Last week, I described the case of a middle-aged male with a vague history of heart failure who had been having progressive shortness of breath for 4-5 days. On the day he called 911, he had been walking a short distance when he syncoped. EMS obtained an ECG:
Inverted T waves are seen in III and aVF, as well as V1-V4.
Compared with the prior ECG, the anterior T wave inversions appeared new.
Subtle S1Q3T3, but no ATWI
What can cause anterior T wave inversion (ATWI)?
There are some rare entities that show up with ATWI; e.g. ARVC. Young women can also have a benign variant, the so-called persistent juvenile T wave pattern.
But in this clinical context, we should consider two main categories: 1) myocardial ischemia, and 2) right ventricular strain.
ATWI and myocardial ischemia
Posterior STEMIs can initially appear as inverted T waves in the right-sided leads, but there is usually a degree (or more!) of ST depression in those same leads.
On the other hand, so-call “anterior ischemia” can cause ATWI too. But this usually is more prominent in the lateral leads, with a “strain” pattern of ST depression as well.
You can also see Wellen’s syndrome in the anterior leads, but these T waves are notable for being deep and/or biphasic.
Clinically, the patient describes days of symptoms, and it seems unlikely that the ECG would appear so benign after days of ischemia that was severe enough to provoke syncope. Also, the echo, while not of the best quality, shows a markedly dilated RV, suggesting that RV strain is more probable than ischemia.
ATWI and right ventricular strain.
Conditions that cause RV enlargement or pressure overload can produce ATWI, as well as S1Q3T3. Clearly, PE is a huge possibility here, but it’s worth remembering that severe COPD can generate this pattern as well, by producing pulmonary hypertension through hypoxic vasoconstriction in the pulmonary arteries. Idiopathic pulmonary hypertension also can produce ATWI and S1Q3T3.
The clear lung sounds do not suggest COPD, and the very recent development of the ATWI means that he likely does not have chronic pulmonary hypertension.
The patient decompensated abruptly during evaluation by the ED physician. Based on the ECG, echo, as well as clinical exam (one leg was significantly swollen), tPA was administered during CPR, but this was unsuccessful. An autopsy confirmed massive bilateral pulmonary emboli.
The ECG can be useful in suspecting PE.
For diagnosing a PE, you basically need an imaging study: CT scan or a V/Q study. The ECG has been derided as being non-specific, missing many cases of PE, or only showing sinus tach.
It was a slow morning in the ED, so I was able to catch the medic as she came in with the patient. “Hey Leigh, what do you have for us? Got an interesting ECG?”
“Well, maybe,” she replied as she wheeled by with a comfortable looking middle-aged male, “here, take a look at it while I give report to the nurse.” She handed me the 12-lead:
After leaving the patient with the RN, Leigh came back. “This is a guy with a history of CHF, with an AICD placement. He’s had shortness of breath for 4 days, worse when he walks. He passed out today when he was walking, so his family called us. He looked fine when we got to him, just needed 2 liters of O2 to keep him at 98%. No chest pain.”
“Yeah,” I said, “he certainly looked fine when you rolled past. Okay, so probably just a CHF admission. I’ll go see him right now.”
“Yeah, it’s probably just his CHF,” she continued, “but I expected worse. His lungs sound just fine, totally clear. Plus, he says it doesn’t get worse when he lays flat. Seems funny for CHF… Plus, I didn’t like my ECG – did you notice the S1Q3T3?”
“Well, I pulled his old ECG, just done a few weeks ago in fact, and I see it looks like there’s a S1Q3T3 too. So, probably doesn’t mean much.” I showed her the ECG I had dug up:
“Okay, Dr Walsh, maybe the S1Q3T3 is old, but I still see…” She paused, and appeared to be looking for a diplomatic way to phrase her thoughts. “How about using the ultrasound, checking to see if there’s any CHF?”
After introducing myself to the patient, gathering a history, and finding that the lungs were, indeed, completely clear, I wheeled over the ultrasound. A quick check of the lungs confirmed that there was no edema in the lungs. I then took a look at the heart. (The image quality is not great, I realize.)
Just so you know what is what:
I then turned to Leigh and asked her “What else did you see on your ECG that you were too polite to point out to me?”
This article is a quasi-cross-post from the website of our good friend Brandon Oto over at EMS Basics. He’s been gracious enough to allow us to adapt the original post from his What it Looks Like series over here. We highly suggest that you go check out the amazing and highly practical writing he does over on his site; it’s the epitome of the high quality content that even a solo blogger can put together in the world of EMS 2.0 and FOAM.
We all know the fundamentals of Basic Life Support (BLS), a lot of us have taken Advanced Cardiac Life Support (ACLS), and some among us have even accrued a collection of advanced resuscitation merit badges. Still, in spite of that, healthcare workers of all fields, training, and experience can stumble when it comes to that most fundamental of steps in the CPR algorithm: recognizing cardiac arrest.
Here we have assembled some of the best videos available on YouTube displaying the physical signs you will encounter when a patient experienced sudden cardiac arrest right in front of you. Thankfully most, but not all, of the patients depicted recovered, and we owe a huge debt to the patients and their families who allowed the footage to be released.
This post isn’t meant to be a critique of the way the codes were managed or how well compressions were performed—we just want to examine what it looks like when a person experiences cardiac arrest so that there is minimum delay before recognition when you encounter this in your practice. Comments that distract from that goal will be deleted.
[To save you time all of the videos link to a point just prior to the patient arresting, but we still highly suggest watching the surrounding footage.]
The Chris Solomon Rescue
Chris Solomon arrived to his morning shift as a dispatcher with the Yorkshire Air Ambulance feeling a bit unwell. He began to develop chest pain and thankfully his colleagues were there to assess him, perform a 12-lead ECG, and identify his STEMI. This entire video is an absolute must-see but take special note of the events surrounding his cardiac arrest.
You’ll note that at exactly 2:18 in the video Chris goes into a V-fib cardiac arrest. There’s no giant display, he just sort of nods off. If you listen closely you can also hear a agonal respirations.
As the crew lowers him to the ground you’ll notice that he immediately begins posturing and displaying the kind of movements that we often associate with seizures. Even as they begin CPR his arms are still moving but make no mistake—and the medics certainly didn’t hesitate—Chris is in cardiac arrest. Even through the first and second defibrillation he maintains his posturing and agonal respirations.
As we see here is not uncommon for a patient to be moving and breathing with their eyes open during a sudden cardiac arrest if high-quality CPR is started early. It is certainly unsettling to perform CPR on someone who seems to be looking at you but it happens and it means that the good-quality CPR is being performed.
This is an amazing save and these providers set a high bar for running a resuscitation, even as it catches them completely off guard in their own dispatch station.
Syncope vs. seizure—at times it is nearly impossible to differentiate the two. That is, unless you have the patient hooked up to a cardiac monitor and video EEG.
This is the case of a 25-year-old female who was referred to a video EEG unit for workup and differentiation of a seizure disorder that was diagnosed eight years prior. When startled she would have episodes of feeling anxious and lightheaded with palpitations before becoming unconscious. One of these episodes was caught while in the video EEG unit. The bottom line displayed on the monitor is her EKG.
This video is hard to watch but that’s a good thing—it means that you’re not comfortable watching someone in cardiac arrest not receive immediate CPR. To ease your mind a bit I will tell you ahead of time that the patient had a full recovery.
At 0:38 in the video the patient goes into torsades de pointes. She immediately begins to feel symptoms and rings her call bell.
She soon becomes unresponsive and begins hyperventilating. This is cardiac arrest and you are seeing very pronounced agonal respirations.
The unit staff, used to seeing and assessing seizures and having been informed that this is what her “seizures” look like, immediately arrive and begin their seizure assessment. Unfortunately there is no cardiac monitor in the room and they do not routinely check pulses on their seizure patients.
At 2:10 she becomes fully apneic except for the occasional agonal respiration. Her EEG also shows a flat-line, as is seen in brain death. More staff arrives and place her in the recovery position and at about 2:23 she spontaneously reverts to normal sinus.
After this event her TdP was recognized and she was diagnosed with a variant of long-QT syndrome, though her resting EKG only had a QTc of 430-480 ms. She chose not to receive an AICD at that time but responded to medical therapy and is apparently doing well.
This case emphasizes both the importance of considering cardiac arrest in anyone presenting with a “seizure.” It also shows that humans can exhibit agonal respirations for a surprisingly long amount of time after cardiac arrest, even with no detectable brain activity on EEG.
This older video, shot for the TLC show “Paramedics,” shows EMS responding to a patient at a local hotel with a chief complaint of chest pain.
Soon after EMS arrival, at about 2:05 in the video, he becomes unresponsive and begins exhibiting agonal respirations. Unsurprisingly, the medic’s first question is whether he has a history of seizures.
This is an extremely common mistake (see the last case).
As he lays back at 2:10 you can see the patient exhibiting posturing very similar to Chris Solomon’s. As they move him to the stretcher the respirations continue and the crew tries to talk to him, apparently still not realizing he is in cardiac arrest. It doesn’t take long to rectify that, however, and he is defibrillated back into a perfusing rhythm.
He was awake and responsive on arrival at the hospital so it seems likely that he had a good outcome.
This video is from the Australian show “Bondi Rescue.” A local man was doing his usual swim at the beach when he started to experience classic cardiac chest pain and requested aid from the lifeguards. Trained in BLS, they called EMS and applied an AED because they recognized the high likelihood of the patient going into cardiac arrest before medics arrived.
At 1:14 in the video, just as the medics arrive on scene, the patient states that he feels like he is going to pass out and goes into cardiac arrest. As in the other cases, he keeps breathing at the start of his arrest and at 1:40 you can clearly see his left arm stiff and raised, in posturing almost exactly like Chris Solomon demonstrated.
Thankfully he responded well to defibrillation and had an excellent outcome. At the hospital they performed an aspiration thrombectomy of a culprit lesion in one of his coronary arteries with immediate resolution of his symptoms and was well enough to visit the lifeguard station a short time later
This video is from the show “Heroes Among Us.” The patient involved was playing basketball with some friends one morning when he suddenly collapsed on the court due to a sudden cardiac arrest. As you can see in the video, after his collapse he was still breathing and the folks nearby thought he was having a seizure. Hopefully you’re noticing a trend at this point.
A bystander who was a physician was walking by and noticed the scene. At 2:20 in the video the patient was still breathing but the physician quickly checked a pulse, didn’t find one, and began immediate CPR.
Yet again, early recognition and early CPR probably contributed to this man having a good outcome and getting back to the point where he could return to playing basketball.
This isn’t true cardiac arrest but it’s a great example of exactly what cardiac arrest can sometimes look like so I had to include it. Plus, it’s pretty much the same mechanism that produces unconsciousness during arrest—global cerebral hypoxia—hence it looks the same, just with a different resolution.
This video shows a diver who experienced significant hypoxia and blacked-out. As you can see, he exhibits pronounced agonal respirations and posturing-type movements that could easily be confused for a seizure.
In this case, after breathing air for a few seconds, he quickly returned back to baseline, just as a typical syncope patient recovers after falling flat.
This is a hard case to discuss. First, it’s only video on our list so far that shows someone who died from their sudden cardiac arrest. Second, we won’t get into the specifics of how his resuscitation was handled, but if you look into Hank Gathers’ story you’ll find that a number of factors aligned that really set him up for a bad outcome.
One factor visible here is that his cardiac arrest was no recognized for a significant amount of time, despite having a known history of malignant arrhythmias.
At 0:37 in the video you see Hank Gathers collapse. He is in cardiac arrest but clearly breathing and exhibiting sporadic muscle movements. After a few seconds he even manages to sit up but quickly collapses back to the court and exhibits seizure-like activity. This ceases a short time later and a couple of minutes after his collapse he is take off the court, having not yet received any CPR.
Anthony Van Loo
This case has a good outcome. Anthony Van Loo was diagnosed with hypertrophic cardiomyopathy (the same condition that killed Hank Gathers) but was able to resume play after receiving an automatic implantable cardioverter defibrillator (AICD). This video shows Anthony, in the top-center of frame, experiencing a sudden cardiac arrest on the field. After a few seconds his AICD shocks him back into a normal rhythm and he almost immediately recovers.
This case emphasizes both how quickly and innocuously sudden cardiac arrest can strike (Anthony had almost no prodrome and showed no readily apparent signs of life on hitting the ground) and how well patients can recover with prompt defribrillation.
This is exactly what we are attempting to replicate in our patients who collapse without an AICD, using CPR to buy time until the defibrillation can arrive.
Another footballer, Miguel García, also collapsed during a match due to sudden cardiac arrest. In the video below you can see him in the far-left background at the 0:18 mark when he starts jogging and suddenly falls to the ground.
Thankfully he also had a good outcome and made a full recovery. Sadly, there are many cases of soccer players experiencing cardiac arrest that were caught on camera (and many more that aren’t) who never recovered, and there is one more in particular we would like to discuss.
One last tragic case with a very important lesson.
As in the past few videos, Antonio Puerta collapsed suddenly during a match. In this video you can see him crouching down before falling over unresponsive.
Soon after the arrival of his teammates and trainers he spontaneously recovered and was actually able to walk back to the locker room.
Syncope is a huge red-flag, especially when it occurs during exercise.
Benign causes of syncope and self-resolved cardiac arrest are undifferentiable from outward appearance. In this case Anthony Puerta experienced a sudden cardiac arrest that resolved on his own. Despite looking perfectly well, only a short time after walking back to the locker room he collapsed again and could not be resuscitated from the arrhythmias that were occurring secondary to arrhytmogenic right ventricular dysplasia (ARVD).
It’s heavy work watching these sorts of videos but it’s important for what we do. Prompt recognition of cardiac arrest is the first link in the Chain of Survival and early CPR and defibrillation are absolutely vital to achieving good outcomes for these patients. Here’s a few final take-home points:
Sudden cardiac arrest is just that—sudden—and can occur without warning.
It is surprisingly difficult to differentiate seizures from early cardiac arrest.
Sudden cardiac arrest that self-resolves is called syncope (H/T to Amal Mattu).
It is nearly impossible to distinguish benign syncope from cardiac arrest until the patient recovers and a thorough history, examination, and workup can be performed.
Any patient presenting with syncope or seizure needs, at the minimum, an EKG.
Last week we presented the ECG of a patient experiencing progressively worsening shortness-of-breath over the course of a day and some marked ECG abnormalities. If you haven’t done so already, it would probably be a good idea to check out the original post first. Strap in, this is going to be a thorough discussion.
Here again is the patient’s initial ECG:
Not a STEMI-equivalent.
This ECG shows:
Sinus tachycardia at a rate of 96 bpm.
First-degree AV-block (PRi of approx 240 ms).
Left anterior fascicular block (LAFB), resulting in…
Old anterior infarction (Q-waves in V1-V3, almost no R-wave in V4).
Moderate ST/T-wave abnormalities in a pattern of diffuse subendocardial ischemia.
ST-depression in I, II, aVL, aVF, V3-V6; ST-elevation in aVR, V1.
Frontal ST-vector of approx 200 degrees, towards the right shoulder.
The #1 take-away from this case is that this ECG is not a STEMI-equivalent. STEMI’s need immediate revascularization and, except in some specific cases, their first stop should be the cath lab. Diffuse subendocardial ischemia is quite the opposite in that it should usually be managed medically in the ED first. Only after initial stabilization and evaluation will select cases proceed to near-immediate or early catheterization.
It has been a popular topic of ECG teaching for the past few years but diffuse ST-depression with ST-elevation in aVR does not necessarily equate with left main coronary artery (LMCA) occlusion. It can be seen in the setting of significant obstruction of the LMCA or significant multi-vessel coronary artery disease, but those can be very different from true 100% occlusion of the left-main.
What you’re seeing when you encounter the above pattern is ischemia affecting the majority of the circumference of the left ventricle, except that it only affects the subendocardial aspect of myocardium, not its full thickness.
Going back to basic cardiac anatomy, there are three major layers that we consider when examining the myocardium in cross-section: the endocardium (inner layer, like the endothelial lining of blood vessels), myocardium (the actual cardiac muscle), and epicardium (outer layer, contiguous with the visceral pericardium, tough to differentiate the two).
Histology slide demonstrating the layers of the atria. The ventricles feature a much thicker myocardium with a thinner endocardium. Click image for source.
When we talk about “subendocardial ischemia,” what we are referring to is ischemia that affects only the heart muscle just below the endocardium, but not extending the full-thickness of the myocardium. This is a little confusing because, if you look at the above slide, you may get the impression that located “below” the subendocardium is the empty space in the cavity of the ventricle. What we are actually discussing is the myocardium that’s adjacent to the endocardium. Terms like “up” and “down” can get a bit confusing when dealing with a hollow and roughly spheroid-shaped organ like the heart.
If you were visualizing localized subendocardial ischemia in the distribution of a non-dominant circumflex artery you might imagine it affecting an area depicted by the yellow shading in the image below.
Localized subendocardial ischemia. Image modified by Vince DiGiulio. Original by Patrick J. Lynch, medical illustrator / CC-BY-2.5, via Wikimedia Commons.
What he means is that even when ST-depression due to subendocardial ischemia appears to show a particular distribution on the ECG (inferior, lateral, etc…), it does not correlate well with actual findings of stenosis on cath. You might think you’re seeing “anterior ischemia” on the ECG but that doesn’t guarantee that there’s a significant stenosis in the LAD causing it.
From my own personal experience, I’ve very rarely seen cases of localized ST-depression that I’ve suspected were due to focal subendocardial ischemia. Perhaps focal subendocardial ischemia isn’t even a distinct electrocardiographic entity, but that’s a digression…
True ischemic ST-depression on the ECG really falls into two broad categories: ST-depression that is reciprocal to STEMI and ST-depression due to diffuse subendocardial ischemia. For more discussion on this and the five sub-categories that fall under those two headings check out this post from Dr. Smith.
So, if subendocardial ischemia affects only the inner portion of the heart muscle, what do we call it when the entire muscle thickness is involved?
Localized transmural ischemia. Image modified by Vince DiGiulio. Original by Patrick J. Lynch, medical illustrator / CC-BY-2.5, via Wikimedia Commons.
Acute transmural ischemia presents as a STEMI on the EKG and, unlike localized subendocardial ischemia, there is excellent correlation between the distribution of the ST-elevation and the region(s) of myocardium involved. Above shows the area of myocardium that would be ischemic during STEMI due to occlusion of a non-dominant left circumflex artery.
Which brings us back to the topic at hand: diffuse subendocardial ischemia.
Diffuse subendocardial ischemia. Image modified by Vince DiGiulio. Original by Patrick J. Lynch, medical illustrator / CC-BY-2.5, via Wikimedia Commons.
This is what our patient in the scenario presented last week is experiencing: diffuse (or “circumferential”) subendocardial ischemia. The majority of the subendocardial region of his myocardium is ischemic but it’s not localized and it doesn’t affect its full thickness. What causes this to happen though?
The reasons why the inner portion of the myocardium is more prone to ischemia than that near the epicardium is a topic of much research with several prevailing theories but, in the most basic sense, the muscle there is a victim of two major factors:
The subendocardium has a less robust blood supply than the subepicardium. Recall that the blood supply to the myocardium penetrates down from the major coronary arteries located at the epicardium, so the blood perfusing the subendocardium has to travel further through smaller arteries and arterioles.
Compared with the subepicardium, the subendocardium experiences more pressure exerted on it by the blood in the left ventricle due to its greater proximity, reducing blood-flow through those already tiny arteries. This is especially true in the setting of high end-diastolic pressure since the myocardium is perfused during diastole.
Alright. So the subendocardium is more prone to ischemia, but why would it ever present as circumferential ischemia affecting the entire left ventricle? This is where the left main coronary artery finally comes into play.
If you fully occlude the left main coronary artery the patient will experience a global STEMI. Example of this are located here and here and here and here and here and here. Below is the region of myocardium experiencing transmural ischemia in the event of a true LMCA occlusion. In this illustration in the best-case scenario of a right-dominant coronary artery distribution, providing at least some perfusion to the infero-posterior wall of the LV.
Diffuse transmural ischemia. Image modified by Vince DiGiulio. Original by Patrick J. Lynch, medical illustrator / CC-BY-2.5, via Wikimedia Commons.
Patients rarely make it to the hospital alive with this degree of transmural ischemia and even fewer survive to PCI. True LMCA occlusion is a rare entity even in prehospital care.
When there is less than 100% occlusion, however, some blood-flow makes it through to the LAD and LCx and the left ventricle experiences diffuse subendocardial ischemia. We see more of these cases because the patients have a better chance of survival thanks to the trickle of blood making it past the obstruction.
Now life would be easy if all subendocardial ischemia correlated with acute subtotal obstruction of the left-main. Unfortunately that’s not the case and the same exact type of ischemia can be produced in a number of settings.
The first is the “left-main equivalent” of multi-vessel coronary artery disease. It’s called that for a couple of reasons:
First, if you have a couple or three major vessels with CAD then the same area of myocardium (i.e. most of it) is going to experience subendocardial ischemia. Your myocardium doesn’t care if there’s one giant artery blocked or several of its subsidiaries; all it knows is that it’s not getting enough perfusion.
Second, like a single significant stenosis in the LMCA, multi-vessel stenoses causing ischemia are usually treated with bypass surgery. Neither scenario does well with attempts at stenting so in both cases patients end up needing CABG.
That’s not entirely straight-forward but at least it’s all issues primarily due to coronary artery disease, right? This is where “elevation in aVR” really falls apart: Anything that causes a global mismatch between oxygen supply and demand by the heart will produce diffuse subendocardial ischemia and the same exact ECG pattern as LMCA stenosis/multi-vessel CAD. Here are some examples in no particular order:
Anemia, causing decreased O2 delivery.
Hypoxia, causing decreased O2 delivery.
Sepsis, causing increased O2 demand.
Severe hypertension, causing increased O2 demand and decreased subendocardial perfusion.
PE, causing decreased O2 delivery and increased O2 demand.
COPD or CHF exacerbation, causing decreased O2 delivery and increased O2 demand.
Hypotension, due to decreased O2 delivery.
Throwing a significant chronic LMCA stenosis or diffuse CAD into the mix with any of the above will only worsen the supply/demand mismatch and increase the amount of ST-deviation.
Also, the same pattern of ST-deviation is also seen in the setting of LVH with “strain” and in patients on digoxin.
As you can see, diffuse subendocardial ischemia really is fraught with pitfalls. In the case of our case presentation, almost everyone who commented fell for the misdirection and assumed the patient needed emergent cath. Andrew Merleman deserves a special shout-out for absolutely nailing the diagnosis and management in his comments on the EKG Club page. Rock on!
In reality the patient was experiencing and acute episode of bilateral pneumonia. The clue here was his increased temperature and gradual onset of the SOB. I wouldn’t blame anyone for thinking it was a CHF exacerbation; the real key was just to avoid assuming that the EKG findings mandated immediate cath. He was admitted to the hospital, treated with BiPAP and antibiotics, and did well. Troponin-I levels (reference < 0.04 ng/mL) were trended and peaked around 1.0 ng/mL.
This patient did indeed experience ACS, but it was demand ischemia due to supply/demand mismatch; known as a type II MI. He certainly had coronary artery disease (as evidenced by his old anterior MI on the initial ECG and significant ST-depression in response to physiologic stress), but it was not the cause of his symptoms and did not mandate invasive investigation or treatment. Once his pneumonia and work of breathing got under control his ECG normalized quite as bit and returned to his baseline.
ECG 2 Days Later. Not normal but normal-enough and matching his baseline.
If you can bear it, stay tuned for an upcoming post where we discuss just what qualifies as a “STEMI equivalent” and which patients with diffuse subendocardial ischemia need immediate cath. This is enough writing for one night…
Also, for those wondering just what the heck is going on with the R-wave in lead V2 in this patient, there will be a post on that as well. It’s due to the left anterior fascicular block, not old posterior MI.
Let me know in the comments if you have any questions or I wasn’t clear about. Subendocardial ischemia is a HUGE topic with many layers so it’s hard to do it justice in one blog post.
You are called to the residence of an 83 year old male with a chief complaint of shortness of breath.
On arrival you find a sick-appearing gentleman working hard to breath. He states that he woke up feeling a bit weak this morning with dyspnea-on-exertion that it has gotten progressively worse over past 12 hours—to the point where his is experiencing respiratory distress at rest. He has also had a productive cough. Noticing that he didn’t sound great on the phone his son came to visit, found him in this state, and called 911.
The patient is in moderate respiratory distress (4-5 word sentences) with a respiratory rate of 28/min and skin that is pale, warm, and diaphoretic. SpO2 is 85% on room air, improving to 92% with a non-rebreather at 15 L/min. Pulse is present at the radials but weak and his NIBP is 97/58 mmHg. Temperature is 38.3 C (oral). Lung sounds show bilateral rales and coarse rhonchi through much of both lung fields.
He denies chest pain, heaviness, tightness—or pain anywhere else for that matter.
His past medical history is significant for CAD with a prior MI, CHF, HTN, DM, dyslipidemia, and GERD.
You obtain the following ECG:
- What do you see?
- How is this ECG going to affect your management? Do you need to activate the cath lab?
- Masters Bonus: What fairly common ECG finding is the cause of that unexpectedly tall R-wave in V2?