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Out-of-hospital cardiacarrest (OHCA) mostly occurs in crowded public places outside hospitals, such as public sports facilities, airports, railway stations, subway stations, and shopping malls. ECMO support therapy for patients with cardiacarrest can be considered when economic conditions permit.
This is the first ever video podcast on EM Cases with Jordan Chenkin from EMU Conference 2017 discussing how to optimize three aspects of cardiacarrest care: persistent ventricular fibrillation, optimizing pulse checks and PEA arrest, with code team videos contrasting the ACLS approach to an optimized approach.
In this part 2 of our 2-part podcast series on CardiacArrest - The When, Why & How, we discuss some of the finer art of cardiacarrest care and answer questions such as: how should we best communicate to EMS, the ED team and the family of the patient to keep the team focused, garner the most important info and keep the flow of the code going?
This 80 year old with a history of CABG had a cardiacarrest. We did a bedside cardiacultrasound. Now, it is true that shortly after a non-ACS cardiacarrest, there can be transient diffuse ST depression, but not ST elevation in a coronary distribution, and there should not be a wall motion abnormality.
The post EM Quick Hits 11 Blunt Cerebrovascular Injury, Physostigmine, TEE in CardiacArrest, Understanding Nystagmus, Subtle Inferior MI, Choicebo appeared first on Emergency Medicine Cases.
Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines. I was there and said, "No, I think this is all due to severe chronic cardiomyopathy and cardiacarrest due to primary ventricular fibrillation, not due to ACS." _ Why did I say that? Here is the initial ED ECG. What do you think?
An emergency cardiacultrasound could be very useful. Appreciation of these subtle ECG findings could have helped to avoid a cardiacarrest and its resulting permanent disability 3. The upright portion of the T-wave in aVF is very large compared to the QRS size. If these remain unchanged, then serial troponins.
He had multiple cardiacarrests with ROSC regained each time. CardiacUltrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. This patient arrested shortly after hospital arrival. Submitted by a Med Student, with Great Commentary on Bias!
A bedside cardiacultrasound was normal, with no effusion. He had the following EKG recorded: Low voltage, suggests effusion. see Ken's discussion of low voltage below) There is a QS-wave in V2. There is minimal, probably normal STE in V2-V6.
Bedside cardiacultrasound showed moderately decreased LV function. See this post: How a pause can cause cardiacarrest 2. (And of course Ken's comments at the bottom) An elderly obese woman with cardiomyopathy, Left bundle branch block, and chronic hypercapnea presented hypoxic with altered mental status. The plan: 1.
We present the case of a man in his 50s, admitted with cardiacarrest secondary to inferolateral STEMI. Successful PPCI was performed via right femoral artery, with access gained under ultrasound guidance.
The post EM Quick Hits 33 Polytrauma Tips & Tricks, Toxic Megacolon, ECG in PE, Patch Calls, CT Before LP, Nebulized Ketamine appeared first on Emergency Medicine Cases.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. If cardiacarrest from hypokalemia is imminent (i.e., As I indicated above, in our cardiacarrest case, after pushing 40 mEq, the K only went up to 4.2 He was managed medically with Clopidogrel.
On arrival, the patient was in shock, was intubated, and had an immediate cardiacultrasound. What does a heart look like on ultrasound when the EKG looks like that? Here you go: It's not the world's greatest cardiacultrasound video, but it does appear to show poor function and low volume. How would you treat?
Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance. . = Smith comment: I agree with starting with a beta blocker such as esmolol, since this is likely to be a hyper-catecholaminergic state.
A bedside cardiacultrasound was recorded: Here is a still image of the echo: The red arrows outline the right ventricle and the yellow arrows outline the left ventricle chamber. Second: what does the ultrasound tell us about the condition? The large RV and small LV on ultrasound make this a right ventricular process.
I suspect this is Type 2 MI due to prolonged severe hypotension from cardiacarrest. The ways to tell for certain include intravascular ultrasound (to look for extra-luminal plaque with rupture) or "optical coherence tomography," something I am entirely unfamiliar with.
But the lack of traditional Sgarbossa criteria is not reassuring enough for such high pretest probability (elderly patient with chest pain, out of hospital cardiacarrest and LBBB), and the Modified Sgarbossa Criteria confirms Occlusion MI in this case. The patient still had chest pain and a third ECG was performed.
It was notable for a normal cardiacultrasound with no pericardial fluid, normal LV and RV function (though the quality was not sufficient to evaluate for wall motion abnormalities) and normal IVC dynamics. Bedside ultrasound is another very important piece. Ultrasound can be very helpful to distinguish causes of hypotension.
A bedside ultrasound was done by the emergency physician, using Speckle Tracking. Here are three more dramatic cases that illustrate RBBB + LAFB Case 1 of cardiacarrest with unrecognized STEMI, died. Unfortunately, that video is unavailable. It appeared to show a lateral wall motion abnormality.
This case was provided by Spencer Schwartz, an outstanding paramedic at Hennepin EMS who is on Hennepin EMS's specialized "P3" team, a team that receives extra training in advanced procedures such as RSI, thoracostomy, vasopressors, and prehospital ultrasound. She was defibrillated and resuscitated. It can only be seen by IVUS.
I would do bedside ultrasound to look at the RV, look for B lines as a cause of hypoxia (which would support OMI, and argue against PE), and if any doubt persists, a rapid CT pulmonary angiogram. There was 100% proximal LAD occlusion with TIMI 0 flow, and cardiacarrest in the cath lab.
His ED cardiacultrasound (which is not at all ideal for detecting wall motion abnormalities, and is also very operator dependent for this finding) was significant for depressed global EF. The patient's initial troponin I was 2.0 ng/mL (99% reference level = 0.030 ng/mL. His prior EF from an ECHO 6 months prior indicated 35% LVEF.
Thirty-six patients (36%) presented with cardiacarrest, and 78% (28/36) underwent emergent angiography. Subendocardial Ischemia from another Cause ( ie, sustained tachyarrhythmia; cardiacarrest; shock/profound hypotension; GI bleeding; anemia; "sick patient"; etc. ).
Case Continued Bedside ultrasound was performed: This shows an anterior wall motion abnormality, and highly suggests the LAD as the infarct artery. The patient was subsequently given 5000 units of heparin, 180 mg of ticagrelor, and defib pads were placed on the patient in the event that he should have a cardiacarrest.
A bedside cardiacultrasound was performed with a parasternal long axis view demonstrated below: There is a large pericardial effusion with collapse of the right ventricle during systole. The beat-to-beat variation in QRS amplitude and morphology is electrical alternans. This patient is only pseudo-stable. She has already had syncope.
He had a previous MI with cardiacarrest 2 years prior. There was an old ECG for comparison: One year prior with no ST segment abnormalities A bedside cardiacultrasound was done by the emergency physician. Case A 47 year old male called 911 for severe chest pain. He was clammy and looked unwell.
Patients who present with chest pain or cardiacarrest and have an ECG diagnostic of STEMI could have myocardial rupture. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual.
They also did an ED bedside ultrasound, shown here : This shows a large amount of pericardial fluid, with some echogenic structures that appear to be thrombi or fibrinous exudate. Patients who present with chest pain or cardiacarrest and have an ECG diagnostic of STEMI could have myocardial rupture. These patients may survive.
Further history later: This patient personally has no further high risk features (syncope / presyncope), but her mother had sudden cardiacarrest in sleep. A bedside cardiacultrasound revealed grossly normal to hyperdynamic systolic function with no obvious areas of wall motion abnormalities.
The clinical significance of ARCA-LCS lies in its potential to cause myocardial ischemia or sudden cardiac death, particularly under physical exertion. Transthoracic echocardiogram, bilateral carotid Doppler ultrasound, and electrocardiogram were normal. No previous history of hypertension or diabetes.
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