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Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. If this EKG were handed to you to screen from triage without any clinical information, what would you think? Do you appreciate any dynamic changes compared to the patient’s prior EKG? What do you think? In fact, Kosuge et al.
A 50-something man presented in shock with severe chest pain. His prehospital ECG was diagnostic of inferior posterior OMI. The patient was in clinical shock with a lactate of 8. Here is his ED ECG: There is bradycardia with a junctional escape. RVMI explains part of the shock. What is the atrial activity?
Her ECG is shown below: What do you think? The conventional machine algorithm interpreted this ECG as STEMI. Alternatively, with STE in V1 and III, and STD in I and aVL, this ECG could represent proximal RCA OMI with right ventricular involvement. What do you do clinically when the ECG looks like this?
Initial ED ECG: What do you think? Then we must consider clinical data other than the ECG, for a pretest probability : Of all wide complex tachydysrhythmias, the majority are VT. Shocked x 2 without effect. Pads were placed with ultrasound guidance, so they were in the correct position. Why did I say that? What to do now?
A closer look, though, also shows the technology of the daya bulky, two-way radio for communicating with EMS, metal gurneys, glass saline bottles, and portable ECG monitors the size of a small shopping cart. Notice the use of the medical anti-shock trousers and the ECG machine. Now, we have ultrasound or CT scans to confirm.
He was unidentified and there were no records available After 7 shocks, he was successfully defibrillated and brought to the ED. Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines. Here is the initial ED ECG. ECG with LBBB and QRS of > 210 ms. What do you think? The QRS is extremely wide.
The below ECG was recorded. The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. This ECG does not have the typical ST-vector of an LAD occlusion. See below for Ken Grauer Comment on the initial ECG: == On arrival, another ECG was recorded: There appears to have been quite a bit of spontaneous reperfusion!
R4 Case Follow-up: SCAD WITH dr. Martella Spontaneous Coronary Artery Dissection (SCAD) is a diagnosis confirmed via imaging: Coronary Angiography, Optical Coherence Tomography, Intravascular Ultrasound Therefore, treatment in the ED is the same as atherosclerotic ACS: ASA, heparin gtt and possible statin.
He had the following EKG recorded: Low voltage, suggests effusion. A bedside cardiac ultrasound was normal, with no effusion. He underwent CPR, and regained a pulse after epinephrine, with an organized narrow complex rhythm at 140, but still with severe shock. Assessment was severe sudden cardiogenic shock. What is it?
He had this ECG recorded. He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. But, remember, we do not evaluate and treat ECGs, we evaluate and treat patients. Are the lungs clear?
She was in shock with thready pulses. A prehospital ECG was recorded: Limb leads: Precordial Leads What is the therapy? The rate is not fast enough to be causing shock, so if it is VT, the priority is still to treat hyperK and secondarily to cardiovert. They thought it was VT, but did not shock. The K returned at 7.4
These diagnoses were not found in his medical records nor even a baseline ECG. An ECG was obtained shortly after arrival: What do you think? There is no evidence of WPW on this ECG, but it is diagnostic for OMI. He reported a history of “Wolf-Parkinson-White” and “heart attack” but said neither had been treated.
No shock was ever delivered. He was in profound shock. A bedside cardiac ultrasound 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. There is no pericardial fluid to account for shock. Sixth: Severe shock (e.g.,
Initial ROSC was obtained, during which this ECG was obtained: What do you think? I sent it to 2 of my ECG nerd colleagues with no clinical information whatsoever, who instantly said: "Looks like afib with subendocardial ischemia and right heart strain pattern." "I CPR was initiated immediately. The rhythm is atrial fibrillation.
Here is his ECG: Original image, suboptimal quality Quality improved with PM Cardio digitization The ECG is highly suggestive of acute right heart strain, with sinus tachycardia, S1Q3T3, and T wave inversions in anterior and inferior with morphology consistent with acute right heart strain. Moreover, there is tachycardia.
Point-of-Care-Ultrasound (POCUS) is a bedside modality that can assist Emergency Physicians (EPs) in differentiating PE from other causes of cardiac arrest. Multiorgan POCUS The diagnostic power of POCUS often resides in combining multiple ultrasound exams. 1-3 As many as 25% of acute PE cases present as sudden cardiac death.
Colin is an emergency medicine resident beginning his critical care fellowship in the summer with a strong interest in the role of ECG in critical care and OMI. An ECG was obtained shortly after arrival: ECG 1 What do you think? The ECG has a lot of artifact, and the amplitude is very small, making interpretation challenging.
Glucose POC ECG: Is this actually sinus tachycardia? Looking at the initial or even repeating the ECG will be helpful here. Additional resuscitation Have we addressed all potential sources of shock for the patient in front of us? Does the patient require blood, a procedure to address obstructive shock, or other source control?
She arrives in the emergency department (ED) with decreased level of consciousness and shock. The EKG shows sinus tachycardia with nonspecific changes and no ST segment elevations, Q waves, or hyperacute T waves. Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients.
An immediate 12-lead EKG was obtained: There is ST elevation in leads aVR and V1, with marked ST depression in I, II, III, aVF, V3-V6. Smith comment: This patient did not have a bedside ultrasound. The ECG cannot diagnose the etiology of ischemia; it only the presence of ischemia, from whatever etiology. What should be done?
If you or your patient do not have a watch capable of providing you with an ECG, consider asking those on board to allow you to borrow theirs. Get a blood gas when possible to help guide your ventilation. Some newer AED's have the capability of providing you with a rhythm strip.
The screening physician ordered an EKG and noted his ashen appearance and moderate distress. Triage EKG: What do you think? Close up of V3 with baseline in red Close up of V4 with baseline in red This ECG alone is highly suspicious for posterior OMI! This is a very specific marker of posterior OMI. Epub 2021 Nov 15.
Past medical history included RBBB without other cardiac history, but old ECG was not available. As for the ECG, it could represent OMI, but RBBB is also a clue that it may be PE. But with prehospital and ED ECGs being ‘STEMI negative’, the ECG was signed off and the patient waited to be seen.
ULTRASOUND IN CHEST PAIN: [BLOG]: It is never a bad idea to throw an ultrasound probe on your patient with chest pain. ECG PATTERN RECOGNITION CARDIAC ARREST AND ST ELEVATION: [BLOG]: Dr. Smith features a brief cardiac arrest case with an ECG pattern that you must know and be able to recognize! Check out his post here.
What is your ECG interpretation and what would you do next? This ECG shows a normal sinus rhythm with a normal conduction pattern (normal PR, normal QRS, and normal QTc), normal axis, late R wave progression (and misplaced V2), normal voltages, ST-elevation in aVR and global ST-depressions. BP was 110 and oxygen saturation was normal.
When the physicians approached him, he was ashen, diaphoretic, and appeared in shock. When the paramedics arrived, they obtained a 12 lead ECG and confirmed the unstable vital signs. EKG is pictured below: What do you think? Why is the patient in shock? He was in profound cardiogenic shock.
Here is his ECG: What is your interpretation? Case Continued 2 days later the patient became increasingly tachycardic, hypotensive, ashen, clammy (in cardiogenic shock) and had a new murmur. This was the 12-lead ECG. This remains consistent with PIRP, as was the first ECG. Exact pain history was difficult to ascertain.
In this case, profound shock for 1 hour would result in the same degree of infarction. A followup ECG was recorded 2 days later: No definite evidence of infarction. The Type 2 MI would then have been a result of the prolonged severe shock while in arrest. For clarity — I’ll again show the initial ECG done in the ED in Figure-1.
Here is the EMS ECG: Obviously massive diffuse subendocardial ischemia, with profound STD and STE in aVR Of course this pattern is most often seen from etoliogies other than ACS. The ECG only tells you there is ischemia, not the etiology of it. This was a point of care ultrasound, not a bubble contrast echo.
Here is his ECG: There is atrial fibrillation at a rate of 95. Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock. If detected early by ultrasound, the patient can be saved. This was the 12-lead ECG.
Consider valvular injury in any patient who appears to be in cardiogenic shock, has hypotension without obvious hemorrhage, or has pulmonary edema. Jeff: Interestingly, the system I work in has prehospital physicians, who do carry US, but I can’t think of a major trauma where ultrasound changed any of the decisions we made.
The paramedics found the patient with ROSC and a GCS 7, and an ECG showing LBBB with possible lateral ST elevation. Below is the first ED ECG, labeled LBBB by the machine. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings.
He had an ECG in clinic which worried the providers because of possible inferior MI, and they sent him to the ED. Here is that ECG: What do you think? He was sent to the ED and had this ECG at t = 1 hour: Similar There are several issues which mitigate against acute inferior MI, and these are the Learning Points: 1.
AEDs are designed to safely deliver the required life-saving shocks to restore a normal heart rhythm during this type of cardiac emergency. These tests can include: Electrocardiogram (Resting ECG). Typically, ECG results appear normal during rest periods. Exercise Stress Test with ECG. Continuous Portable ECG Monitoring.
AEDs are designed to safely deliver the required life-saving shocks to restore a normal heart rhythm during this type of cardiac emergency. These tests can include: Electrocardiogram (Resting ECG). Typically, ECG results appear normal during rest periods. Exercise Stress Test with ECG. Continuous Portable ECG Monitoring.
Here is her ECG on arrival to the ED: What is your differential? The ECG is quickly reviewed and shows sinus rhythm with normal QRS complexes. Her prior ECG on file is shown below: What are your next steps? Learning Points: The ECG is always just one piece of the clinical puzzle. What are your next steps?
Here is her EKG: What is unusual about this? Her bedside cardiac ultrasound was normal We decided to cardiovert her since the time of onset was very recent. Here is the ECG after ibutilide: What do you notice? Here is the post-cardioversion ECG: Sinus rhythm, still with the longer QT interval. She was on no medications.
Here was his ED ECG, which was identical to the prehospital ECG. ST vector In this ECG, the ST vector is both posterior (away from V3 and V4), upward, away from aVF, and rightward (away from I, II, V5, V6 and towards aVR. This is unfortunate in my view, as it complicates the retrospective analysis of the ECG!!
Individualize the choice of using inotropes, vasopressors, or fluids to treat post-CA hypotension and to target the likely cause(s) contributing to the shock and hemodynamic state (100%, 23/23). In patients with enteral intolerance or shock, start with trophic EN (rates of 10–20 mL/h) and adjust according to tolerance (91%, 19/21).
Nachi: Each year, in the US, approximately 10,000 patients present with electrical burns or shocks. Pay attention to the entry and exit sites, as the pathway of the shock is predictive of the potential for myocardial injury and arrhythmia. Those with low voltage injuries and a normal EKG do not require monitoring.
The ECGs An initial ECG was obtained as the pain was rapidly resolving: Minimal upsloping ST Elevation in III, with a steeply biphasic T wave, and with reciprocal ST depression in leads I and aVL. Often, intravascular ultrasound or intravascular optical coherence tomography is requeried to make the diagnosis. Lobo et al.
Here was his prehospital ECG, which I viewed immediately while the resident performed cardiac ultrasound: What do you think? Here is the cardiac ultrasound which the resident performed as I viewed the ECG: This shows a huge pericardial effusion. An ED ECG was recorded: What do you think? Is is sinus?
So I immediately left the room to get an ultrasound machine. While calling for some help and arranging to have her transported to our critical care zone, I got this quick ultrasound which confirmed my suspicion: This quick view was all I was able to obtain in the circumstances. Why did she go from stable to shock in seconds?
Given her reported chest pain, shortness of breath, and syncope, an ECG was quickly obtained: What do you think? A bedside cardiac ultrasound was performed with a parasternal long axis view demonstrated below: There is a large pericardial effusion with collapse of the right ventricle during systole. This patient is only pseudo-stable.
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