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Bedside cardiac ultrasound with no obvious wall motion abnormalities. This confirms that the pain was ischemia and is now resovled. BP initially 160s/90s, O2 sats 95% on room air. The cardiology fellow agreed with plan for emergent cath and escorted the patient to the cath lab.
No ischemia. A bedside cardiac ultrasound performed by a true EM expert (Robert Reardon, who wrote the cardiac ultrasound chapter in Ma and Mateer) showed an inferior wall motion abnormality. We already know that the ischemia is ongoing, though mild (because of the persistent pain). Q-waves are even more pronounced.
Coronary Intravascular Ultrasound (IVUS) equipment consists of an IVUS catheter, pullback device and the imaging console. Incomplete stent apposition can be detected by intravascular ultrasound. Transient ischemia may occur while negotiating tight stenosis or small vessels.
The secondary outcomes included ischemia-driven target lesion revascularization, target vessel myocardial infarction, death, cardiac death, target vessel revascularization, stent thrombosis, and major adverse cardiac events. Circulation, Ahead of Print. The 2 coprimary outcomes were target lesion revascularization and myocardial infarction.
This EKG is diagnostic of transmural ischemia of the inferior wall. If it is angina, lowering the BP with IV Nitroglycerine may completely alleviate the pain and the (unseen) ECG ischemia. Transmural ischemia (as seen with the OMI findings on ECG) is not very common with demand ischemia, but is possible.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. What should be done? Should the cath lab be activated?
This suggests diffuse subendocardial ischemia. However, along with that subendocardial ischemia, there is also STE in lead III with reciprocal ST depression in aVL, and some STE in V1. If there is also subendocardial ischemia, the ST depression vector remains leftward, with a reciprocal ST Elevation vector also to the right.
Bedside cardiac ultrasound showed moderately decreased LV function. It should be kept in mind that on occasions, beta-one agonist can result in increased ventricular ectopy e.g., in severe myocardial ischemia (by increasing myocardial demand), or sometimes with congenital long-QT syndrome. She was intubated.
There is also STE in lead III with reciprocal depression in aVL and I, as well as some subendocardial ischemia pattern with STD in V5-V6 and STE in aVR. Aslanger's is a combination of acute inferior OMI plus subendocardial ischemia, and due to the ischemia vectors , it has STE only in lead III. Now another, with ultrasound.
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If this STD were due to LVH or to subendocardial ischemia, rather than posterior OMI, it would be maximal in V5 and V6. A bedside ultrasound was done, with dozens of clips, and was even done with Speckle Tracking. There was no cough or fever, the CXR looks like pulmonary edema, the ultrasound showed classic pulmonary edema B lines.
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.
Such T-waves are almost always reciprocal to ischemia in the region of aVL (although aVL looks n ormal here) , and in a patient with chest pain are nearly diagnostic of ischemia. An emergency cardiac ultrasound could be very useful. Ischemia on the ECG can be very subtle and is easily missed. Lesson : 1.
The differential is: Posterolateral OMI or subendocardial ischemia The distinction between posterior OMI and subendocardial ischemia can be important and sometimes difficult. Bedside ultrasound is another very important piece. Ischemic ST depression includes posterior OMI and subendocardial ischemia.
Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall. Similarly, STD in aVL is usually reciprocal to inferior ST elevation, not "lateral ischemia."
There is no definite evidence of acute ischemia. (ie, Simply stated — t he patient was having recurrent PMVT without Q Tc prolongation, and without evidence of ongoing transmural ischemia. ( Some residual ischemia in the infarct border might still be present. Both episodes are initiated by an "R-on-T" phenomenon.
He arrived in the ED and had an immediate bedside cardiac ultrasound while this ECG was being recorded. The bedside ultrasound (video not available) reportedly showed only a slightly reduced LV function. The patient was given 6mg, then 12 mg, of adenosine, without a change in the rhythm. Here is the ECG: What do you think?
In terms of ischemia, there is both a signal of subendocardial ischemia (STD max in V5-V6 with reciprocal STE in aVR) AND a signal of transmural infarction of the inferior wall with Q wave and STE in lead III with reciprocal STD in I and aVL. Now another, with ultrasound. The rhythm is atrial fibrillation. What is the Diagnosis?
His response: “subendocardial ischemia. Smith : It should be noted that, in subendocardial ischemia, in contrast to OMI, absence of wall motion abnormality is common. With the history of Afib, CTA abdomen was ordered to r/o mesenteric ischemia vs ischemic colitis vs small bowel obstruction. Anything more on history?
There is ST depression beyond the end of the wide QRS in I, II, aVF, and V4-V6, diagnostic of with subendocardial ischemia. 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 ST elevation.
I performed a bedside cardiac ultrasound and the posterior wall appeared to be contracting and shortening normally. A posterior ECG was done and showed no ST elevation, not even 0.5 mm in only one posterior lead is highly sensitive and specific for posterior STEMI).
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There was a gradual progression of CKD from mild to severe stages between days 7 and 28 identified by a combination of hematological (creatinine, blood urea nitrogen, and total protein) and imaging (MRI, μCT, dual-energy X-ray absorptiometry, and ultrasound) markers.
One very useful adjunct is ultrasound: Echo of his heart can distinguish aneurysm from acute MI by presence of diastolic dyskinesis, but it cannot distinguish demand ischemia from ACS. Furthermore, notice the well-formed Q-waves in inferior leads. These must raise suspicion of old MI with persistent ST elevation.
1.196 x STE60 in V3 in mm) + (0.059 x computerized QTc) - (0.326 x RA in V4 in mm) Third, one can do an immediate cardiac ultrasound. A bedside ultrasound was done by an emergency physician and simultaneously read by a cardiologist. greater than 23.4 is likely anterior STEMI). LV aneurysm is very different for inferior vs. anterior MI.
A majority (62.5%) of those presenting with ‘normal’ ECGs had the cath lab activated without any ECG being labeled ‘STEMI’ by automated interpretation – based on signs of Occlusion MI including ECG changes, regional wall motion abnormality on bedside ultrasound, or refractory ischemia. Hughes KE , Lewis SM , Katz L , Jones J.
Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. So there is now high pre-test probability + refractory ischemia + Modified Sgarbossa + dynamic ECG changes. The patient still had chest pain and a third ECG was performed. Learning points 1.
I do not think this ECG is by itself diagnostic of OMI (full thickness, subepicardial ischemia ), b ut comparison to a previous might reveal this ECG as diagnostic of OMI. Thus, they obscure the last possible indication for emergent reperfusion in "NSTEMI" (all guidelines recommend emergent cath for refractory ischemia in NSTEMI).
This suggests further severe ischemia. The problem is difficult to study because angiographic visualization of arteries is not perfect, and not all angiograms employ intravascular ultrasound (IVUS) to assess for unseen plaque or for plaque whose rupture and ulceration cannot be seen on angiogram. And yet the arteries remain open.
My opinion was that it was not a cath lab case, but I did suggest they do a bedside ultrasound to look for an anterior wall motion abnormality. I had not seen the cardiac ultrasounds at this time. I did not have more information at the time. To the ED providers, the patient denied CP, SOB, or drug use.
Down-up T-waves in inferior leads are almost always reciprocal to ischemia in the territory underlying aVL. This is not normal and is a tip off that there is posterior ischemia accompanying the ischemia in aVL. Data from stress testing proves that the ST depression of ischemia does not localize.
This proves that the first one was, surprisingly, due to ischemia!! After rethinking the case, he remained concerned about ACS and subsequently performed a point-of-care ultrasound in order to evaluate for regional wall motion abnormality. A second troponin had been drawn 3 hours after arrival and was again less than 0.30ng/mL.
This is an ultrasound (a bit like the type that we use on pregnant women to look at the baby). An ultrasound will allow you to visualise the heart, measure the sizes of the chambers, assess the heart valves and work out how well the heart functions as a pump. It is still possible to have ischemia without coronary disease.
However the patient continued to have chest pain and bedside ultrasound showed hypokinesis of the septum with significantly reduced LVEF. Possible mechanisms of ventricular arrhythmias elicited by ischemia followed by reperfusion. The receiving emergency physician consulted with interventional cardiology who stated there was no STEMI.
A bedside ultrasound was done by the emergency physician, using Speckle Tracking. Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was Was the ST elevation due to transient demand ischemia, or is it false positive? Unfortunately, that video is unavailable.
Normally, concavity in ST segments suggests absence of anterior ischemia (though concavity by itself is not reassuring - see this study ). His ED cardiac ultrasound (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.
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. Alternation in ST segment appearance ( or in the amount of ST elevation or depression ) — is often linked to ischemia. She has already had syncope.
Case continued: All the physicians were very worried about LAD occlusion and recorded a couple bedside ultrasounds: This shows a profound apical and septal wall motion abnormality, perfectly consistent with LAD OMI. These ultrasounds confirm LAD occlusion. Pain will resolve with completed infarct or with resolution of ischemia.
ALL TROPS WERE UNDETECTABLE A formal ultrasound was done: Normal estimated left ventricular ejection fraction at rest. This ST-T wave appearance in the lateral chest leads of ECG #2 is consistent with L V “ S train” vs ischemia. The initial troponin returned undetectable. No wall motion abnormality at rest.
Dr. Nossen performed a bedside ultrasound which was interpreted as normal. Learning Points: Ectopic atrial rhythm can produce atrial repolarization findings that can be confused for acute ischemia, STEMI, or OMI.
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. Takotsubo is a sudden event, not one with crescendo angina.
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. Therefore, we performed ultrasound-guided pericardiocentesis. Is is sinus?
This strongly suggests reperfusing RCA ischemia. Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. Often, intravascular ultrasound or intravascular optical coherence tomography is requeried to make the diagnosis.
This was diagnosed by IVUS (intravascular ultrasound) as a ruptured plaque. This was clearly severe subepicardial ischemia causing ST Elevation, but it was not of a long enough duration to result in measurable infarct. Values: STE60V3 = 2.0, QRS V2 = 10, RAV4 = 15.5, QTc = 377 by computer 4-variable formula value = 16.2, But maybe not.
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