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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.
He was defibrillated into VT. He then underwent dual sequential defibrillation into asystole. But cardiac arrest is a period of near zero flow in the coronary arteries and causes SEVERE ischemia. See these related cases: Cardiac arrest, defibrillated, diffuse ST depression and ST Elevation in aVR. They started CPR.
2 Standard management for VT and VF involves the use of electrical defibrillation, high-quality chest compressions, and epinephrine. Initial guidelines defined “refractory” as VT or VF occurring despite three shocks from a cardiac defibrillator. Tips for use of dual sequence defibrillation 11 : Use the same model of defibrillator.
Defibrillation is the treatment of choice in these cases but does not often result in sustained ROSC ( Kudenchuk et al 2006). Acute coronary syndrome (ACS) is responsible for the majority (60%) of all OHCAs in patients. Half of these arrests are witnessed with the other half being un-witnessed.
More past history: hypertension, tobacco use, coronary artery disease with two vessel PCI to the right coronary artery and circumflex artery several years prior. VF was refractory to amiodarone, lidocaine, double-sequential defibrillation, esmolol, etc. It is unknown when this pain recurred and became constant.
Indication for emergency invasive coronary angiography or had coronary angiography within 1 hour of arrival. Known obstructive coronary artery disease or known coronary stent. Known cardiac defibrillator. Excluded: Obvious cause for OHCA prior to SDCT or on hospital arrival. Pre-existing DNR order.
She was unable to be defibrillated but was cannulated and placed on ECMO in our Emergency Department (ECLS - extracorporeal life support). After good ECMO flow was established, she was successfully defibrillated. Here is a case of ECMO defibrillation with near shark fin that was due to proximal LAD occlusion. The K was normal.
He denied any known medical history, specifically: coronary artery disease, hypertension, dyslipidemia, diabetes, heart failure, myocardial infarction, or any prior PCI/stent. Despite immediate chest compressions, and multiple rounds of defibrillation, he could not be resuscitated. Breath sounds were clear in all lung fields.
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.
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 C-LD. COR 3, No benefit, LOE B-R.
The ST segment changes are compatible with severe subendocardial ischemia which can be caused by type I MI from ACS or potentially from type II MI (non-obstructive coronary artery disease with supply/demand mismatch). The arrhythmia spontaneously converted before defibrillation was achieved. This is an ominous sign.
Below is the version standardized by PM Cardio app Meyers interpretation: Findings are specific for posterior (and also likely inferior) wall transmural acute infarction, most likely due to acute coronary occlusion (OMI). There is a relatively normal QRS yet there is STD maximal in V2-V4, which resolves from V4 to V6.
Among patients with left bundle branch block, T-wave peak to T-wave end time is prolonged in the presence of acute coronary occlusion. Finally, do a coronary angiogram Possible alternative to pacing is to give a beta-1 agonist to increase heart rate. Coronary Angiography No angiographic significant obstructive disease.
We can, therefore, put down the defibrillation pads, set aside the amiodarone, and look further at the ECG. The coronary angiogram revealed no critical stenosis, or acute plaque ulceration. Paradoxically, though, the third green arrow identifies a QRS that is more narrow than the RBBB complexes surrounding it.
After amiodarone and several defibrillations and about 20 minutes after initial arrest, stable ROSC was achieved. Other coronaries were normal. How did the PM Cardio Queen of Hearts perform: Not OMI with low confidence. ECG#3 Resuscitation efforts were ongoing. ROSC was achieved shortly before new episodes of ventricular tachycardia.
He underwent coronary angiography which showed severe multivessel disease, and he agreed to proceed with workup for CABG. But artifact is "alive and well" — and learning to recognize it will amaze many of your colleagues ( and may serve to avoid an unnecessary defibrillation or two ).
He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. The next day, and angiogram showed normal coronary arteries. This young male had ventricular fibrillation during a triathlon. On his bib it stated that he had a congenital heart disorder. His initial ECG is shown here. He awoke and did well.
She was found to be in ventricular fibrillation and was defibrillated 8 times without a single, even transient, conversion out of fibrillation. She was immediately intubated during continued compressions, then underwent a 9th defibrillation, which resulted in an organized rhythm at 42 minutes after initial arrest. References : 1.
After resuscitation and defibrillation , there were no more episodes of TdP. A coronary angiogram was done that did not show significant coronary artery disease. A coronary angiogram was done that did not show significant coronary artery disease. Below is the patient’s 12 lead ECG following defibrillation.
There are a few subtle signs of coronary occlusion here. He was defibrillated. He had an ECG recorded: Sinus Rhythm. This was read as normal by the emergency physician and by the computer. QTc is 400 ms. What do you think? First , look at V4-V6. The T-wave is almost as tall as the R-wave. This should not be. Anterolateral STEMI.
Even though the primary suspicion was not ischemic heart disease, a CT angiogram was performed, and it revealed normal coronary arteries. This ruled out coronary disease as the cause of conduction system disease. She was given CRT-D (Cardiac Resynchronization Therapy-Defibrillator).
The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. During angiogram in the cath lab, the patient suffered two episodes of ventricular fibrillation for which he was successfully defibrillated. Two stents were placed with resultant TIMI 3 flow. Just another NSTEMI.
Here is the post shock ECG: Cardiology was called stat for ischemic VT, query SCAD vs thrombotic occlusion vs coronary vasospasm. Cath lab was activated: There was no coronary artery disease, but there was spontaneous coronary artery dissection (SCAD) of the distal LAD, which was narrowed by 95%, and treated medically.
Accuracy of OMI findings versus STEMI criteria for diagnosis of acute coronary occlusion myocardial infarction. DIagnostic accuracy oF electrocardiogram for acute coronary OCClusion resulTing in myocardial infarction (DIFOCCULT study). Transient ST-segment myocardial infarction: a new category of high risk acute coronary syndrome?
The assay at my institution, for example, is frequently negative until 4-6 hours after acute coronary occlusion. After the second defibrillation the patient had an organized rhythm: Bradycardic escape/agonal rhythm, with large ST deviations. It should have been shocked at least 10 seconds ago.
Acute coronary occlusion is the most common and most treatable cause of this pattern, but it is not the only cause. Takotsubo, spasm, low flow with a preexisting stable coronary lesion, etc. He was defibrillated immediately and had return of normal mental status.
12 minutes later, the patient went back into VFib arrest and underwent another 15 minutes of resuscitation followed by successful defibrillation and sustained ROSC. In total, he received approximately 40 minutes of CPR and 7 defibrillation attempts. Coronary spasm causing massive current of injury with shark fin ECG.
This page summarises the most current recommendations for the management of acute coronary syndromes with persistent ST-segment elevations (i.e This page summarises the most current recommendations for the management of acute coronary syndromes with persistent ST-segment elevations (i.e
When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully. 90% stenosis of the proximal ramus intermedius, pre procedure TIMI II flow The ramus intermedius is a normal variant on coronary anatomy that arises between the LAD and LCX.
A patient had a cardiac arrest with ventricular fibrillation and was successfully defibrillated. The proof of this is that only 5% of patients enrolled had acute coronary occlusion. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. This study failed to do so. 5% vs. 58%!! As per Dr.
He was defibrillated, but they also noticed that he was being internally defibrillated and then found that he had an implantable ICD. He was unidentified and there were no records available After 7 shocks, he was successfully defibrillated and brought to the ED. There was no bystander CPR. Cardiology agreed. Initial trop ~200.
He underwent further standard resuscitation EXCEPT that we applied the Inspiratory Threshold Device ( ResQPod ) AND applied Dual Sequential Defibrillation (this simply means we applied 2 sets of pads, had 2 defib machines, and defibrillated with both with only a fraction of one second separating each defibrillation.
She was defibrillated and resuscitated. 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. One need not have obstructive coronary disease to have occlusive thrombus!
She spontaneously converted (Defibrillation was not performed). Most such rhythms in the setting of ischemia are VF and will not convert without defibrillation. The patient was referred for coronary angiography which did not reveal any atherosclerotic changes. A repeat magnesium level was not drawn prior to coronary angiography.
Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. Ventricular fibrillation is not only caused by acute coronary syndrome. Much depends on the post resuscitation ECG and its evolution shortly after defibrillation.
She was never defibrillated. Angiogram --Minimal coronary atherosclerosis --No obstructive epicardial coronary artery disease or evidence of plaque rupture noted to explain prolonged QT or ventricular fibrillation cardiacarrest, suspect nonischemic mechanism Echo The estimated left ventricular ejection fraction is 45 %.
It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. He reportedly told his family "I think I'm having a heart attack", then they immediately drove him to the ED, and he was able to ambulate into the triage area before he collapsed and became unresponsive. CPR was initiated immediately.
A defibrillator should be immediately available as a precaution. Acute coronary syndrome (including myocardial infarction ) within the last 30 days. A maximum of two infusions can be given. Each infusion should be completed, even if the patient reverts to sinus rhythm. Normal dilution: 4 mg/ml.
Today's case reminds us of the intuitive logic that if a patient has a shockable arrest ( ie, VFib ) — and following successful defibrillation shows evidence of acute OMI ( even if STEMI criteria are not necessarily fulfilled ) — that such patients have much to gain from immediate cath with PCI. (
Takeaway lessons * In any sudden loss of pulse/consciousness, particularly in a known cardiac patient, the presumption should be for a shockable arrhythmia and rapid defibrillation should be prioritized above all else. A diastolic BP above 3540 mmHg, measured from the arterial line during cardiac arrest, suggests adequate coronary perfusion.
Written by Pendell Meyers A woman in her 70s with known prior coronary artery disease experienced acute chest pain and shortness of breath. Her history and ECG were interpreted as very concerning for acute coronary syndrome which might benefit from acute reperfusion therapy. KEY Points: DSI does not indicate acute coronary occlusion!
Written by Willy Frick with edits by Ken Grauer An older man with a history of non-ischemic HFrEF s/p CRT and mild coronary artery disease presented with chest pain. The most common way is by delivering a lead into the coronary sinus ostium in the RA, which wraps around the posterolateral portion of the LV. ECG 1 What do you think?
She underwent coronary angiography which showed thrombotic occlusion of an RPL branch s/p aspiration thrombectomy. Throughout this process, the patient had repeated VF and was defibrillated 8 times. Written by Willy Frick A young woman with a history of paroxysmal nocturnal hemoglobinuria presented with acute substernal chest pain.
The submitter started the patient on amiodarone and arranged implantation of a defibrillator. == MY Comment , by K EN G RAUER, MD ( 12/27 /2024 ): == Superb discussion by Dr. Frick in today's case, that highlights a series of important points regarding the ECG recognition of stable VT ( V entricular T achycardia ).
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