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She was brought in by ambulance and received aspirin and nitroglycerin en route. link] Case continued She arrived in the ED and here is the first ED ECG. CORONARY ARTERIES: Exam was not directly tailored for coronary artery evaluation, noting recent diagnostic coronary angiogram. Stroke-volume:50 ml.
He advises, however, recurrent syncopal episodes for the past six months, some of which have resulted in ED admission, yet no identifying mechanism could be determined. 3,4] The final 12 Lead ECG does not meet any Smith-modified Sgarbossa criteria, so the T wave signatures are characteristic of improved coronary flow, but not necessarily MI.
He arrived to the ED by helicopter at 1507, about three hours after the start of his chest pain while chopping wood around noon. He arrived to the ED by ambulance at 1529, only a half hour after the start of his chest pain around 1500 while eating. Patient 2 , EKG 1: What do you think? It was stented. This was a large OMI.
His wife contacted the ambulance service after the patient experienced an episode of loss of consciousness. The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch).
Written by Bobby Nicholson, MD 67 year old male with history of hypertension and hyperlipidemia presented to the Emergency Department via ambulance with midsternal nonradiating chest pain and dyspnea on exertion. Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. What do you think?
A 40-something male presented by ambulance with one hour of chest pain that was improving after sublingual nitroglycerine and 325 mg of aspirin, chewed. Here is his initial ED ECG: What do you think? Or had not had a prehospital ECG on the ambulance. Then the ED doc would be dependent on that first ECG.
The ambulance report says "BP continued to drop during transport and pt remained cold and clammy." Frick — an all-too-common misconception is that the absence of obstructive coronary disease on cardiac catheterization rules out acute coronary occlusion as the cause of the patient's acute event. This is not the case.
Turns out that it was a 50-something patient with no previous cardiac history who had called 911 for chest pain and had presented 75 minutes earlier by ambulance to triage (as the entire ED was overloaded). All triage ECGs are immediately shown to triage ED faculty.
Ambulated to ambulance for eval. The coronaries were clean (this is not the gold standard, however, as some patients with ischemic ST elevation may have clean coronaries). ACTUAL CORONARY ANATOMY: Dominance: Right LM: A 5 mm vessel which bifurcates into the LAD and LCx coronary artery.
This is her pre-hospital ECG: This is her first ECG in the ED: What do you think? The nitro she took in the ambulance did not help. She also received an additional nitro in the ED after receiving aspirin and nitro via EMS. Her first EKG in isolation has no hard findings that are diagnostic for an acute coronary occlusion.
He reportedly told his family "I think I'm having a heart attack", then they immediately drove him to the ED, and he was able to ambulate into the triage area before he collapsed and became unresponsive. The value of Stat Echo in the ED for confirming clinical and ECG suspicion of acute PE cannot be overstated!
Study idea: We should look at all OMIs who had a chest CT and compare to all patients with Non-OMI pathology who had a contrast chest CT and have radiologists blindly interpret the perfusion of the myocardium The cardiology fellow came down to the ED and said: "What are you worried about? This ST depression?" 2022.08.750 Section 5.2.2,
It was a constant ache on the left side of his chest that forced him to stop cycling and call for an ambulance. He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronary artery disease with a near-occlusive culprit lesion in the RCA, possibly reperfused.
He rehydrated and had no orthostatic symptoms prior to discharge, ambulated well. - Discussion Thus, no further ECGs were recorded and there was no angiogram or stress test or CT coronary angiogram. No previous study for comparison. Clinical Course: - He had no events on cardiac monitoring overnight. -
They did not have an ultrasound on the ambulance (some local crews are starting to utilize POC limited US in our service areas). Also, the RV appears large and hypokinetic The patient kept having recurrent syncopal episodes in the ED and was subsequently intubated for stabilization and airway protecting prior to going to the cath lab.
Some of the critical differentials include pulmonary embolism, acute decompensated heart failure, pneumonia, pneumothorax, and acute coronary syndrome. Anginal chest pain, chest heaviness, or evidence of fluid overload suggest acute coronary syndrome or acute decompensated heart failure. Signs and symptoms of systemic infection (e.g.,
Cardiology wanted a CT of the aorta to rule out dissection, presumably partly due to the very high blood pressure readings, but also because it is hard for people to believe that a 20-something woman could have acute thrombotic coronary artery. They also recommended a NTG drip, after which she reported complete resolution of pain.
The patient was then sent to the ED for evaluation not by ambulance but driven to the ED by his wife. In this case report the 69-year old woman ( who incidently had a history of both coronary disease and cardiomyopathy ) remained in sustained VT for 5 days without hemodynamic deterioration.
He was worked up non-emergently in the ED with pain recurring and resolving multiple times during his stay. As such, the patient was placed on a heparin drip and transferred by ambulance to a cardiac cath-capable facility. Three years later, the patient presented again to the ED with chest pain. Another EKG was eventually taken.
This case was a 69 year old male, brought in by ambulance, after being found unresponsive in bed by family earlier that day. On arrival to the ED, he was breathing spontaneously, had faint pulses, and was cool to the touch. He received an additional 300 mg rectal aspirin and 5000 unit heparin bolus in the ED.
The cath lab was deactivated by cardiologist on arrival at ED because it was "not a STEMI". Initial 4th generation troponin I was 10 ng/mL is consistent with large MI due to acute coronary occlusion (OMI). He presented to the ED for evaluation chest pain. There are moderate coronary artery calcifications.
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