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This was sent by anonymous The patient is a 55-year-old male who presented to the emergency department after approximately 3 to 4 days of intermittent central boring chestpain initially responsive to nitroglycerin, but is now more constant and not responsive to nitroglycerin. It is unknown when this pain recurred and became constant.
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?
A 56 year old male with PMHx significant for hypertension had chestpain for several hours, then presented to the ED in the middle of the night. He reported chestpain that developed several hours prior to arrival and was 5/10 in intensity. The pain was located in the mid to left chest and developed after riding his bike.
No ChestPain, but somnolent. The fact that this is syncope makes give it a far lower pretest probability than chestpain, but it was really more than syncope, as the patient actually underwent CPR and had hypotension on arrival of EMS. Here is the ED ECG (a photo of the paper printout) What do you think?
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? Also: How did this happen? Is this just right bundle branch block?
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. His prehospital ECG was diagnostic of inferior posterior OMI. He appeared gray in color, with cool skin.
Case An 82 year old man with a history of hypertension presented to the ED with chestpain at 1211. He described his chestpain as pleuritic and reported that it started the day prior while swinging a golf club. His pain suddenly became much worse in the ED and he became acutely diaphoretic, dizzy, and hypotensive.
This was sent to me by a former resident from a community hospital: A middle-aged woman complained of chestpain and was seen in triage. The computer interpreted the ECG (GE Marquette 12 SL) as: "Sinus Bradycardia. Here it is: Computer interpretation: "Sinus bradycardia. She had a ECG recorded. Normal ECG."
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.
Submitted and written by Megan Lieb, DO with edits by Bracey, Smith, Meyers, and Grauer A 50-ish year old man with ICD presented to the emergency department with substernal chestpain for 3 hours prior to arrival. At this time he reported ongoing chestpain and was given aspirin and nitroglycerin.
Written by Jesse McLaren, with edits from Smith and Grauer A 60 year old with no past medical history presented with two hours of chestpain radiating to the left arm, with normal vitals. Unfortunately, the reality is — that many ( most ) WPW patients who present with chestpain do not manifest intermittent preexcitation.
The patient’s chestpain spontaneously resolved before he was evaluated and has a repeat ECG obtained at 22:12 obtained shown below. Soon afterward, the patient’s symptoms return along with lightheadedness, bradycardia, and hypotension. It is unclear if he received aspirin at triage. This ECG is more difficult.
The patient has acute chestpain. Instead — my thoughts were as follows: The rhythm is sinus , with marked bradycardia and a component of sinus arrhythmia. This was texted to me in real time. What do you think? Here was my answer: "Not ischemia. Maybe HOCM or another form of LVH. I would not activate cath lab.
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.
The patient with no prior cardiac history presented in the middle of the night with acute chestpain, and had this ECG recorded during active pain: I did not see any ischemia on this electrocardiogram. Their apparently excessive length (QT interval) is due to bradycardia. This is a case I had quite a while back.
Written by Pendell Meyers A woman in her 50s presented with acute chestpain and lightheadedness since the past several hours. Here is her triage ECG during active symptoms: What do you think? The ED physician read this as "Normal sinus rhythm. Marked ST abnormality, possible anterior subendocardial injury."
A middle-aged woman with a history of hypertension presented with typical chestpain. Here was her presenting ECG, with chestpain: Inferior leads show hyperacute T-waves and reciprocal STD in aVL, with a reciprocally hyperacute T-wave in aVL. Her BP was 160/80. This is all but diagnostic of inferior OMI.
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. To improve visualization — I've digitized the original ECG using PMcardio ).
This ECG could easily be seen in an ED chestpain patient, and I have seen many) What do you think? Description Sinus bradycardia. Comment I (Smith) have seen many similar ECGs in ED chestpain patients. I have seen this innumerable times in chestpain patients in the Emergency Department.
He did not have chestpain. Chestpain in high risk patient. Syncope and Bradycardia Syncope in a 20-something woman Long QT: Do not trust the computerized QT interval when the QT is long An Alcoholic Patient with Syncope Cardiac Arrest. Here is his triage ECG: What do you think? Is it STEMI? What is going on here?
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.
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.
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 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?
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 chestpain: V5 and V6 sure look like a STEMI For this ECG and chestpain in the ED, the Cath lab activated. But the angiogram was clean.
All of the patients presented with chestpain , and they are all in triage. Triage is backed up, and 10 minutes into your shift one of the ED nurses brings your several ECG s that has not been overread by a physician. Which, if any, of these patients has OMI, with myocardium at risk and need for emergent PCI?
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.
This is the initial ED ECG of a 46 year old male with chestpain: The QTc was 420 ST Elevation at 60 ms after the J-point in lead V3 = 2.5 ng/ml) A 45 year old male called 911 for chestpain: The QTc was 400 ST Elevation at 60 ms after the J-point in lead V3 = 3.5 100% LAD occlusion. He underwent CABG. QRS V2 = 15.5
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 55 year old with no previous cardiac history presented with 3 hours of chestpain. The pain was persistent and reportedly still present at the time of the ECG. He has now implemented the Queen of Hearts in his hospital. He wanted to share one of the first cases. This will be corrected in Version 2, coming soon.
The relationship between low RHR and CI has yet to be described.Purpose:We hypothesize that resting sinus bradycardia (low RHR) could be a predictor of chronotropic incompetence and reduced exercise capacity.Methods:The derivation cohort consists of 201 patients with normal Bruce protocol treadmill stress echocardiogram. x age in years).Results:The
If you experience any symptoms, such as chestpain, dizziness, unusual tiredness or fatigue, shortness of breath, or irregular heartbeat, your doctor would want you to go for an ECG test to find out the underlying cause. A fast heartbeat is called tachycardia, while a slow heartbeat is called bradycardia in medical terms.
Written by Willy Frick A 46 year old man with a history of type 2 diabetes mellitus presented to urgent care with complaint of "chest burning." The ECG shows sinus bradycardia but is otherwise normal. The patient said his chestpain was 4/10, down from 8/10 on presentation. The following ECG was obtained.
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 ).
The combination of absence of chestpain and history of LV aneurysm made it easy to assess that this patient does not have acute OMI. In view of the History with the current admission ( ie, presenting to the ED for vertigo — with no new chestpain ) — I interpreted ECG #1 as no OMI.
We have borderline sinus bradycardia with 1 ° AVB and occasional PACs. ECG diagnosis: Borderline sinus bradycardia, 1st degree AVB, RBBB, and occasional PACs. Case Review EMS is called to the residence of a 69 y/o M with a chief complaint of chestpain. What’s the rhythm? Is that a supraventricular rhythm?
His first electrocardiogram ( ECG) is given below: --Sinus bradycardia. In a patient with ongoing, severe chestpain — the subtle-but-real ST-T wave changes are "dynamic" indication of an ongoing acute cardiac event — therefore prompting the need for cardiac cath! As he seemed very agitated, fentanyl and diazepam were given.
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.
Even if you don't see the OMI, you can usually prevent such a long delay to reperfusion by recording serial ECGs every 15 minutes for a patient with persistent chestpain. The rhythm in ECG #1 is sinus bradycardia and arrhythmia. Record serial ECGs every 15 minutes!! Hillinger et al.
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. What do you think?
Now chestpain free. There is a junctional bradycardia. Another ECG was recorded: ECG 2: Findings are still present and have evolved to a smal l degree At time 6 hours, Troponin T returns at between 0.50 ng/mL (not giving exact number, but significantly high) Now having frequent PVCs. She was taken to the cath lab.
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.
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.
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