The managing editor of the EP Lab Digest recently interviewed me about the PH12ECG blog.
You can see the interview here.
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There’s an interesting case study posted over at Dr. Smith’s ECG blog called Right Bundle Branch Block with Acute ST Elevation Best Seen on Prehospital ECG.
Dr. Smith makes the point that RBBB should not distort the ST segment the way LBBB does. He’s right, but sometimes the ECG diagnosis of STEMI can be difficult with RBBB as his case study demonstrates.
The prehospital 12 lead ECG is a scanned copy, but you can easily make out ST segment elevation in leads V2-V6 and I and aVL. The ST segment elevation is concordant to the terminal deflection of the QRS complex in leads V2-V4.
The cardiac cath lab was activated by EMS while the patient was still in the field.
En route, the patient experienced VF a couple of times and was shocked by the treating paramedic. The patient was awake on arrival in the emergency department and a very interesting ECG was recorded that you can see here.
The S waves have retured in the precordial leads and the T waves are now appropriately discordant to the terminal deflection of the QRS complex. The ST segments are straight (non-concave) which is worrisome and still elevated in leads I and aVL, but as Dr. Smith says:
[W]ere it not for the arrest and the prehospital ECG, this would not be a slam dunk diagnosis.
He finishes with this teaching point:
[T]he prehospital ECG is critical, as was early prehospital cath lab activation. Were it not for this prehospital ECG and the cardiac arrest, the diagnosis may have been significantly delayed. Had this happened, the artery may have re-occluded prior to angiography, with resultant recurrent cardiac arrest and/or shock and death.
Thanks for sharing, Dr. Smith!
You can also see Dr. Smith’s recent post on hyperacute T waves here.
Next there is a recent post at Peter Canning’s Street Watch: Notes of a Paramedic called 12-Lead ECG in ROSC.
This is also the title of an article in JEMS by Keith Wesley MD in which he reviews:
Müller D, Schnitzer L, Brandt J, et al, The accuracy of an out-of-hospital 12-lead ECG for the detection of ST-elevation myocardial infarction immediately after resuscitation. Annals of Emergency Medicine. 52(6):658-64, 2008.
Peter explores the issue of performing a prehospital 12 lead ECG on cardiac arrest patients after they experience return of spontaneous circulation.
It’s definitely a good idea! See #8 in my recent blog post Prehospital 12 Lead ECG – What Are the Indications?
Here are some interesting ECGs from the first cardiac arrest I worked according to the “new” science (i.e., 2 minutes of CPR prior to the first shock and minimizing interruptions to chest compressions).
Here’s the 12 lead ECG we captured after ROSC:
As a side note, what is the cardiac rhythm? If you know, leave a comment.
Capturing a 12 lead ECG is particularly important if you need to justify transporting a cardiac arrest patient with ROSC to an interventional facility (PCI-hospital).
In reference to the study, Keith Wesley MD concludes:
One last interesting note on this article is that the physicians used 1 mm of ST elevation in the inferior leads but 2 mm in the precordial leads for diagnosis of infarction. Studies have shown that using 1 mm for both increases the sensitivity but captures a significant number of additional STEMIs. It would be interesting to know how this would’ve impacted the 77 patients in this study.
With respect to Keith Wesley MD, I actually agree with using 2 mm of ST-segment elevation in the right precordial leads as the standard, particularly for younger male patients, for whom 1 mm of ST segment elevation in leads V1-V3 is a normal finding (not a normal variant).
*** UPDATE ***
The American Heart Association published a policy statement on out-of-hospital cardiac arrest in January 2010.
Regional systems of care for out-of-hospital cardiac arrest: A policy statement from the American Heart Association. Circulation. 2010 Feb 9;121(5):709-29. Epub 2010 Jan 14
This part is particularly relevant to our discussion:
“Up to 71% of patients with cardiac arrest have coronary artery disease, and nearly half have an acute coronary occlusion. There is a high incidence (97%) of coronary artery disease in patients resuscitated from OOHCA who undergo immediate angiography and a 50% incidence of acute coronary occlusion. However, the absence of ST elevation on a surface 12-lead electrocardiogram after resuscitation of circulation from cardiac arrest is not strongly predictive of the absence of coronary occlusion on acute angiography. A case series of patients with unsuccessful field resuscitation suggested that in such patients, VF is more likely to be due to coronary disease than is asystole or pulseless electric activity…these studies suggest that patients who are resuscitated from out-of-hospital VF have a high likelihood of having an acute coronary occlusion.
“The feasibility and efficacy of primary PCI in patients who survive cardiac arrest with STEMI have been well established. The combination of mild therapeutic hypothermia with primary PCI is feasible, may not delay time to start of primary PCI in well-organized hospitals, and is associated with a good 6-month survival rate and neurological outcome…
“Patients resuscitated from OOHCA with STEMI should undergo immediate angiography and receive PCI as needed. Immediate coronary angiography is reasonable for patients resuscitated from VF and may be considered in patients resuscitated from other initial rhythms who do not have a clear noncardiac cause of cardiac arrest…Because emergent coronary angiography is not widely available, patients resuscitated from out-of-hospital VF or from OOHCA with STEMI should be transported as soon as it is feasible to a facility that is capable of performing these procedures. Field providers treating such patients should bypass referral hospitals and go directly to a cardiac resuscitation receiving hospital so that these patients can receive angiography within 90 minutes…”
I’d like to announce a couple of outstanding additions to the blogosphere!
My friend and colleague Pete Reid started a blog called Star of Life Law. In addition to being a firefighter/paramedic at my fire department, Pete is also an attorney. He’s also a heck of a nice guy. Check him out!
Firehouse Zen is a blog put together by Mick Mayers, a good friend who is also a battalion chief at my fire department (yes, I know, we’re a literate bunch). Mick’s blog focuses on leadership and change. Gee, why would the fire service need any help with that? 
Then check out BarefootNurse. She’s an excellent nurse with lots of experience in the emergency department. She’s also the accreditation officer of a hospital, and a graduate student studying to be a Clinical Nurse Specialist. She also loves sea turtles and has impeccable fashion sense.
I would also like to acknowledge my Norwegian friend Klaus over at The ECG Blog. If there was ever a man (besides Nick) who could rival me in terms of ECG dorkiness, it’s Klaus. He also teaches me really cool Norwegian words, and even sends me custom .mp3 files when I’m having difficulty with the pronunciation!
Last but not least, I’d like to thank “Rads” over at Rain Makes Everything Wet. Not only did she take my tutorial on axis determination. She liked it! If not for my deep respect for Klaus, I would probably rename this The Nerdy EKG Blog.
For those who weren’t aware, “nerdy” is a term of endearment. The jury is still out on “dorky”.
Every time I’ve defended Southern California’s use of the GE-Marquette 12SL interpretive algorithm in their STEMI system I’ve taken some flack for it (see the comments section here and more recently in the EMS Responder forum here).
I agree that in a perfect world, paramedics would receive extensive 12 lead ECG training as part of their core education (including how to identify the STE-mimics and how to identify AMI in the presence of the STE-mimics).
Unfortunately, the vast majority of paramedics in the country are not receiving this level of training in school, and it’s not possible to read a 12 lead ECG at this level after an 8 hour crash course in 12 lead ECG interpretation.
That being the case, if you want to regionalize STEMI care, then there are only three options.
- Provide specialized training to paramedics (in my opinion it should be at least 24 hours) and allow them to bypass non-PCI hospitals based on their own interpretation.
- Provide less specialized training and use a computerized interpretive algorithm (i.e., when the computer says ***ACUTE MI SUSPECTED*** and the paramedic agrees the patient is taken to a PCI hospital).
- Provide less specialized training and transmit the ECG off-site for physician evaluation.
None of these solutions is perfect and some locations are using a combination of methods. I applaud Southern California for building a highly functional regional STEMI system. Is it perfect? No. Is there room for improvement? Of course.
It’s easy to criticize.
While it’s true that the GE-Marquette 12SL interpretive algorithm has a high specificity when it gives the ***ACUTE MI SUSPECTED*** message or ***ACUTE MI***, it’s not perfect. In fact, Southern California has a problem with false positives ECGs.
Note: the Philips MRx uses a different interpretive algorithm but the Physio-Control LP12 and ZOLL M and E series use the GE-Marquette 12SL interpretive algorithm, as do the majority of systems inside the hospital. To my knowledge, one is not been proven superior to the other.
Since some EMS systems are using the interpretive algorithms to influence whether or not patients are taken to PCI hospitals, I thought I would devote some time to discussing how to get the most out of them.
Interpretive algorithms are a tool like any other. They have limits and they require understanding. For example, you can get a false positive from the computer when you capture an ECG with poor data quality (which is one of the reasons I spend a lot of time talking about data quality).
Capturing a 12 lead ECG with good data quality is a sign of professionalism. Conversely, handing over (or transmitting) an ECG to the hospital with poor data quality shows a lack of professionalism.
There have been a couple of times in my career that no matter what I did, I couldn’t get a good tracing (Parkinson’s disease, bad electrodes, broken leads, combative patient) but it’s rare.
In addition to poor data quality, sometimes tachycardias can fool the interpretive algorithm, especially atrial flutter.
The specificity of the computerized interpretive algorithm is maximized when you capture the ECG with excellent data quality, the chief complaint is chest pain, and the heart rate is less than 100.
Even with these caveats, you will occasionally run into false positives.
Consider the following ECG.
You will notice that the data quality is pretty good (just a little bit of wandering baseline in lead V4).
The computer is giving the ***ACUTE MI SUSPECTED*** message.
Why?
Here is the story.
Patient is a 76 year old male. No known medical history, no meds, excellent physical condition, walks every day.
Two days prior the patient experienced some shortness of breath while walking, but the sensation went away with rest. Approximately 30 minutes prior to EMS arrival, patient walked outside to get the newspaper, bent down, and experienced some mild chest discomfort. The patient walked back inside and felt like someone was "standing on his chest." At this time the patient's spouse called 9-1-1.
At the time of EMS arrival, the patient appears acutely ill. He is slightly diaphoretic but not overly anxious. He admits to 8/10 chest pain and mild dyspnea. He denies nausea, vomiting, or palpitations. No JVD. Breath sounds are clear bilaterally.
Vital signs are assessed:
RR: 18
Pulse: 58
BP: 155/90
SpO2: 98 on RA
The cardiac monitor is attached.
A 12 lead ECG is captured.
What now?
Let us assume for the sake of discussion that you live in a rural community.
You are 25 minutes away from your local receiving hospital (no cath lab) and 55 minutes away from a hospital in the next county over that is capable of primary PCI.
Do you bypass the local community hospital?
Should the cardiac cath lab be activated prior to your arrival?
Who makes the decision?
Let's take a look at another case.
This was one of the first ECGs ever transmitted to my local receiving hospital on the Lifenet Receiving Station. It was definitely the first STEMI.
The data quality of the first 12 lead ECG wasn't the greatest. This is the second ECG, with lead V4 in the position of V4R.
Unfortunately, I can't seem to locate the details of this case. All I remember is that it was a male patient with chest pain.
This is an interesting ECG for several reasons.
There is ST segment elevation in leads II, III, and aVF which suggests acute inferior STEMI. You can also make out ST segment elevation in leads V5 and V6.
But where are the reciprocal changes? Normally we'd expect to see something in leads I and aVL. In this case, we don't even have so much as a flattening of the ST segment.
Very unusual indeed!
The only places I can see ECG changes that could be construed as reciprocal changes are in leads aVR and V1.
Is this a STEMI? I wouldn't blame you if you gave serious consideration to another diagnosis like pericarditis.
It is a STEMI.
Let's look at lead V4R. Do you see ST segment elevation?
No.
In fact, there appears to be about 1 mm of ST segment depression.
Is there right ventricular involvement?
No.
The culprit artery isn't even the RCA. It's the circumflex (LCX).
Take a look at the image to the right from an editorial in the New England Journal of Medicine by HJ Wellens.
You will note that lead V4R in this case looks almost identical to the third example, which indicates occlusion of the circumflex artery.
When I contacted the director of cardiovascular services at the hospital, he confirmed that the circumflex was 100% occluded.
If you remember your coronary anatomy from Part I, it's the right coronary artery (RCA) that typically supplies the right atrium and right ventricle before reaching the inferior wall of the left ventricle.
In a minority of patients, the circumflex (LCX) supplies the inferior wall of the left ventricle. Occlusion of this artery generally does not threaten the right ventricle.
So what have we learned? Is it always necessary to check the right sided precordial leads in the setting of acute inferior STEMI? Or at least lead V4R? It certainly isn't going to hurt. I won't discourage it.
Consider this comment left by Shaggy in Part II.
I work in a busy ED and one day the medics brought in a hypotenisive patient with an inferior wall MI on their 12 lead. I asked the attending if she wanted me to do a 12 lead with V4R. Her answer which I heard from others was if it is inferior and hypotensive, consider it right sided and treat as such. However, after reading this post, I see the importance of checking the right side on a normotensive patient with an inferior MI. I am glad you are around. I just wish I didn't have to keep reviewing your posts.
I tend to agree with the attending. I would simply include patients who are technically normotensive but on the low side of "normal" especially if they are bradycardic or "shocky" in appearance!
SoCal Medic alluded to another trick in a comment he left for Part I.
I have been taught two different ways, the first by obtaining V4R and evaluating that for ST Segment changes and the second by comparing Lead II to Lead III.
You will notice that in Part II, the ST segment elevation in lead III is > than the ST segment elevation in lead II. An examination of lead V4R confirms right ventricular involvement.
In this case, the ST segment elevation in lead II is > than the ST segment elevation in lead III. An examination of lead V4R confirms that there is not right ventricular involvement.
Is it really that simple? Actually, it is.
Consider this table from Eskola et al. How to Use ECG for Decision Support in the Catheterization Laboratory – Cases With Inferior ST Elevation Myocardial Infarction. Journal of Electrocardiography Vol 37 No. 4 October 2004.
See also:
Right ventricular infarction – Part I
Right ventricular infarction – Part II
Right ventricular infarction – Part III
Additional resources:
From the March 2008 issue of EMS Magazine:
Recognition and Treatment of Right Ventricular Myocardial Infarction by Gene Gandy
Let’s look at a case study that demonstrates the potential danger associated with right ventricular infarction.
EMS is called to the residence of a 68 year old female with chest pain.
On arrival, the patient is anxious, cool, pale, and diaphoretic.
Vital signs are assessed.
Resp: 20
Pulse: 68
BP: 105/55
SpO2 95 on RA
A 12 lead ECG is captured showing acute inferior STEMI.
“Time is therapy” for STEMI patients, so the most important issue to consider is how this patient is going to be reperfused.
The other issue to consider is how you’re going to manage the patient.
The paramedic in charge of the call wisely suspected the possibility of right ventricular involvement and decided to capture another 12 lead ECG using modified lead V4R.
Basically, this is lead V4 moved over to the right side of the chest (hence the addition of the letter ‘R’ which stands for ‘right’).
When lead V4R shows at least 1 mm of ST segment elevation in the presence of inferior STEMI, it’s a highly sensitive marker for right ventricular involvement.
Does this mean that every patient with right ventricular involvement will develop the hypotensive syndrome? No. But it means the patient is at risk and drugs like nitroglycerin and morphine should be used with caution!
Here is the 12 lead ECG with lead V4 in the position of V4R.
Is there at least 1 mm of ST segment elevation in lead V4R?
Yes!
Even if there wasn’t quite 1 mm of ST segment elevation in this lead, because the QRS complex is so small, you’d want to consider the amount of ST segment elevation relative to the size of the QRS complex (thanks for this tip Dr. Smith).
To fully appreciate this point, look at the same cardiac cycle in lead V4R “stretched” vertically, which makes it easier to see the ST segment elevation relative to the size of the QRS complex.
This is the inverse of the rule for LBBB (and LVH) where the deeper the S wave, the higher the ST segment.
So we have a patient with acute inferior STEMI with right ventricular involvement.
Now what?
Place the patient on oxygen, start an IV, and give the patient a fluid bolus!
These patients can handle a lot of fluid, and it helps maintain their pressure, especially if you’re even thinking about a trial of nitroglycerin!
The paramedic on this call gave the patients a bolus of 500 ml 0.9% NS which brought the patient’s pressure up to 124/68.
A single dose of SL NTG brought the patient’s pressure down to 90/48.
Can you imagine what would have happened had the paramedics not performed a preemptive fluid bolus?
The paramedics withheld NTG for the remainder of the transport and repeated the fluid bolus of 500 ml 0.9% NS which brought the patient’s pressure back to 110/55 (almost what they started with).
On arrival at the hospital, the lead paramedic gave a report to the on duty ED physician, who was completely dismissive when the paramedic showed her the 12 lead ECG with lead V4 in the position of V4R.
Please note, I have the highest respect for the medical profession. I have nothing against emergency physicians. I’m just telling it like it was.
The physician immediately ordered NTG and morphine.
The paramedic sat down to write the report, and within 5 minutes he heard a nurse yell out “I need help in here!”
The patient was crashing. Fast.
Here is a 12 lead ECG that was captured after the patient’s pressure plummeted (I never found out how low it went).
Do you notice anything about the ST segment elevation?
Suffice it to say, we are not doing our patients a favor when we put them into uncompensated cardiogenic shock.
The patient was stabilized after several tense minutes and sent up to the cardiac cath lab.
Here is an ECG taken before the intervention.
Here is an ECG taken after.
As far as I know, the patient made a full recovery.
See also:
Right ventricular infarction – Part I
Right ventricular infarction – Part II
A visitor to the PH12ECG blog from Birmingham, United Kingdom made me smile today, and I’m sure s/he had no idea! 
Now that’s entertainment!
Peter Canning over at Street Watch: Notes of a Paramedic has a recent post entitled STEMI Interpretation that’s worth checking out.
In it, he observes:
When we take a class in STEMI recognition, the ECGs, once you know how to read them, are all pretty clear cut. You can flash the 12-leads on the screen and a well-taught class will call out in unision “Inferior, Anterior, Anterior, Inferior, Lateral,” etc. You get tricky and you throw in the ST imposters, but they catch on. “Left Bundle, Right Bundle, LVH, Inferior, Anterior, Left Bundle,” etc.
The problem is when you get back on the street not all 12-leads are so cut and dried…
I couldn’t have said it better myself.
Unfortunately, a lot of paramedics feel so good about themselves after taking a basic 12 lead ECG STEMI recognition class that they buy into the mindset that paramedics can interpret an ECG as good as a physician.
In 99% of cases, it simply isn’t true. Not because paramedics can’t be taught to read an ECG as good as a physician, but because paramedics aren’t taught to read an ECG as good as a physician.
Peter goes on to discuss a recent article published in the American Journal of Cardiology that essentially shows that interpretation of ST segment elevation on the 12 lead ECG can be difficult, even for cardiologists.
This finding is not surprising. I have written about the problem of ST segment elevation in a previous post.
Peter goes on to quote the study’s “bottom line”:
This study’s findings reflect the diagnostic limitations encountered by cardiologists when the ECG is used as the sole diagnostic tool for STEMI. If experienced readers, using the current criteria and guidelines, cannot accurately and consistently distinguish between STEMI and NISTE, less-experienced readers cannot be expected to do so.
And then adds
So take heart, paramedics, we aren’t expected to be seers. Just do the best you can to identify what you can. Cast a wide net when you do your 12-leads. Do serial 12-leads. One that is not obvious can soon grow into a not subtle one. Call the obvious ones, and bring attention to the possible ones. Evaluate based on patient presentation and ECG.
I am mostly in agreement, especially with regard to performing serial 12 lead ECGs. However, while we may not be expected to “be seers” in all situations, we can “be seers” in most situations.
With the proper training.
Tomas Garcia MD, author of “12 Lead ECG – The Art of Interpretation” once told me the most common reason cardiologists fail their board exams is ECG interpretation.
ECG interpretation can be difficult. Admitting that is the first step to developing real expertise. It’s sort of the same as tracheal intubation in this regard. Just because you can intubate a patient with typical anatomy doesn’t mean you can handle a difficult airway.
Just because you can identify a homerun STEMI after an 8-hour introduction to 12 lead ECG class doesn’t mean you’re going to pick up on ventricular aneurysm.
There are always going to be false positive cardiac cath lab activations. If it never happens, you’re not being aggressive enough. If it happens too often, you’re being too aggressive.
A case like this from the Lost on the Floor blog (brought to my attention by Klaus of The ECG Blog) could fool almost anyone, especially without an “old” ECG for comparison.
Can you be taught to identify the mimics of acute STEMI?
Yes.
Can you be taught to identify acute STEMI in the presence of baseline abnormalities that mimic acute STEMI?
Yes!
It’s difficult but it’s not impossible.
*** Update 02/16/09 ***
Peter had posted this ECG from the study and reported that only 5 out of 15 experienced ECG interpreters called it correctly.
In the comments he reports:
5 out of 15 experts correctly said this was a STEMI.
“A 57-year-old man with chest pain. There were QS waves in V1–V2. There was mild STE in V1–V2. There was terminal T-wave inversion V2–V6. There was T-wave inversion in I and aVL. Peak troponin I 26.84 ng/ml. Peak CKMB 29.6 ng/ml. Coronary angiography showed proximal left main stenosis 40%, proximal left anterior descending artery stenosis 95%, left circumflex artery 60%. The patient underwent PPCI of his proximal left anterior descending artery. STEMI was diagnosed by 5/15 readers (33%).”
I had guessed the ECG showed left ventricular aneurysm.
Consider this ECG from Brady WJ, ST Segment and T Wave Abnormalities Not Caused by Acute Coronary Syndromes. Emerg Med Clin N Am 24 (2006) 91-111.
As I noted in the comments, ventricular aneurysm is a difficult mimic because it’s not really a mimic at all. It’s an “old” MI with persistent ECG abnormalities.
It would be interesting to know if an acute thrombosis was found during intervention, of if this was one of those patients for whom chronic atherosclerosis finally became so occlusive that it caused cardiac injury.
My guess is that the ECG didn’t look a whole lot different after stenting.
By the way, Stephen Smith from Dr. Smith’s ECG Blog has as a decision rule to help you distinguish between acute anterior STEMI and left ventricular aneurysm (of course he does)!
Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J of Emerg Med 2005 May; 23(3):279-287
See also:
ECG Challenges from AACN Advanced Critical Care (links to article about STEMI mimics)
Left ventricular hypertrophy – Part I
Left ventricular hypertrophy – Part II
41 year old male CC: Chest pain
41 year old male CC: Chest pain – Answer
Wolff-Parkinson-White Syndrome (WPW) – STEMI Mimic
41 year old male CC: Chest pain (looks like BER, proves to be acute STEMI)
23 year old male CC: Chest pain (benign early repolarization)
Right ventricular infarction. What is it and why should you care?
Depending on what you read, right ventricular infarct may complicate up to 40 or 50% of all inferior MIs.
Remember, when we say “inferior MI” or “anterior MI” we’re talking about the inferior wall of the left ventricle or the anterior wall of the left ventricle.
If you look at the typical patient’s coronary anatomy, the right coronary artery comes off of the aortic root and runs down the right side of the heart, supplying the right atrium, right ventricle, and the inferior wall of the left ventricle.
That’s why the right coronary artery (RCA) is usually the “culprit artery” for an inferior wall MI.
But where in the RCA is the occlusion located?
If it’s a proximal occlusion (high up in the RCA) then the occlusion may actually be affecting the right ventricle and the inferior wall of the left ventricle.
Why is this a problem? Simple.
Look at this cross section of the heart.
When compared to the left ventricle (which is essentially a muscular tube) the right ventricle is thinner and attaches to the left ventricle like a pocket.
Remember, the right ventricle is only responsible for pulmonary circulation (lower pressure) where as the left ventricle (higher pressure) has to pump blood to the entire body and back.
In the setting of right ventricular infarction, the right ventricle can become “stunned” and fail to pump blood effectively. It essentially becomes a conduit through which blood flows. When this occurs, the patient becomes highly dependent on central venous pressure to maintain adequate cardiac output.
Sometimes, this is referred to as being “pre-load dependent” which is a term that I find amusing. In the first place, it’s become a catch phrase, but more importantly, raise your hand if you’re not pre-load dependent!
Because patients with a stunned right ventricle are dependent on central venous pressure to maintain cardiac output, it can be dangerous to give these patients nitroglycerin, which is a potent vasodilator. Morphine can cause problems for the same reason.
Patients with right ventricular infarction (almost always associated with inferior wall MI) tend to start out with borderline blood pressures. This is due in part to right ventricular stunning, but also because inferior MI often stimulates the Bezold-Jarisch reflex, which leads to a state of hypervagotonia. It’s no accident that sinus bradycardia is the most common arrhythmia associated with inferior MI!
Granted, it’s possible for a proximal occlusion of the RCA to upset the blood supply to the SA node, which could cause sinus bradycardia, but the percentage of inferior MIs that present with sinus bradycardia is far higher than this phenomenon could explain.
It’s also worth mentioning that varying degrees of AV block are known to occur with inferior MI, usually with a narrow complex escape rhythm.
So how do you know if a patient with inferior MI has an associated right ventricular infarct? After all, it might change your treatment! Or should it?
In Part II, we’ll discuss how to identify right ventricular infarct (RVI) on the 12 lead ECG, and in Part III, I’ll share my theory as to whether or not it’s necessary to apply electrodes to the right side of the patient’s chest.
See also:
Right ventricular infarction – Part I
What is the differential diagnosis of tall R waves in lead V1?
From Mattu, Brady, et al., Prominent R Wave in Lead V1: Electrocardiographic Differential Diagnosis. Am J Emerg Med 2001; 19:504-513. PMID: 11593472
- Right bundle branch block
- Left ventricular ectopy
- Right ventricular hypertrophy
- Acute right ventricular dilation (acute right heart strain)
- Type A Wolff-Parkinson-White syndrome
- Posterior myocardial infarction
- Hypertrophic cardiomyopathy
- Progressive muscular dystrophy
- Dextrocardia
- Misplaced precordial leads
- Normal varient
Can you identify all of these conditions? The most important to know are RBBB, RVH, WPW Type A, and posterior MI.
RBBB is characterized by a superaventricular rhythm with a QRS duration = or > 120 ms, a terminal R wave in lead V1, and a slurred S wave in lead I. See an example here.
RVH is characterized by a right axis deviation, a tall R wave in lead V1, and often a right ventricular “strain pattern” in the right precordial leads. See an example here.
WPW Type A is characterized by a short PR interval, delta waves, and positive concordance of the precordial leads. See an example from the ECGPedia here.
Posterior MI is often associated with inferior MI. When present, the R wave in lead V1 is at the very beginning of the QRS complex (not the end of the QRS complex as is the case with RBBB). We’ll cover this topic more in-depth in a future discussion.
As for “left ventricular ectopy” just remember that ventricular complexes that originate in the left ventricle show RBBB morphology in lead V1. Conversely, ventricular complexes that originate in the right ventricle show LBBB morphology in lead V1.
Among other things, this means you can determine which ventricle a PVC comes from if you’re monitoring lead V1.
It’s astonishing that some people alive on the Earth today have literally seen technology go from “horse and buggy” to “space shuttle”.
Sort of like my recent switch from the Motorola i530 to the Apple iPhone G3. One things I can say about the Motorola i530 is that it’s rugged. I bought it because the salesman said I could drop it without breaking it.
He was right.
Something tells me I’m going to have to be a little more careful with the iPhone.
Anyone know how to send a text message?
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