The original presentation of this case appeared as "What's Wrong with Mr. Wilson?"… You can read the original post here.
Much has been written lately about RBBB abnormalities that were missed.
First, let's review the 12 lead of a typical RBBB. When learning to recognize abnormalities, we must first be intimately familiar with what "normal" looks like.
Editors note: Some astute readers may notice some subtle abnormalities of the ST segments here (so technically, not a normal ECG). I use this example to illustrate typical morphologies of the QRS complex:
*image credit LITFL
Typical features of an uncomplicated RBBB:
- Widened QRS of at least 120 ms
- rSR' in V1-V3
- Widened S wave in the lateral leads, most notably in leads I and aVL
- Should follow the rule of "appropriate discordance" (if you are unfamiliar with this rule, refer to this previous post: Right Bundle Branch Block–Part II
Instead of the typical rSR' pattern in V1, you may in fact see any of the following morphologies:
It is not abnormal to have a small amount of discordant ST depression in the right precordial leads. However, ST elevation in the right precordial leads is never normal. In fact, the ST segments should not be distorted enough in RBBB to cause ST elevation at all. This is precisely why RBBB does not confound STEMI interpretation in the way that LBBB does, where ST elevation may be a normal finding.
Now let's take a look at the 12 lead of our 57 year old male patient who complained of feeling "really sick":
- There is sinus rhythm at a rate of about 80 bpm, with RBBB
- Left axis deviation (bi-fasicular block)
- Abnormally upright T waves in V1-V3
- Questionable T wave in lead I
- Slight elevation of the ST segment in V1-V2
- Significant abnormal Q waves in V1-V4 with loss of initial R wave
Overall, this is an ugly ECG. There should never be any ST elevation, and certainly the Q waves in V1-V3 are very abnormal and significant.
If we look at a normal RBBB and our patient's ECG side by side, the abnormalities become obvious:
From the previously mentioned RBBB posts by Dr. Stephen Smith (links above):
- RBBB should not have ST elevation at baseline.
- In RBBB, there should be some ST depression in V2 and V3. An isoelectric ST segment may represent relative ST elevation.
- The presence of such well developed anterior Q waves suggest completed transmural STEMI.
Dr. Smith elaborates further on the Q waves:
"The wide Q waves suggest "transmural" MI (completed MI with infarction of the entire thickness of the ventricle). This was common before the days of reperfusion of STEMI, but still happens in patients who present late and therefore do not get timely reperfusion therapy"
The story of our patient:
The ECG recorded above was taken at admission to the cath lab. He was found to have a 99% lesion of his LAD. His ejection fraction was in the 30s.
He received a stent and a balloon pump, and was admitted to the ICU. His prognosis questionable.
Two weeks prior, he had started to feel very short of breath, along with a cough. On exertion, he felt "much more tired than normal".
After a few days he went to his PCP. His hx was significant for hypertension and smoking. It is unknown whether or not an ECG was acquired at that time.. He was, however, diagnosed with an URI and sent home with antibiotics.
He started to feel slightly better after a day or two, then began to decline again. He found himself without the energy to walk across the room. He had his wife drive him to the ED.
At the ED, they found him to be hypotensive (86/58) and not improving after the antibiotics. An ECG very similar to the one recorded above was acquired. Although it was not found to be diagnostic, there was concern that his issues could be cardiac. He was scheduled for a non-emergent cath a few days later.
At that time, the above ECG was acquired and the lesion was found.
- ECG abnormalities can be missed at many levels of care.
- Become the "expert"– you can save lives!
- You can not discover an abnormality until you are crystal clear on what "normal" looks like
- Missed abnormalities can lead to delays in much needed patient care and possibly worsened outcomes
For more information, be sure to read our series on RBBB:
This is the conclusion to 53 year old male: Severe leg pain. You may wish to review the case.
Before we begin, my apologies for the delay in posting this conclusion. I live in coastal NY, and we got hammered by Hurricane Sandy. It has taken me a little time to get all caught up.
This is not an easy case. Our patient's chief complaint is of sudden onset of severe leg pain, and chest pain. Also notable is the measured hypertension.
Here is another look at the second 12 lead, which showed the following changes from the first:
There is sinus tachycardia, at a rate slightly above 100 bpm. There is physiologic left axis deviation. There are no signs of chamber enlargement, and the QRS is normal width. There is slight ST elevations in I and aVL, with ST depressions in the inferior leads, as well as V2 and V3.
At this point, our list of DDX should probably include:
- Possible aortic dissection
The patient's complaint sounds like it could be DVT, as many readers pointed out. We might expect to see swelling and redness as well, and this was not noted by the EMS crew. These signs and symptoms are not sensitive, however, as about 50% of people with DVTs will not have them.
The patient is hypertensive, with chest pain, which led some of you to suggest an aortic dissection. Usually there is sudden onset of maximal chest pain, 10/10, with a "ripping" or "tearing" sensation. We do not have those typical signs and symptoms here by history.
The patient does have ischemic signs on the 12 lead, consistent with lateral STEMI, but the patient's main complaint seems to be leg pain, not the chest pain.
So, how do we manage this patient?
For starters, I think this is a tough patient to figure out. We have three good possibilities on our list of DDX, and two of them are immediately life threatening.
I look at it this way, and of course it is with the benefit of hindsight. There seems to be more going on here than DVT, based on the patient's presentation, chest pain and 12 lead ECG.
STEMI seems to be a reasonable assumption based on the 12 lead, but I would be thinking that as an atypical presentation (leg pain), this would almost be off the charts. It just doesn't seem like STEMI.
We also know that other conditions can cause ischemic changes on the ECG, and a dissecting aorta is one of them.
Of course, O2 and IV access are indicated. NTG is a good possibility because it would be beneficial in either scenario.
With that in mind, I would at least make sure we are transporting the patient to a hospital that can handle both STEMI and surgery for dissecting aorta.
If a dissection progresses in a retrograde direction towards the aortic root, an acute total or partial occlusion of one of the main coronary arteries can occur. Usually, it is the RCA that is involved, but unusually, it can involve the left main. In the ED, heart rate and blood pressure will be controlled until surgery is performed. You can read more about this phenomenon here.
As you have probably surmised by now, this was the fate of our patient. Once in the ED, a CT scan revealed a dissection of the ascending aorta. This dissection caused a partial occlusion of the LMCA. The patient underwent extensive surgery to repair the aorta. He was expected to make a strong recovery.
We hope you enjoyed this unusual case! As always, comments are encouraged!
This is the conclusion to a 51 year old female CC: Near Syncopal Episode. If you haven't read the first part we highly recommend it!
When we left off, our crew was attending to a 51 year old female who had almost passed out in a stadium tunnel during a college football game. We received a few questions as to the type of football, which could be important to the diagnosis, so we will clarify that this was an American Football game.
Our crew had found her to be hypotensive, first bradycardic and then tachycardic, with concerning changes on the 12-Lead. A nasal cannula at 4 L/min was initiated and they established bilateral IV's and were rapidly infusing nomal saline to restore perfusion.
Let's take a look at the initial rhythm strip:
The initial rhythm strip shows a narrow complex tachycardia at ~130 bpm, without clear P-waves. Retrograde P-waves can be seen in numerous complexes T-waves, leading to a presumptive diagnosis of a junctional tachycardia.
The longer rhythm strip shows sinus complexes followed by runs of junctional tachycardia. Astute readers will note Wenckebach conduction of the retrograde P-waves!
This finding alone would be highly concerning given our patient's present condition and history, however, when we move onto the 12-Lead her diagnosis is clinched:
The initial 12-Lead ECG again shows a junctional tachycardia, with markedly hyperacute T-waves and ST-elevation in the anterior precordials with downsloping ST-depression in the inferior leads. The degree of which the T-waves tower over the R-waves in V4 is truely impressive!
The crew immediately recognized the extensive anterior wall infarct with cardiogenic shock, and given the concurrent finding of a junctional tachycardia presumed there to be gross insult to the AV nodal tissue. They placed defibrillation pads on the patient and helped the arriving crew package the patient. The patient was able to follow commands and 324 mg aspirin was given PO. After 1 liter of fluid the patient remained hypotensive and another bolus was started. Oxygen was titrated to maintain an SpO2 of >96%.
Eventually the patient stated she had some dull pressure in her chest, but otherwise denied pain or shortness of breath. An early STEMI notification was given and while enroute to a STEMI receiving center the crew ran multiple 12-Leads, capturing the evolution of the myocardial infarction.
In this 12-Lead we can clearly see periods of alternating tachycardia and bradycardia, an ominous sign given the evolving MI. V5 and V6 were removed and adjusted closer to V4 and V7 so that defibrillation pads could be placed.
The patient was taken directly to a cath lab suite and found to have a 100% occlusion of the LAD and after the placement of a stent the patient's ECG normalized and her hypotension resolved.
This case illustrates the amazing evolution of an extensive anterior myocardial infarction and highlights the role the LAD can play in AV nodal function. We hope you enjoyed these ECG's as much as we did!
When we last left off, our patient was a 63 year old male complaining of substernal chest pain which awoke him from sleep. We obtained standard, right-sided, and posterior ECG's which cardiology deemed non-specific. Our patient continued to have persistent chest pain even after maximal therapy.
Coronary catheterization was performed later that morning, and a total occlusion of the first obtuse marginal (OM1), a branch of the circumflex artery, was found. A drug eluting stent was placed, and his subsequent hospital course was unremarkable.
Could we have guessed this from the start? Let's take a look at his ECG's again:
Reviewing our patient's first ECG we see horizontal ST segment depression of 1 mm was seen in II and aVF, 3 mm ST depression in V2, and 1 mm ST depression in V3 and V4, all with upright T waves. An early R-wave transition was noted, with a height of 13 mV and an R/S of 1 in V2. Lead III showed T wave inversion.
The right-sided ECG featured only ST segment depression and inverted T-waves.
Reviewing the posterior leads, we see some interesting changes. Notably ST segment elevation of 0.5 mm in V7 and V8, and an unchanged appearance of the limb leads.
So, Dr. Walsh, what can we take away from this case?
Devoted readers of EMS 12-Lead will already know much about posterior MI, so I'll just do a brief review of the basics. I encourage you to search for the tag "posterior STEMI" for more information. As always, Dr. Stephen Smith's website also has plenty of examples and teaching about posterior MIs.
There is a small amount of controversy about what anatomic area of the heart a "posterior" MI actually affects. Some have suggested that the infarct is actually in the infero-basal region, while others have evidence that it should be viewed as a lateral infarct.
Regardless of the name, however, it generally is the result of an occlusion of the left circumflex coronary artery (link to cool animation). This territory is generally regarded as "electrically silent" in the standard ECG leads. As such, diagnosis relies on indirect evidence in the standard leads, as well as the use of non-standard "posterior" ECG leads.
So, how can we be Posterior STEMI Rock Stars, Doc?
For years, the standard teaching on identifying a posterior MI has emphasized some common elements. Brady summarized the most important of these:
- Horizontal ST depression in V1-V4
- Tall, broad R waves (>30ms)
- Upright T waves
- Dominant R wave (R/S ratio > 1) in V2
So, a typical posterior STEMI looks like this:
Inferioposterior STEMI courtesy of LifeInTheFastLane.
Note the ST elevations in the inferior and lateral leads; in general, a posterior MI usually shows signs of a STEMI in either of these two regions the majority of the time. It's pretty obvious that evidence of STEMI in one area (e.g. inferior) certainly strengthens suspicion for a posterior MI.
However, here's an example of a posterior MI that does not show any inferior or lateral involvement:
Posterior STEMI without inferiolateral changes. (PubMed)
Using posterior leads (V7-V9) can show ST elevation, but the magnitude may not be as dramatic as that seen in the "usual" STEMIs. Many experts consider, for example, 0.5 mm of elevation to be significant, instead of the usual > 1 mm criteria, and that elevation in just one lead is sufficient.
So what's wrong with the conventional thinking?
There's a short-cut way to diagnose a posterior MI, that involves "flipping" the ECG. The idea is that the ST depression in the anterior leads is a "mirror" view of ST elevation in the posterior wall, and that the tall R-waves are actually deep Q-waves.
For example, a blow-up of lead V2 from the isolated posterior MI above (the second ECG) looks like this:
It fulfills all the criteria I reviewed above, so it's a classic example of how we currently define a posterior MI. And if we "flip" it, we get this:
Yep Doc, that looks like a regular STEMI now!
For many people (MDs included!), the diagnosis of a posterior MI starts, and ends, with this flipping.
I'll tell you what has always bothered me though. Look at the R-wave in the un-flipped image. This is just the mirror image of the Q-wave, and our "flipped" image reinforces that. In fact, the Q-wave in our flipped image looks pretty darn old, like the MI has progressed far along already.
Furthermore, the T-wave in our "flipped" image hardly looks hyper-acute. In fact, it looks like the T-waves are in the process of returning to baseline, another indication that our "classic" posterior MI is old.
Here's an example of an subacute/old inferior MI, for comparison. Also note the resolving, partially inverted, T-waves in III and aVF:
Old Inferior MI courtesy of LifeInTheFastLane.
It looks instead like our description of posterior MI is training us to look for old, completed MIs!
Let's look at this from another angle. Look at this typical inferior STEMI, and focus on lead aVF:
That's a classic STEMI, no doubt. Tiny Q-waves, tall T-wave – everything suggests that this is very acute.
Now, instead of being lead aVF, let's pretend it were lead V9. What would the "flipped" view of this lead be? Let's flip it and see!
This view shows a small R-wave, and a fully inverted and deep T-wave. Now, if we take a look back at the criteria listed above for a posterior MI, however, it would not meet much of the description of a posterior MI we listed before.
We're teaching people to pick up on old posterior MIs, and training them to miss the acute presentations.
Interesting, so how can we avoid this, Doc?
Well, I may have had this thought kicking around in my head, but some cardiologists actually wrote down these thoughts! Birnbaum et al. just published the article Common pitfalls in the interpretation of electrocardiograms from patients with acute coronary syndromes with narrow QRS: a consensus report. This wasn't a prospective controlled trial, but they managed to get 13 cardiologists to agree on a few things.
One of those was that our standard description of the morphology of posterior MI on the ECG is likely wrong. Helpfully, they proceed to describe what we ought to be looking for!
After reviewing the usual evolution of LCx-occlusion MI, they conclude that the standard definition, that relies on tall R-waves and upright T-waves is:
… the late “mirror image” of fully evolved ST-segment MI (STEMI) (Q waves with terminal T-wave inversion) and not the acute phase of STEMI.
By contrast, they give an example of what they consider to be an acute posterior STEMI:
If we blow up lead V2…
…we see that there is a small R-wave, and fully inverted T-waves, and an R/S < 1. It meets none of Brady's criteria above. But if we flip it…
It looks like a regular ol' STEMI!
Bring it home for us, doc.
The usual description of posterior MI may be in need of revision. The posterior leads, however, remain useful to reveal acute cardiac ischemia.
Thank you again to Dr. Brooks Walsh for this case and his insight into posterior STEMI!
- Did you catch the posterior STEMI?
- Does your service allow you to activate a posterior STEMI?
This is part II to 59 year old male–"Lifting Boxes". You may wish to review the case.
Let's review the ECG:
There is sinus rhythm at about 90 bpm. Some of you saw a slight bit of ST elevation in the inferior leads, and maybe an abnormal aVL. Perhaps? Perhaps not? V1-V4 look possibly abnormal, but there is an awful lot of artifact. There appears to be a bit of ST depression in V5-V6. Is this an ischemic ECG? Looks concerning from what we can decipher.
Sometimes on blog posts, we get used to crisp ECGs and tidy scenarios. Nothing wrong with that. Sometimes, though, our cases on the street just don't go like that. Often there is much to learn from those, but I digress.
There are a couple of real concerns with this case;
- As correctly pointed out in the comments, the quality of the ECG is poor. This leads to all sorts of interpretation problems. If we put effort into it, we can usually get a pretty good tracing. On occasion though, it can be tough.
- Another issue is that the 12 lead was not acquired early on. The crew acquired the ECG in the ambulance after the following: assessment, history, physical exam, O2, ASA, bathroom break, change of clothes, etc. This is not what we are after, and we could miss important findings by waiting this long.
As most of the comments reflect, the timing of the ECG and poor quality make it tough to interpret, and tough to activate the cath lab. I know some of you saw findings that led to you say you would activate, but doing so based on this one poor quality ECG is tough to do. Just is.
So off to the community hospital he went.
Calls are run like this every day. We all know it. In fact, it is one of the reasons we discuss cases such as this.
Could this patient have benefited if the call was handled differently?
Fortunately, we know that he did!
In a contrasting plot twist, this call was actually handled quite differently:
In reality the crew obtained the history and vitals previously mentioned. However, undaunted by the patient's reluctance they convinced him to allow a 12 lead to be acquired immediately. This is what they found:
Due to the patients girth and breathing patterns, it was difficult for the crew to acquire a totally clean ECG. However, this one clearly shows ST elevation inferiorly, as well as V5 and V6. We can also see ST depression in V2-V4 with tall R waves. There is also slight ST depression in aVL: Infero-postero-lateral STEMI.
The crew acquired another 12 lead with V4R which revealed about 1mm of ST depression in V4R:
The ECGs were transmitted, and the patient was emergently transported to the cath lab, where he underwent PCI and had a successful outcome.
For comparison, note how much the ST segments resolved from the first 12 lead to the one acquired in the ambulance:
After just a short period of time from the first ECG, obvious ST elevation in II and III has mostly resolved. Timing is everything!
The point of all of this is to clearly illustrate the importance of early 12 leads and good data quality. The prehospital care of this patient could have gone either way. We see it every day. How we handle those first minutes, and the quality of the data we acquire will have a huge impact on the care our patients receive.
What are your thoughts? I'm sure you have experiences similar to this one!
Here is the conclusion to 51 year old male: Chest Pain. You may wish to review the case.
Here is the ECG again:
There is a regular sinus rhythm at a rate of about 70. The QRS is narrow. The axis is normal, at about 15 degrees.
Let's take a look at the constellation of ST changes:
There is ST elevation in leads I, aVL, V2-V6. There is slight ST depression in III and aVF (and arguably in lead II) with ugly looking T wave inversions. Some of you also noted the suspicious looking Q waves in III and aVF.
Pericarditis and Early Repol were put forth as possibilities. Remember though, that neither of those will have reciprocal changes (excepting myocarditis, which may present as STEMI). Here, we have reciprocal changes inferiorly. If you were inclined to be thinking about STEMI mimics in this case, those changes should put ischemia at the top of the list. In addition, as some of you pointed out, the ST changes do not look like Early Repol, and the amount of ST elevation here is alarming.
The crew in this case, along with the physician, decided this was STEMI. The patient was given Heparin, ASA, anti-emetics, and Morphine. His condition improved enroute, and his BP climbed to 124/75.
Upon arrival at the hospital, he was taken directly to the cath lab. There was a complete blockage of the LAD.
Here is the cath lab image showing the blockage:
Here is the image after revascularization:
I don't know about you, but I always find these images amazing. Fortunately, our patient was discharged from the hospital to cardiac rehab a few days later. He was expected to recover nicely.
Enjoy the holiday!
This is the discussion to "What Happened?" You may wish to review the case here.
Ok, let's review the initial 12 Lead:
Just about everyone picked up on the infero-posterior STEMI.
Where it got interesting for me, was determining what the rhythm was! At first glance, the rhythm was for the most part regular (note the computer interpretation of Atrial Fibrillation with RVR!) and narrow, with a rate just a touch faster than 100. I did not see P waves before most of the QRS complexes, and I initially thought it was a junctional tachycardia.
As the STEMI was most likely due to an RCA occlusion, it is not surprising to have conduction disturbances. The pause, followed by an apparent sinus beat (circled in red above), had me wondering if this was indeed junctional with a sinus "escape" after the pause, or some kind of sinus rhythm with AV block.
In keeping with our spirit of "Peer Sourcing", I ran this strip by electrophysiologist Dr. Nick Tullo, of the ECG Academy.com. A review done by Life in the Fast Lane of Dr. Tullo's excellent academy can be found here. This is the conversation I had with Dr. Nick about this rhythm:
Me: Thanks for the help Dr. Nick. Now, what the heck is this?? Junctional, or sinus/AV block?
Dr. Nick: I would call it "Atypical Wenckebach" –essentially 13:12. You can see a sinus P following the fourth beat, and then a similar pause just before the end of the tracing. The pause is less than two times the previous R-R, and the PR of the second beat following the pause is longer than the PR that interrupts the pause (what you are calling accelerated juntional is really sinus rhythm with a first degree AV block, but you can't see the P easily because it's buried in the previous T). In the setting of acute IWMI it's due to the same high-vagal-tone mechanism that would cause the usual 3:2 or 4:3 Wencheback (or even complete heart block in some patients) but the AV node is mostly keeping up.
Me: Wow… OK! But, how do we know it's not a junctional rhythm with a sinus beat escaping from the pause?
Dr Nick: You have to look hard for the P waves. If it was a junctional rhythm you'd see consistent P's at the end of the QRS or maybe in the very early part of the ST segment. If I'm right, the P wave will be on the T-wave somewhere and not always in the same spot (since it's not directly connected to the previous QRS). Granted, the ST elevation makes it hard to see the Ps. But I see the answer clearly:
Look at V5…see how the first beat has a concave upslope of the T wave while the second beat looks like it has a bump on it? That bump is the P wave. Assuming that the R-R interval midway through the "junctional rhythm" is equal to the atrial rate (since the PR doesn't change midway through an Atypical Wencheback cycle) measure back from the visible P preceeding the third beat in V5…doesn't it land right at the bump? The reason the T looked concave the beat before that is because that P wave is on the peak of the T.
I've put together some graphics to help illustrate the important points.
First is Lead V5, which Dr. Nick referenced, blown up. I've done the same with lead II. Note the subtle morphology changes in the two T waves. This is the last P wave of the cycle, which does not conduct. the P wave following the pause is the first of the cycle, and has the shortest PR interval:
I know, you're thinking, "Really? Do those little blips/bumps really measure out?" Don't take my word for it. I've got one more illustration to show you. I took a mid cycle R-R interval (1), as Dr. Nick suggested, and used that to measure back and see where the P wave should be in leads II and V5 (2,3):
As you can see, right on cue, those blimps/bumps are right where the P wave should be. And there we have it: 13:12 Atypical Wenckebach, with a PVC at the very end of the strip.
My sincere thanks to Dr. Nick Tullo for his help with this case, and kudos to Jason, who expertly picked up on this in the comments section.
Now for the second 12 Lead:
The patient was treated with thrombolytics (TNK), and as many of you commented the resulting rhythm was an accelerated idioventricular rhythm (AIVR). AIVR appears similar to VT, but slower (slower than 120). In the thrombolytics era, this transient rhythm was noted to be a marker of reperfusion, although not all patients with a reopened coronary artery have AIVR. When it appears it rarely causes hemodynamic instability, and usually requires no treatment. For more information about AIVR, see here.
Of course, you will notice that I have circled several leads in the 12 lead above. In keeping with this case, in which nothing seems to be typical, you will notice that in fact the ST segments have not resolved during the AIVR. The inferior ST elevations remain, as do the ST depressions in V1-V4, and aVL.
When asked about this, Dr. Smith, of Dr. Smith's ECG Blog had this to say: "This is one of the few cases of AIVR I've seen that was not associated with reperfusion."
In this case, our patient failed thrombolytics. He was immediately sent for rescue PCI. Unfortunately, we don't have any additional information.
There was a lot of information in this discussion. I sure learned a lot!
I look forward to your comments, and as always, thanks for reading!
This is the discussion for Elderly Female: Chest Pain. You may wish to review the case.
Ok, this was not an obvious case, at least, not until the end. As far as the patient goes, I think we all agree about the differentials: ACS vs. possible aortic dissection (due to the pain radiating to her back).
The patient had no history of problems with aneurisms, but no history of CAD either. Pain starting while under exertion, with substernal chest pain, and diaphoresis sure sounds like ACS. You could check for differences in BP in each arm, which the crew did, but this finding in a dissecting aortic aneurism is often absent. But, never bad to keep in mind other possibilities of what's going on. Now, let's review the initial ECG:
The patient had a hard time sitting still due to her discomfort, and the resulting wandering baseline and irregular rhythm present challenges to interpretation. We have a rhythm that is A-Fib. We have slight ST elevation in V1-V3 (possibly slight in V4), and ST depression in V5 and V6. Anterior MI? Maybe, but maybe not.
Several of you astutely noted that the morphology appeared to resemble LVH with secondary reploarizaion abnormalities, the so called "Strain Pattern". One addition challenge here, is that this printout does not appear to let the QRS complexes run into eachother, rather it cuts them off at the level of the overlying or underlying QRS complex. This makes it difficult to measure.
The monitor interpretation did indeed say that voltage criteria for LVH was met. However, as Tom B has mentioned so many times on this site, it is more important to recognize the morphology of Strain Pattern, than actually know the voltage criteria. Here is a snapshot of Strain morphology typical in the lateral precordial leads:
Here are leads V5 and V6 from our patient:
Similar morphology? Looks like it… we would like to see the degree of depression proportional to the height of the R wave, but unfortunatlely the complexes are chopped by the machine, adding another challenge to the interpretation. No history of MI, and the "QS" looking complexes of the right precordials sure add to the look of Strain pattern. For more on LVH and Strain pattern, check out this previous case from ems12lead.com.
What about the ST depression in the inferior leads? Let's take a look:
Could this be attributed to Strain pattern? Strain pattern can manifest itself in the inferior leads, but according to Dr, Smith of Dr. Smith's ECG Blog, "usually you can tell because the voltage will be high in the limb leads, as usually measured in aVL". That was not the case here, so I think the ST depression in the inferior leads looks to be very suspicious.
Another thought proposed about this was the possibility of "Dig Effect". Here is an example of what Dig effect looks like (note the "scooped" appearance of the ST segment):
In our patient, I see flatter, downward sloping ST depression, but the baseline is wandering somewhat and it's not an easy call. It's hard to argue if you had it on your list of differentials though, especially with the history of AF.
So what do we have? A patient who seems to have ACS with an ECG that looks like Strain pattern, but also has concerning ST depression in the inferior leads. In the comments section of this case, I think VinceD summed it up best when he said: "We'd have to watch her like a hawk and worry about worst first with this clinical picture. She doesn't qualify for urgent PCI (at the moment)…" At the moment is the key.
That is precisely the same take the crew had, and they decided to watch her like a hawk and do serial ECG's… Once again, here was the clinching ECG acquired moments from the community hospital:
In less than twenty minutes, you can see the side by side changes here:
We can see the ST elevation increased in V2 and V3 from approximately 1mm to approximately 3mm, and in V4 the increase was from about isolectric to an astounding 5mm! In addition, the ST depression in the inferior leads increased by about 1mm. Indeed, they were born out to be reciprocal changes. Keep in mind it took less than 20 minutes for these changes to be recorded on the 12 leads.
The key to this case was the serial 12 leads done by the crew. While I don't think anyone could find fault with the cath lab not being activated after the first 12 lead, it was too late to send her directly to the cath lab by the time the last one, which revealed the STEMI, was acquired. The cath lab was activated as soon as possible, and ground transportation to it was dispatched immediately. Unfortunately an unavoidable delay still occured. A D2B time of <90 minutes could not be achieved.
Although the STEMI was recognized, this case does not have a happy ending. The bloodwork showed a highly elevated Troponins (exact value unknown), but upon arrival at the cath lab, for reasons unknown, she refused all treatments.
Key Learning Points:
1- Know your morphologies and differentials. It helps you get a better patient history, and helps you figure out what's going on with the ECG.
2- In the words of Dr. Corey Slovis: "One ECG begets another"… DO SERIAL ECG'S! And, espcially if the patient's presentation changes, get another 12 lead. Many STEMI's are missed because serial 12 leads are not done. One ECG is a snapshot in time. Like one set of vitals. But they are also dynamic, and as we've seen in this case and others on this blog, they can change dramatically in very short periods of time.
This is the conclusion to 41 year old female: chest pain.
I think we would all agree the patient presentation is suspicious for ACS. Let's review the first 12 Lead:
The rhythm is sinus tach. There is about 1mm of ST elevation in V1, and depending on where you spot your J point, little to no elevation in leads V2, V3. There is about 1mm of ST depression in leads I, II, and V6. Lead III also has a Q wave and an inverted T wave. However, both a Q wave and an inverted T wave in lead III may be normal. One could definitely argue this is a suspicious looking 12 Lead, but I'm not sure if any of us would activate the cath lab based on this ECG alone. If serial ECG's are not done, the cath lab is not activated, and likely nothing will be discovered to change that.
But, you are all well aware of the importance of serial ECG's, and so was the Medic on this call. So let's take a look at the second 12 Lead, taken only 7 minutes later:
There are obvious dynamic changes here. For starters, there are now hyperacute T waves that tower over the QRS in leads V2 and V3, and are much larger than they were in V4. They are localized to leads V2-V4 and "point" to the area of infarct. The ST elevation in leads V1 and V2 is now 3mm, and in V3 is 3-4 mm. The ST depression in leads I, II, and V6 have deepened slightly. The T wave inversion in lead III has deepened, and there is now measurable ST depression in aVF. Also, there is subtle loss of the R wave in leads V2-V3. On its own, this ECG is probably diagnostic of STEMI, but with the dynamic changes compared to the first one, it is virtually assured.
In the third 12 Lead:
The hyperacute T waves are not as towering as they were…the ST elevation in V1-V3 are now 1-2mm, and the ST depression has greatly resolved. The inverted T wave in lead III is now mostly upright. These changes are likely the result of the treatments given by the Medic, perhaps some reperfusion of the culprit artery.
To illustrate how dynamic these changes were over the course of the three ECG's, have a look at leads V1-V3 side by side:
At the cath lab, the patient was found to have an occlusion of the LAD, for which she was stented.
Some key points to take away:
- The importance of serial ECG's can not be overstated.
- Subtle changes,such as straightening of the ST segment or subtle enlargement of the T wave may be the first change on the ECG.
- Hyperacute T waves are localized, and "point" to the area of infarct.
- ST deviations may normalize after treatments such as ASA, NTG… Failure to do serial ECG's may delay patient care if these deviations are missed. For additional information on this point, see this excellent post on Dr. Smith's ECG Blog.
Here's an interesting case sent in by faithful reader Carl R. Christiansen, Paramedic, from Norway. As usual, changes have been made to protect patient confidentiality.
It's an early Sunday morning when you are dispatched to a hotel for a 41 year old female with chest pain.
You and your partner enter the hotel room and find the woman lying in bed. As she sits up to greet you, you notice the color of her face is pink, but she seems to be slightly uncomfortable and restless. She tells you that she woke up at about 8 am with chest pain in the center of her chest, which does not move anywhere. She isn't short of breath or lightheaded…no nausea or vomiting, or anything else out of the ordinary other than the chest pain. The pain doesn't change with breathing, movement, or palpation. She adds that she's had some similar pain come and go over the last three or four days, but never as bad as this. You ask her to rate her discomfort, and she tells you 9/10.
As you assess her appearance, you don't see anything abnormal… no JVD, no edema. Her pulse feels rapid but regular, and her lung sounds are clear bilaterally. Inspection and palpation of her chest and back are normal. You do a FAST screening, which shows nothing abnormal. All she can tell you is that she had a couple of glasses of wine with dinner the night before, and slept through the night until the pain woke her up this morning.. She has no relevant medical history, and takes no medications.
While you are getting the history, your partner takes a set of vitals:
- Pulse: 104 and regular
- BP: 210/155
- RR: 18 and regular
- CTC: Pink, warm and dry
- SpO2: 99%
You acquire the following 12 Lead ECG:
What do you think? What would you do next?
The treating paramedic gave the following treatments:
- One SL NTG
- 300 mg ASA
- IV established
- 2.5 mg of Morphine IV
- 600 mg Plavix orally
As the above are being done, a second 12 Lead is acquired:
After the treatments were given, the patient's blood pressure dropped to 129/84, and her heart rate dropped to and remained at about 80. The Paramedic called a Code STEMI and transported the patient to a PCI center. Upon arrival there, this last 12 Lead was acquired by the crew:
What do you see on these 12 Leads?
Would you have called a Code STEMI?
What would your treatment have been for this patient?
This is the discussion for 63 year old male: Chest Pain.
Many of you thought the original 12 leads showed Wellens' Syndrome.
Lets review some key points about the T wave inversions of Wellens' for a moment:
- They occur when an occluded artery is reperfused, spontaneously or otherwise
- They are always recorded during a pain free period
- They are most prominent in V2-V4, rarely extending out to V6
- QTc is usually greater than 425
- T wave in III is usually upright
Let's take a look at the 12 Lead:
Initially, I also thought this was Wellens'. I decided to seek the opinion of Stephen Smith, M.D. of Dr. Smith's ECG Blog, and with his permission, here's what he had to say:
"I don't think this is Wellens'. I think it is benign T-wave inversion. QT on the short side, distinct J-waves, extension out to V5-V6. It is a baseline of benign TWI followed by LAD occlusion." Indeed, the QTc in the first two 12 leads were 422 and 418 respectively. In his experience, the QT is prolonged in Wellens', and this is one way to differentiate it from benign T wave inversion (BTWI), which normally has a QTc < 400-425."
Now for the obvious STEMI:
Due to the deterioration of the patient's condition upon arrival to the hospital, he was brought directly to the acute area. Through translators, they were able to explain that patient was working out earlier this morning and developed right shoulder pain, which prompted the first EMS response. His symptoms resolved by EMS' first arrival and he sent them away. He subsequently took a shower and again began to feel the right shoulder pain, shortness of breath and lightheadedness again, which prompted him to recall EMS.
A hospital ECG at 10:01 revealed improvement in patient's ST elevation (no copy was retained). Heparin was administered, and the patient was moved to the cath lab. The angiogram revealed single vessel coronary artery disease. The mid LAD had 95% acute plaque disruption. A thrombectomy was performed, and a white and pink thrombus was retrieved. The artery was stented, and TIMI-3 flow was restored. Door-to-Balloon time was 34 minutes.
Here are the before-and-after angiograms:
This is the conclusion to 54 year old female CC: BLS intercept.
I did not expect to get so many comments! Great discussion on many points. It even afforded an opportunity to review atrioventricular blocks.
Going back to the case let’s look at the initial 12-Lead ECG.
As many readers noted, there is a lot of baseline wander. This is not the most helpful of 12-Leads. On scene the crew attempted multiple 12-Leads, however, the patient would not sit still and that was the best one.
I think a close look at the Initial 12-Lead has enough information to make a field diagnosis.
Leads III and aVF have subtle ST-elevation and Q-waves, which without any cardiac history are likely new. More importantly, the ST-elevation in III and aVF is proportionately large compared to the QRS amplitude. Leads aVL, V2, and V3 all have at least 1mm of ST-depression without question. I’ve borrowed Tom’s technique of using PowerPoint to stretch the leads vertically while preserving the ST/QRS ratio to help illustrate these findings.
Is ST-elevation present in two or more contiguous leads?
Additionally, we should take into account all of our findings which strongly suggest an MI.
- Chest pain which awoke the patient from sleep
- Left sided paresthesia
- ST-elevation in two contiguous leads, with reciprocal changes
- 3° AV Block, with a junctional escape
This constellation of findings would be expected with an occlusion of the RCA, potentially with right ventricular and/or posterior involvement. We can solidify our hunch with knowledge that the AV node is fed by the RCA in right-dominant individuals. ST-elevation in Lead III > Lead II is suggestive of RCA occlusion.
The crew in this case activated the cath lab from the field. They gave 324 mg ASA, started bilateral lines, gave multiple fluid boluses, placed pads for pacing, and administered 0.5 mg atropine while preparing the patient for transcutaneous pacing.
At the receiving facility, after they switched to the ED’s monitor, the patient’s rhythm changed to a 2° AV Block Type II with a ventricular rate of 70, easily palpable radials, and improved skin color.
In the cath lab, the following was found:
Diagnosis: Acute ST-elevation myocardial infarction.
Christopher A. Watford from the My Variables Only Have 6 Letters blog has submitting a very interesting case study (actually he submitted two but you’ll have to wait for the other one).
EMS is called to the residence of a 69 year old male complaining of chest pain.
On arrival the patient is found sitting in a kitchen chair.
He appears acutely ill.
Skin is ashen, cool, and very diaphoretic.
Levine’s sign is present.
It is obvious that the patient is anxious and in severe pain.
Onset: Sudden onset approx 20 minutes before EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Severe pressure
Radiate: The pain does not radiate
Time: No previous episodes
Breath sounds are clear bilaterally.
Vital signs are assessed.
Pulse: 60 R
SpO2: 90 on RA (increases to 96 with oxygen via NRB @ 15 LPM)
No known drug allergies.
Denies any significant medical history other than “indigestion”.
The cardiac monitor is attached.
A 12-lead ECG is captured.
Another 12-lead ECG is captured with modified chest leads V4R, V5R and V6R.
How would you treat this patient?
Is there anything about this case that surprises you?
*** Update 12/13/2010 ***
What Christopher and I both found unusual about this case is that the GE-Marquette 12SL interpretive algorithm was not giving the ***ACUTE MI SUSPECTED*** message, even though it was giving messages like “ST-elevation consider anterolateral or acute infarct” and “inferior injury pattern” which I had always thought automatically trigged an accompanying ***ACUTE MI SUSPECTED*** message.
This is especially important because some EMS systems require the ***ACUTE MI SUSPECTED*** message in order for paramedics to bypass the local non-PCI hospital for the STEMI Receiving Center!
So, I contacted a friend at Physio-Control who put me in touch with the person responsible for the computerized interpretive algorithm. He was also surprised that the ***ACUTE MI SUSPECTED*** message was not present on these 12-lead ECGs. So he turned to a “veteran 12SL designer”.
Together they figured out the problem.
Mystery solved! The 12SL expert said that the 12SL algorithm would definitely give the Acute MI statement for the first cse that you sent me. So I turned to the setup choices (LP12 Operating Instructions, chapter 9). One of the setup menu items is “ACUTE MI”. The description is “Print Acute MI message”. Further explanation says, “ON: Prints on the 12-lead reports when criteria are met.”
I think that the LP12 is set up with the ACUTE MI option turned off. I suggest that you get back to the customer and have them turn ACUTE MI on in the setup menu for this LP12 and any others that they have.
So, if you have a Lifepak 12 and you’re not receiving the ***ACUTE MI SUSPECTED*** message for obvious acute STEMIs, you might want to check this parameter.
Thanks for all the comments! I’m not allowed to blog while I’m on duty (the policy has nothing to do with me personally) so if it seems like I’m not responding, I’m probably just at work.
The paramedic who submitted this case has requested the follow-up information from his supervisor, but unfortunately she’s out-of-town for the next 2 weeks.
In the meantime, we can lay out the issues.
Obviously, this is a scary looking ECG because there is significant ST-elevation in the precordial leads.
However, this ECG also meets the voltage criteria for LVH.
Could it be a strain pattern (typical secondary repolarization abnormality)?
It’s difficult to tell with the wandering baseline throughout this ECG, but if you line up the point at which the PR-segment hits the QRS complex in leads V1, V2, and V3 you can see that each of these leads shows approximately 4 mm of ST-elevation.
You will recall that with a “strain pattern” the degree of ST-elevation is proportional to the depth of the S-wave in the opposite direction! So the lead with the deepest S-wave should have the most significant ST-T wave abnormality in the opposite direction.
It’s not easy to tell the exact depth of the S-wave because the complexes are running together, but these measurements are probably fairly close.
There’s no way that a typical strain pattern would show the same amount of ST-elevation in one lead with S-waves that are 22.5 mm deep and another with S-waves that are only 6 mm deep.
Here’s the most disturbing finding, in my opinion.
There appears to be reciprocal behavior between the inferior leads and the high lateral leads.
So, if this is a STEMI mimic (for example, benign early repolarization superimposed on top of left ventricular hypertrophy) it’s a darned good one! I wouldn’t blame any paramedic for calling in a STEMI Alert for this patient.
So what should the hospital do when they are in receipt of a patient like this? I asked Stephen Smith MD from Dr. Smith’s ECG Blog and here’s what he said.
“If I were the ED physician, I would aggressively treat the blood pressure with NTG (up to 250 mcg/min or even higher) until the BP came way down. I would do a bedside cardiac ultrasound and look for anterior wall motion. If pain did not go away, and echo did not definitely show good wall motion, I would activate the cath lab.”
It’s always nice to get Dr. Smith’s perspective! I’ve learned a lot from his blog over the past 2 years. If you’re not familiar with his website you should take the time to check it out! His case studies are top notch!
Hopefully we’ll have the outcome in about 2 weeks.
I find this case to be extremely interesting for a variety of reasons. (Click HERE to see the original post).
As many of you pointed out, the history and clinical presentation isn’t exactly screaming “Acute Coronary Syndrome!”
But then, as others have pointed out, the elderly often have atypical or vague symptoms.
Let’s look at the 12-lead ECG itself (I will post the serial ECGs to the original case study so you can see those, too).
First question, does it meet the ACC/AHA STEMI criteria (imperfect though it may be). I have to admit, when I first reviewed this case I didn’t see it, but the answer is, “Yes.”
Hyperacute T-wave are visible in several leads, the most noticeable of which are leads V4 and V5.
Here’s an important teaching point, courtesy of Dr. Smith from Dr. Smith’s ECG Blog in reference to this case.
“The T-wave is the best indicator of viable myocardium at risk.”
Is ST-elevation also present?
Some of you have been taught that 2 mm of ST-elevation is required in two contiguous precordial leads. That is only the case for leads V2 and V3. This is probably due to the fact that leads V2 and V3 often have deep S-waves.
In this case, lead V4 has about 2 mm of ST-elevation and lead V5 has 1 mm of ST-elevation.
Couldn’t this be benign early repolarization? In theory, yes, although BER is not particularly common in elderly female patients.
There’s also another way to tell. Look at the R-wave progression in leads V1-V4. It’s non-existent, which points away from benign early repolarization.
Do any other leads show ST-elevation?
As some of you mentioned in the comments, ST-elevation is present in the high lateral leads I and aVL. However, it’s less than 1 mm. So it’s not significant. Right?
It’s significant due to the low amplitude of the QRS complex! You have to consider proportionality.
To illustrate this point consider the following graphics that “stretch” leads I and aVL vertically while preserving the ST/QRS ratio.
This is the same image side-by-side but the image on the right has been “stretched” vertically. It’s a single cardiac cycle in lead I. It looks much worse when it’s stretched, doesn’t it? But the ST/QRS ratio is exactly the same!
Here’s another example of lead I.
Here’s lead aVL, normal on the top and “stretched” vertically on the bottom.
If only there were reciprocal changes to firm up the diagnosis!
You will notice a flattening of the ST-segment in leads III and aVF that by itself would not seem particularly significant in a 76 year old female with a history of emphysema. However, it’s all about context! Over and over again I have preached Tomas Garcia, MD’s admonition to “consider the company” that any ECG abnormality keeps.
A flattening of the ST-segments in the inferior leads when the anterior and high lateral leads are suspicious for acute STEMI should be considered reciprocal changes.
Now what do you think? Are you sold or do you still have doubts?
Here’s an awesome case submitted by Nathan Stanaway of Grady EMS in Atlanta, GA.
The patient is a 53 year old female c/o chest discomfort and mild dyspnea.
The pain is described as “severe” and she gives the pain a 10/10.
Past medical history is significant for migraine headaches and anxiety.
Patient is a poor historian and does not know what meds she takes.
Drug allergy: ASA
The patient is found sitting in a car in the middle of the road.
Skin: pale and very diaphoretic.
RR: 24 shallow
HR: 84 R
SpO2: 98 on RA
Breath sounds: clear bilaterally.
A 12-lead ECG is captured.
What should the paramedic do next?
Here’s another case from a faithful reader who wishes to remain anonymous.
No, these are not all from the same anonymous reader!
EMS responds to a 58 year old male complaining of chest discomfort.
Onset: 30 min ago while mopping hot tar on roof
Provoke: Nothing makes the pain better or worse
Quality: Dull pressure
Radiate: The discomfort does not radiate
Time: Persistent with no previous episodes
The patient is found supine on the ground appearing acutely ill and diaphoretic.
The patient was moved to air conditioned room, skin dried.
Pt denies SOB, allergies, meds, history.
SpO2: 99 on RA
Breath sounds: clear bilaterally
12-lead ECG was captured.
Crew initiates CP protocol to include O2, ASA, NTG.
The patient declines intravenous access.
Vital signs remained unchanged.
The patient stated that he felt better and did not want to be transported to the emergency department.
The EMS crew was concerned about the patient’s decision and spent the next 40 minutes persuading the patient to be seen at the hospital.
Finally the patient agreed.
The patient was loaded for transport, the monitor was re-attached, and en route other 12 lead ECG was captured.
Are you noticing a trend here?
An 81 year male reports to the fire station to have his blood pressure checked.
He tells the paramedics he had just finished a round of golf and was sitting in the clubhouse when he felt, “cold and shaky.”
He relocated to his car with the windows rolled up and the A/C turned off. The ambient temperature was very warm but he still felt cold.
That’s when he decided to drive to the fire station.
At the time of evaluation his BP was 120/70 and his pulse was 76 and regular, which was consistent with the other vital signs recorded on his BP card over the past 2 weeks.
When he left the fire station he did not appear acutely ill.
Two hours later an ambulance was dispatched for a male patient with shortness of breath.
The paramedics recognized the man standing on the side of the road wearing a jogging suit as the same man who was at the fire station earlier for a BP check.
He states that he called his doctor who was out of town, and the on-call physician advised him to call 9-1-1.
The man was helped into the back of the ambulance and undressed from the waist-up. A surgical scar is noted down the center of his chest.
Past medical history: MI and CABG x3 in 1985
His vital signs were assessed.
SpO2: 96 on RA
He states that “nothing has really changed” since he was at the fire station.
When asked about shortness of breath, he denies it.
The cardiac monitor is attached.
When specifically asked about chest discomfort he states, “Well, I do a little bit of chest pressure, but it’s nothing like when I had my heart attack.”
A 12-lead ECG is captured.
What is your impression?
When it comes to regionalized STEMI care, we treat all STEMI patients the same. But are they the same?
The answer is, "No!"
Most EMS protocols include a maximum ground transport time of 30-60 when bypassing non-PCI hospitals (AHA Mission: Lifeline calls them "STEMI Referral Hospitals").
The idea is that when the "first medical contact-to-balloon" interval exceeds 90 minutes, the patient would be better served by transport to a non-PCI hospital for fibrinolytics.
Is this true?
The answer is, "Maybe!"
Consider Hospital delays in reperfusion for ST-elevation myocardial infarction: implications when selecting a reperfusion strategy. Circulation. 2006 Nov 7;114(19):2019-25
According to this table, the three variables to consider are:
- Symptom duration ( 120 min.)
- Age of the patient ( 65 years)
- Infarction location (anterior vs. non-anterior)
For early presenters (< 120 min. symptom onset) the point at which primary PCI loses its benefit over fibrinolytic therapy is an additional 94 minutes (that's door-to-balloon minus door-to-needle or D2B-D2N).
For late presenters (> 120 min. symptom onset) primary PCI loses its benefit at 190 min. (D2B-D2N).
For patients 65 years of age primary PCI loses its benefit at 155 min. (D2B-D2N).
For anterior infarction primary PCI loses its benefit at 115 minutes (D2B-D2N)
For non-anterior infarction primary PCI loses it benefit at 112 minutes (D2B-D2N).
The following graph illustrates how these variables interact.
This suggets that young patients who present early with anterior STEMI should probably receive fibronolytics prior to transfer.
On the other hand, late presenters and/or patients > 65 years of age should probably be transferred for primary PCI even when transport times are prolonged.
An elderly patient who presents early with acute anterior STEMI is right on the edge (assuming other "high risk" criteria are not met) at 107 minutes (D2B-D2N).
EMS is called to the residence of a 77 year old male complaining of palpitations.
Upon arrival, paramedics find the patient lying in bed. He is awake but lethargic. He is oriented to person, place, and time.
The patient’s skin is cool, pale, and diaphoretic.
He admits to chest discomfort and mild shortness of breath. Breath sounds are clear bilaterally.
Past medical history is significant for HTN and CABGx3 (a year and a half ago).
Vital signs are assessed.
RR: 22 and shallow
Pulse: Too rapid to count
SpO2: Does not register
The cardiac monitor is attached.
How would you treat this patient?
*** UPDATE ***
The patient was transported to the emergency department where he immediately received synchronized cardioversion.
EMS is called to the parking lot of a local fast food restaurant for a 66 year old male complaining of chest pain.
On arrival, the patient appears acutely ill. His skin is pale/ashen but dry. He is rubbing his chest and there is a grimace on his face. He is not conversant but he answers simple questions with yes or no answers and seems quite content to jump on the gurney and go to the hospital.
Onset: 30 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: He describes the pain as “crushing” in the center of his chest
Radiate: The pain does not radiate to the arms, back, neck or jaw
Severity: The patient gives the pain a 10/10
Time: No previous similar episodes
Vital signs are assessed.
SpO2: 97 on RA
He admits to mild dyspnea but breath sounds are clear bilaterally.
The cardiac monitor is attached.
*** UPDATE ***
Here is the 12-lead ECG that was captured on arrival at the hospital.
EMS is called to the doctor’s office to evaluate a 54 year old male complaining of chest pain.
On arrival, the patient is alert and oriented to person, place, time, and event. However, he is anxious and his skin is pale and diaphoretic.
He is on oxygen via NC @ 4 LPM. An IV has been started and is running KVO. The patient has been giving 4 baby aspirin and administered 1 SL NTG spray prior to your arrival.
Onset: 2 hours ago while at work
Provoke: Nothing makes the pain better or worse
Quality: Described as a heavy pressure leaving him breathless
Radiate: The pain radiates up to the neck and jaw
Severity: Patient reluctantly gives the pain an 8/10
Time: No previous episodes
Past medical history: Depression, hyperlipidemia
Vital signs are assessed.
SpO2: 99 on RA
The cardiac monitor is attached.
*** UPDATE ***
A serial ECG is obtained en route to the hospital.