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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.
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 ).
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. The resultant rhythm after cardioversion is shown in Figure-2.
. = 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.
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.
during which sinus bradycardia and arrhythmia are seen but not to a degree that produces symptoms. The easy way to remember the arrhythmias most commonly associated with SSS is to think of what one might expect if the SA node became sick. New slow AFib reflects a combination of these rhythm problems. 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.
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?
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?
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 ).
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?
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.
He has a family history concerning for arrhythmia. Given the circumstances of his car crash, we presume it was due to an underlying arrhythmia. He has a family history concerning for arrhythmia with his father requiring some sort of device (PPM, ICD, unclear) at a young age.
Here was my answer: "Not ischemia. Instead — my thoughts were as follows: The rhythm is sinus , with marked bradycardia and a component of sinus arrhythmia. WPW Cardiac arrhythmias ( especially AFib ). This was texted to me in real time. The patient has acute chest pain. What do you think? I would not activate cath lab.
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 ).
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. In this case, there is diffuse ischemic ST depression of subendocardial ischemia, of course with accompanying reciprocal STE in aVR.
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). The "usual rules" of cardiac arrhythmias are simply not always followed in critically ill patients. There is STE in aVR.
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. By this I mean — that it includes all arrhythmias in which the rate is “ T achycardic” ( ie, ≥100/minute in an adult ) — and , in which the rhythm is “ S upra V entricular” ( ie, originating at or above the AV node ). There are nonspecific ST-T abnormalities. This is a “ generic ” term.
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