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The ECG shows sinus tachycardia with RBBB and LAFB, without clear additional superimposed signs of ischemia. The Initial ECG in Today's Case: As per Dr. Meyers — the initial ECG in today's case shows sinus tachycardia with bifascicular block ( = RBBB/LAHB ). Sinus Tachycardia ( common in any trauma patient. ).
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.) This is sinus tachycardia (rhythm) with complete heart block (AV node function) with ventricular escape rate just below 30. Never forget that sinus tachycardia is the scariest arrhythmia.
Here was his initial ED ECG: There is sinus tachycardia at a rate of about 140 There is profound ST Elevation across all precordial leads, as well as I and aVL. I said I think there is a fixed stenosis in the LAD and the tachycardia and stress caused a type 2 STEMI.
There is a narrow complex tachycardia at a rate of 130. ECGs: there is a regular narrow complex tachycardia still at a rate of exactly 130, with no P-waves and also no change since the prehospital ECG. During tachycardia, in this case, the baseline continuously undulates especially in leads II, aVR and V1; very good for atrial flutter.
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?
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. For review — GO TO: The June 4, 2018 post ( LA-LL reversal ).
Tachycardia and ST Elevation. == MY Comment , by K EN G RAUER, MD ( 7/7 /2024 ): == Among the most rewarding type of case for me during my days working in the ED — would be seeing a patient who presented with acute CP ( C hest P ain ) — who I would be able to “cure” simply by recognizing and treating their arrhythmia. Would you give lytics?
Here is his 12-lead: There is a wide complex tachycardia with a rate of 257, with RBBB and LPFB (right axis deviation) morphology. Read about Fascicular VT here: Idiopathic Ventricular Tachycardias for the EM Physician Case Continued He was completely stable, so adenosine was administered. See Learning point 1 below. Arch Intern Med.
Here was the ECG: There is sinus tachycardia. Our chief of cardiology, Gautam Shroff, interprets it differently and thinks this is indeed ischemia. This was sent by a reader. A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenic shock. and K was normal. This is "Shark Fin" morphology.
First, we have a narrow-complex, regular tachycardia, with a rate of about 135-140. This narrows our differential for the rhythm down to sinus tachycardia, paroxysmal supraventricular tachycardia (PSVT, or SVT), and atrial flutter. Tachycardia and ST Elevation. She was discharged home. Christmas Eve Special Gift!!
Given the rapid rate of the tachycardia and the amorphous shape of the QRS — the decision was made to sedate the patient and cardiovert. This phenomenon may sometimes be seen following an episode of a sustained tachycardia — in which marked ST-T wave abnormalities not due to infarction may be seen for a period of hours, or even days!
The ECG there reportedly showed an irregular tachycardia, and the patient was immediately referred to the emergency room. Here is her ECG on arrival: There is a wide complex tachycardia that is irregularly irregular (this is difficult to determine at these very high rates). Vitals were within normal limits other than heart rate.
My Comment , by K EN G RAUER, MD ( 7/5/2018 ): This blog post provides an excellent example of how a patient with SSS ( = S ick S inus S yndrome ) may present. Because the SA node is sick the SA node recovery time is often prolonged, which is why long pauses most commonly follow episodes of tachycardia ( which produced SA node suppression ).
Ruling out other potential causes of bradycardia ( ie, recent ischemia-infarction; hypothyroidism ). 2 short runs of SVT ( presumably atrial tachycardia ). 2 short runs of SVT ( presumably atrial tachycardia ). Bradycardia was not limited to nighttime hours. No pause beyond 2.0 Bradycardia was not limited to nighttime hours.
These include ( among others ) — acute febrile illness — variations in autonomic tone — hypothermia — ischemia-infarction — malignant arrhythmias — cardiac arrest — and especially Hyperkalemia. Sinus Tachycardia ( common in any trauma patient. ). mm ( generally ≥2 mm ) in ≥1 right precordial lead, followed by a positive T-wave. —
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. We have often referred to this almost magical m irror- i mage r elationship for ST-T waves in leads I II and aV L — which when present, means a cute i nferior O MI until you prove otherwise ( See My Comment on the 8/9/2018 SSmith Blog Post ).
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. 2) Tachycardia to this degree can cause ST segment changes in several ways. Again, not an expected outcome with diltiazem).
The first task when assessing a wide complex QRS for ischemia is to identify the end of the QRS. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). What do you think?
There is appreciable STE aVR with near-global STD that appropriately maximizes in Leads II and V5, and thus suggesting a circumstance of generic, diffusely populated, circumferential subendocardial ischemia versus occlusive coronary thrombus. [1] There is evolution from Wellens Pattern A to Pattern B, now inclusive of V6.
This is critical for the EMS provider, or ED clinician, as identification of Grade I ischemia (aka, HATW’s) addresses the culprit lesion at the earliest opportunity with excellent downstream prognosis for the patient. [2] 2] But there is also Sinus Tachycardia! Chapter 6: Introduction to Myocardial Ischemia and Infarction.
After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. A Very Wide Complex Tachycardia. 72; Issue 9; 2018 ) — A ) Brugada-1 ECG pattern, showing coved ST-segment elevation ≥2 mm in ≥1 right precordial lead, followed by a negative T-wave. — Use Lewis Leads!!
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. She was ventilated by bag-valve-mask by EMS on arrival and was quickly intubated with etomidate and succinylcholine. A rectal temperature was obtained which read 107.9
During observation in the ED the patient had multiple self-terminating runs of Non-Sustained monomorphic Ventricular Tachycardia (NSVT). That said there were no clinical symptoms or ECG findings suggestive of ongoing ischemia. This patient very likely has some form of idiopathic ventricular tachycardia.
Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Among potential conditions that may produce Brugada Phenocopy are infarction and ischemia. Ischemia or infarction. Hyperkalemia 2.
It is possible there is microvascular dysfunction producing residual transmural ischemia. But this is most common when there is prolonged ischemia, and this patient had the fastest reperfusion imaginable! Here is the final angiogram following placement of a stent in the ostial RCA. Circulation Research , 114 (12), 18521866. Galiuto, L.,
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