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But cardiacarrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. After cardiacarrest, I ALWAYS wait 15 minutes after an ECG like this and record another. See these related cases: Cardiacarrest, defibrillated, diffuse ST depression and ST Elevation in aVR.
There was concern that the rhythm might represent ventricular tachycardia, so lidocaine was given and one attempt at cardioversion was performed. A woman in her 50s with dyspnea and bradycardia A patient with cardiacarrest, ROSC, and right bundle branch block (RBBB). HyperKalemia with CardiacArrest.
A small proportion of patients with STEMI treated via primary PCI experienced late ventricular tachycardia (VT) or ventricular fibrillation (VF), occurring one or more days following the procedure, but late VT or VF with cardiacarrest occurred rarely, especially among patients with uncomplicated STEMI, according to a study published in JAMA Network (..)
This certainly looks like an anterior STEMI (proximal LAD occlusion), with STE and hyperacute T-waves (HATW) in V2-V6 and I and aVL. How do you explain the anterior STEMI(+)OMI immediately after ROSC evolving into posterior OMI 30 minutes later? This caused a type 2 anterior STEMI.
The ECG in Figure-1 — was obtained from a middle-aged man who presented to the ED ( E mergency D epartment ) in cardiacarrest. Prompt cath is therefore advised if the post-ROSC shows an acute STEMI. Continuing with assessment of ECG #1 in Figure-2: The rhythm is sinus tachycardia at ~110/minute.
He had multiple cardiacarrests with ROSC regained each time. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest") Learning Points: Sudden witnessed CardiacArrest due to ACS is almost always due to dysrhythmia. This patient arrested shortly after hospital arrival.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? Comments: STEMI with hypokalemia, especially with a long QT, puts the patient at very high risk of Torsades or Ventricular fibrillation (see many references, with abstracts, below). There is atrial fibrillation.
In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0 Elevated troponin does not, however, guide any treatment strategies to minimize myocardial injury.
Are Some Cardiologists Really Limited by Strict Adherence to STEMI millimeter criteria? I was texted these ECGs by a recent residency graduate after they had all been recorded, along with the following clinical information: A 50-something with no cardiac history, but with h/o Diabetes, was doing physical work when he collapsed.
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. 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. A near 60 year old male called 911 for increasingly severe fever and SOB.
Past medical history included RBBB without other cardiac history, but old ECG was not available. The prehospital and ED computer interpretation was inferior STEMI: There’s normal sinus rhythm, first degree AV block and RBBB, normal axis and normal voltages. Vitals were normal except for oxygen saturation of 94%. Vitals were normal.
ECG is consistent with severe hypokalemia and/or hypomagnesemia causing prolonged QT (QU) at high risk of Torsades (which is polymorphic ventricular tachycardia in the setting of a long QT interval). Polymorphic Ventricular Tachycardia Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management CardiacArrest.
She was diagnosed with a Non-STEMI and kept overnight for a next day angiogram. Medics recorded the above ECG and called a STEMI alert. The patient went into arrest pre-hospital. Her symptoms at the time ECG #1 was obtained were CP and SOB — yet interpretation of this initial tracing prompted a STEMI alert.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). The below ECG was recorded. He required multiple defibrillations within a period of a few hours.
Other than tachycardia, Other than slight tachycardia, vitals were within normal limits (including oxygen saturation). The provider contacted cardiology to discuss the case, but cardiology "didn't think it was a STEMI, didn't think he needed emergent cath." The whole paradigm is literally called "STEMI" vs. "NSTEMI."
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. aVR ST segment elevation: acute STEMI or not? aVR ST Segment Elevation: Acute STEMI or Not?
Here is the ECG: Sinus tachycardia. Discussion See this post: STEMI with Life-Threatening Hypokalemia and Incessant Torsades de Pointes I could find very little literature on the treatment of severe life-threatening hypokalemia. If cardiacarrest from hypokalemia is imminent (i.e., This patient presented with severe DKA.
There is sinus tachycardia (do not be fooled into thinking this is VT or another wide complex tachycardia!) This pattern is essentially always accompanied by cardiogenic shock and high rates of VT/VF arrest, etc. Code STEMI was activated. Plus recommendations from a 5-member panel on cardiacarrest.
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? Here are other posts on hyperK, large calcium doses for hyperK, and ventricular tachycardia in hyperK Weakness, prolonged PR interval, wide complex, ventricular tachycardia Very Wide and Very Fast, What is it? How would you treat?
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". After initiating treatment for hyperkalemia, repeat ECG showed resolution of Brugada pattern: The ECG shows sinus tachycardia. Steve, what do you think of this ECG in this CardiacArrest Patient?" HyperKalemia with CardiacArrest.
See many examples of Pseudo STEMI due to hyperkalemia at these two posts: Acute respiratory distress: Correct interpretation of the initial and serial ECG findings, with aggressive management, might have saved his life. But the rate is ~130/minute — which is a bit fast for sinus tachycardia. No followup EKG was recorded!!
Otherwise vitals after intubation were only notable for tachycardia. An initial EKG was obtained: Computer read: sinus tachycardia, early acute anterior infarct. 2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. A rectal temperature was obtained which read 107.9 Bicarb 20, Lactate 4.2,
There is ST depression in II, III, and aVF that is concerning for reciprocal depression from high lateral STEMI in aVL, where there is some ST elevation. There is also ST depression in precordial leads, greatest in V3 and V4, concerning for posterior STEMI. The patient died is spite of resuscitative efforts. It is found on 1% to 3.5%
ECG met STEMI criteria and was labeled STEMI by computer interpretation. J waves can also be induced by Occlusion MI (5), STEMI mimics including takotsubo and myocarditis complicated by ventricular arrhythmias (6, 7), and subarachnoid hemorrhage with VF (8). Take home : Not all STEs are STEMIs or OMIs. What do you think?
There is sinus tachycardia and also a large R-wave in aVR. 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. Her temperature was 106 degrees. As part of the workup, she underwent an ECG.
A 12-lead was recorded, showing "STEMI," but is unavailable. There was never ventricular fibrillation (VF) or ventricular tachycardia (VT), no shockable rhythm. The patient was unconscious BEFORE the cardiacarrest, at the same time that she had strong pulses. Therefore, cardiacarrest is NOT the etiology of the coma.
It is a wide complex regular tachycardia at a rate of 120. Is it ventricular tachycardia? I fear that many learners would also not easily recognize where the QRS actually ends, and I fear that some may think that this is ventricular tachycardia due to inability to distinguish QRS from ST segment. The ST Elevation is NOT typical.
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. Unexplained cardiacarrest or documented VF/polymorphic VT: +3 3. Unexplained sudden cardiac death (3 categories) (+0.5 - +2) 4.
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