ECG Blog #443 — A 40s Man with CP and Dyspnea

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?

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.
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• 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).
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• 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. 
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• 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).
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• 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).

PEARL #5: The KEY for being able to suspect acute PE from the ECG — is when you see a constellation of ECG findings potentially consistent with this diagnosis (as listed below in the ADDENDUM in Figure-7) — in a patient with a suggestive history. 

• 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).
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• 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).

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?

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".
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• 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. 
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• 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."
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• 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.

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.

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).
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• 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”. 

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ADDENDUM #1 (8/16/2024): 

I've included below some review material regarding the ECG diagnosis of acute PE (Pulmonary Embolus) and RV "strain".

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).

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?

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).

Follow-Up: Pulmonary CT scan confirmed an acute submassive PE.