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ECG Blog #532 — A Surprise Diagnosis ...
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The ECG in Figure-1 was obtained from a middle-aged man — who presented to the ED (Emergency Department) with a 1-week history of intermittent "burning chest pain" — with some "shortness of breath".
QUESTIONS:
- How would YOU interpret the ECG in Figure-1?
- Should you activate the cath lab?
- — Should you do anything else at the bedside?
-USE.png) |
| Figure-1: The initial ECG ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
MY Thoughts:
The ECG in Figure-1 was sent to me with the above history. I wrote back that my initial interpretation of this tracing was the following:
- This is a very worrisome ECG!
- There is sinus tachycardia — which of itself is a worrisome sign, since sinus tach tends to be an uncommon finding with acute MI — unless "something else" is going on (ie, heart failure, shock, etc.).
- There are inferior Q waves in a "qRS" pattern — which in the inferior leads usually means that an inferior MI has occurred at some point in time.
- At the least — there is DSI (Diffuse Subendocardial Ischemia) — as indicated by ST elevation in lead aVR, with ST depression in the other 5 limb leads (as well as in the lateral chest leads).
- I suspect there is a Precordial "Swirl" pattern — with clearly abnormal ST elevation and T wave inversion in lead V1 — and ST segment straightening with ST elevation in leads V2,V3 — and what looks to be some J-point depression in lead V6 (A "Swirl" pattern is typically seen with acute or recent proximal LAD occlusion — and the loss of R wave from V2-to-V3 suggests anterior infarction).
- I asked the following: i) Any prior history of heart disease in this patient? — and, ii) Any prior ECGs available?
- I suggested that, "The patient needs prompt cath" — with my suspicion of an LAD "culprit" artery.
QUESTION:
- BUT — What did I not mention in my above comments?
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CASE Follow-Up:
- The patient was admitted to the Intensive Care Unit with a diagnosis of acute ACS (Acute Coronary Syndrome).
- While contemplating the best approach to management — bedside Echo was done. Surprisingly — bedside Echo showed a markedly dilated RV with a "D-shaped" septum.
- CTPA (CT Scan Pulmonary Angioram) was then performed — which confirmed the diagnosis of massive acute PE (Pulmnary Embolism).
- The patient was treated with injection of low molecular weight heparin (Enoxaparin) — and rapidly improved.
- Bedside Echo can be extremely helpful in confirming acute MI when ECGs are equivocal — IF — Echo shows a localized wall motion defect.
- The caveat is that if the patient is no longer having CP (Chest Pain) at the time that Echo is done — then nothing is ruled out if the Echo is normal. But if CP persists and the Echo shows perfectly normal LV function — this makes an acute MI much less likely.
- Bedside Echo may suggest Takotsubo Cardiomyopathy if there is "apical ballooning" due to apical akinesis or hypokinesis with preserved or hypercontractile basal segments (Izumo and Akashi — Cardiovasc Diagn Ther 8(1):90-100, 2018).
- In today's case — Echo was the KEY Clue that led providers away from the diagnosis of ACS (Acute Coronary Syndrome) — and to the correct clue of massive acute PE! (See ECG Blog #443 — for a case in which I review the findings of Bedside Echo and CTPA in a patient with a large acute PE).
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What Did We Miss?
In cases like this one — I find it helpful to "soul-search" and GO BACK to try and learn from any clinical clues that may have been missed.
- "Some shortness of breath" was mentioned in the brief history we were given. It's hard to know how significant the symptom of dyspnea was in today's case from words on the printed page. Sometimes — "Ya just gotta be there!" ( = at the bedside!).
- PEARL #2: In my experience — by far, the most commonly overlooked vital sign is the respiratory rate! Much of the time — the clinician at the bedside simply does not take the time to COUNT the respiratory rate.
- Nurses also (in my experience) do not always count the respiratory rate. Instead — they sometimes just put down 12 or 15/minute if the patient "seems OK".
- Clinical Reality: Unless you spend a conscious moment in which you truly LOOK at the patient — it is all-too-easy to miss a patient taking small but rapid breaths — unless you actually COUNT the breaths per minute. And if the patient was breathing 25-30/minute at rest ==> that's tachypnea, which should serve as an important clue that an acute pulmonary problem may be the cause!
Taking Another Look at Today's ECG ...
In addition to the history of CP (described as a "burning" chest pain in today's case) — the ST elevation in the anterior leads in the initial ECG (in Figure-1) led me to suspect an acute cardiac event as my primary diagnosis.
- PEARL #3: Instead of the anterior ST depression or T wave inversion of RV "strain" — anterior lead ST elevation may sometimes be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016).
- Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2,V3 in today's initial ECG).
What I also found confusing about the initial ECG in today's case — was the question of whether there is (or is not) ST depression in multiple leads.
- The answer to this question depends on how you define the ST segment baseline — which sometimes is not an easy task.
- As review — I include below in Figure-2 my approach for determining the ST segment baseline in any given tracing.
.png) |
| Figure-2: "My Take" on defining the ST segment baseline (from Grauer K: ECG Pocket Brain-2014 ePub). |
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With PEARL #3 and Figure-2 in mind — I'll add Figure-3 below, which is my summarizing chart of the ECG Findings associated with acute PE — which I then reapply to today's initial ECG in Figure-4.
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| Figure-3: ECG Findings associated with acute PE (updated since ECG Blog #443). |
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Figure-4: Another Look at Today's Initial ECG ...
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| Figure-4: I've labeled today's initial ECG. |
KEY Point: With the above information in mind — Today's ECG (that I've labeled in Figure-4) — could be consistent with the diagnosis of acute PE, albeit without the typical appearance of RV "strain", in which T wave inversion is seen in anterior and/or inferior leads. Among the ECG findings in Figure-4 potentially consistent with acute PE are the following:
- Sinus tachycardia (Here at a rate of ~115/minute).
- S waves in multiple leads (ie, Leads I,II,III; aVF; V4,5,6).
- ST elevation in lead aVR.
- RV "strain" (Here in the form of ST depression in the inferior leads — assuming one uses the TP baseline for judging if there is ST elevation or depression).
- Anterior lead ST elevation — which as noted in PEARL #3, can be a sign of acute PE.
- ST depression in the remaining chest leads (V4,V5,V6) — again assuming one uses the TP baseline for judging if there is ST depression.
PEARL #4: ECG findings in Figure-4 against acute PE are: i) Q waves in each of the inferior leads (YELLOW arrows in leads II,III,aVF); — and, ii) Loss of r wave between lead V2-to-V3, with a QS wave in lead V3.
- In this patient who presented with a 1-week history of "burning" CP and some "shortness of breath" — this ECG leaves us with trying to distinguish between acute LAD occlusion vs acute PE (with the additional possibility of Takotsubo Cardiomyopathy — given diffuse ST-T wave abnormalities, and what appears to be a prolonged QT interval).
- KEY Point: Until bedside Echo was done in today's case — I strongly suspected acute proximal LAD occlusion as the diagnosis.
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"Take Home" Message:
On occasion — acute PE may present with a "pseudo-infarction pattern, as it did in today's case.
- Bedside Echo made the diagnosis in a matter of minutes.
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Acknowledgment: My appreciation to Mohammed Elsisi (from Cairo, Egypt) for the case and these tracings.
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Related ECG Blog Posts to Today’s Case:
- ECG Blog #443 and ECG Blog #496 — Review challenging cases on the ECG diagnosis of acute PE.
- ECG Blog #313 and ECG Blog #435 — Review more cases on the ECG diagnosis of acute PE.
- ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
- ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
- My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
- ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
- ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”.
- ECG Blog #380 — Reviews the concept of Precordial "Swirl".
- ECG Blog #483 — Reviews the concept of DSI (Diffuse Subendocardial Ischemia) in Pearl #1 of this blog post.
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ECG Blog #443
https://ecg-interpretation.blogspot.com/2024/08/ecg-blog-443-40s-man-with-cp-and-dyspnea.html
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The ECG in Figure-1 was obtained from a man in his 40s — who presented to the ED (Emergency Department) because of CP (Chest Pain) and shortness of breath.
QUESTIONS:
- In view of the above history — How would YOU interpret the ECG in Figure-1?
- Based on the history and the patient's initial ECG — the cath lab was activated. Do you agree?
-USE.png) |
| Figure-1: The initial ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio). |
MY Thoughts on this CASE:
Not being there — I am unaware of physical exam parameters (blood pressure, respiratory rate; oxygen saturation; heart and lung auscultation, etc.). What we can comment on, given the brief history of new CP and dyspnea — is the initial ECG shown in Figure-1. I see the following:
- There is sinus tachycardia (upright P wave with fixed PR interval in lead II) — at the rapid rate of ~130/minute.
- Regarding intervals — the PR interval is normal — the QRS is of normal duration. Given the rapid rate — it is hard to say much about the QTc.
- There is RAD (Right Axis Deviation) — in that that QRS is slightly more negative than positive in lead I ( = estimated frontal plane axis about +100 degrees).
Regarding chamber enlargement — LVH is not present. Although frank criteria for RVH (Right Ventricular Hypertrophy) are not present — there are a number of ECG findings consistent (if not suggestive) of acute RV "Strain" (See Figure-2).
- PEARL #1: Before going further — We need to consider the possibility of acute PE (Pulmonary Embolism)! Acute PE remains one of the most commonly overlooked diagnoses. As per links that I provide below — IF the diagnosis of acute PE is not thought of, this entity will be missed! (See ECG Blog #435 — ECG Blog #313 — as well as My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog).
I review the ECG diagnosis of acute RV "strain" and acute PE in the ADDENDUM below (See Figures-7, -8, -9). For now — Let's continue with ECG signs consistent with and suggestive of acute RV "Strain".
- Sinus Tachycardia and RAD — as already noted above.
- PEARL #2: In the absence of associated heart failure (cardiogenic shock) — sinus tachycardia is not a common finding in acute MI. As a result — the finding of sinus tachycardia in today's patient, who presents with both CP and shortness of breath (especially to as rapid a heart rate as the ~130/minute seen here) — should immediately prompt consideration of something other than acute coronary occlusion.
- Although criteria for RAA (Right Atrial Abnormality) are not strictly satisfied (P wave amplitude in lead II does not attain 2.5 mm in amplitude) — the P wave in lead II is more peaked and pointed than it usually is (within the RED oval in Figure-2). In the context of a suggestive clinical history and other ECG signs of acute RV "strain" — I interpret more-than-expected inferior lead P wave peaking as suggestive of RAA, therefore another supportive (albeit subtle) indication of RV "strain" (See ECG Blog #75 — for more regarding ECG criteria for RAA).
- S1Q3T3 — Whereas the diagnostic value of this pattern is limited when seen as an isolated finding — a definite S1Q3T3 pattern (as seen in Figure-2) — is very helpful in today's case, given association with other ECG evidence pointing to the possibility of acute PE.
- PEARL #3: ST-T wave findings of acute RV "Strain" — are most often seen in the form of anterior T wave inversion (and/or anterior ST depression). The other ECG area to look for RV "strain" — is in the inferior leads, though it is less common in my experience to only see RV "strain" inferiorly without also seeing ST-T wave changes anteriorly.
- As a result — I admittedly, was initially deterred from the diagnosis of acute PE because of the lack of anterior T wave inversion in ECG #1. That said — ST-T wave changes of acute RV "strain" are present in each of the inferior leads (BLUE arrows in leads II,III,aVF in Figure-2).
- PEARL #4: Instead of anterior lead T wave inversion — there is some ST elevation in leads V1 and V2, with ST segment straightening in lead V3. On occasion — such anterior lead ST elevation (instead of T wave inversion) can be seen with acute PE (Zhan et al — Ann Noninvasive Electrocardiol 19(6):543-551, 2014 — and — Omar HR — Eur Heart J: Acute Cardiovascu Care (5(8): 579-586, 2016).
- Right-sided leads such as leads III, aVR and V1 — face the anterior region of the RV. If the RV is enlarged — then leads V2 and V3 may also face the anterior region of the RV — and — if there is severe transmural ichemia of the RV, any of these leads may show ST elevation (as is seen in leads aVR and V1,V2 in Figure-2).
- Today’s patient presented to the ED not only with chest pain — but also with shortness of breath, therefore with a history potentially consistent with the diagnosis.
- Easily attainable bedside findings that further support the diagnosis of acute PE include a low oxygen saturation — and — an increased respiratory rate. To emphasize — Count the respiratory rate yourself! (Reading the respiratory rate off of nursing notes is not necessarily accurate in my experience — so spending 15-20 seconds simply looking at the patient breathing and counting breaths is well worth this short amount of your time).
- ECG Signs (in addition to those already mentioned above) — that are consistent with acute PE in today’s tracing (as per the Table in Figure-7) include: i) Poor R wave progression, with persistence of S waves through to lead V6; and, ii) The rSr' morphology seen in lead V1, which in association with the narrow terminal s waves in lateral leads I and V6 — is consistent with a IRBBB proxy (See labeled Figure-2 below).
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| Figure-2: I've labeled the initial ECG in today's case. |
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QUESTION:
Although today’s initial ECG is potentially consistent with acute PE — I would not be 100% convinced of this diagnosis from the tracing shown in Figure-2 alone.
- What could be done at the bedside within no more than a few minutes to verify the diagnosis of acute PE?
ANSWER:
- A POC (Point-Of-Care) ECHO — will sometimes be diagnostic of acute PE. When it is — this may greatly expedite clinical decision-making for anticoagulation and/or thrombolysis.
- The sensitivity of POC Echo is not perfect. That said — the specificity of Echo for acute PE can be excellent IF certain echocardiographic findings are present. This is especially true for larger, more hemodynamically significant PEs — with prognostic insight provided depending on the degree of impairment of RV function (On and Park — Korean J Intern Med: 38(4);456-470, 2023 and Hritani et al — Cleveland Clin J Med 85(110: 826-828, 2018).
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The ECHO on Today's Patient:
In Figure-3 — I've labeled the 4-chamber view from the Echo on today's patient. In Figure-4 — I've included the video recording of this view. What do you think?
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| Figure-3: Still picture of the Echo 4-chamber view. |
Figure-4: Video recording of this 4-chamber view. I include a slow-motion section to facilitate recognition of the diagnostic Echo sign described below.
Figures-3 and -4 on Today's Echo:
For orientation — the 4 chambers are shown in Figure-3:
- The RV (Right Ventricle) is clearly dilated, and appears to be even larger than the LV. As a result of RV overload — the IVS (InterVentricular Septum) is shifted toward the left side of the heart. In a patient with a suggestive history and ECG findings consistent with acute PE — seeing this degree of RV dilation on Echo strong favors acute PE as the diagnosis. That said — seeing RV dilation on Echo does not distinguish between acute vs chronic causes of RV "strain".
- PEARL #6: In contrast to the finding of RV dilation (that could be a longstanding condition) — the McConnell Sign is a dynamic echocardiographic finding that is specific for conditions causing acute RV "strain", such as acute PE.
- A McConnell Sign is said to be present when 2 echocardiographic findings are seen: i) There is RV free wall akinesis (seen as per the YELLOW arrow in Figure-3 — as an outward movement of the RV free wall as a result of increased pressure in the dilated RV chamber); and, ii) The RV apex manifests hypercontractility, as a result of being "tethered" to the LV (RED arrow moving inward). This sign is positive in the video recording shown in Figure-4 — in which the RV apex has been described as "a trampoline bouncing up and down while the rest of the RV remains still."
- References on Echo for PE Diagnosis: Oh and Park - Korean J Intern Med 38(4):456-470, 2023 — and — Hritani et al - Cleveland Clin J Med 85(11):826-828, 2018 — and — IF you want an excellent 5-minute video review on recognition of the McConnell Sign on Echo — WATCH_this_VIDEO by Dr. Christopher Voscopoulos.
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Diagnostic CTPA on Today's Patient:
Final confirmation of acute PE in today's case was obtained by CTPA ( = Pulmonary Angiography in Figure-5).
- Excellent review of diagnostic testing for acute PE (Moore et al — Cardiovasc Diagn Ther 8(3):225-243, 2018).
- For a 10-minute video review on reading Pulmonary CT Scan — WATCH_this_VIDEO by Dr. Jake Gibbons.
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| Figure-5: CTPA view in today's case — showing large clot burden in the right and left main pulmonary arteries. |
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CASE Follow-Up:
The "good news" in today's case — is that the patient received thrombolytics, and ultimately did well. That said — the diagnosis of acute PE was delayed for a number of hours, because providers were initially more concerned about an acute MI. As a result — diagnostic Echo was not performed until after cardiac cath was found to be normal.
- PEARL #7: Echo at the bedside is a fast test that takes only minutes! In today's case — the Echo could have been done while waiting for cath facilties to get ready. Had this been done — the dramatic RV dilation and positive McConnell Sign seen in Figures-3 and -4 — would have allowed immediate confirmation of acute PE that could have avoided any need for cardiac cath, thereby expediting initiation of thrombolytic therapy.
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Repeat ECG After Thrombolytic Therapy:
I found it of interest to compare the follow-up ECG obtained after successful thrombolytic therapy (Figure-6).
- Sinus tachycardia has resolved.
- Right axis deviation in ECG #2 is much less (predominant positivity of the R wave in lead I has returned).
- RV "strain" is no longer evident (resolution of ST depression in the inferior leads).
- Right-sided ST elevation that had been present in leads aVR, V1,V2 of ECG #1 — is no longer seen in the repeat tracing.
- S waves no longer persist through to lead V6.
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| Figure-6: Comparison between the initial ECG in today's case — with the repeat ECG obtained following thrombolytic therapy. |
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Acknowledgment: My appreciation to Magnus Nossen (from Fredrikstad, Norway) for the case and these tracings.
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Related ECG Blog Posts to Today’s Case:
- ECG Blog #313 and ECG Blog #435 — Review cases on the ECG diagnosis of acute PE.
- ECG Blog #233 — Reviews a case of Acute PE (with discussion of ECG criteria for this diagnosis).
- ECG Blog #119 — Reviews a case of Acute PE (and ECG criteria for this diagnosis).
- My Comment at the bottom of the page in the June 17, 2024 post in Dr. Smith's ECG Blog (regarding a case similar to today's ECG Blog).
- ECG Blog #234 — Reviews ECG criteria for the diagnosis of RVH and RV "Strain".
- ECG Blog #77 — Another review of ECG criteria for the diagnosis of RVH and RV “Strain”.
ADDENDUM #1 (8/16/2024):
I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".
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| Figure-7: ECG Findings associated with acute PE (from ECG Blog #435). |
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PEARL #8: The "Note" under the S1Q3T3 finding in Figure-7 — refers to data from Kosuge et al (Am J Cardiol 99(6): 817-821, 2007 — and the March 4, 2023 post in Dr. Smith's ECG Blog) — that state that when there is T wave inversion in the chest leads, if T waves are also inverted in leads III and V1 — then acute PE is far more likely than acute coronary disease (See the Addendum ECG in Figure-10 below).
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| Figure-8: Summary of KEY findings in the ECG diagnosis of acute PE (from my ECG-2014-ePub). |
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| Figure-9: Summary (Continued) of KEY findings in the ECG diagnosis of acute PE. |
ADDENDUM #2 (8/17/2024):
My thanks to Konstantin Tikhonov (from Moscow, Russia) — who sent me the following illustrative ECG and case the very next day after I posted this ECG Blog #443.
- The patient whose ECG is shown in Figure-10 — had progressively increasing dyspnea over a 10 day period.
- Considering the ECG findings shown above in Figure-7 (with attention to PEARL #8) — How many ECG findings of acute PE can you identify?
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| Figure-10: Addendum ECG (My thanks to Konstantin Tikhonov for sending me this case). |
ANSWER:
The ECG in Figure-10 shows the following findings in favor of acute PE:
- Sinus tachycardia.
- S1Q3T3.
- Persistent precordial S waves (through to lead V6).
- Acute RV "strain" (here in the form of deep, symmetric chest lead T wave inversion that is maximal in leads V2,V3,V4 — and as per PEARL #8, shows T wave inversion in lead V1 and lead III, as well as in lead aVF).
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