Friday, August 12, 2022

Inferior ST Elevation and Hyperacute T-waves, but Patient is Pain Free. What is going on?

A 60-something female presented with episodes of chest pain for the previous 2 days that lasted 20 to 30 minutes each.  On the day of presentation, her episode lasted much longer and she came to the emergency department.  In the ambulance, she was given nitro and her pain was relieved.  On arrival to the emergency department she was pain free.

What do you think?

Here is an ECG from 3 years prior

This is classic Wellens' pattern B morphology, and fits with the entire presentation.  

So it is Wellens' syndrome The ECG is so classic that when I saw the ECG on the system, I knew it was the full syndrome and wrote that "this patient would be pain free at this moment."  Then I confirmed that when I went to the chart.

See important description of Wellens' syndrome below.

The providers who saw the patient were concerned about inferior OMI due to the subtle STE in inferior leads, and STD in aVL.

How do we KNOW it is not active inferior OMI?  
1. The patient is completely pain free and 2. Such inferior STE, and even apparent hyperacute T-waves, are commonly reciprocal to anterior and high lateral reperfusion.

Here is a similar case: 

How do you explain these inferior hyperacute T-waves?

1 hour later:

Further evolution (deepening) of symmetric T-wave inversion in precordial leads


Acute MI Non ST Elevation Myocardial Infarction .

Culprit is 90% stenosis in the proximal LAD .

After PCI:

2 days later

Wellens' syndrome 

Wellens' syndrome is a syndrome of Transient OMI (including transient STEMI) of the LAD, in which the ECG was not recorded at the time of the anginal pain, but only after sponaneous resolution of the pain, at which time the ECG shows reperfusion T-waves in the LAD distribution.  Pattern A = terminal T-wave inversion (biphasic); Pattern B shows deep symmetric T-wave inversion.  Wellens' syndrome also requires preservation of R-waves. 
Thus, in Wellens' syndrome, the patient is: 
1) Pain free after an episode of angina,
2) Has a typical T-wave inversion morphology (not all T-wave inversion is Wellens!!), 
3) Will have preserved R-waves
4) Will have evolution of the T-wave inversion, 
5) Will always have some rise and fall of troponin, 
6) Will have an OPEN artery OR good collateral circulation (the myocardium is perfused)
7) At high risk of re-occlusion (with pseudonormalization of T-waves if it occurs)

Such T-wave inversion also occurs in all the other coronary distributions.

See these posts for a variety of Wellens and mimics:


MY Comment, by KEN GRAUER, MD (8/12/2022):


An appreciation of Wellens' Syndrome is a must in emergency care. The "beauty" of this clinical entity is 3-Fold: i) Awareness of what to look for in the History and in the ECG allows diagnosis within seconds (as per Dr. Smith's instant analysis in today's case)ii) Recognition of Wellens' Syndrome tells you the anatomy (ie, accurate prediction of a high-grade proximal LAD stenosis)andiii) Recognition of Wellens' Syndrome prompts the need for timely cath and life-saving treatment
  • In addition to today's case — we've posted numerous examples of Wellens' Syndrome on Dr. Smith's ECG Blog (See the June 28, 2018 post — and the December 14, 2018 post — to name just 2 instances).
  • Unfortunately, despite the above expert commentary by Dr. Smith in today's case — Wellens' Syndrome remains a misunderstood diagnosis by all too many healthy care providers.

The History of Wellens' Syndrome:
It's hard to believe that the original manuscript describing Wellens' Syndrome was published 40 years ago! As I contemplated today's case — I thought it would be insightful to go back to this original manuscript (de Zwaan, Bär & Wellens: Am Heart J 103: 7030-736, 1982):
  • The authors (de Zwaan, Bär & Wellens) — studied 145 consecutive patients (mean age 58 years) admitted for chest pain, thought to be having an impending acute infarction (Patients with LBBB, RBBB, LVH or RVH were excluded). Of this group — 26/145 patients either had or developed within 24 hours after admission, a pattern of abnormal ST-T waves in the anterior chest leads without change in the QRS complex.
  • I've reproduced (and adapted) in Figure-1 — prototypes of the 2 ECG Patterns seen in these 26 patients. Of note — all 26 patients manifested characteristic ST-T wave changes in leads V2 and V3.
  • Most patients also showed characteristic changes in lead V4.
  • Most patients showed some (but less) ST-T wave change in lead V1.
  • In occasional patients — abnormal ST-T waves were also seen as lateral as in leads V5 and/or V6.

  • Half of the 26 patients manifested characteristic ST-T wave changes at the time of admission. The remaining 13/26 patients developed these changes within 24 hours after admission.

  • Serum markers for infarction (ie, CPK, SGOT, SLDH) were either normal or no more than minimally elevated.

ECG Patterns of Wellens' Syndrome:
The 2 ECG Patterns observed in the 26 patients with characteristic ST-T wave changes are shown in Figure-1:
  • Pattern A — was much less common in the study group (ie, seen in 4/26 patients). It featured an isoelectric or minimally elevated ST segment takeoff with straight or a coved (ie, "frowny"-configuration) ST segment, followed by a steep T wave descent from its peak until finishing with symmetric terminal T wave inversion.
  • Pattern B — was far more common (ie, seen in 22/26 patients). It featured a coved ST segment, essentially without ST elevation — finishing with symmetric T wave inversion, that was often surprisingly deep. 

Figure-1: The 2 ECG Patterns of Wellens' Syndrome — as reported in the original 1982 article (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982).

ST-T Wave Evolution of Wellens' Syndrome:
I've reproduced (and adapted) in Figure-2 — representative sequential ECGs obtained from one of the patients in the original 1982 manuscript.
  • The patient whose ECGs are shown in Figure-2 — is a 45-year old man who presented with ongoing chest pain for several weeks prior to admission. His initial ECG is shown in Panel A — and was unremarkable, with normal R wave progression. Serum markers were negative for infarction. Medical therapy with a ß-blocker and nitrates relieved all symptoms.
  • Panel B — was recorded 23 hours after admission when the patient was completely asymptomatic. This 2nd ECG shows characteristic ST-T wave changes similar to those shown for Pattern B in Figure-1 (ie, deep, symmetric T wave inversion in multiple chest leads — with steep T wave descent that is especially marked in lead V3).

  • Not shown in Figure-2 are subsequent ECGs obtained over the next 3 days — that showed a return to the "normal" appearance of this patient's initial ECG (that was shown in Panel A of Figure-2). During this time — this patient remained asymptomatic and was gradually increasing his activity level.

  • Panel C — was recorded ~5 days later, because the patient had a new attack of severe chest pain. As can be seen — there is loss of anterior forces (deep QS in lead V3) with marked anterior ST elevation consistent with an extensive STEMI. Unfortunately — this patient died within 12 hours of obtaining this tracing from cardiogenic shock. Autopsy revealed an extensive anteroseptal MI with complete coronary occlusion from fresh clot at the bifurcation between the LMain and proximal LAD.

Figure-2: Representative sequential ECGs from one of the patients in the original 1982 article. Panel A: The initial ECG on admission to the hospital; Panel B: The repeat ECG done 23 hours after A. The patient had no chest pain over these 23 hours. NOTE: 3 days after B — the ECG appearance of this patient closely resembled that seen in A ( = the initial tracing)Panel C: 5 days later — the patient returned with a new attack of severe chest pain. As seen from this tracing (C) — this patient evolved a large anterior STEMI. He died within hours from cardiogenic shock (Figure adapted from de Zwaan, Bär & Wellens: Am Heart J 103:730-736, 1982 — See text).

Relevant Findings from the 1982 Article:
The ECG pattern known as Wellens' Syndrome was described 40 years ago. Clinical findings derived from the original 1982 manuscript by de Zwaan, Bär & Wellens remain relevant today.
  • One of the 2 ECG Patterns shown in Figure-1, in which there are characteristic anterior chest lead ST-T wave abnormalities — was seen in 18% of 145 patients admitted to the hospital for new or worsening cardiac chest pain.
  • Variations in the appearance of these 2 ECG patterns may be seen among these patients admitted for chest pain. Serial ECGs do not show a change in QRS morphology (ie, no Q waves or QS complexes developed). Serum markers for infarction remain normal, or are no more than minimally elevated.
  • Among the subgroup of these patients in this 1982 manuscript who did not undergo bypass surgery — 75% (12/16 patients) developed an extensive anterior STEMI from proximal LAD occlusion within 1-2 weeks after becoming pain-free.

LESSONS to Be Learned:

At the time the 1982 manuscript was written — the authors were uncertain about the mechanism responsible for the 2 ECG patterns of Wellens' Syndrome.
  • We now know the mechanism. A high percentage of patients seen in the ED for new cardiac chest pain that then resolves — with development shortly thereafter of some form of the ECG patterns shown in Figure-1 — had recent coronary occlusion of the proximal LAD — that then spontaneously reopened.

  • The reason Q waves do not develop on ECG and serum markers for infarction are normal (or at most, no more than minimally elevated) — is that the period of coronary occlusion is very brief. Myocardial injury is minimal (if there is any injury at all).

  • What spontaneously occludes — and then spontaneously reopens — may continue to reocclude, and then reopen — until eventually a final disposition is reached (ie, with the "culprit" vessel staying either open or closed).

  • As per the above discussion by Dr. Smith — We can know whether the "culprit" artery is either open or closed by correlating serial ECGs with the patient's history of chest pain. For example, in today's case — the finding of deep, symmetric T wave inversion in virtually all chest leads in association with resolution of the chest pain immediately told Dr. Smith that the LAD had spontaneously reopened.

  • The importance of recognizing Wellens' Syndrome — is that it tells us that timely cardiac cath will be essential IF we hope to prevent reclosure. In the de Zwaan, Bär & Wellens study — 75% of these pain-free patients with Wellens' ST-T wave changes went on to develop a large anterior STEMI within the ensuing 1-2 weeks if they were not treated.
  • Thus, the goal of recognizing Wellens' Syndrome — is to intervene before significant myocardial damage occurs (ie, diagnostic criteria for this Syndrome require that anterior Q waves or QS complexes have not developed — and serum markers for infarction are no more than minimally elevated).
  • It is not "Wellens' Syndrome" — IF the patient is having chest pain at the time the ECG patterns in Figure-1 are seen. Active chest pain suggests that the "culprit" artery has reoccluded.
  • Exclusions from the 1982 study were patients with LBBB, RBBB, LVH or RVH. While acute proximal LAD occlusion can of course occur in patients with conduction defects or chamber enlargement — Recognition of the patterns for Wellens' Syndrome is far more challenging when any of these ECG findings are present.

  • Finally — a word about the ECG Patterns of Wellens' Syndrome shown in Figure-1 is in order. Pattern A — is far less common, but more specific for Wellens' Syndrome IF associated with the "right" history (ie, prior chest pain — that has now resolved at the time ST-T wave abnormalities appear).
  • Unlike the example in Figure-1Pattern B may be limited to symmetric T wave inversion without the finding of steep T wave descent into terminal negativity in any lead. This is the pattern seen in today's case — which given the history, was immediately diagnosed as Wellens' Syndrome by Dr. Smith.

In Conclusion — the 145 pts studied by de Zwaan, Bär & Wellens in 1982 continue to provide clinical insight into the nature of Wellens' Syndrome some 40 years after this manuscript was written.
  • P.S.: And sometimes — there may be a similar evolution of ECG findings indicative of acute occlusion and spontaneous reperfusion (corresponding to changes in chest pain severity) in not only anterior leads — but also in the inferior leads. As per Dr. Smith in today's case — this is not active acute inferior OMI — but rather a "reciprocal part" of the Wellens' Syndrome evolution.

Saturday, August 6, 2022

A man in his 40s with multitrauma from motor vehicle collision

Submitted and written by Andrew Yde MD, peer reviewed by Meyers, Grauer, Smith

A man in his 40s presented after motor vehicle collision in which he was the unrestrained driver in a vehicle moving at high speed. He was found by EMS to be obtunded at the scene of the accident, and was intubated in the field. On initial ED evaluation the patient was found to be hypotensive and tachycardic, with multiple obvious orthopedic injuries. He received emergent transfusion and bilateral chest tubes. FAST exam was indeterminate, but did not show a large amount of free fluid. He was deemed stable for CT scans.

CTs revealed the following injuries: left hemopneumothorax, right pneumothorax, pneumomediastinum, sternal fracture, right anterior rib fractures 2-6, left sided flail chest of ribs 2-9, L2 transverse process fracture, left clavicle fracture, grade 1-2 liver laceration, and a grade 1 splenic laceration. The patient was admitted to the surgical trauma ICU.

That night, he exhibited multiple episodes of ectopy, and what appeared to be NSVT. Electrolytes were found to be within normal limits, and the following EKG was obtained:

What do you think?


The patient had no prior EKGs in the system for comparison. The ECG shows sinus rhythm with a right bundle branch block (RBBB). The STD and T waves following the RBBB in V1-V3 are unusual in morphology and potentially excessively discordant compared to normal RBBB. Also, the lateral precordial leads are unusual in that they still have the R', instead of the slurred S wave we see in I and aVL, suggesting that the lateral chest leads are misplaced medially (probably because of the left chest tube in place).

Cardiac contusion was suspected. Remember: other important considerations for ECG changes in the setting of trauma include traumatic coronary dissection or laceration.

A troponin was ordered, along with a repeat EKG, seen below.

Mostly unchanged.


The high sensitivity troponin I (normal less than 20 ng/L) resulted at 20,973 ng/L, and cardiology was consulted. Cardiology recommended an echocardiogram and trending troponins, stating that cardiac contusion was their initial impression. 

The repeat troponin overnight into the following morning was>25,000 ng/L (the lab does not report higher values).

By this time, a formal echocardiogram had been obtained, which revealed normal left ventricular ejection fraction (LVEF), with a severely hypokinetic right ventricle. These findings were interpreted as consistent with cardiac contusion. Cardiology continued to follow, but no cardiac catheterization was deemed necessary. Cardiology cleared the patient for rib plating.

After induction of anesthesia in the operating room, awaiting rib plating, the patient had a run of what was assumed to have been Non-Sustained Ventricular Tachycardia (NSVT), though this telemetry strip was not available for review. He then went into a bradydysrhythmia, and the procedure was aborted. On returning to the ICU, the ECG below was taken, revealing atrial fibrillation with a PVC.

Atrial fibrillation, narrower RBBB than before, one PVC. There appears to be STE and possibly hyperacute appearing T waves in some leads such as I, II, aVF, V6, compared to prior ECGs.

The troponin had begun to downtrend significantly, down to 2,243 ng/L. by hospital day 3. 

A repeat echocardiogram revealed no left ventricular wall motion abnormalities and normal EF, but reduced RVEF and akinesis of the RV free wall and mid ventricle to apex., with biatrial enlargement. The patient was placed on an amiodarone drip, and ultimately converted back to sinus rhythm. He remained hemodynamically stable.

More ECGs were obtained at days 6 and 9 below:


These ECGs show progressive resolution of the RBBB and significant improvement in prior concerning ST changes. 

The remainder of the patient’s hospital course was characterized by many complications. He was finally discharged to rehab after about a month in the hospital.

See our other cases of myocardial contusion and related cases (some of which have an important diagnosis OTHER THAN myocardial contusion!):

A Child with Blunt Trauma -- See how the ECG can be definite for myocardial contusion, but subtle, and what happens if you miss it.   


This is a case where clinical context is of vital importance, because the EKG manifestations of cardiac contusion are fairly unpredictable. Intramyocardial hemorrhage, edema, and necrosis of myocardial muscle cells are characteristics of cardiac contusion. All of these cause troponin elevation, making troponin a very specific marker for cardiac injury. It is suggested that a troponin that is within normal reference range at about 4-6 hours from the inciting event suggests strongly the absence of cardiac injury in blunt chest trauma (Sybrandy).

The EKG is not generally sensitive for cardiac contusion. The right ventricle comprises the majority of the anterior heart which is most susceptible to direct injury in blunt chest trauma. Cardiac contusion can manifest on the ECG in a number of ways, including: ST segment elevation or depression, prolonged QT, new Q waves, conduction disorders such as RBBB, fascicular block, atrioventricular (AV) nodal conduction disorders (1,2, and 3 degree AV block), and arrhythmias such as sinus tachycardia, atrial and ventricular extrasystoles, atrial fibrillation, ventricular tachycardia, ventricular fibrillation, sinus bradycardia, and atrial tachycardia (Sybrandy). RBBB in blunt chest trauma seems to be indicative of several RV injury. Atrial fibrillation is also a predictor of worse outcomes in this case (Alborzi).

See these publications for more information

Overall, management for cardiac contusion is mostly supportive unless surgical complications develop, involving appropriate treatment of dysrhythmias and hemodynamic instability. Ultimately, a normal ECG and normal troponin at 4-6 hours from initial traumatic incident is highly predictive of a lack of future cardiac complications in blunt chest trauma.
Between 81-95% of life-threatening ventricular dysrhythmias and acute cardiac failure occur within 24-48 hours of hospitalization. Troponins and EKGs should be trended until normalization (Sybrandy).  

Delayed cardiac rupture is a potential consequence, especially if there is any ST Elevation.  See this case, this case, and this case.  In patient's at risk, physical activity should be limited for several months after the injury.


Alborzi, Z., Zangouri, V., Paydar, S., Ghahramani, Z., Shafa, M., Ziaeian, B., Radpey, M. R., Amirian, A., & Khodaei, S. (2016, April 13). Diagnosing myocardial contusion after blunt chest trauma. The journal of Tehran Heart Center. Retrieved July 2, 2022, from

Moyé, D. M., Danielle M. Moyé From the Division of Cardiology, Dyer, A. K., Adrian K. Dyer From the Division of Cardiology, Thankavel, P. P., Poonam P. Thankavel From the Division of Cardiology, & The Data Supplement is available at to Poonam Punjwani Thankavel. (2015, March 1). Myocardial contusion in an 8-year-old boy. Circulation: Cardiovascular Imaging. Retrieved July 2, 2022, from

Sybrandy, K. C., Cramer, M. J. M., & Burgersdijk, C. (2003, May). Diagnosing cardiac contusion: Old Wisdom and new insights. Heart (British Cardiac Society). Retrieved July 2, 2022, from 

MY Comment by KEN GRAUER, MD (8/6/2022):
Excellent review by Drs. Yde and Meyers — regarding multi-trauma with resultant Cardiac ContusionI focus my comment on a number of additional specific aspects of the serial ECGs obtained in today's case.

As per Drs. Yde and Meyers — the ECG is less than optimally sensitive for detecting cardiac injury following blunt trauma. This is because the anterior anatomic position of the RV (Right Ventricle), and its immediate proximity to the sternum — makes the RV much more susceptible to blunt trauma injury than the LV. But because of the much greater electrical mass of the LV — electrical activity (and therefore ECG abnormalities) from the much smaller and thinner RV are more difficult to detect. To REVIEW (Sybrandy et al: Heart 89:485-489, 2003 — Alborzi et al: J The Univ Heart Ctr 11:49-54, 2016 — and Valle-Alonso et al: Rev Med Hosp Gen Méx 81:41-46, 2018) — ECG findings commonly reported in association with Cardiac Contusion include the following:
  • None (ie, The ECG may be normal — such that not seeing any ECG abnormalities does not rule out the possibility of cardiac contusion).
  • Sinus Tachycardia (common in any trauma patient ...).
  • Other Arrhythmias (PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib).
  • RBBB (as by far the most common conduction defect — owing to the more vulnerable anatomic location of the RV). Fascicular blocks and LBBB are less commonly seen.
  • Signs of Myocardial Injury (ie, Q waves, ST elevation and/or depression — with these findings suggesting LV involvement).
  • QTc prolongation.

  • NOTE: Prediction of cardiac contusion "severity" on the basis of cardiac arrhythmias and ECG findings — is an imperfect science.

Additional KEY Points:
Despite the predominance for RV (rather than LV) injury — use of a right-sided V4R lead has not been shown to be helpful compared to use of a standard 12-lead ECG for detecting ECG abnormalities.
  • In addition to ECG abnormalities related to the blunt trauma of cardiac contusion itself — Keep in mind the possibility of other forms of cardiac injury in these patients (ie, valvular injury, aortic dissection, septal rupture) — as well as the possibility of a primary cardiac event (ie, acute MI may have been the cause of an accident that led up to the trauma).
  • ECG abnormalities may be delayed — so repeating the ECG if the 1st tracing is normal is appropriate when concerned about severe traumatic injury.
  • That said (as per Drs. Yde and Meyers) — IF troponin is normal at 4-6 hours and IF the ECG is normal — then the risk of cardiac complications is extremely low.

How Did YOU Interpret the Initial ECG?
I found the initial ECG in today's case extremely interesting. Clearly, this patient with severe multi-trauma following a motor vehicle accident suffered a cardiac contusion — confirmed by the presence of obvious ECG abnormalities and marked troponin elevation.
  • While the literature acknowledges the difficulty trying to predict "severity" of cardiac contusion from ECG findings — there are a number of concerning ECG abnormalities present in the initial tracing (Figure-1).

Figure-1: I've reproduced and labeled the initial ECG in today's case.

MY Thoughts on the Initial ECG:
  • The rhythm in ECG #1 is sinus (RED arrow in lead II— at a rate of ~90/minute. 
  • The PR interval looks to be slightly prolonged (especially considering the relatively rapid rate). Among the conduction defects seen with cardiac contusion is 1st-degree AV block.
  • The QRS complex is widened — and the predominantly wide qR pattern in lead V1, in association with the wide terminal S wave in lead I — is diagnostic of RBBB (Right Bundle Branch Block).

  • NOTE: The ECG in Figure-1 provides an excellent example of how QRS width may vary depending on which lead is being looked at. I've added vertical time lines to clarify the beginning and end of the QRS complex (RED and PURPLE dotted lines, respectively). Despite obvious QRS widening — Note how narrow the QRS looks in simultaneously-recorded lead II, due to the fact that much of the last part of the QRS in this lead lies on the baseline.

  • The QRS appears to be very wide and fragmented in leads V1,V2,V3. While I did not find literature to support this degree of widening and amorphous QRS morphology as a predictive factor of cardiac contusion severity — I thought the observation over serial tracings of progressive QRS narrowing, with return to a more normal triphasic RBBB morphology supported the concern regarding this initial tracing.
  • Additional evidence of abnormal ECG findings in Figure-1 was present in the form of: i) Deep Q waves in leads III and aVF; ii) Overly peaked (hyperacute?) T waves in leads I, II, aVL and aVF; andiii) Excessive ST-T wave depression in the anterior leads (that clearly exceeds that expected with simple RBBB).

  • Did YOU notice how atypical the lateral chest leads are for RBBB? (QRS complexes within the dotted BLUE rectangles). Normally with RBBB — lateral chest leads show an upright R wave with a wide terminal S wave — and not persistence of similar-looking triphasic-notched complexes with persistent ST-T wave depression. I suspect the reason for this atypical QRST morphology in leads V4,V5,V6 — is that electrode lead placement had to be altered in this patient with multi-thoracic traumatic injuries requiring chest tubes, splinting, bandages, etc. NOTE: The relevance of recognizing this atypical RBBB morphology relates to its potential effect on comparing serial ECGs.

  • Did YOU notice the prominent J waves (? Osborn waves) in the inferior leads? There is also prominent negative notching in leads I and aVL (BLUE arrows in the limb leads). We've previously noted how such prominent J waves may be seen not only with hypothermia — but also with other conditions, including myocardial ischemia — and that ischemia-induced J-waves have been found to increase the risk of developing malignant ventricular arrhythmias (See My Comment in the September 23, 2020 post of Dr. Smith's ECG Blog)
  • J waves have also been shown to be a marker of significant increased risk following penetrating cardiac trauma (Nicol and Navsaria: J Injury 45:112-115, 2014)
  • Regardless of whether you call these deflections prominent J waves or Osborn waves — I found it "telling" that these deflections were present in both of the first 2 ECGs done in today's case — that an episode of presumed VT, followed by significant bradycardia was seen shortly thereafter in the OR — but that these J-point deflections were no longer seen in the last 3 ECGs (which were done after those life-threatening arrhythmias resolved).

What Happened on Serial ECGs?
I've selected 3 of the 5 ECGs from today's case with the goal of highlighting the evolution of ECGs changes that developed over the course of this patient's hospital admission (Figure-2).

Figure-2: Comparison between 3 of the 5 ECGs recorded in today's case.

MY Thoughts on these Serial ECGs:
I found it interesting to trace progressive improvement of ECG abnormalities over the course of this patient's hospital admission:
  • I've already discussed the notable findings in ECG #1.

  • ECG #3 — was obtained following the episode of presumed VT and marked bradycardia that necessitated stopping the operative procedure. Compared to ECG #1, there is now: i) AFib with a PVC; ii) Some narrowing of the QRS, with appearance of a more distinct triphasic complex in anterior leads (that is now much more typical of RBBB morphology); iii) Much less ST-T wave depression in the anterior leads; iv) Development of significant ST elevation in leads I and II (and to a lesser extent in leads aVL and aVF); v) Loss of the prominent J-point notching that was seen in ECG #1; andvi) A change in QRS morphology in the lateral chest leads that seems more consistent with an RBBB conduction defect (perhaps a result of improved electrode lead placement?).

  • ECG #4 (done on Hospital Day #6) — There is now: i) Return to normal sinus rhythm at a slower rate; ii) Further narrowing of the QRS — that is now consistent with an incomplete RBBB pattern; iii) Reduced size of the Q wave in lead III — with resolution of the Q wave in lead aVF; and iv) Continued improvement in ST-T wave abnormalities.

  • In SUMMARY: While the literature does not provide us with specific ECG criteria for assessing severity of cardiac contusion — today's case does provide insight as to how clinical correlation with serial ECGs can confirm that the patient is recovering. I thought it significant that this severely injured multi-trauma patient initially showed an extremely wide QRS (with RBBB and an amorphous QRS morphology) — that gradually narrowed and took on a more distinct RBBB morphology (with eventual resolution of the conduction defect). Along the way — the patient manifested ST-T wave elevation and depression, changing size of Q waves, and a series of rhythm changes (VT, bradycardia, AFib, PVCs) — with eventual improvement of all these ECG findings that corresponded with his progressive recovery.

Wednesday, August 3, 2022

What happens if you don't recognize Hyperacute T-waves?

The origin of these ECGs cannot be revealed.  

Time 0:

Sinus rhythm with an intraventricular conduction delay (QRS is about 120 ms)

Hyperacute T-waves in V2-V5, Diagnostic of Proximal LAD occlusion, but without ANY ST Elevation except for less than 1 mm in aVL, and 0.25 mm in lead I.

There is also minimal STE in aVL with reciprocal STD in II, III, aVF.

Notice that there is plenty of R-wave in V2 and V3.

This should be an obvious case of acute proximal LAD Occlusion.  However, it was missed.

In this, case the Hyperacute T-waves are preceded by subtle ST Depression in V2 and V3.  Thus, they are specifically the hyperacute T-waves called "de Winter's T-waves."

Note that hyperacute T-waves are not just tall.  In fact, they frequently are NOT tall.  They are "bulky" and this bulk is always in proportion to the QRS.

"Bulk" is a result of the area under the curve (AUC), in proportion to the QRS amplitude/AUC.

Such high AUC is a result of:
1) JT interval (total duration of T-wave)
2) Degree of upward concavity
3) Symmetry
4) Amplitude

Old ECG:

Ventricular Paced Rhythm with some native beats which show inferior OMI.  
(There is a also a pacer spike in the midst of the native QRS -- it comes to late to pace the ventricle)
The paced beats in V2 and V3 show posterior OMI

3 hours:

T-waves remain hyperacute, but not as tall.  
Q-waves developing in V2-V4 and aVL.  
QS-wave in V2.

12 hours:

T-waves slightly less prominent
Q-waves definite

21 hours

T-waves much less prominent, which is evidence that there is less viable ischemic myocardium.
It is possible that there is some reperfusion as etiology of resolving ST Elevation.  Evidence for this is the abrupt downturn of the T-wave. 
But any reperfusion is AFTER significant myocardial loss, as evidenced by QS-wave in V2 and new QR-wave in V3

I do not have the corresponding angiogram, troponins, echo.  But these ECGs definitively show the irreversible loss of myocardium that happens if Hyperacute T-waves go unrecognized.  They are a definite sign of OMI, and if the patient does not have reperfusion (either by lucky spontaneous reperfusion or by intervention), then lots of myocardium will be lost.

Result: lots of lost myocardium.

See here for many examples of hyperacute T-waves:

Comment by KEN GRAUER, MD (8/3/2022):
An important part of the process of assessing serial ECGs — is comparison with a prior ("baseline" ) tracing. The goal of determining which changes are new was instantly evident in today's case by review of the old ECG ( = the 2nd ECG shown above in Dr. Smith's discussion of this patient's serial tracings).

I found the Old ECG in today's case to be fascinating — so I focus my comment on its analysis. For clarity — I've reproduced this 2nd tracing in Figure-1. At the time this Old ECG was done — the patient had a pacemaker. As per Dr. Smith — the rhythm in ECG #2 shows intermittent ventricular pacing with evidence of infero-postero infarction at some point in time.

No clinical information was available in association with the ECG in Figure-1. All we know — is that this ECG was recorded at some point in the past.
  • How would you date the infarction in Figure-1?
  • Is the pacemaker functioning appropriately?
  • What is the underlying cardiac rhythm? (ie, WHY do you think the pacemaker was needed?).

Figure-1: The previous ECG in today's case. (To improve visualization — I've digitized the original ECG using PMcardio).

MY Thoughts on the Old ECG:
The art and science of cardiac pacing continues with breathtaking advances. It is no longer easy (or even possible) to fully assess pacemaker function solely from the ECG without knowledge of pacing specifications for that particular patient. That said — we often can get a quick idea as to how a pacemaker is functioning, especially when one or more spontaneous beats are present. For the ECG that appears in Figure-1 — there is more to be learned!
  • The "good news" — is that modern pacemakers can be interrogated remotely by means of a wireless, telemetered, external programming device (Brief review by Safavi-Naeini and Saeed — Texas Heart Inst J 43:415-418, 2016 on the basics of pacemaker troubleshooting).
  • The 2nd piece of "good news" — is that modern pacemakers are truly amazing devices with an astonishing performance record. Pacemaker malfunction does occur (and it is important to recognize this when it happens) — but most of the time, the pacemaker will be right! So I generally begin my assessment of pacemaker tracings with the mindset that even when I see unusual or unexpected findings — there may be a physiologic reason for why the pacemaker is appropriately functioning in this way (the details of which can then be sorted out when the pacemaker is interrogated).

Assessing the Pacemaker:

In Figure-2 — I've labeled the long lead II rhythm strip from ECG #2.

  • RED arrows in Figure-2 reveal that there is an underlying regular sinus rhythm in ECG #2. Note that the PR interval that precedes each of the narrow beats (ie, beats #1, 4, 7) is the same! Therefore — beats #14 and 7 are sinus-conducted (albeit with a prolonged PR interval of 0.24 second = 1st-degree AV block).
  • The vertical PINK lines in Figure-2 highlight pacemaker spikes. The fact that wide, paced complexes immediately follow pacemaker spikes to produce beats #2,3; 5,6; and 8 — confirms that there is at least some ventricular capture!
  • The R-R interval of the first 3 pacemaker spikes is 6 large boxes. This corresponds to a pacing rate of 50/minute — which presumably is the rate the pacer was set at to fire if no spontaneous beats are sensed.

WHY does the 4th pacer spike occur early?
  • Note that beat #4 is a spontaneous sinus-conducted beat! If the pacemaker was only sensing the QRS — then we would not see this 4th pacemaker spike that occurs just after beat #4!
  • As stated a moment ago — spontaneous beats in Figure-2 are conducting with a prolonged PR interval. So it must be that the reason the 4th pacer spike in Figure-2 occurs early — is that there is dual chamber pacing (of both atria and ventricles) — and since no QRS complex was sensed after 0.23 second at this point in the cardiac cycle, the pacemaker fired. The 7th pacer spike in Figure-2 also occurs early for the same reason. This implies that the pacemaker is appropriately sensing the atria. (Simple adjustment could reprogram the pacer to accept a slightly longer PR interval before firing).
  • That the pacer is appropriately sensing the ventricles — is evident from the 5th pacer spike — which once again waits the programmed amount of 6 large boxes after the previous pacer spike before firing. This provides the patient with a guaranteed ventricular rate of at least 50/minute — while still providing adequate opportunity for spontaneous conduction to occur.

Figure-2: I've labeled P waves (RED arrows) and the pacemaker spikes (PINK lines) that are seen in the long lead II rhythm strip from ECG #2.

How to "Date" the Infarction in Figure-1?
Now that we've determined from Figure-2 that beats #1, 4 and 7 are spontaneously conducted — We can return to Figure-1 to assess QRS morphology of these sinus-conducted beats.

  • Focusing on beat #1 in leads II and III — reveals a large Q wave in lead III. The ST-T wave of these beats (as well as the ST-T for sinus-conducted beat #4 in lead aVF) looks hyperacute, albeit without frank ST elevation.
  • Sinus-conducted beat #4 in lead aVL manifests reciprocal change (ie, mirror-image opposite ST-T wave depression — compared to the ST-T wave appearance in lead III). This suggests a recent inferior OMI (perhaps just after the stage of ST elevation). The hint of terminal T wave positivity in aVL (and of beginning T wave inversion in the inferior leads) may portend reperfusion.
  • No spontaneous beats are seen corresponding to the 2 QRS complexes in leads V1,V2,V3 — but ST-T wave morphology of paced beats #5 and 6 suggests abnormal ST segment flattening with excessive T wave peaking (that is also seen for beat #8 in lead V4). I interpreted this ST-T wave appearance as indicative of posterior OMI reperfusion T waves.

  • BOTTOM Line: My hunch is that there was a recent infero-postero OMI — and that we are now see reperfusion changes.

What is the Underlying Rhythm in Figure-1?
So WHY was the pacemaker needed for ECG-2? The answer to this is best explained by laddergram (Figure-3):

  • For clarity — I labeled the sinus-conducted P waves in Figure-3 with RED arrows.
  • YELLOW arrows highlight those P waves that are not conducted. Since some P waves are conducted but others aren't — some form of 2nd-degree AV block is present.

  • PEARL: Since we know this patient has just had an infero-postero OMI — and there is group beating with sinus-conducted beats that manifest a narrow QRS with 1st-degree AV block — the odds are overwhelming that the type of conduction disturbance will turn out to be 2nd-degree AV block of the Mobitz I Type ( = AV Wenckebach)!

  • GREEN arrows highlight non-conducted P waves that do not have a "chance" to conduct — because they either occur just before or just after paced beats.
  • The small BLUE circles at the bottom of the laddergram correspond to pacer spikes. As already noted — the pacer spikes that appear just after sinus-conducted beats #1, 4 and 7 are appropriately sensing the preceding P wave — but do not pace the ventricles because of sinus conduction.

  • BOTTOM Line: It is impossible to tell IF the GREEN arrow P waves would be able to conduct if given a chance to do so (which is why I added ??? in the AV nodal Tier of the laddergram). That said — as per the above Pearl — statistical odds overwhelmingly favor Mobitz I 2nd-degree AV block as the conduction disturbance — with the "good news" that AV Wenckebach in this setting often resolves as the patient's condition stabilizes.

Figure-3: My proposed laddergram for the rhythm in ECG #2 from Figure-1.

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