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See our other countless hyperkalemia cases below: General hyperkalemia cases: A 50s year old man with lightheadedness and bradycardia Patient with Dyspnea. A woman with near-syncope, bradycardia, and hypotension What happens if you do not recognize this ECG instantly? HyperKalemia with CardiacArrest. With a twist.
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.
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 ). Principal adverse cardiac effects of Quinidine include QRS widening and QTc prolongation. The below ECG was recorded.
Polymorphic Ventricular Tachycardia Long QT Syndrome with Continuously Recurrent Polymorphic VT: Management CardiacArrest. A New Seizure in a Healthy 20-something More cases of long QT not measured correctly by computer (these are all fascinating ECGs/cases): Bupropion Overdose Followed by CardiacArrest and, Later, ST Elevation.
Despite the clinical context, Cardiology was consulted due to concerns for a "STEMI". Hyperkalemia causes peaked T waves and the "killer B's of hyperkalemia", including bradycardia, broad QRS complexes, blocks of the AV node and bundle branches, Brugada morphology, and otherwise bizarre morphology including sine wave. With a twist.
In any case, there is bradycardia. It was a PEA or bradyasystolic arrest , not a shockable rhythm. Although most cardiacarrest from MI is due to ventricular fibrillation, some is due to high grade AV block, and so this could indeed be due to large acute STEMI. No shock was ever delivered. Sixth: Severe shock (e.g.,
The provider contacted cardiology to discuss the case, but cardiology "didn't think it was a STEMI, didn't think he needed emergent cath." About two hours after admission, he suffered a cardiacarrest (whether it was VF/VT or PEA is not available) and expired. The whole paradigm is literally called "STEMI" vs. "NSTEMI."
There is sinus bradycardia with one PVC. There is "Shark Fin morphology" I saw this and thought for certain that this was going to be an LAD or left main occlusion as etiology of arrest, and etiology of profound ST Elevation in I, II, aVL, and V3-V6, and ST depression in III, V1 and V2. She then had a 12-lead: What do you think?
If it is STEMI, it would have to be RBBB with STEMI. This ECG pattern may be diagnostic of B rugada S yndrome IF seen in association with: i ) a history of cardiacarrest; polymorphic VT; or of non-vagal syncope; and / or ii ) a positive family history of sudden death at an early age; and / or iii ) a similar ECG in relatives.
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. No followup EKG was recorded!!
A prehospital ECG was recorded (not shown and not seen by me) which was worrisome for STEMI. A previous ECG from 4 years prior was normal: This looks like an anterior STEMI, but it is complicated by tachycardia (which can greatly elevate ST segments) and by the presentation which is of fever and sepsis.
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. Smith comment: 1) Brugada ECG may have ST shifts in limb leads as well as precordial leads. Bicarb 20, Lactate 4.2,
ECG met STEMI criteria and was labeled STEMI by computer interpretation. This ECG shows a sinus bradycardia with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, normal R-wave progression, normal voltages. Hypothermia can also produce bradycardia and J waves, with a pseudo-STEMI pattern.
Further history later: This patient personally has no further high risk features (syncope / presyncope), but her mother had sudden cardiacarrest in sleep. Regardless of further evaluation, she should avoid bradycardia, AV nodal blockers, Na channel blockers, and fevers. --If Syncope and ST Segment Elevation.
A 12-lead was recorded, showing "STEMI," but is unavailable. 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. She was BVM ventilated and suctioned. Shortly thereafter, pulses were lost.
Theres sinus bradycardia, borderline PR interval, narrow QRS; normal axis/R wave progression; low precordial voltages, and subtle peaked T waves (most obvious in V2, but all T waves are symmetric with a narrow base). Theres no prior ECG to compare - but the bradycardia, prolonged PR and peaked T waves could all be from hyperkalemia.
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