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In addition — there is transmural ischemia of the septum , most often resulting from occlusion proximal to the 1st septal perforator branch of the LAD. The rhythm in both tracings in Case #2 shows AFib with a controlled ventricular response ( with a PVC in the 2nd tracing ).
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. WPW Cardiac arrhythmias ( including AFib ).
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.
These findings suggest that instead of VT — the rhythm in Figure-1 is AFib with a fairly rapid ventricular response. Since the rhythm is supraventricular (ie, AFib ) — we can accurately assess QRS morphology. Shark Fin" ST segment elevation is most often a sign of severe transmural ischemia that results from acute coronary occlusion.
M y I MPRESSION : The rhythm in Figure -1 is almost certain to be very rapid AFib in a patient with WPW. NOTE #2: Surprisingly, it is not uncommon for patients in AFib with WPW to be hemodynamically stable — despite having exceedingly rapid ventricular rates. ECG Blog #284 — Reviews a case similar to today's Very Fast AFib.
. = My Comment by K EN G RAUER, MD ( 3/15 /2023 ): = I found today’s case highly instructive in highlighting a number of important aspects regarding the presentation and initial treatment of a patient who presents to the ED with new AFib. I focus my comment on a few additional aspects regarding new AFib.
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 rhythm is rapid AFib. Atrial fib may cause Occlusion mimic."
Many patients have a T achy- B rady syndrome in which tachyarrhythmias ( most commonly rapid AFib ) alternate with periods of bradycardia. New slow AFib reflects a combination of these rhythm problems. Thus, it is not those episodes of rapid AFib seen in patients with Tachy-Brady that qualify. second in duration.
There was no evidence of ischemia. C linical P oints R egarding E CG # 1 : We are told that the patient is a middle-aged woman and that she previously had been in AFib with LBBB. While I agree that AFib + complete AV block is the most likely rhythm diagnosis I'd like to see additional monitoring strips to be sure.
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?
Thoughts about Today's CASE: On occasion — a patient may present for acute care because of CP ( C hest P ain ) due solely to a tachyarrhythmia ( including new AFib, a reentry SVT or VT ). Figure-1: The initial ECG in today's case. ( To improve visualization — I've digitized the original ECG using PMcardio ).
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
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. WPW Cardiac arrhythmias ( including AFib ). Voltage for LVH ( the R wave in lead aVL easily surpassing 12 mm ).
Here is her post-cardioversion ECG: ECG#2 - Immediately post cardioversion: Appropriate ST depression maximal in V5-6 and lead II, secondary to subendocardial ischemia, likely residual from the preceding tachycardia. Patient was referred to electrophysiologic testing due to suspicion of afib and WPW. She was sedated and cardioverted.
The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ). Chest trauma was suspected on initial exam. Here is his initial ECG around 1330: What do you think?
I see the following: Although there is no long lead rhythm strip — we can see that the rhythm is AFib with a controlled ventricular response ( ie, irregularly irregular rhythm without P waves — and with a heart rate between ~70-110/minute ). Regarding Intervals: There is no PR interval ( since the rhythm is AFib ).
MY THOUGHTS on ECG #1: My initial impression on looking at the ECG in Figure-1 — was that the rhythm was either rapid AFib in a patient with WPW — or — PMVT ( P oly M orphic VT ). The reason I initially thought the underlying rhythm was AFib — is that no atrial activity is seen in any lead and the rhythm “looks” irregular. See text ).
Here was my answer: "Not ischemia. WPW Cardiac arrhythmias ( especially AFib ). This was texted to me in real time. The patient has acute chest pain. What do you think? Maybe HOCM or another form of LVH. I would not activate cath lab. Abnormal ST-T wave abnormalities. Conduction defects (ie, LBBB, IVCD ).
These include ( among others ) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiac arrest — and especially Hyperkalemia. Other Arrhythmias ( PACs, PVCs, AFib, Bradycardia and AV conduction disorders — potentially lethal VT/VFib ).
In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished. First , there can simply be diffuse ST depressions (which obligates reciprocal STE in aVR) associated with tachycardia which are not indicative of ischemia.
(Harvard University Heart Letter) A clinical polygenic risk score test for diseases ranging from atrial fibrillation (AFib) to breast cancer was piloted by scientists. Stroke) A Danish study indicated that combining nitrates and PDE5 inhibitors isn't always a terrible idea for men with ischemic heart disease and erectile dysfunction.
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The rhythm is atrial fibrillation. The QRS complex is within normal limits. These include.
This ST depression appears to be maximal in leads V3-to-V5 — which could reflect acute posterior OMI ( O cclusion-based M yocardial I nfarction ) — most probably with multi -vessel disease ( ie, diffuse subendocardial ischemia suggested by the ST depression with ST elevation in aVR>V1 ). This patient has new CP — and — he is hypotensive.
When I was shown this ECG, I said it looks like such widespread ischemia that is might be a left main occlusion, or LM ischemia plus circumflex occlusion (high lateral and posterior OMI). There is STE in aVR. Thus, there is high lateral OMI with diffuse ST depression. Moreover, left main occlusion often presents near death.
The QRS is wide in B — but the rhythm is irregularly irregular with no sinus P waves — so this most probably represents rapid AFib with an atypical RBBB/LPHB morphology. We now see that QRS morphology in lead II during sinus rhythm is similar to the QRS morphology in lead II during rapid AFib (beats #1-5 in lead II in A).
While patients with repolarization variants or acute ischemia ( including the DeWinter T wave pattern ) often manifest peaked T waves the T waves with ischemia or repolarization variants tend not to be as pointed as is seen with hyperkalemia and, the base of those T waves tends not to be as narrow as occurs with hyperkalemia.
There is no evidence of infarction or ischemia. There is a large peaked P-wave in lead II (right atrial enlargement) There is left axis deviation consistent with left anterior fascicular block. There are nonspecific ST-T abnormalities. Troponin I was 0.054 ng/mL NT-ProBNP was 8316 (0-900 pg/mL). "
Compared to TTE from 7/3/24: the anterior regional wall motion abnormality is new and is consistent with ischemia/infarction in the LAD territory == MY Comment , by K EN G RAUER, MD ( 11/20 /2024 ): == There are several insightful aspects of today's case. Regional wall motion abnormality--mid anterior akinesis.
That said — the diagnosis of acute PE continues to be overlooked ( and the ECGs of such patients continue to be misinterpreted as acute ischemia or infarction — instead of being recognized as diagnostic of acute PE ). Meyers' discussion — he lists more than 20 links to cases that we've presented related to this entity on Dr. Smith's ECG Blog.
Discussion: This patient was very lucky that she had a doctor who understood her initial ECG, advocated for her, performed serial ECGs, and that her serial ECGs happened to have temporary lack of RBBB which reduces the complexity of the ischemia interpretation. Regularity of the rhythm rules out AFib. Many patients are not this lucky.
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