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Written by Jesse McLaren A healthy 75 year old developed 7/10 chestpain associated with diaphoresis and nausea, which began on exertion but persisted. Below is the first ECG recorded by paramedics after 2 hours of chestpain, interpreted by the machine as “possible inferior ischemia”. What do you think?
Written by Willy Frick A man in his 50s with history of hypertension, hyperlipidemia, and a 30 pack-year smoking history presented to the ER with 1 hour of acute onset, severe chestpain and diaphoresis. preceding each of the fascicular beats — indicating a faster rate for the escape rhythm compared to the sinus bradycardia ).
A 50-something man presented in shock with severe chestpain. 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. The February 11, 2020 post ( LA-RA reversal ). The March 18, 2020 post ( LA-RA reversal ).
The patient presented due to chestpain that was typical in nature, retrosternal and radiating to the left arm and neck. He denied any exertional chestpain. It is unclear if the patient was pain free at this time. He has a medical hx notable for hypertension, hyperlipidemia and previous tobacco use disorder.
The patient presented with chestpain. I was taught that the tell-tale sign of ischemia vs an electrical abnormality was in the hx, i.e. chestpain for the ischemia and potential syncope for brugada. Only 5-18% of ED patients with chestpain have a myocardial infarction of any kind. Bradycardia.
The rhythm is sinus bradycardia at a rate just over 50/minute. Although difficult to measure ( because of marked overlap of the QRS in multiple chest leads ) — there appears to be greatly increased QRS amplitude, consistent with voltage for LVH. The February 11, 2020 post ( LA-RA reversal ).
I see the following: The rhythm is sinus bradycardia at ~55-60/minute. PEARL # 2: Applying PEARL #1 to today's case — the fact that this patient's symptoms began before ECG #1 was obtained, and that his chestpain had resolved by the time ECG #1 was recorded — strongly suggests that the "culprit" artery may have spontaneously opened.
He woke up alert and with chestpain which he also had experienced intermittently over the previous few days. The history in today's case with sudden loss of consciousness followed by chestpain is very suggestive of ACS and type I ischemia as the cause of the ECG changes. What do you think?
The patient in today’s case is a previously healthy 40-something male who contacted EMS due to acute onset crushing chestpain. The pain was 10/10 in intensity radiating bilaterally to the shoulders and also to the left arm and neck. Written By Magnus Nossen — with edits by Ken Grauer and Smith. The below ECG was recorded.
He arrived to the ED by helicopter at 1507, about three hours after the start of his chestpain while chopping wood around noon. He arrived to the ED by ambulance at 1529, only a half hour after the start of his chestpain around 1500 while eating. Angiography revealed a 30% nonobstructive stenosis of the mid LAD.
This middle aged male with h/o GERD but also h/o stents presented to the ED with chestpain. The computer called "Sinus Bradycardia" only (implying that everything else is normal. The overreading Cardiologist called it only "Sinus Bradycardia" with no other findings. There is zero ST Elevation.
He denied any chestpain or shortness of breath and stated he felt at his baseline yesterday prior to drug use. They recommended repeating his ECG and awaiting troponin since the patient did not have any chestpain. He complained of generalized weakness and left lower extremity numbness. What is it? Activate the Cath Lab?
Apparently he denied chestpain. JAMA 2000) showed that 1/3 of patients with STEMI, and 1/3 of patients with NSTEMI, present without chestpain. Chestpain and Concordant ST Depression in a patient with aortic valve and previously normal angiogram Right Bundle Branch Block and ST Depression in V1-V3.
A 40-something male with no previous cardiac disease presented with chestpain. The pain continued and the first high sensitivity troponin I returned at 105 ng/L Another ECG was recorded: The ST segment in aVF has flattened a bit, revealing that there is some STD in addition to the non-specific findings in III and aVL.
There was no chestpain. For example — bradycardia and AV conduction disturbances are not uncommon with Hyperkalemia , with these conduction disturbances most often resolving once serum K+ is corrected. This was written by Magnus Nossen The patient is a female in her 50s. She was feeling fine prior to the last seven days.
This fantastic case and post was written by Jesse McLaren (@ECGcases), edited by Smith Case You’re shown an ECG from a patient in the waiting room with chestpain. Sinus bradycardia, normal conduction, normal axis, normal R wave progression, no hypertrophy. JAMA Cardiol 2020 5. -- Litell JM, Meyers HP, Smith SW.
He said that his pain does not feel like his previous episode of pericarditis, and is not related to meals. He denied chestpain, shortness of breath, nausea, fever, chills, rashes, cough, and leg pain. He admitted to lifting some heavy objects a few days ago but denied trauma.
After the heart rate increased slightly, here was the repeat ECG: Sinus bradycardia, only slightly faster rate than prior. See these similar cases: A man in his sixties with chestpain Why is there inferior ST elevation, and would you get posterior leads? Sudden CP and SOB with Inferior ST Elevation and in STE in V1.
Smith and Myers found that in otherwise classic Wellens syndrome – that is, prior anginal chestpain that resolves with subsequent dynamic T wave inversions on the ECG – even the T waves of LBBB behave similarly. [2] 2] Although the clinical context in today’s case does not fit these descriptors for Type I OMI (e.g. 5] Isnard, R.
A recent similar case: A 40-something with chestpain. 3 of the 4 have similarly bizarre PVCs. == MY Comment by K EN G RAUER, MD ( 4/29/2020 ): == Cardiac Arrest with Bizarre PVCs/Torsades de Pointes: Intriguing case with many interesting features. Is this inferior MI? There is a bigeminy with very Bizarre looking PVCs.
It was from a patient with chestpain: Note the obvious Brugada pattern. The elevated troponin was attributed to either type 2 MI or to non-MI acute myocardial injury. There is no further workup at this time. Smith: Here is a case that was just texted to me today from a former resident. This patient ruled out for MI.
days of chestpain that started as substernal and crushing in nature awakening him from sleep and occasionally traveling to right side of neck. The pain was described as constant, worse with deep inspiration and physical activity, sometimes sharp. He reported 1.5
Despite the baseline artifact theres sinus bradycardia, convex ST elevation in III, reciprocal ST depression in aVL and possible anterior ST depression indicating inferoposterior OMI. He was given two separate sprays of nitroglycerin sublingually, neither of which improved his pain but did cause him to become briefly hypotensive ( 600 ng/L.
Case A 68 year old man with a medical history of hypertension, hyperlipidemia, and CAD with stent deployment in the RCA presented to the emergency department with chestpain. A post-cath EKG was recorded at 0719: The computer interpretation read Sinus bradycardia, otherwise normal ECG. He had an EKG recorded right away.
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