Wednesday, January 13, 2021

A 47-year-old man with abdominal pain and heart rates approaching 300 bpm

 Written by Pendell Meyers


A 47-year-old man with known WPW syndrome presented to the ED complaining of left abdominal pain, diarrhea, and chills. He denied palpitations, but is found to have a heart rate of 170 bpm at triage. He states that he occasionally has episodes of tachycardia which usually lasts about 1 hour, which he was instructed to "ride out at home unless they persist."  Other than his heart rate, his other vitals were within normal limits, and the patient did not show any signs of compromised cardiac output or distress.


Here is his initial ECG:

What do you think?




The ECG shows an irregularly irregular polymorphic tachycardia at approximately 186 bpm. Occasional beats are conducted with narrow, normal morphology, but most are conducted aberrantly with a nonspecific intraventricular conduction delay pattern, which is not actually very wide despite the abnormal conduction. While most of the abnormally conducted beats have the same morphology, the morphology becomes more polymorphic when the rate increases, as seen twice during this ECG, with lead V1 best demonstrating significantly different morphology between QRS complexes. Several beats are conducted at approximately 300 msec after the previous beat, which is extremely unlikely to be the result of a normal AV node conduction.

Because it is irregularly irregular, polymorphic, and has R-R intervals approaching less than 300 msec, the diagnosis is atrial fibrillation with WPW (also called pre-excited atrial fibrillation) until proven otherwise.

Here is his baseline ECG:

Sinus rhythm with very short PR interval and subtle delta waves. The QRS morphology matches the most common beats in the presentation ECG above, implying that this is his most common QRS pattern as a result of simultaneous activation via the AV node and accessory pathways.



Although the patient remained clinically stable and never showed any signs of distress or shock, his heart rate gradually accelerated over the course of the next 30 minutes.  He never showed any signs of deterioration, and cardioversion was not attempted. All nodal blockers (BB, CCBs, amiodarone, adenosine) were avoided.

A repeat ECG was performed:

Extremely rapid rates, approaching 260-280 bpm. It is technically polymorphic (again V1 is most clear), although I must say it is slightly less polymorphic than other examples of AF + WPW that I have seen at rates like this. It is also still irregularly irregular, so it must still be AF.


We (Smith and Meyers) believe that the best course of action for this persistent dysrhythmia at a rate of nearly 280 bpm, even if the patient is not clinically unstable, is probably just to perform synchronized cardioversion at this time, without waiting for infusions such as ibutilide or procainamide. Dysrhythmias like this which are persistent at such high rates and polymorphic have a high chance of deterioration into VT/VF. We would give etomidate and perform synchronized cardioversion for this. In my practice, it takes a significant amount of time to actually obtain and administer ibutilide or procainamide. If it recurs after cardioversion, of course an infusion will be required.

In this case, however, electrical cardioversion was not performed and the patient did not deteriorate.

Cardiology advised starting ibutilide (a class III antidysrhythmic medication which blocks K channels, increasing the duration of the refractory period, which inhibits conduction and propagation of dysrhythmias). Procainamide (a class Ia Na channel blocker) would also have been reasonable.

Ibutilide was started, followed by conversion to sinus rhythm approximately 20 minutes later.


Here is his repeat ECG:

Sinus rhythm similar to baseline ECG.


The patient was admitted for observation and treatment of the underlying illness.


Learning Points:

Irregularly irregular polymorphic (usually wide, but not always greater than 120 msec) tachycardia should be assumed to be atrial fibrillation with WPW until proven otherwise.

Adenosine should never be given to any rhythm that is irregular or polymorphic.

Any AV nodal blocker is considered contraindicated in AF with WPW for fear of enhancing conduction through the bypass tract, which theoretically could result in deterioration of the rhythm.

Unstable patients should be cardioverted. For stable patients, procainamide or ibutilide are both accepted pharmacologic agents for this scenario. Synchronized cardioversion with sedation is a reasonable and safe option as well, however it would not be appropriate if the rhythm is intermittently terminating and recurring (because it will simply recur after your cardioversion). Even for seemingly stable patients, the greater the heart rate and more polymorphic the QRS, the more likely the rhythm will deteriorate, and the more appropriate synchronized cardioversion becomes.

Please refer to our tachycardia algorithm (found on our "teaching images" tab: http://hqmeded-ecg.blogspot.com/p/teaching-images.html), and/or our EMRAP Corependium chapter on Tachydysrhythmias for more information.

See other examples of this rare rhythm here:

A Clinical Scenario to Recognize- Irregular WCT



Monday, January 11, 2021

A wide complex tachycardia

Submitted by Van Wall M.D., Written by Pendell Meyers


Let's go back to the basics for a common and classic scenario.

A middle-aged patient presents with shortness of breath and palpitations. The patient was stable without signs of low cardiac output or distress. Her ECG is shown below (first see what you think without using the baseline): 

What do you think?






There is a (minimally) wide complex, regular monomorphic tachycardia at a little faster than 150 bpm. I measure the QRS duration at almost exactly 120 ms. The differential would include ventricular tachycardia, any cause of narrow complex regular tachycardia plus added conduction aberrancy (such as a bundle branch block), or other causes of QRS widening like hyperkalemia or sodium channel blockade. Of course, the interpreter should always start by assuming that a wide complex monomorphic tachycardia is due to ventricular tachycardia and/or life threatening hyperkalemia, until proven otherwise.

This demonstrates why it is so important to be able to recognize RBBB, LBBB, and paced rhythms (pacer spikes) so quickly. This ECG has perfect RBBB morphology, one of the rare times that we can be confident that a regular wide complex rhythm is not classic ventricular tachycardia. 

For more discussion on features of SVT vs. VT, see these prior posts:





A prior baseline showing identical RBBB morphology during sinus rhythm would prove this definitively. 


Here is the prior baseline ECG on file:

This shows the same RBBB morphology in sinus rhythm.



They applied Lewis leads to see if they could get a better look at the atrial rhythm:

I can't say that I see clear atrial activity.



They gave 12 mg adenosine (a perfectly reasonable and guideline-endorsed option for any rhythm that is regular and monomorphic, regardless of QRS width):



Flutter waves are revealed.

The rhythm soon returned to 2:1 atrial flutter, of course. The patient was then rate controlled and did well.


Learning Points:

Assume that wide complex regular tachycardia is VT and/or hyperkalemia. Then work backwards and prove that assumption false, if possible. VT is more likely statistically, and the likelihood of VT increases further with age, cardiac pathology, and QRS duration.

Recognizing classic RBBB or LBBB morphology may enable the diagnosis of SVT with aberrancy. This can be basically definite if the morphology is shown to be identical to prior known RBBB or LBBB morphology on baseline ECG.

Adenosine is contraindicated in irregular or polymorphic QRS complex rhythms. It is not contraindicated for wide complex regular monomorphic tachycardia, and is very reasonable in this scenario.


Friday, January 8, 2021

Acute chest pain, ST Depression in V2 and V3, relief with Nitroglycerine, "normal" coronaries, and apical ballooning. Is it takotsubo?

This was submitted by Michael Fischer, one of our outstanding 2nd year EM residents at Hennepin Healthcare.

Case

A previously healthy female in her 40s presented 1 hour after abrupt onset 10/10 crushing chest pain that started while brushing her hair that morning. The pain radiated to her bilateral jaw and right shoulder, and did not seem to be exertional or pleuritic in nature.  

 

Here is her pre-hospital ECG: 



What do you think?












Smith: V2 and V3 have some minimal ST depression with downsloping.  This is highly suggestive of posterior MI.



This was read by EMS as non-specific. Aspirin 324mg was given by EMS. Nitroglycerin spray x3 was also given which brought her pain down to 3/10 upon arrival to the ED. She was vitally stable with systolic BP of 140s. No cardiac history, not taking any medications, but does have 1st degree relatives with CAD.  

 

Here is her first ED ECG:


The ST Depression is more pronounced, and has extended to V4







This was interpreted as ST-depression in V2-V4. Additional sublingual nitro was given x2, bringing her pain to 0/10 in her chest, however she still had pain in her jaw.  

 

Given the abrupt onset of pain, aortic pathology was also a concern. Bedside echocardiography revealed grossly intact left ventricular function, non-dilated aortic root. Suprasternal view of the aorta revealed normal caliber aorta with no obvious dissection flap. Upper extremity pulses were equal. D-dimer was sent as further rule out for dissection.  

 

A repeat ECG was obtained with her chest pain resolved after nitroglycerin: 


Almost completely resolved




This was interpreted as resolved anterior ST-depression. 

 

Over the course of the next 30 minutes while labs were pending, her chest pain slowly returned. Her troponin returned at 0.682 ng/mL (upper reference limit of 0.045 ng/mL), D-dimer negative. At this point, interventional cardiology was consulted and recommended medical management with plan for the catheterization lab that afternoon. She remained vitally stable with systolic BP in the 130-140s. She was started on a nitro drip and was heparinized.  

 

Her chest pain continued to wax and wane on the nitro infusion. She additionally received hydromorphone and ondansetron. Interventional cardiology was consulted again regarding her waxing and waning pain, at which time they took the patient to the catheterization lab.  

 

Given her rapid improvement on nitro, it was thought that her symptoms could be due to coronary vasospasm given her overall lack of CAD risk factors. Ruptured plaque and coronary dissection remained leading differentials as well.  

 

Angiogram report: 

Normal coronary arteries.  

Left ventriculogram demonstrated apical ballooning and hypercontractile base consistent with stress-induced cardiomyopathy.  

 

Takotsubo Cardiomyopathy- The Great Imitator! 

As previously discussed in this blog, Takostubo cardiomyopathy may manifest as T-wave inversion or ST elevation that can mimic a STEMI. This patient’s ECG with anterior ST depression is an atypical ECG presentation in takotsubo, and diagnostic of posterior MI, prompting angiography to rule out acute coronary occlusion.  


On chart review, there was no inciting stressor thought to precede her symptoms. She did well and was discharged on an ACE-inhibitor and beta-blocker. 


Smith comment: This ECG is very unusual for takotsubo.  And although it correlates mostly closely with posterior transmural ischemia (posterior STEMI), it would not be unusual for subendocardial ischemia due to LAD spasm or LAD subtotal thrombosis.  Thus, I am not entirely convinced of takotsubo in this case.  


All management was appropriate.  The cath lab certainly needed activation.  The coronaries were clean.  There was apical ballooning on ventriculogram.  


However, the cath report does not mention whether the LAD wraps around to the inferior wall, and there was no intravascular ultrasound (IVUS) to prove absence of ruptured plaque that does not manifest on plain angiogram (which only shows the lumen of the artery and, unlike IVUS, does not show extraluminal plaque).


Moreover, the onset of chest pain was without inciting event, as usually happens with takotsubo, and was relieved with nitroglycerin, which strongly suggests some element of coronary ischemia.


Thus, we may never know whether this was LAD ACS, LAD spasm, or a very strange sort of takotsubo.


Monday, January 4, 2021

ECG with Aslanger's Pattern. CT Pulmonary Angiogram Reveals LAD Ischemia (Septal Transmural). But this is not Contradictory.

A 52 y.o. male presented with persistent central chest pressure, without radiation, SOB or diaphoresis, which began at rest approximately one hour prior to arrival.   He had never had pain like this before.  He felt slightly nauseous earlier but no vomiting.  He is denying any back pain or abdominal pain.  

An ECG was recorded during pain:

What do you think?








This shows significant ST depression in I, II, and V4-V6, with reciprocal ST Elevation in aVR.  This suggests diffuse subendocardial ischemia.  

However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1.  These suggest inferior OMI with possible RV involvement.

Both of these patterns together suggest Aslanger's pattern, recently published in J Electrocardiology: A new electrocardiographic pattern indicating inferior myocardial infarction.  https://pubmed.ncbi.nlm.nih.gov/32526537/

This newly recognized ECG pattern is defined as "(1) any STE in III, but not in other inferior leads, (2) STD in any of leads V4 to V6, (but not in V2) with a positive or terminally positive T-wave, (3) ST in lead V1 higher than ST in V2."  

One might argue that this case does not apply because of the ST depression in V2, but 1) V2 is probably misplaced and 2) it is not enough ST depression to negate the rule.

Here, we will ignore lead V2 because it doesn't make any sense at all: the R/S ratio is higher than in either V1 or V3, which suggests misplacement.

Here is an illustration of the ST vector in Aslanger's pattern:

The label of leads II and III are reversed -- Sorry

The right side of the inferior wall manifests ST Elevation, resulting in an ST vector directly to the right. Thus, even though there is inferior OMI, there is no STE in II or aVF, only in III.  Moreover, this means there will be MORE reciprocal STD in lead I than in lead aVL, and this is indeed the case with our ECG above.  If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.  With the ST vector all to the right, the only leads with ST Elevation are III, aVR and V1.

Thus, this pattern was associated with simultaneous inferior MI AND diffuse ischemia due to LAD, Left Main, or 3 vessel disease.

HOWEVER, there is yet another entity which could produce this, and it is transmural septal ischemia.  Could this be Septal STEMI (STE in V1 and aVR, with reciprocal ST depression in V4-V6?), with ADDED STE in III?  

Aslanger added in the limitations in his article: 

"Theoretically, an isolated basal inferoseptal infarction or an acute inferior MI in the presence of previous infarctions that may change the orientation of lesion vector can also cause a similar picture. Lastly, this pattern may represent a chronic change from a previous ischemic insult as seen in a limited number of the patients in the control group".

Vectors

In diffuse subendocardial ischemia, which when due to ACS, is usually from LAD or Left Main insufficiency, all walls would have a negative vector pointing from the endocardium to the epicardium (positive vector from epicardium to endocardium, the opposite of OMI).  Since there is no ventricular wall at the top ("base") of the heart (there are only atria), then the addition of all those negative vectors points towards the apex; if the entire heart has subendocardial ischemia, then the ST depression vector points towards the apex (II, V5), with a reciprocal STE vector towards aVR (and even V1).   

In Septal STEMI, transmural ischemia of the septum is recorded by the overlying lead V1 as ST Elevation.  aVR is similarly (but not exactly) placed and can show STE.  Lead III is also on the right and might manifest ST Elevation in Septal STEMI.

It is important to remember that the ST depression of subendocardial ischemia does not localize.  Here, the ST depression is in "lateral" leads, but this does not mean there is "lateral" ischemia.  It may either be reciprocal to Septal STEMI, or due to subendocardial ischemia from the LAD insufficiency.

Case Continued

Bedside ultrasound was performed:

This shows an anterior wall motion abnormality, and highly suggests the LAD as the infarct artery.  Often patients with subendocardial ischemia on the ECG do NOT have a wall motion abnormality, which contrasts with patients with OMI/STEMI who always have a wall motion abnormality, at least if the echo is of high enough quality and uses bubble contrast.

The patient was slightly tachypneic and mildly hypoxic in the stabilization room and therefore the physicians obtained a CT pulmonary angiogram as well as aortogram to rule out dissection and PE.

The initial Abbott hs troponin I returned at 52 ng/L (Upper reference limit for males is less than or equal to 34 ng/L).  FYI: 52 ng/L is the threshold for "rule in" by European studies as it has a high positive predictive value in the setting of chest pain.

The D dimer was undetectable, so CTPA was probably unnecessary, but it did have interesting findings:

Top left: conventional CT.  

Top right is colored iodine overlay; Blue areas of myocardium are ischemia.  

Bottom left is plain iodine map.  

Bottom right is low Kilo Electron Volt image which brings out iodine.  See the 2 very dark areas, one in the septum and one near the apex.  Notice that they correlate with blue on the colored spectral CT (blue is ischemia on spectral CT).

These areas of hypoperfusion are in the septum and apexstrongly suggesting LAD ischemia.  In addition, they are indeed transmural!

This CT interpretation was made with moderate certainty

Contrast this CT transmural ischemia here with this CT subendocardial ischemia. 


Below we can see a coronal image of the heart:

Notice the inferior wall (lower part of image) is subtly transmurally darker than the remainder.
If prospectively interpreted in blinded fashion, this is not definitively diagnostic, according to our CT Guru, Gopal Punjabi (https://twitter.com/CtSpectral)
This suggests inferior OMI but is by no means diagnostic.


Case continued

The patient was placed on a nitroglycerin drip and chest pain gradually resolved.  The emergency medicine faculty spoke directly with cardiology faculty and the decision was made to activate the cath lab via "pathway B."  (Our "Pathway A" is for clear STEMI; "Pathway B" is intensive evaluation and discussion for patients who might need the cath lab emergently for possible OMI, but it is not as clear as with STEMI).  The patient was subsequently given 5000 units of heparin, 180 mg of ticagrelor, and defib pads were placed on the patient in the event that he should have a cardiac arrest. 

Angiogram

Culprit Lesion: 90% mid LAD stenosis with evidence of plaque rupture, TIMI III flow on angiography.

Troponin profile:

Unfortunately, they were not measured to peak, which would help determine if this was indeed Septal STEMI or Non-Occlusive Subendocardial Ischemia.


ECG after PCI:

Left axis deviation, but otherwise normal


Formal Echo:

The estimated left ventricular ejection fraction is 71%.

There is no left ventricular wall motion abnormality identified.

So the wall motion has recovered (remember we showed a definite WMA during the ischemia).  Such quick recovery is uncommon in STEMI/OMI unless there is very quick reperfusion.  If this case was indeed OMI, then there was very fast spontaneous reperfusion, as in indicated by the open artery with TIMI III flow.  When reperfusion is not so fast, wall motion recovery may require many days to weeks.  When recovery is delayed, it is often called "myocardial stunning."


Wednesday, December 30, 2020

Chest pain after motor vehicle collision with an abnormal ECG - blunt cardiac injury? OMI? normal variant?

Submitted and written by Morgan Penzler MD, with edits by Pendell Meyers


A man in his early 40s with no significant past medical history was involved in a motor vehicle collision, in which another car struck his driver's side at high speed after running a red light. He was seat-belted, and both side and front airbags deployed. The patient had no symptoms preceding the collision. He required complex extrication from the vehicle by EMS. He was immediately taken to the nearest emergency department, where he had normal vital signs but was complaining of worsening left sided and substernal chest pain. Trauma workup revealed multiple left rib fractures, a small left pneumothorax, a moderate splenic laceration, and some minor pelvic fractures.

The patient reported worsening chest pain, and so an ECG and troponin were ordered.

Here is the initial ECG at 1723:

What do you think? 







Annotated with J points identified in all leads



The ECG shows sinus rhythm with RBBB. The ST segments and T waves are abnormal for RBBB, because there is STE in II, III, aVF, V5 and V6. The STE is concordant in III and aVF. Interestingly, there is no reciprocal STD in aVL. There are large volume T waves in the same leads that are concerning for hyperacute T waves. Overall, this ECG is concerning for lateral and inferior (or apical) OMI. If the RBBB is new, this would be another feature concerning for LAD occlusion (because the LAD supplies the RBB), or blunt cardiac injury in this setting.



Here is a normal (baseline) RBBB for reference:






Initial high sensitivity troponin I returned elevated at 51 ng/L (limit of detection = 6 ng/mL, URL = 12 ng/mL).

Beside echo reportedly showed no clear wall motion abnormalities (I would expect a formal contrast enhanced echo probably should show WMA).

The patient was given aspirin and fentanyl for pain. Given his traumatic injuries, as well as concerning ECG and elevated troponin with concern for blunt cardiac injury, he was transferred immediately to a tertiary care center with both trauma services as well as interventional cardiology.

The second troponin I resulted at 84 ng/L.


Another ECG was recorded at 1759:
I do not see much change. The STE in V4 is slightly greater.



On arrival to the ED at the tertiary care center, the patient complained of ongoing chest pain. An ECG was recorded at that time (1946):

Inferior leads show an obvious STEMI now. There is huge reciprocal STD in aVL now. New STE in V3, and progression of OMI in the lateral leads. STD in V2 would suggest posterior involvement.


Right sided leads were recorded at 2010:
Leads V4-V6 appear to be on the right chest now, and they show only a hint of STE in "V6." I can't be sure, but it appears to me that V3 has not been moved to V3E. In other words, I believe only V4-V6 have been moved to V4R-V6R. Normally, right sided leads should be fully reversed in V1-V6.


The ED team spoke immediately with the interventionalist, and they agreed that the patient should have immediate cardiac catheterization despite the traumatic mechanism and injuries. 

The angiogram revealed a dissection of the mid-LAD (a wraparound LAD) with acute thrombotic occlusion. The RCA was normal. During attempt to open the thrombotic occlusion, the patient suffered a catheter induced dissection of the left main and proximal LAD. The left main, proximal LAD, and mid LAD were all stented, with resultant TIMI 3 flow in all coronaries.

For platelet inhibition (while also in the setting of internal traumatic bleeding), they decided initially on IV cangrelor infusion which can be turned off quickly if need be. The plan was to switch to plavix after traumatic bleeding had been definitively controlled.

The patient was then transferred to interventional radiology for catheter-directed embolization of the splenic laceration.

Repeat troponins were 19,790 and 21,932, then no further troponins were ordered.


The patient had no further significant events during hospitalization and was discharged home on day 5.


Discussion:

Significant cardiac trauma occurs in approximately 10% of patients with severe blunt chest trauma. Isolated coronary artery dissection from blunt trauma is a very rare event. Traumatic dissections are most often seen in the LAD, followed by the RCA and LCX. It is thought that this is due to the relative anterior position of the LAD. 

The ECG is a report from the myocytes of their condition. They do not know the etiology of acute complete ischemia. No matter if its typical ACS, traumatic dissection causing acute occlusion, or spasm, it is the same result to the myocytes, and the same findings can be present on the ECG. 


References:

Allemeersch, G. J., Muylaert, C., & Nieboer, K. (2018). Traumatic Coronary Artery Dissection with Secondary Acute Myocardial Infarction after Blunt Thoracic Trauma. Journal of the Belgian Society of Radiology, 102(1), 4.

James et al.: Dissection of the left main coronary artery after blunt thoracic trauma: Case report and literature review. World Journal of Emergency Surgery 2010 5:21.

Nikparvar, M., Asghari, S. M., & Farshidi, H. (2019). Delayed diagnosis of myocardial infarction in a young man with a blunt chest trauma. Journal of cardiovascular and thoracic research11(3), 251–253. 

Saturday, December 26, 2020

A 50 year old man with sudden altered mental status and inferior STE. Would you give lytics? Yes, but not because of the ECG!

Submitted by Alex Bracey, written by Pendell Meyers

A man in his 50s was hunting with a friend when he suddenly "fell out" (similar to syncope), but then did not return to baseline, and instead had persistent altered mental status. His friend was able to get him into the truck and drive him to a nearby community hospital (non-PCI center). 

When he arrived, his mental status had deteriorated further, to the point that he was quickly intubated on arrival. After intubation, vital signs were all within normal limits. He was quickly rushed to the CT scanner and a noncontrast head CT was completely normal.

Side note: The differential of sudden persistent loss of consciousness with adequate hemodynamics is relatively short: seizure, intracranial hemorrhage, basilar artery occlusion. After a negative noncontrast head CT the next step is looking for a hyperdense basilar artery sign AND to perform a CT cerebral angiogram).

An ECG was recorded quickly on return to the ED:

(sorry for poor quality, cannot get originals)

What do you think?







There is a narrow complex regular rhythm at a rate of approximately 120 bpm. There is the appearance of STE in inferior leads II, III, and aVF (with STD in aVR), but this is entirely due to flutter waves which are only seen in those leads. 

Also, the atrial flutter in this case is relatively slow like in many other cases we've shown. Normal atrial size and conduction rate typically results in a flutter circuit of about 300 bpm, with 2:1 conduction causing resultant ventricular rate of about 150 bpm. Here the flutter rate is approximately 240 bpm, with ventricular rate around 120 bpm. This implies a large atrium, slowed conduction (due to, for instance, Na channel blocking agents), or both.

We have shown countless examples of this same phenomenon (atrial flutter mimicking inferior STE or STD). We have also shown several cases in which atrial flutter hides true, active ischemia.

Christmas Eve Special Gift!! Prehospital Cath Lab Activation: What do you think?




The treating team did not identify the flutter waves and they became worried about possible "STEMI" (despite the unusual clinical scenario). They called their transfer center cardiologist on call, who reviewed the case on the phone with them, as well as the ECG. The EM provider asked if the cardiologist thought it was a "STEMI." The cardiologist also did not see atrial flutter, and advised giving thrombolytics for perceived "inferior STEMI."

The patient received thrombolytics and then was transferred to the PCI referral center. 

On arrival to the PCI center's Emergency Department, the receiving team recorded an ECG on arrival:

Persistent atrial flutter, however this time the QRS occurs on a slightly different portion of the flutter wave. In my opinion this makes the flutter waves slightly easier to recognize in this ECG.


Atrial flutter was recognized at this time. On arrival, apparently the patients mental status was improved compared to his initial presentation, because he was noticed to be pulling at his tube and gagging, requiring sedation.

The case was reviewed by the receiving team who had concerns for acute stroke or other cause of acute altered mental status. 

A CT angiogram of the head and neck was performed which showed a basilar artery thrombus which was concerning for brainstem stroke as the inciting cause. There was again no intracranial hemorrhage. Serial troponins were negative. 

The patient was admitted for stroke management. No obvious adverse events were attributed to the thrombolytics. Long-term outcome is unknown.

Thus, it seems that two mistakes may have inadvertently led accidentally to the appropriate administration of thrombolytics!! They mistook atrial flutter for STEMI, and did not recognize the clinical presentation of basilar artery occlusion. Correct, but for the wrong reason!

So the answer to the title of this post is: "Yes, I have a patient with a devastating stroke, and I do not have neurointerventional capabilities, so I will give thrombolytics!"


Discussion

Flutter waves are well known to mimic ST deviations, as well as to hide true ischemic ST deviations from the interpreter. In many cases of flutter waves mimicking ST deviations, the expert electrocardiographer can see the morphology of the flutter waves as the cause of apparent STE or STD. Likewise, in some cases of ischemia concealed by flutter waves, the ischemia can be seen despite the flutter waves, whereas in other cases the dysrhythmia must be terminated before the ischemia can be clearly distinguished. 


Even when flutter waves conceal true ST segment deviations, the cause and effect relationship may be unclear. Tachycardia to this degree can cause ST segment changes in several ways. First, there can simply be diffuse STD (which obligates reciprocal STE in aVR) associated with tachycardia, which are not even necessarily indicative of ischemia. Second, the increased demand created by extreme tachycardia may exceed the ability of the coronary arteries to supply sufficient blood (due to preexisting three vessel or left main disease, with or without ACS). In this case, there is diffuse ischemic STD of subendocardial ischemia, of course with accompanying reciprocal STE in aVR. Finally, if a region of the myocardium supplied y a severely flow-limiting (but not necessarily fully occluded) lesion suddenly undergoes massively increased demand due to acute tachycardia, the supply-demand mismatch may be so great that the tissue undergoes acute transmural ischemia, both subendocardial and subepicardial, which may result in infarction (just as in the case of classic thrombotic occlusion MI). This case represents the same physiologic event as OMI in terms of the result on the myocardium, therefore with identical ECG features, however, ACS may not even be present.







Wednesday, December 23, 2020

ST Depression Maximal in V1-V4 and Angio shows 3 Vessel Disease. Is it posterior? Which is the culprit?

A 70-something woman had acute chest pain.

The ECG was texted to me with the words: "Acute chest pain. Could this be posterior MI? What do you make of the ST depression in V4-V6?"

What do you think?














My response: "The ST depression is maximal in V1-V4.  This is most consistent with a posterior MI.  If it sounds clinically like acute MI then this is good for activating the cath lab."

Her response: "Yeah, I did activate.  But the cardiology fellow told me he was sure it would not be a posterior MI because of diffuse ST depression.  He suggested that we should have consulted cardiology rather than activating the cath lab, and treated this like a NonSTEMI."

My response: "That is not true.  It is possible that it is not posterior, but about 80-90% of the time it is posterior if the STD is maximal in V1-V4.  So if it turns out not to be, that does not mean he was right.  He was not right."

She did give nitroglycerine, and the pain improved but did not resolve, then recorded this ECG:
The ST depression persists but is not as profound


I did not know this at the time, but because of a widened mediastinum on CXR, they did a CT aortogram that was negative (I use one CT image below to illustrate "posterior" MI).

The first troponin I returned at 4100 ng/L -- quite high for a very acute MI, usually seen in subacute MI.

Angiographic findings (done approximately 150 minutes after 1st ECG):

Brisk, TIMI III flow into all coronaries. Severe distal vessel tortuosity and moderate left coronary calcium.

1. Left main: normal.

2. LAD: Type III. Long (~35 mm) moderately calcified 70% proximal to mid LAD stenosis.

      A diagonal branch distal to the stenosis has luminal irregularities.

3. LCX: Tortuous, mildly calcified with luminal irregularities in the proper vessel and a 80-90% stenosis in the proximal OM followed by a 70% stenosis downstream after two 90 degree bends. A smaller OM has luminal irregularities. 

4. RCA: Long (>35 mm), 70% mid RCA stenosis stenosis. It supplies a medium sized RPDA and small RPLA 


So there is severe 3 vessel disease, but all arteries are open with good flow.  This seems to imply that the fellow was correct in this case, but this is not true.  The arteries were clearly not all widely patent (open) at the time of ECG recording, 150 minutes earlier.  Spontaneous reperfusion with TIMI-3 (normal) flow is very common, occurring in up to 19% of proven STEMI (1).  When there is such full reperfusion of an occlusion (OMI), it makes it difficult to identify the culprit on angiogram unless there is clearly an ulcerated plaque on the angiogram, which apparently there was not, or the angiographer would have found it.

However, had the angiogram been done at exactly the same time as the first ECG, the culprit would have been apparent.

The fact that the proximal OM (obtuse marginal branch off the circumflex) had such a tight stenosis makes it a likely culprit for the acute plaque rupture, but not certain.

Furthermore, the arteries were "tortuous" (full of twists and turns) and so any PCI was going to be technically difficult, so it was deferred at that point in order to discuss Coronary Bypass surgery (CABG).

The troponin peaked over 21,000 ng/L. This is very high and a level more consistent with STEMI/OMI than with NonSTEMI, although there is quite a bit of overlap.  Most STEMI have troponin I over 10 ng/mL (roughly equivalent to 10,000 ng/L), and most NonSTEMI have troponin I below 10 ng/mL.  

The formal bubble contrast echocardiogram: "Findings are most consistent with ischemia/infarct in the diagonal and OM vascular territories."  This confirms Posterior MI.


The patient refused Bypass Surgery (CABG), and so was taken back for another angiogram and intervention.


2nd angiogram, with intervention:

Culprit Lesion (s): 80% stenosis of proximal OM1 in the setting of significant tortuosity.  Successful PCI of proximal OM stenosis.


All subsequent ECGs continued to have ST depression (not shown), suggesting a No Reflow phenomenon.  No further troponins were measured.


Learning points:
1. Precordial ST Depression, when maximal in V1-V4 (vs. V5-V6) is reciprocal to ST Elevation in the wall opposite those leads (i.e, posterior wall, which is now often and confusingly called "Lateral" -- see below) and indicates posterior OMI in 80-90% of cases.
2. Diffuse ST depression, maximal in II, V5 and V6 is more often due to diffuse subendocardial ischemia and has reciprocal ST Elevation in aVR.
3. Even when there is 3-vessel disease, one of them is usually the acute culprit, whether it can be identified or not.  Intervening can be hazardous however, which is one reason that CABG is often recommended.
4. 15-20% of OMI are reperfused by the time of the ECG.  A very high troponin (TnI over 10.0 ng/mL or 10,000 ng/L; TnT over 1.0 ng/mL or 1000 ng/L) can help to ascertain whether there was occlusion at the time of the ECG.  This is a crucial part of our ECG research -- when we assess the ECG, we need to figure out what the state of the artery was during its recording.
5. Echocardiogram can help to determine if precordial ST depression is due to subendocardial ischemia (absence of wall motion abnormality, or at least not in posterior location) vs. posterior (posterior or lateral WMA).
6.  Posterior MI is now frequently called "Lateral" (see articles by Bayes de Luna below).  I prefer the old terminology of "Posterior" (see image and explanation below) because it differentiates OMI with ST depression ONLY (V1-V4) from OMI that has ST Elevation, with or without ST depression.  See this:

This is the CT scan image of this patient
The area of transmural infarct is outlined in red.
It is the lateral wall.
--However, due to rotated orientation in the chest, the lateral wall of the heart is oriented towards the posterior thorax, directly opposite V1, V2, and V3.
--Posterior leads V7-V9 would have shown STE if the voltage was high enough.  
--All that lung between the heart and V7-V9 can result in insufficient QRS or ST-T voltage!
--V1-V3 are directly opposite the wall with STE (under leads V7-V9), and therefore show reciprocal ST Depression.
--Therefore, it is more appropriate to call this a posterior STEMI than a "lateral" STEMI.
--A lateral STEMI would show STE on the 12-lead in V5 and V6 (or high lateral in I, aVL)

1. Cox DA, Stone GW, Grines CL, et al. Comparative Early and Late Outcomes After Primary Percutaneous Coronary Intervention in ST-Segment Elevation and Non–ST-Segment Elevation Acute Myocardial Infarction (from the CADILLAC Trial). Am J Cardiol [Internet] 2006;98(3):331–7. Available from: http://www.sciencedirect.com/science/article/pii/S0002914906007168

Articles by Bayes de Luna which attempt to eliminate the idea of a "Posterior MI".  

I find that these ideas only confuse the acute treatment of any Occlusion MI (OMI) that only manifests ST depression in leads V1-V4.  By propagating the idea that there is no posterior MI, they propagate the idea that patients who do not have ST Elevation do not have OMI (or STEMI equivalent with ST Elevation vector pointing towards the posterior thorax).

… R wave in V1 is caused by a lateral not posterior myocardial infarction—new evidence based on contrast-enhanced cardiac magnetic resonance—electrocardiogram …

A BayĆ©s de Luna, D Rovai, G Pons Llado… - European Heart …, 2015 - academic.oup.com
Paperpile
Since 1964, a tall and broad R wave in V1–V2, in the absence of right ventricular
hypertrophy, complete right bundle-branch block, or Wolff–Parkinson–White syndrome, has
been considered the sign of a posterior myocardial infarction (MI). 1 According to this theory … Cited by 21 Related articles All 10 versions Import into BibTeX

Concordance of electrocardiographic patterns and healed myocardial infarction location detected by cardiovascular magnetic resonance

AB de Luna, JM Cino, S Pujadas… - The American journal of …, 2006 - Elsevier
Paperpile
Q-wave myocardial infarction (MI) location is generally based on a pathologic correlation
first proposed> 50 years ago. Despite the proved reliability of contrast-enhanced
cardiovascular magnetic resonance (CE-CMR) imaging to detect and locate infarcted areas  Cited by 84 Related articles All 7 versions Import into BibTeX

A new terminology for left ventricular walls and location of myocardial infarcts that present Q wave based on the standard of cardiac magnetic resonance imaging: a …

Bayes de Luna, G Wagner, Birnbaum, K Nikus… - Circulation, 2006 - Am Heart Assoc
Paperpile
The ECG is the most frequently used tool for evaluating myocardial infarction (MI). The ECG
provides an opportunity to describe location and extent of infarction expressed as
pathological Q waves or their equivalents. The terminology used for the left ventricular (LV) …

 


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