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link] A 62 year old man with a history of hypertension, type 2 diabetes mellitus, and carotid artery stenosis called 911 at 9:30 in the morning with complaint of chest pain. Challenge QUESTION: The relative change in T-QRS-D is not the only thing that changes during period of time that passed between recording of the 2 ECGs shown in Figure-1.
Thanks in part to rapid bedside diagnosis, the patient was able to avoid emergent coronary angiography. Here is lead I from ECGs 1 and 2 shown side-by-side to highlight the change in axis from borderline right to completely normal. While not completely ruling out acute coronary disease — another cause should be considered.
Written by Willy Frick A man in his 50s with a history of hypertension, dyslipidemia, type 2 diabetes mellitus, and prior inferior OMI status post DES to his proximal RCA 3 years prior presented to the emergency department at around 3 AM complaining of chest pain onset around 9 PM the evening prior. ECG 1 What do you think? Grines, C.
Coronaries were clean. I agree, however: 1) I don't think you can get a good enough ech o without bubble contrast. 3) E cho is another step that takes time. I agree, however: 1) I don't think you can get a good enough ech o without bubble contrast. 3) E cho is another step that takes time. Time is myocardium.
Moreover , the patient has ongoing symptoms and has an unexplained elevated troponin, so she is having an MI and the only question is whether it is type 1 or type 2 due to hypertension. Case continued She was loaded with aspirin 325 mg, and repeat troponin drawn around the time of EKG 1 resulted at 267 ng/L. At midnight.
Pain improved to 1/10 after EMS administers 324 mg aspirin and the following EKG is obtained at triage. C Examination notable for diaphoresis, 1+ bilateral lower extremity edema, regular heart rate and rhythm, and no signs of respiratory distress with normal breath sounds. What do you think? In fact, Kosuge et al. Stein et al.
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. Learning Point: 1. As is often emphasized on Dr. Smith's ECG Blog — the evolution of an acute OMI is not necessarily static — but may be "dynamic".
Initial vital signs include: NIBP 99/58 HR 150-160 (trend) RR 10 (spontaneous, but shallow) SpO2 86 (RA) BBS CTA The initial rhythm strip is attached: Figure 1 There is a wide complex tachycardia of varying morphology, amplitude, and R-R cycle length. A prominent vertical scar, however, is noted at the sternum.
A prior ECG from 1 month ago was available: The presentation ECG was interpreted as STEMI and the patient was transferred emergently to the nearest PCI center. The patient proceeded to cath where all coronaries were described as normal with no evidence of any CAD, spasm, or any other abnormality. So maybe she is better than I am.
Two recent interventions have proven in randomized trials to improve neurologic survival in cardiac arrest: 1) the combination of the ResQPod and the ResQPump (suction device for compression-decompression CPR -- Lancet 2011 ) and 2) Dual Sequential defibrillation. Figure-1: The initial ECG in today's case — obtained after ROSC.
This was a very complex case and the details are too much for an ECG Blog, but suffice it to say that, s hortly thereafter, the patient had an asystolic arrest and was resuscitated. Learning Points: 1. If the situation is not right for acute coronary occlusion, then the ECG findings probably do not represent acute coronary occlusion.
We recorded an ECG in which V1-V3 were put in the position of V4R-V6R, and V4-6 were placed in V7-9 to (academically) confirm posterior OMI. 1 mg of Atropine was given and the heart rate increased transiently to 60. Atropine usually works in junctional rhythm with a narrow complex 9. What to do? RVMI explains part of the shock.
The pain is described as located in the midsternal area, radiating to the right arm, described as 8-9/10 and worse with deep inspirations. In the evening, he became diaphoretic and complained of 9/10 continuous chest pain. If there is NO WMA, then it is not coronary occlusion, but if there IS one, then you still don't have a diagnosis.
It is unclear to me whether this case could represent 1) simple supply/demand mismatch due to increased demand from epinephrine, 2) Kounis syndrome (usually described as mast cell mediated coronary vasospasm during allergic reaction), 3) brief autolysed left main or LAD ACS with no findings on later echo and CT coronary angio, or 4) something else.
Vittinghoff, E. Metoprolol and atenolol are overwhelmingly beta-1 cardioselective. Beta-1 blockade decreases inotropy and chronotropy and has no vasoconstrictive effects. The prohibition against beta blockade in cocaine toxicity, causing "unopposed alpha" stimulation, needs to be re-examined. is intuitive, and not surprising.
mm of ST segment elevation, V2 and V3 have 1 mm of elevation, v4 has 2 mm of elevation and v5 around 1.5 Hospital Course The patient was taken emergently to the cath lab which did not reveal any significant coronary artery disease, but she was noted to have reduced EF consistent with Takotsubo cardiomyopathy. What do you think?
Queen: #1: NOT OMI, HIGH CONFIDENCE Queen: #2: NOT OMI, HIGH CONFIDENCE ECG 1 Interpretation: there is terminal T-wave in V3-V6. LEARNING POINT : 1. Along the way to acquiring more experience in recognizing the ECG findings of acute coronary occlusion — is incorporation of a number of KEY ECG Features into one's clinical acumen.
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. As you take another LOOK at ECG #1 — What is the relevance of the findings that I've labeled in Figure-1 ?
On review of systems the patient reported back pain for approximately 1 week which he was treating with NSAIDs with minimal relief. As we have described multiple times on this blog, false positive "pericarditis" kills by distracting the clinician from actual emergencies including OMI, dissection, PE, and others. 15-9/6/2017 ).
He was taken emergently to the cardiac catheterization lab and found to have multi-vessel coronary artery disease with a near-occlusive culprit lesion in the RCA, possibly reperfused. Slow TIMI 2 initially with brisk flow status post percutaneous coronary intervention with 18mm drug-eluting stent.
Easy LINK — [link] — My New E CG P odcasts ( 5/28/2024 ): These podcasts are part of the Mayo Clinic Cardiovascular CME Podcasts Series ( "Making Waves" ) — hosted by Dr. Anthony Kashou. And regarding arrhythmias: For more on the regular WCT — See My Comment in the May 5, 2020 post and in the April 15, 2020 post in Dr. Smith's ECG Blog.
And so it is wise to look at the coronary arteries. Here they are: Learning Points: 1. This ECG certainly looks like myocarditis, and was due to myocarditis, but missing acute coronary occlusion is not acceptable. In acute MI, the T-wave is large, and the T/ST ratio is high. This is much more typical of myocarditis.
4 important features that indicate acute right hear strain: 1. In this study, (quote) "negative T waves in leads III and V 1 were observed in only 1% of patients with ACS compared with 88% of patients with APE (p less than 0.001). They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6%
He had episodes of chest pain off and on all night, until about 1 hour prior to arrival when the pain became constant, crushing, 10/10 chest pain that radiated to both arms. Proven STEMI has an open artery in 19% to 36% of cases, depending on whether it is TIMI −1, −2, or −3 flow. 25] Stone et al found that 72% have TIMI 0 or 1 flow.
But these cases show the potential dangers of delayed recognition and treatment of inferior reperfusion Take away 1. ECG’s can be labeled as ‘normal’ by the computer (and confirmed by cardiology) even with diagnostic signs of occlusion or reperfusion References 1. JAMA Intern Med 2019 9. Am J Med [Internet] 2017;130(9):1076–83.e1.
Ct coronary angiogram showed normal coronary arteries. Smith note: I think CT coronary angiogram is reasonable with the elevated troponins and symptoms. Regarding the History: It sounds from the History as if this patient has at least a significant component of EIA ( E xercise- I nduced A sthma ).
This ECG is quite obvious for long-time readers, and you may think this far too easy to be presented on this blog. mm in just one lead V7-9), but as far as I can tell all of these documents specifically avoid calling this condition STEMI and specifically avoid using any terminology similar to "STEMI equivalent." Comment from K.
The coronaries were clean (this is not the gold standard, however, as some patients with ischemic ST elevation may have clean coronaries). ACTUAL CORONARY ANATOMY: Dominance: Right LM: A 5 mm vessel which bifurcates into the LAD and LCx coronary artery. QRSV2 = 16 RAV4 = 14 Value = 20.24 (The cutoff of 18.2
2020;71(1):235-246. Plt 37×10^9/L and 40×10^9/L, SOC and TEG, respectively) All patients enrolled had an upper endoscopy and verified the source of bleeding. Article: Kumar M et al. Thromboelastography-Guided Blood Component Use in Patients With Cirrhosis With Nonvariceal Bleeding: A Randomized Controlled Trial.
There are two main etiologies of ischemic ST-depression: 1) subendocardial ischemia 2) reciprocal to ST-elevation in an opposite wall Here there are distinct R-waves with marked ST-depression throughout most of the precordium. Tips for recognizing Acute Posterior STEMI: 1. References: 1. This can help in confirmation.
Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. Baseline Q-wave surpasses time from symptom onset as a prognostic marker in ST-segment elevation myocardial infarction patients treated with primary percutaneous coronary intervention. J Am Coll Cardiol 53(17):1503-9. Very unlikely.
A 40-something male presented with dyspnea and left arm numbness, and perhaps some chest tightness, for 11/2 hours. E CG # 1 = the initial Triage ECG ( TOP ) — As per Dr. . = Here is his triage ECG: There is massive STE in V3-V6, and also STE in II, III, aVF. Why is this important? Thelin et al. Mokhtari et al.
Although acute anterior STEMI frequently has narrow QR-waves within one hour of onset (1. He found 2 ECG patterns of atypical T-wave development in PIRP: 1) persistently positive (upright) T-waves 48 hours after AMI onset. Lessons : 1. Although rupture has a high mortality, it is not uniformly fatal References 1.
Is this due to coronary occlusion? The medic activated the cath lab but was refused by the interventionalist, who did not believe that this ECG represented acute coronary occlusion. Important Learning Point: "STEMI" is defined by millimeter criteria (1 mm in limb leads), which this does not meet. Why did I say this? Look at aVF.
The Differential Diagnosis is: SVT with aberrancy(#) [AVNRT vs. WPW (also called AVRT*)] Atrial flutter with 1:1 conduction, with aberrancy VT coming from the anterior fascicle ( fascicular VT )@ *AVRT = AV Reciprocating Tachycardia (Tachycardic loop that uses both the AV node and an accessory pathway. See Learning point 1 below.
Angiogram showed a 99% left main thrombotic occlusion with TIMI-1 flow (this is considered "occlusion" even though there is some flow. not left main occlusion == MY Comment by K EN G RAUER, MD ( 1/16/2020 ): == I did not correctly identify the “culprit artery” in this case. mEq/L Her BP with pressors came up to 80, then 100.
Learning Points: 1. Smith was asked to interpret without the benefit of any clinical information ( = ECG #1 in Figure-1 ). There are frequent PVCs ( on this tracing — 3 PVCs in the space of 10 seconds = beats #3, 9, 14 ). Thus, the patient may be pain free from infarct alone, even without spontaneous reperfusion.
1 week later (about 1 week prior to the tamponade visit) she had a follow up outpatient visit and this ECG was recorded: Appears to show resolving findings. For an excellent review of the pathophysiological explanation of signs and symptoms associated with Pericardial Tamponade SEE this Review by Jensen et al in the e-Journal Card.
Cardiac Syncope ("True Syncope") Independent Predictors of Adverse Outcomes condensed from multiple studies 1. Palpitations preceding syncope (highest value on EGSYS score) 9. It's complicated, but they derived a score based on these variables: 1. h/o heart disease (+1) 3. Troponin greater than 99th percentile (+1) 5.
Whether your program is primarily 9-1-1, interfacility transport (IFT), or a combination of both, the likelihood of being responsible for the safe and expeditious transport of a STEMI patient is high for anyone in the out-of-hospital care setting. There, we would find two coronary ostias, left and right. Sir Isaac Newton.
Moreover, it does not follow a coronary distribution very well. The coronaries were clean. Today's patient unfortunately developed PEA ( P ulseless E lectrical A ctivity ) arrest shortly after arrival of the medic team. This is unusual in acute OMI. In addition, there is STE in V3-V6, so there is massive injury. From this site.
I suspect most blog readers did not struggle with this one. Pendell Meyers , Aaron E. Puskarich Abstract Objectives Data suggest patients suffering acute coronary occlusion myocardial infarction (OMI) benefit from prompt primary percutaneous intervention (PPCI). PEARL #2: The above said Remember the rule of "N = 1".
1:45, case start To orient you to this screen, the top is obviously ECG waveforms. The arterial pressure waveform is transduced using the coronary catheter. But in the case of an ostial lesion, there is little or no space between the outside of the catheter and the wall of the coronary artery.
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