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Both of these features make inferior + RV MI by far the most likely ( Pseudoanteroseptal MI is another name for this ) There is also sinus bradycardia and t he patient is in shock with hypotension. A narrow complex bradycardia without any P-waves is also likely to respond to atropine, as it may be a junctional rhythm.
The ECG shows sinus bradycardia but is otherwise normal. Although it is statistically unlikely, multiple plaque ruptures are possible. On intravascular ultrasound (IVUS), the mid RCA plaque was described as "cratered, inflamed, and bulky," and the OM plaque was described as "bulky with evidence of inflammation and probably ulceration."
I will leave more detailed rhythm discussion to the illustrious Dr. Ken Grauer below, but this use of calipers shows that the rhythm interpretation is: Sinus bradycardia with a competing (most likely junctional) rhythm. preceding each of the fascicular beats — indicating a faster rate for the escape rhythm compared to the sinus bradycardia ).
There is sinus bradycardia with one PVC. If the arrest was caused by acute MI due to plaque rupture, then the diagnosis is MINOCA. Here is my comment on MINOCA: "Non-obstructive coronary disease" does not necessarily imply "no plaque rupture with thrombus." She then had a 12-lead: What do you think? FFR can be useful.
There are multiple possible clinical situations that could account for diffuse subendocardial ischemia that is not due to ACS and plaque rupture. As per Dr. Nossen — today's initial ECG ( LEFT tracing in Figure-2 ) shows sinus bradycardia with QRS widening due to bifascicular block ( RBBB/LAHB ).
A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms. Coronary artery disease Excessive cholesterol builds up plaque that blocks the arteries supplying blood to the heart. Arrhythmia In simple words, arrhythmia refers to an irregular heartbeat.
plaque disruption), the T waves still manifest markings of a previous state of suboptimal coronary flow that resolved: Type II supply-demand mismatch in the setting of extreme bradycardia. 2] Although the clinical context in today’s case does not fit these descriptors for Type I OMI (e.g.
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. Mechanisms of plaque formation and rupture. Coronary plaque disruption. He told the patient this horrible news. The other point in favor of RCA is junctional rhythm. Virmani, R.,
Influenza-like illness can also trigger plaque rupture. Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI.
There are 2 main options: Overdrive pacing could be considered and in the right clinical situation, this is often effective for reducing ventricular arrhythmias ( especially in the case of preventing pause induced or bradycardia-induced arrhythmias in association with QTc prolongation ). There were no plaques or stenoses.
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