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Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead. This was deemed “non-specific” by the ED physicians. Type I ischemia.
The ECG does not show any definite signs of ischemia. Why Was Cardiac Cath Negative for Coronary Disease? Use ß-blockers with caution ( as they may aggravate coronary spasm ). Given the potential triggering effect of smoking on coronary spasm — absolute abstinence from smoking is essential! The below ECG was recorded.
But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. Then assume there is ACS. Confirmation of sinus tachycardia should be easy to verify when the heart rate slows a little bit ( as the patient's condition improves ) — allowing clearer definition between the T and P waves.
Category 1 : Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates. It’s judicious, then, to arrange for coronary angiogram. Supply-demand mismatch (non-occlusive coronary disease, or exacerbation of preexisting flow insufficiency) a.
Background: Historically, we have treated acute coronary syndrome with supplemental oxygen regardless of the patient ’ s oxygen saturation. More recent evidence, however, demonstrates that too much oxygen could be harmful ( AVOID Trial ) by causing coronary vasoconstriction and increasing oxidative stress. Low O2 protocol: 3.1%
Note that as many as 7% of patients with acute coronary syndrome have chest pain reproducible on palpation [Lee, Solomon]. which reduces the pre-test probability of acute coronary syndrome by less than 30% [McGee]. In an attempt to clarify language, a consensus definition was developed. per 100,000 to 11 per 100,000 [Rosso].
RBBB + LAFB in the setting of ACS is very bad. Some patients have baseline RBBB with LAFB, but in patients with likely ACS, these are associated with severe infarction with cardiac arrest, cardiogenic shock or impending shock. Patients with ACS and RBBB/LAFB usually have a left main vs. proximal LAD. Learning Points: 1.
There were zero patients in this study with a "normal" ECG who had any kind of ACS! Old ‘NSTEMI’ A history of coronary artery disease and a stent to the same territory further increases pre-test likelihood of acute coronary occlusion, including in-stent thrombosis. So this study is actually worthless.
This was texted to me from a former resident, while working at a small rural hospital, with the statement: "I can’t convince myself of anything here, but he’s a 63-year-old guy with prior stents and a good story for ACS." We don't know if he had a stress test, a CT Coronary angiogram, or they just decided to do an angiogram.
ACS then becomes less likely. Before the lab values returned this patient had a n emergent coronary CT angiogram done that ruled out CAD. A false positive cath lab activation is also off course acceptable for this diagnosis if you cannot get an emergent coronary CT angiogram. There are no coronary stenoses.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. This is diagnostic of ACS; it appears to be a reperfused acute inferior OMI. The 3rd inferior lead ( = lead II ) — shows definite ST-T wave flattening.
The commonest causes of MINOCA include: atherosclerotic causes such as plaque rupture or erosion with spontaneous thrombolysis, and non-atherosclerotic causes such as coronary vasospasm (sometimes called variant angina or Prinzmetal's angina), coronary embolism or thrombosis, possibly microvascular dysfunction. This is not the case.
Thus, this does NOT meet STEMI criteria (though, as of 2022, it is a formal "STEMI equivalent", assuming everyone agrees that this is de Winter morphology, for which there is currently no objective definition). Even if a patient's ECG does meet STEMI criteria, it may not be perceived so. What a farce.
He reported a history of ischemic cardiomyopathy with coronary stent placement approximately 10 years prior, but could not recall the specific artery involved. 1, 2] The most clinically useful definition to account for this entire constellation is intraventricular conduction delay. Attached is the first ECG. Isn’t VT ALWAYS “wide”?
However , this patient is having chest discomfort, and by definition then she should be considered not to be stable. Ischemia from ACS causing the chest discomfort, with VT another consequence (or coincidence)? If the patient is hemodynamically stable, iv amiodarone could be considered in such a clinical situation. Is this: 1.
Serial ECGs enhance the diagnosis of acute coronary syndrome. Similarly, the OMI paradigm respects ACS as a dynamic process in which ECG changes reflect the phase of myocardial injury and risk stratify which patients may benefit from emergent PCI. Perform serial ECGs even if symptoms are constant. In fact, use of antidyrhythimcs (e.g.,
A CT Coronary angiogram was ordered. Here are the results: --Minimally obstructive coronary artery disease. --LAD Although a lesion is not visible anatomically on this CT scan, coronary catheter angiography could be considered based on Cardiology evaluation." A repeat troponin returned at 0.45 CAD-RADS category 1. --No
Therefore, this does not meet the definition of myocardial infarction ( 4th Universal Definition of MI ), which requires at least one troponin above the 99% reference range. You can see the deficiency of the definition of MI. Two negative troponins do not exclude the possibility of short-lived acute coronary occlusion.
When Pendell and I are coding ECGs for the Queen's training, this is one category: "Definite ischemia, difficult to differentiate between posterior OMI and subendocardial ischemia." In our opinion it should not be given in ACS unless you are committed to the cath lab. In my opinion, I think it looks more like subendocardial ischemia.
Click here for Direct Download of the Podcast Paper: Aykan AC et al. PMID: 23102885 Aykan AC et al. Because the lungs receive 100% of cardiac output, it has been hypothesized that a lower dose of thrombolytic therapy may still be effective with a better safety profile [3][4]. Clin Exp Emerg Med 2023. JACC Cardiovasc Interv 2018.
This pattern occurs regardless of whether the cause is ACS (decreased supply) or any other cause of decreased supply or increased demand. You must understand that this pattern does not differentiate ACS from other causes of supply/demand mismatch.
Distilling this case into its most salient components, a man with multiple risk factors for coronary disease is presenting with several days of chest pain and markedly elevated troponin with no other reason to explain the lab abnormality ( e.g. sepsis). The patient has ACS by history, active pain, and an elevated troponin.
80%) and definitely too much for hour to hour. However, the Definition of MI requires at least one value above the 99th percentile, which for a male is 34 ng/L (16 ng/L for women). Thus, these troponins are very concerning for ACS, and subsequent ones will probably be diagnostic of acute MI. of the time.
-See this study showing an association between morphine and mortality in ACS: Use of Morphine in ACS is independently associated with mortality, at odds ratio of 1.4. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative.
We who know ischemic ECGs know that really when T-wave inversion is specific for coronary thrombosis that it indicates reperfusion of the artery, not active occlusion. that is, show a pattern of labile ST-T wave changes not due to an acute coronary event. I personally can hardly wait for that future version! Some patients do this.
The biphasic T wave is consistent with recent reperfusion of an occluded coronary artery supplying the inferior region. Here’s the angiogram of the RCA : No thrombus or plaque rupture in the RCA (or any coronary artery) was found. This MI wasn’t caused by a ruptured plaque of CAD - it was a coronary artery dissection of the RCA.
References: 1) See this study showing an association between morphine and mortality in Non-STE-ACS: Meine TJ, Roe M, Chen A, Patel M, Washam J, Ohman E, Peacock W, Pollack C, Gibler W, Peterson E. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative.
The fire department, who operate at an EMT level in this municipality, arrived before us and administered 324 mg of baby aspirin to the patient due to concern for ACS. Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries). An angiogram is a "lumenogram;" most plaque is EXTRALUMINAL!!
Here is an article I wrote: Updates on the ECG in ACS. Was this: 1) ACS with ischemia and spontaneous reperfusion? The patient was taken for an angiogram and had an 80% LAD lesion, but it could not be definitely determined whether this was an acute thrombotic lesion or a chronic stable lesion. References : 1. J Electrocardiol.
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. Sensitivity of POCUS even for definite wall motion abnormalities is far from perfect. The ECG only tells you there is ischemia, not the etiology of it.
There is perhaps a tiny J-wave in several of the QRS complexes in V3, but it would not be enough to definitively say there is a J-wave. Lead aVL, for example, has a definite J-wave. link] He was admitted to the cardiology unit for serial troponin measurements and concern for possible ACS. Stat echo would also be helpful.
But because the patient had no chest pain or shortness of breath, it was not deemed to be from ACS. They were less likely to have STEMI on ECG, and more likely to be initially diagnosed as non-ACS. Dialysis patients have a high rate of ACS without chest pain and high rate of delayed diagnosis and delayed reperfusion 2.
He underwent coronary stenting (uncertain which artery). Therefore, even with a normal or non-diagnostic ECG, a 50 year old male patient should undergo serial ECGs and troponins and be admitted to a monitored bed until MI or ACS can be ruled out. The patient went home and, in front of his wife, he collapsed.
Some providers were worried about ACS because of this ECG. My answer alleviated their concern for ACS and no further workup was done for ACS. showed that , when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. Kosuge et al.
When he showed it to me, I said "Ouch, looks like an acute coronary occlusion. no LBBB or paced rhythm), acute coronary occlusion MI (OMI) is diagnosed in approximately 75% of cases. The Smith-Modified Sgarbossa Criteria Accurately Diagnose Acute Coronary Occlusion in Emergency Department Patients With Ventricular Paced Rhythm.
The diagnostic coronary angiogram identified only minimal coronary artery disease, but there was a severely calcified, ‘immobile’ aortic valve. Author continued : STE in aVR is often due to left main coronary artery obstruction (OR 4.72), and is associated with in-hospital cardiovascular mortality (OR 5.58).
Rather it is due to coronary insufficiency due to a tight left main or 3-vessel disease with inadequate coronary flow. Fourteen (16%) of the 86 patients who had CT also had immediate cardiac catheterization for acute ischemic changes; 7 of which had primary percutaneous coronary intervention (PCI).
Fortunately, Dr. Cho was not looking for STEMI ECG criteria but for an acute coronary occlusion. As he documented, “This patient is experiencing chest pain consistent with an acute coronary syndrome. Start using the terms acute coronary occlusion and occlusion MI. That’s exactly what happened in this case.
The ECG is diagnostic for acute transmural infarction of the anterior and lateral walls, with LAD OMI being the most likely cause (which has various potential etiologies for the actual cause of the acute coronary artery occlusion, the most common of which is of course type 1 ACS, plaque rupture with thrombotic occlusion).
This is acute ACS, but it almost always seen in a pain free state. So this ECG was immediately recorded: Indeed, as predicted, a patient with previous Wellens' waves who now definitely has chest pain has acute Occlusion, with new ST elevation in I, aVL, V2-V5. An ED ECG, if recorded with pain, should show LAD OMI.
The 50-something patient with history of coronary stenting and slightly reduced LV ejection fraction. There is definite reperfusion. which would suggest reduced rates of major adverse cardiac events with coronary artery bypass grafting." This alone could be due to LVH, but V4 could NOT be due to LVH. He awoke with naloxone.
Immediate and early percutaneous coronary intervention in very high-risk and high-risk Non-STEMI patients. Smith comment: We have shown that use of opiates is associated with worse outcomes in ACS: Bracey, A. Opioids in ACS may reduce the pain score, but do not provide reperfusion for ongoing ACS. Lupu L, et al.
Electrocardiographic Diagnosis of Acute Coronary Occlusion Myocardial Infarction in Ventricular Paced Rhythm Using the Modified Sgarbossa Criteria. Immediate ECG diagnosis of an acute coronary lesion resulting in occlusion myocardial infarction is critical in the modern reperfusion era. Annals of Emergency Medicine 2021.
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