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For more on this subject — SEE the September 3, 2020 post in Dr. Smith’s ECG Blog with 20-minute video talk by Dr. Meyers on The O MI M anifesto. ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ).
ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
The ECG does not show any definite signs of ischemia. IMPRESSION: The finding of sinus bradycardia with 1st-degree AV block + marked sinus arrhythmia + the change in PR interval from beat #5-to-beat #6 — suggests a form of vagotonic block ( See My Comment in the October 9, 2020 post in Dr. Smith's ECG Blog ).
My written interpretation on a tracing such as this one would read, "Marked LVH and 'strain' and/or ischemia — with need for clinical correlation." BOTTOM LINE: ECG changes of LV "strain" and/or ischemia that we see on today's initial ECG — were not present 9 years earlier. Please see ECG Blog #73 for additional details ).
The history and associated deep anterior S waves (ie, the reciprocal of tall lateral lead R waves ) will suggest LVH rather than Precordial Swirl ( See ECG Blog #254 and My Comment at the bottom of the page in the February 6, 2020 and June 20, 2020 posts in Dr. Smith's ECG Blog ). Cardiol 27:674-677, 2004 ).
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. Nevertheless, the clinical situation made other etiologies unlikely.
In any case, the ECG is diagnostic of severe ischemia and probably OMI. So this could be myocarditis but in my opinion needs an angiogram before making that diagnosis. == Dr. Nossen Comment/Interpretation: Evaluation of ischemia on an ECG can be very challenging. Concordant STE of 1 mm in just one lead or 2a.
As a result, the ST elevation ( with especially tall, peaked T wave in lead V2) — is not indication of acute ischemia. As suggested by Figure-4 below in the ADDENDUM — assessment of the ST-T waves in leads V2,V3 and V5,V6 — is consistent with ischemia and / or LV "strain".
In this patient's case, the RV ischemia manifested as dramatic anterior hyperacute T waves. This degree of STE is a bit atypical for LAD ischemia. Remember that the RV is the most anterior chamber. Here is a transverse image of a CT showing this. A few clues that might have suggested this are: There is marked STE in V1.
Subendocardial Ischemia from another Cause ( ie, sustained tachyarrhythmia; cardiac arrest; shock or profound hypotension; GI bleeding; anemia; "sick patient" , etc. ). To EMPHASIZE: This pattern of diffuse Subendocardial Ischemia does not suggest acute coronary occlusion ( ie, it is not the pattern of an acute MI ).
In the days before I learned to look for OMI, back when I was counting ST elevation boxes, I used to save ischemia for last.) I interpret tracings systematically in "real time" ( including my assessment for acute ischemia ). The February 11, 2020 post ( LA-RA reversal ). The March 18, 2020 post ( LA-RA reversal ).
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia.
Are you confident there is no ischemia? Primary VT , and the VT with tachycardia is causing ischemia with chest discomfort (supply-demand mismatch/type 2 MI)? Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? Do you agree with this strategy? How can you better assess the ST segments?
Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall. Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."
ACUTE MI (I allowed Acute MI to be in the report because I knew there would be an elevated troponin from ischemia, which is the definition of acute MI -- but in this case it would most likely be a Type 2 MI from tachycardia) There is also LA-RA lead reversal. The February 11, 2020 post ( LA-RA reversal ).
I thought this finding consistent with the finding of ST depression in lateral leads I; V4,V5,V6 — and possibly indicative of multivessel disease ( ie, Diffuse Subendocardial Ischemia — as discussed in ECG Blog #400 ). ECG Blog #400 — Reviews the concept of " dynamic " ST-T wave changes ( and also Diffuse Subendocardial Ischemia ).
Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. In practice — It appears that electrical alternans is most often seen in association with regular SVT rhythms ( See the example in My Comment at the bottom of the page, in the September 7, 2020 post in Dr. Smith's ECG Blog ).
Osborn waves have been reported with hypercalcemia, brain injury, subarachnoid hemorrhage, Brugada syndrome, cardiac arrest from VFib — and — severe, acute ischemia resulting in acute MI ( See My Comment in the November 22, 2019 post on Dr. Smith’s Blog ). Rituparna et al — as well as Chauhan and Brahma ( Int.
Recognizing hyperacute T waves — patterns of leads — an OMI ( though not a STEMI ) — See My Comment at the bottom of the page in the November 8, 2020 post on Dr. Smith's ECG Blog. ECG Blog #400 — Reviews the concept of " dynamic " ST-T wave changes ( and also DSI = Diffuse Subendocardial Ischemia ).
It is due to transmural ischemia not only of the anterior wall and apex, but due to transmural ischemia of the septum, usually due to occlusion proximal to the first septal perforator. Is this Acute Ischemia? The voltage is high but not huge. Read the case. More on LVH. This is LVH only, not OMI. This is LVH Only, not OMI.
The same reciprocal relationship is seen in severe subendocardial ischemia, just with opposite vector direction where V1 can show ST elevation) Below you can find the 3D model of the heart and coronary vessels. Each main coronary artery (LAD, RCA and LCx) are shown in separate images.
The fact that R waves 2 through 6 are junctional does make ischemia more difficult to interpret -- but not impossible. Back to the assessment of ischemia: Returning to the ECG, the leads that catch my eye first are -- I, II, V4, V5, V6. Ischemia can be disguised by a wide escape rhythm, which decreases the sensitivity of ECG.
--The STD in V2-V6 might be interpreted as subendocardial ischemia, but with the inferior STE, it is far more likely to represent posterior OMI. In subendocardial ischemia, cath lab is indicated if the pain persists in spite of medical therapy (aspirin, anticoagulant, IV nitro). At 100 minutes, the above ECG was recorded.
My interpretation was: RBBB with hyperacute T-waves in V4-V6 that are all but diagnostic of LAD occlusion vs. post ROSC ischemia. For more on the application of this Trace-down; Copy-over technique with Shark Fin ST segment deviations — See My Comment in the May 19, 2020 post in Dr. Smith's ECG Blog.
Learning Point: Concordant ST segment elevation can arise from profound ischemia triggered by ventricular tachycardia (VT), or it may represent an exaggerated basal ST change accompanying tachycardia. See My Comment at the bottom of the page in the May 19, 2020 post in Dr. Smith's Blog ). A peak troponin level of 70 ng/L was observed.
5] Back to the case The patient had serial ECGs over the next hour with no significant change: The first troponin came back at 1,400 ng/L (normal <26 in males and <16 in females), confirming MI – and the patient’s refractory ischemia indicated this was an Occlusion MI.
Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. She was taken to the cath lab and her coronaries were clean!! There was no MRI, but the presumptive diagnosis is myocarditis. I have seen this pattern in severe acute AI also."
There is probably a trickle of flow which is why there is both subendocardial ischemia (ST depression) and early subepicardial ischemia (hyperacute T-waves). Academic Emergency Medicine 27(S1): S220; May 2020. I sent the last one to the Queen of Hearts #PMCardio app and here is the verdict: My response: "It’s not even subtle.
Time 17 minutes Not much different One month earlier This is Left Bundle Branch Block (LBBB) without any sign of ischemia. If so, one would expect that the chest pain is diminishing or gone & that the culprit would be the LAD. It turns out that she spends much of her time in LBBB (see ECGs below) What is going on??? link] Shvilkin et al.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. Thus, they obscure the last possible indication for emergent reperfusion in "NSTEMI" (all guidelines recommend emergent cath for refractory ischemia in NSTEMI).
ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
2] Here there is no posterior ST elevation, but the anterior ST depression is also less—so it is dynamic, confirming acute ischemia. The absence of STE in V7-V9 is often due to resolution of ischemia, as seen by resolution of ST depression in V7-V9. non-occlusive ischemia) JAHA 2021 3. -- Meyers HP, Bracey A, Lee D, et al.
Final diagnosis of cerebral ischemia was made in 662/1043 patients (63.5%) and stroke mimic was diagnosed in 381/1043 patients (36.5%). Detailed chart review was conducted to extract both the variables needed to apply the mimic scales the final diagnosis confirmed by final imaging and discharge diagnosis (cerebral ischemic vs stroke mimic).
ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
The unique " shape " of the prominent ST-T wave abnormalities in this tracing — that are much more suggestive of some significant form of LVH ( L eft V entricular H ypertophy ) rather than ischemia. For more on Giant T waves — See My Comment at the bottom of the page in the June 22, 2020 and September 19, 2022 posts in Dr. Smith's ECG Blog ).
Does this mean that the ST depression in V3 represents "anterior" subendocardial ischemia, and not posterior OMI? This is most consistent with ischemia/infarction in the distribution of the left circumflex coronary artery. non-occlusive ischemia) 2. Thus, they have much less voltage. They have ZERO ST Elevation.
Smith : the profound persistent STE suggests either persistent occlusion or " no reflow " with persistent downstream ischemia. It makes you think you have done something for the ischemia when you have not! Academic Emergency Medicine 27(S1): S220; May 2020. Long term outcome unknown but obviously bleak. Abstract 556.
Am J Emerg Med 2020 3. We are told that the Stress Echo that was performed showed objective evidence of inducible ischemia ( confirmed apparently by both wall motion abnormalities and ECG changes ). Was this objective evidence of inducible ischemia accompanied by chest pain? Int J Cardiol 2013 2. Shin YS, Ahn S, Kim YJ.
ECG Blog #184 — illustrates the "magical" mirror-image opposite relationship with acute ischemia between lead III and lead aVL ( featured in Audio Pearl #2 in this blog post ). ECG Blog #271 — Reviews determination of the ST segment baseline ( with discussion of the entity of diffuse Subendocardial Ischemia).
Below is the first ECG recorded by paramedics after 2 hours of chest pain, interpreted by the machine as “possible inferior ischemia”. As Smith and Meyers explained in a 2020 article in EM News : “What should we do in the meantime while we are still stuck in the STEMI paradigm in daily practice? What do you think?
The Queen was not able to see this one: Of course we do not know for certain that the inferior findings represent ischemia. The only way to PROVE that ECG findings are due to the alleged OMI/ischemia is to show evolution in that territory. It could have been a false positive ECG, but if it had been, no harm done. It was not.
This suggests further severe ischemia. There is 1 mm of ST segment elevation in lead aVR — which in the context of ST segment flattening in most other leads, suggests that there may be a component of subendocardial ischemia from underlying coronary disease. Detailed coronary artery evaluation not performed. Downstream vasospasm?
24: Joint American College of Cardiology/Journal of the American College of Cardiology Late-Breaking Clinical Trials (Session 402) Saturday, April 6 9:30 – 10:30 a.m. ET Main Tent (Hall B1) This session offers more insights from key clinical trials presented at ACC.24 24 and find out what it all means for your patients.
Santa Clara, CA, USA) semi compliant balloon adapted from cardiovascular literature which showed a pre‐dilation angioplasty capability in coronary stenotic lesions.MethodsWe performed a retrospective review of prospectively maintained mechanical thrombectomy (MT) databases of 2 comprehensive stroke centers between November 2020, and May 2023.
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