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A 45-year-old male with a history of chronic obstructive pulmonary disease (COPD), asthma, amphetamine and tetrahydrocannabinol (THC) use, and coronary vasospasm presented to triage with chest pain. During assessment, the patient reported that a left heart catheterization six months prior indicated spasms but no coronary artery disease.
Compensatory enlargement was defined as being present when the total coronary arterial cross-sectional area at the stenotic site was greater than that at the proximal nonstenotic site. We documented that the majority of stenotic lesions had compensatory enlargement and thus exhibited remodeling. As was emphasized by Dr.
An unknown EP reviews the report, determines that there is no reason to notify the patient, and documents nothing. Autopsy shows coronary atherosclerosis and marked cardiomegaly with a thickened left ventricular wall. It wasn’t, so you weren’t called, nor did the doc need to document anything.
The most likely would be #2) initially normal, then #3) subtle OMI, then #4) obvious STEMI, and then #1) reperfusion: In other words, the patient with an initially normal ECG develops an acute coronary occlusion, with ECGs that progress from subtle to obvious, and then reperfuse after angiography. But that’s not always the case.
Past medical history includes coronary stenting 17 years prior. Cardiology was consulted and the patient underwent coronary angiogram which showed diffuse severe three-vessel disease. Coronary angiogram shows diffuse severe three-vessel disease. Initial ED ECG: What do you think? How Can We Prove that ECG #1 is VT?
This document covers high sensitivity troponin, risk disposition pathways, and STEMI equivalents. STEMI vs. NSTEMI dichotomy is not sensitive for true occlusion MI or acute coronary occlusion.
Triage documented a complaint of left shoulder pain. For the same reason, you should not delay coronary angiography because pain resolves with morphine. A few hours later, the patient underwent coronary angiography, which showed complete occlusion of her mid left circumflex artery. The patient said, "I just don't feel good."
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]. Cardiology consult note written around that time documents that "Pain improved with NTG, morphine in ED but still present."
The providers documented concern for ST elevation in the precordial and lateral leads as well as a concern for hyperkalemic T waves in the setting of succinylcholine administration. Preliminary findings documented in the cath lab were “Anterior STEMI and no significant coronary artery disease.” (!!!) Potassium resulted as 4.9,
showed that among patients with either acute coronary syndrome or acute pulmonary embolism and negative T waves in the precordial leads (V1-V4), that inverted T waves in leads III and V1 were present in only 1% of patients with acute coronary syndrome and 88% of patients with pulmonary embolism. In fact, Kosuge et al.
It shows a proximal LAD occlusion, in conjunction with a subtotally occluded LMCA ( Left Main Coronary Artery ). Upon contrast injection of the LMCA, the patient deteriorated, as the LMCA was severely diseased and flow to all coronary arteries ( LAD, LCx and RCA ) was compromised. He was taken immediately to the cath lab.
The documentation does not describe any additional details of the history. They also documented "Reproducible chest tenderness." We know that even high-sensitivity troponin may not exceed the "normal" range for a period of hours in certain patients with acute coronary occlusion. The following ECG was obtained.
The patient is an older woman with known coronary disease and an ICD-Pacemaker implanted because of a history of VT ( V entricular T achycardia ). 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.
And you can see why: the artery may sponstaneously reperfuse, as it did here well before angiography, and documented with resolution of pain and evolution of the ECG to typical full reperfusion pattern Peak troponin I was 8544 ng/L. This is typical for a brief LAD OMI.
It is well documented with continuous 12-lead monitoring that acute re-occlusion is frequently asymptomatic. It is important to recognize that coronary thrombosis is dynamic , with spontaneous opening and lysing of the thrombus in the infarct-related artery (we all have endogenous tPA and plasmin to lyse thrombi). Akkerhuis KM, et al.
Dr. Smith and other authors showed the utility of Speckle Tracking Strain Echo in this case report: Diagnosis of acute coronary occlusion in patients with non–STEMI by point-of-care echocardiography with speckle tracking Repeat ECG: Slightly less hyperacute T waves, likely indicating improving flow compared to the first ECG.
He had no previously documented medical problems except polysubstance use. Serial ECGs enhance the diagnosis of acute coronary syndrome. Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the Crusade Quality Improvement Initiative. Perform serial ECGs even if symptoms are constant.
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%
This patient had known coronary artery disease (CAD), and previously required drug eluting stents to the obtuse marginal and diagonal arteries. 1 Despite the rarity of dextrocardia, coronary artery disease can occur with a similar frequency to that of the general population. Coronary heart disease in situs inversus totalis.
6] Among 394 emergency department Code STEMI patients with acute culprit lesion requiring coronary interpretation, 16 (4.1%) presented with an ECG labeled ‘normal’ or ‘otherwise normal’ by computer interpretation. have published a number of warnings about the previous reassuring studies.[4,5]
Their OMI Manifesto details how use of standard STEMI criteria results in an unacceptable level of inaccuracy, in which an estimated 25-30% of acute coronary occlusions are missed! The finding of dynamic ST-T wave changes on serial tracings in association with a change in chest pain symptoms ( SEE My Comment in the July 21, 2020 post ).
K EY P oints : This patient has known coronary disease. In this patient with documentedcoronary disease — these q waves could reflect prior lateral infarction ( especially in view of the Q in lead aVL ). I would have loved to see an ECG on this patient prior to development of coronary disease. It was stented.
What They Did: Single-center, pilot prospective observational cohort trial in Turkey Thrombolysis 25mg of alteplase without a bolus was administered over 6 hours by peripheral IV infusion If hemodynamic instability persisted despite first dose of thrombolysis, a second 6hr infusion of 25mg alteplase without bolus was administered (No patients in the (..)
Notoriously elusive, with a high misdiagnosis rate, thoracic aortic dissection (AD) can mimic many conditions, including acute coronary syndrome (ACS, the most common), gastroesophageal reflux disease (GERD), stroke, and spinal-cord compression. 1 Opioids or anxiolytics are often given to patients whose diagnosis of AD is missed or delayed.
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. As cardiology documented, “possible STEMI. Start using the terms acute coronary occlusion and occlusion MI.
This is of course diagnostic of an acute coronary occlusion MI (OMI) that also meets STEMI criteria. The condition of the coronary artery at the time of angiogram may be different than it was 30 minutes prior during recording of the ECG. A 40-something woman had sudden chest pain. She called 911. The proposed mechanism is complex.
I was not worried for a coronary etiology. Possible explanations include: i ) Coronary vasospasm, with a brief period of coronary occlusion; ii ) Supply-demand mismatch ( Type II MI ) — precipitated by amphetamine-induced catecholamine surge; and / or , iii ) Catecholamine-mediated platelet aggregation with subsequent thrombus formation.
STEMI criteria is bad at differentiating between normal variant and acute coronary occlusion or reperfusion, and initial troponin levels don't differentiate between occlusive and non-occlusive MI 3. the presence of J waves from early repolarization doesn’t rule out an acute coronary occlusion 4.
You can easily imagine this patient getting one of several diagnoses -- vasospasm, MINOCA , pericarditis, or maybe even no diagnosis at all beyond "non-obstructive coronary artery disease." Another option would be to use Optical Coherence Tomography for Coronary Imaging ). That plaque is at risk of thrombosing again.
But it does prove that the patient has coronary disease and makes the probability that his chest pain is due to ACS very very high. Instantaneous wave-free ratio is performed using high fidelity pressure wires that are passed distal to the coronary stenosis. Acute T-waves are large, even if not necessarily hyperacute.
To realize — Assessment of ECG #1 is complicated by knowing: i ) That today’s patient has a history of documented CAD ; and , ii ) The lack o f a prior tracing for comparison at the time the initial ECG was interpreted. Figure-1: Comparison between the first 3 ECGs in today’s case. What We Learn from the Prior Tracing?
[link] An angiogram was done: It showed no culprit and no coronary disease, but did show a myocardial bridge in the mid LAD. An excellent review of myocardial bridging, with full text: [link] Myocardial bridging is when the coronary artery, usually the LAD, dives into the myocardium.
Emergent CT coronary angio also likely has a role in such cases. Like they would for any other acute arterial occlusion syndrome (such as suspicion of acute large vessel stroke), they take the patient across the hall and perform an immediate CT (coronary) angiogram, showing patent coronaries.
Early coronary angiography in post-CA patients with no ST-segment elevation on the presenting ECG may still be of benefit by potentially salvaging myocardium and decreasing the incidence of systolic heart failure in survivors (95.7%, 22/23). Individualize RBCTs to the clinical situation (81%, 17/21).
The P wave is positive in lead aVL of ECG #3, which means it is a low atrial (or probably coronary sinus) rhythm — which of itself is not necessarily “abnormal” in a child if there is no other sign of underlying heart disease. As we see in ECG #3 — the regular rhythm is NOT sinus, because the P wave is negative in lead II.
Ongoing pain noted throughout all documentation, but after nitro drip and prn morphine, "pain improved to 2/10." Association of intravenous morphine use and outcomes in acute coronary syndromes: Results from the CRUSADE Quality Improvement Initiative. Repeat ECG: New developing Q waves in V2 and V3, further confirming evolving OMI.
Acute myocardial infarction with normal and near normal coronary arteries. Documentation with coronary arteriography within 12 1/2 hours of the onset of symptoms in two cases (three episodes). Electrical injuries in the emergency department: an evidence-based review. Emerg Med Pract. 2018 Nov;20(11):1-20. Am J Cardiol.
The 2 clinical areas of most potential benefit to emergency care from computerized interpretations are: i ) Cardiac arrhythmias; and , ii ) Rapid detection of acute coronary O cclusion ( ie, detection of acute O MI ) in cases for which easily recognizable STEMI-criteria are not present.
After admission he undergoes another ECG, though it is unclear from documentation whether there was a change in his chest pain. Documentation strongly suggests that this finding was what ultimately convinced the cardiologists that this was not pericarditis. After this result he was given therapeutic enoxaparin. Teaching points: 1.
The patient was in his 50s with history of hypertension, diabetes, seizure disorder, and smoking, but no known coronary artery disease. No patient should have to be "lucky" by having a positive troponin to be taken seriously as a possible acute coronary occlusion. 418 of these 1788 (23%) had acute coronary occlusion.
His HEAR score (before troponin resulted) was documented at 3, with documentation stating "low suspicion for ACS." Chest pain is documented as ongoing. Repeat 0157 with ongoing chest pain: Basically the same features diagnostic of LAD occlusion. QOH: "OMI High confidence". Physician interpretation: "No STEMI."
We assume that at some point the patient's pain returned, but it is not documented, so exactly when this happened is uncertain. Immediately after the second ECG was performed, the patient's pain resolved completely. After reviewing the case, cardiology requested that the patient be admitted to observation for stress testing the next morning.
. == It is certainly possible that IF the timing had been such that this patient’s initial ECG was normal ( as it was for ECG #2 in Figure-1 ) — that the severity of this patient’s underlying coronary disease could have been overlooked. Chest Pain scores can be misleading.
The patient proceeded to cath where all coronaries were described as normal with no evidence of any CAD, spasm, or any other abnormality. Our patient had a Brugada Type 1 pattern elicited by an elevated core temperature, which is also a documented phenomenon. PM Cardio digitized version.
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