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There is sinus bradycardia with one PVC. This is a troponin I level that is almost exclusively seen in STEMI. So this is either a case of MINOCA, or a case of Type II STEMI. If the arrest had another etiology (such as old scar), and the ST elevation is due to severe shock, then it is a type II STEMI.
Looking first at the long-lead II rhythm strip — there is significant bradycardia , with a heart R ate just under 40/minute. But the point to emphasize — is that it should only take seconds to recognize that there is bradycardia from significant AV block. = Would you approve her for a nonemergent surgical procedure?
Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. Step 1 to missing posterior MI is relying on the STEMI criteria. A prospective validation of STEMI criteria based on the first ED ECG found it was only 21% sensitive for Occlusion MI, and disproportionately missed inferoposterior OMI.[1]
Later, I found old ECGs: 5 month prior in clinic: V5 and V6 look like OMI 9 months prior in clinic with no chest symptoms: V5 and V6 look like OMI 1 year prior in the ED with chest pain: V5 and V6 sure look like a STEMI For this ECG and chest pain in the ED, the Cath lab activated. But the angiogram was clean. There was no OMI.
Whatever today's rhythm turns out to be — the "good news" is that the bradycardia and degree of AV block is likely to improve as soon as there is reperfusion of the "culprit" artery ( Therefore need for prompt cath with PCI ). ECG Blog #218 — Reviews HOW to define a T wave as being H yperacute ?
Triage physician interpretation: -sinus bradycardia -lateral ST depressions While there are lateral ST depressions (V5, V6) the deepest ST depressions are in V4. In this case, the vessel supplied a portion of the posterior LV circulation. The screening physician ordered an EKG and noted his ashen appearance and moderate distress.
Here is his ED ECG: There is obvious infero-posterior STEMI. What are you worried about in addition to his STEMI? There is also bradycardia. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. Bradycardia puts patients at risk for "pause-dependent" Torsades de Pointes. mEq/L, from 1.9
The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI. Is there STEMI? Circulation Research , 56 (2), 184–194. Circulation , 63 (2), 333–340. About one hour later his high sensitivity troponin I resulted at 3,000 ng/L (reference 3-54 ng/L). Do not treat AIVR. Moffat, M.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. There was no evidence bradycardia leading up to the runs of PMVT ( as tends to occur with Torsades ). With longterm use there may be — bradycardia, AV conduction defects and risk of Torsades de Pointes ( especially in patients also on Digoxin ).
2) The STE in V1 and V2 has an R'-wave and downsloping ST segments, very atypical for STEMI. Cardiology was consulted and they agreed that the EKG had an atypical morphology for STEMI and did not activate the cath lab. Circulation, 117, 1890–1893. [3]: See additional image at the bottom of this post. Bicarb 20, Lactate 4.2,
They recorded this ECG: Obvious inferior STEMI/OMI What else? There is also STE in V1 which is diagnostic of right ventricular OMI in this situation , and partly explains the syncope and hypotension (along with the bradycardia). Medics recorded a BP of 79/52 with pulse of 47. As I wrote in that Nov. The cardiac cath was "normal".
Within ten minutes, she developed bradycardia, hypotension, and ST changes on monitor. Bradycardia and heart block are very common in RCA OMI. Circulation Research , 114 (12), 18521866. Circulation , 92 (3), 657671. Circulation , 125 (3), 491496. Circulation , 145 (13), 10021019. link] Bentzon, J.
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