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The ECG in Figure-1 — was obtained from a middle-aged woman with positional tachycardia and diaphoresis with change of position from suprine to sitting. My THOUGHTS on the ECG in Figure-1: The rhythm is sinus tachycardia at ~105/minute ( ie, The R-R interval is regular — and just under 3 large boxes in duration ).
ischemia) or it can be secondary to abnormal depolarization (e.g Discussion: The ECG in today's case does not have typical ST depression vector of diffuse subendocardial ischemia. The ST vector in subendocardial ischemia (SEI) usually has the largest amount of ST depression in leads II and V5, towards the apex of the heart. (ST
CT of the chest showed no pulmonary embolism but bibasilar infiltrates. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. She was intubated.
Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead. The CXR demonstrated no pulmonary edema. Type I ischemia.
This is ischemic ST depression, and could be due to increasing tachycardia, with a heart rate over 130, but that is unlikely given that the patient is now complaining of crushing chest pain and that there was tachycardia all along. Xray was consistent with pulmonary vascular congestion. There is widespread ST depression.
Here is his ECG: Original image, suboptimal quality Quality improved with PM Cardio digitization The ECG is highly suggestive of acute right heart strain, with sinus tachycardia, S1Q3T3, and T wave inversions in anterior and inferior with morphology consistent with acute right heart strain. Moreover, there is tachycardia.
An Initial ECG was performed: Initial ECG: Sinus tachycardia with prolonged QT interval (QTc of 534 ms by Bazett). She was admitted to the ICU where subsequent ECGs were performed: ECG at 12 hours QTc prolongation, resolution of T wave alternans ECG at 24 hours Sinus tachycardia with normalized QTc interval. No ischemic ST changes.
The patient was transported to the CCU for further medical optimization where a pulmonary artery catheter was placed. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
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. ).
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. The estimated pulmonary artery systolic pressure is 37 mmHg + RA pressure. QTc was 374, and the formula value was quite high, consistent with LAD occlusion.
This usually represents posterior OMI, but in tachycardia and especially after cardiac arrest, this could simply be demand ischemia, residual subendocardial ischemia due to the low flow state of the cardiac arrest. This rules out subendocardial ischemia and is diagnostic of posterior OMI. V4-5 continue to show STD.
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. The rhythm is atrial fibrillation. The QRS complex is within normal limits.
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.
Whenever you see tachycardia with bundle branch block, you should suspect that it is rate related BBB. After resolution, there was T-wave inversion in V1-V3, highly suggestive of ischemia. There are features of the T-wave inversion, however, which argue against ischemia. Moreover, and importantly, there was sinus tach.
Advanced cardiac imaging especially in atypical presentations, can aid in early diagnosis.Case:A 59 year-old man with history of biopsy-proven pulmonary sarcoidosis presented with non exertional chest pain for 2 months. Stress echocardiogram ruled out myocardial ischemia.
His prehospital ECG showed "inferior" ST depression and high voltage, with tachycardia. I suspected no OMI, that this could be due to LVH plus tachycardia. The estimated pulmonary artery systolic pressure is 29 mmHg + RA pressure. On arrival to the ED, the patient was diaphoretic, tachycardic. and had dilated pupils.
The bedside echo showed a large RV (Does this mean there is a pulmonary embolism as the etiology?) The flutter waves can conceal or mimic ischemic repolarization findings, but here I don't see any obvious findings of OMI or subendocardial ischemia. Obviously he has multiple reasons to have pulmonary hypertension.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" That said, complete LM occlusion would be expected to have subepicardial ischemia (STE) in these myocardial territories: STE vector 1.
ECG in a person with persistent anginal pain for the past several hours showing significant ST segment depression anterolateral leads along with sinus tachycardia. Clinical evaluation and X-Ray chest showed features of pulmonary edema. ST segment elevation is noted in aVR.
They include myocardial ischemia, acute pericarditis, pulmonary embolism, external compression due to mass over the right ventricular outflow tract region, and metabolic disorders like hyper or hypokalemia and hypercalcemia. According to a recent systematic review and meta-analysis, spontaneous type 1 ECG had 2.4%
The ECG shows sinus tachycardia, a narrow, low voltage QRS with alternating amplitudes, no peaked T waves, no QT prolongation, and some minimal ST elevation in II, III, and aVF (without significant reciprocal STD or T wave inversion in aVL). It is difficult to tell if there is collapse during diastole due to the patient’s tachycardia.
These findings are concerning for inferior wall ischemia with possible posterior wall involvement. C linically — the rhythm we see in the long lead II of ECG #3 behaves similar to MAT, even though there is no tachycardia. A majority of patients with MAT have longstanding pulmonary disease. No significant changes, ongoing pain.
The only time you see this without ischemia is when there is an abnormal QRS, such as LVH, LBBB, LV aneurysm (old MI with persistent STE) or WPW." Here is the patient's troponin I profile: These were interpreted as due to demand ischemia, or type II MI. ng/mL is seldom a result of demand ischemia (type 2 MI). First was 2.9
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. If there is polymorphic VT with a long QT on the baseline ECG, then generally we call that Torsades, but Non-Torsades Polymorphic VT can result from ischemia alone. He appeared to be in shock. Serum potassium level (range 2.5
and the patient was converted to veno-venous (V-V) ECMO due to persistent pulmonary insufficiency. Use of objective evidence of myocardial ischemia to facilitate the diagnostic and prognostic distinction between type 2 myocardial infarction and myocardial injury. He remained supported on an intraaortic balloon pump.
If the patient has Abnormal Vital Signs (fever, hypotension, tachycardia, or tachypnea, or hypoxemia), then these are the primary issue to address, as there is ongoing pathology which must be identified. Evidence of acute ischemia (may be subtle) vii. Aortic Dissection, Valvular (especially Aortic Stenosis), Tamponade. Left BBB vi.
The status of the patients chest pain at this time is unknown : EKG 1, 1300: There is sinus tachycardia and artifact of low and high frequency. However, there is also significant tachycardia , with heart rate of 116, and known hypoxia. She arrived to the ED with a nonrebreather mask. Her blood pressure on arrival was 153/69.
Smith : This is classic for pulmonary embolism (PE). Acute pulmonary embolism was confirmed on CT angiogram: The patient did well. See our other acute right heart strain / pulmonary embolism cases: A man in his 50s with shortness of breath Another deadly triage ECG missed, and the waiting patient leaves before being seen.
For right or wrong reasons, the world of electrophysiology has pushed us into a belief system that, if it is AF, the culprit must be pulmonary veins. In fact, non-pulmonary vein origins can be a staggering 70% in some series. If we look at the above map,RA prevails over LA convincigly in termes of focal atrial tachycardia.
There was never ventricular fibrillation (VF) or ventricular tachycardia (VT), no shockable rhythm. she had severe pulmonary edema. This is the etiology of the blood from her nose and mouth (frothy bloody pulmonary edema) This is what frothy bloody pulmonary edema looks like. There is sinus tachycardia at ~115/minute.
August 2024 Approvals Minima Stent System (P240003) (Approval Date: August 28, 2024) The Minima Stent System is an expandable cobalt-chromium metal mesh tube to reopen blood vessels in neonates, infants, and children with Coarctation of the Aorta and Pulmonary Artery Stenosis, specifically designed to expand as younger patients grow.
Bedside POCUS showed very poor LV function and a few pulmonary B lines. A Chest X-ray did not show pulmonary edema. This ECG was recorded: It is difficult to appreciate P-waves, but I believe this is sinus tachycardia. Negative trops and negative angiogram does not rule out coronary ischemia or ACS. He was put on BiPAP.
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