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Case continued Another ECG was recorded 3 hours later, still 1/10 pain: There is sinus bradycardia with RBBB. But there are also new Q-waves, stronly suggesting new infarction. So we know there is myocardialinfarction and the patient has persistent pain, but it is very mild. They only mask the underlying pathology.
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.
However the patient continued to have chest pain and bedside ultrasound showed hypokinesis of the septum with significantly reduced LVEF. AIVR is not always the result of significant pathology, but is classically associated with the reperfusion phase of acute myocardialinfarction. Do not treat AIVR.
Troponin T peaked at 38,398 ng/L ( = a very large myocardialinfarction, but not massive-- thanks to the pre-PCI spontaneous reperfusion, and rapid internvention!! ). Some residual ischemia in the infarct border might still be present. Over the next couple of days the patient was weaned off of mechanical circulatory support.
Here is his ED ECG: There is bradycardia with a junctional escape. Case continued A bedside ultrasound showed diminished LV EF and of course bradycardia. Posterior wall involvement attenuates predictive value of ST-segment elevation in lead V4R for right ventricular involvement in inferior acute myocardialinfarction.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Literature on Hypokalemia as a risk for ventricular fibrillation in acute myocardialinfarction.
The ECG shows sinus bradycardia but is otherwise normal. So there is probability of myocardial injury here (and because it is in the correct clinical setting, then myocardialinfarction.) The documentation does not describe any additional details of the history. The following ECG was obtained. ECG 1 What do you think?
Use of drugs producing bradycardia like beta blockers in stages III and IV may precipitate low output state. J Cardiovasc Ultrasound. J Cardiovasc Ultrasound. In stage IV, this restrictive filling pattern remains fixed even during Valsalva maneuver. Initial stages (I to III) are considered reversible with treatment. Ha J et al.
There is sinus bradycardia with one PVC. MINOCA: MyocardialInfarction in the Absence of Obstructive Coronary Artery Disease). The ways to tell for certain include intravascular ultrasound (to look for extra-luminal plaque with rupture) or "optical coherence tomography," something I am entirely unfamiliar with.
Electrocardiographic Differentiation of Early Repolarization FromSubtle Anterior ST-Segment Elevation MyocardialInfarction. Patient presentation is important This was a 60-something with acute chest pain: There is sinus bradycardia at a rate of 44. In case you were wondering about the T-waves and bradycardia, the K was normal.
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. Ischemic ST-Segment Depression Maximal in V1-V4 (Versus V5-V6) of Any Amplitude Is Specific for Occlusion MyocardialInfarction (Versus Nonocclusive Ischemia).
Check : [vitals, SOB, Chest Pain, Ultrasound] If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Frequent or repetitive PACs ii. orthostatic vitals b.
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