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They started CPR. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. Then assume there is ACS. Smith's ECG Blog ( See My Comment in the March 1, 2023 post) — DSI does not indicate acute coronary occlusion! It also does not uniformly indicate severe coronary disease.
The paramedics achieve return of spontaneous circulation (ROSC) after CPR, advanced cardiac life support (ALCS), and Intubation. Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients. EMS arrives and finds the patient in monomorphic ventricular tachycardic (VT) cardiac arrest.
There was no bystander CPR. I was there and said, "No, I think this is all due to severe chronic cardiomyopathy and cardiac arrest due to primary ventricular fibrillation, not due to ACS." _ Why did I say that? For this reason we did not believe this was an acute coronary event and did not activate the cath lab.
Emergent coronary angiography is not recommended over a delayed or selective strategy in patients with ROSC after cardiac arrest in the absence of ST-segment elevation, shock, electrical instability, signs of significant myocardial damage, and ongoing ischemia (Level 3: no benefit). COR 2b, LOE B-R. COR 2b, LOE C-LD. COR 2a, LOE B-R.
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. It is unknown when this pain recurred and became constant.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" Furthermore, among 35 patients with acute left main coronary artery occlusion, 9 presented with RBBB (mostly with LAFB) on the admission ECG.
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.
It was witnessed, and CPR was performed by trained individuals. She arrived in the ED 37 minutes after 911 was called, with continuing CPR. Here is an article I wrote: Updates on the ECG in ACS. Was this: 1) ACS with ischemia and spontaneous reperfusion? Updates on the Electrocardiogram in Acute Coronary Syndromes.
However, vertical flow can result in myocardial injury secondary to coronary artery spasm. This is supplied via alternating current (AC), increasing the risk of titanic contraction of skeletal muscle, leading to kids holding on to the electrical power source. AC and DC shocks may result in different injury patterns.
He underwent immediate CPR, was found to be in ventricular fibrillation, and was successfully resuscitated. He underwent coronary stenting (uncertain which artery). See explanation below. The patient went home and, in front of his wife, he collapsed. I do not have the post-resuscitation ECG. Did the ECG offer unseen hints?
CPR was initiated immediately. If this is ACS with Aslanger's pattern , the ST depression vector of subendocardial ischemia (due to simultaneous 3 vessel or left main ACS) is directed toward lead II (inferior and lateral). It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation.
Medics found her apneic and pulseless, began CPR, and she was found to be in asystole. Rather it is due to coronary insufficiency due to a tight left main or 3-vessel disease with inadequate coronary flow. A middle-age woman with h/o hypertension was found down by her husband.
He underwent CPR and then was shocked out of VF. ST depression maximal in V1-V4, in the context of ACS symptoms and unexplained by QRS abnormality or tachydysrhythmia, should be considered posterior OMI until proven otherwise. Today's patient is high-risk ( ie, in a high "prevalence" group for having an acute coronary event ).
CPR was initiated and she subsequently entered into V-Fib storm. ACS can be a very dynamic process. For example, a coronary plaque ruptures: the vessel can undergo occlusion, spontaneous reperfusion, maybe reocclusion, again reperfusion, etc. Shortly after this ECG she suddenly went unresponsive and into V-Fib.
Is there likely to be fixed coronary stenosis that led to demand ischemia during pneumonia? --Was It is highly associated with proximal LAD occlusion or severe left main ACS and with bad outcomes. Here is a parasternal long axis without speckle tracking: There is very good function, but the lateral wall is not in this view.
Data that do not establish neurological risk stratification in the first 6 hours after CA include the patient’s age, duration of CPR, seizure activity, serum lactate level or pH, Glasgow motor subscore in patients who received NMB or sedation, pupillary function in patients who received atropine, and optic nerve sheath diameter (95.3%, 20/21).
In total, he received approximately 40 minutes of CPR and 7 defibrillation attempts. Coronary spasm causing massive current of injury with shark fin ECG. I would not expect ST-E to vanish in four beats with dissolving thrombus (also we know that the coronaries were clean). I suspect LAD or LM.
He underwent CPR, and regained a pulse after epinephrine, with an organized narrow complex rhythm at 140, but still with severe shock. And so it is wise to look at the coronary arteries. This ECG certainly looks like myocarditis, and was due to myocarditis, but missing acute coronary occlusion is not acceptable.
The arterial pressure waveform is transduced using the coronary catheter. Normally, the diameter of the coronary artery ostium is much greater than the diameter of the catheter so that catheter engagement does not significantly impair antegrade coronary perfusion. Here is the ECG and arterial waveform during RCA angiography.
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