightening, with slight-but-real J-point ST elevation and hyperacute T wave appearance are never “normal” findings in this lead.
  • Lead V1’s appearance is in sharp contrast to what we see in lead V2 — in which the usual slight, gently upsloping ST elevation that is normally seen in this lead — has been replaced by an isoelectric, straightened ST segment (RED arrow). In a patient with new CP — this suggests posterior OMI until proven otherwise.
  • Additional definitely abnormal ST-T waves are seen in the 2 leads within the BLUE rectangle. In leads V5 and V6 — BLUE arrows highlight “ledge-like” and significant ST depression.
  • BLUE arrows in lead I add support to the validity of the finding that there clearly is abnormal, straightened ST depression in the lateral leads.

IMPRESSION:
In a patient with new CP — today’s initial ECG has to be interpreted as clearly abnormal until proven otherwise.
  • As enthusiastic as I am about the amazing (and ever increasing) accuracy of the QOH AI application — I believe that optimal clinical management must also depend on capable provider assessment of emergency ECGs. Optimal use of QOH can best be achieved by joint effort (ie, Pre-hospital and hospital providers seeing the ECG first — and then supplementing their interpretation by what they learn from QOH input).
  • Therefore — an important benefit of QOH — is that providers can (and should) learn from this application — so that with time, the interpretations of all providers (pre-hospital, emergency clinicians and cardiologists) will improve regarding faster and more accurate recognition of acute OMI.

  • Regarding specifics of today's case — I fully acknowledge that I found myself unable to predict the “culprit” artery based solely on the initial ECG. That said — I nevertheless was able to strongly suspect acute OMI based on the history of new CP and the initial ECG. I believe recognition of the ST-T wave abnormalities I highlight in Figure-1 should be within the skill set of experienced prehospital providers, emergency physicians, and those cardiologists called on to perform acute cath lab activation.
  • At the least — if technical issues (such as the overly wavy baseline in the limb leads from today’s case) prevent valid interpretation — then the ECG should be promptly repeated. The decision of whether or not to activate the cath lab hangs in the balance.
  • And, if after assessment of a technically adequate tracing there is still uncertainty about whether this higher risk patient with new CP is having an acute OMI — then serial ECGs should be repeated frequently (ie, within every 10-30 minutes, or so)  until such time that joint decision-making between clinician with QOH input can comfortably rule in or rule out acute OMI


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