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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. Then assume there is ACS. It also does not uniformly indicate severe coronary disease. They started CPR.
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. The QRS is extremely wide.
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.
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.
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. VF was refractory to amiodarone, lidocaine, double-sequential defibrillation, esmolol, etc.
Does this patient have ACS? Again, it is common to have an ECG that shows apparent subendocardial ischemia after resuscitation from cardiac arrest, after defibrillation, and after cardioversion. He did not have ACS. Ventricular fibrillation is not only caused by acute coronary syndrome. Learning Points: 1.
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.
He was resuscitated with chest compressions and defibrillation and 1 mg of epinephrine. ACS would be highly unusual in a young athlete, and given the information on his race bib, one must first suspect that the abnormal ST elevation is due to demand ischemia, not ACS. The next day, and angiogram showed normal coronary arteries.
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.
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.
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.
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. She was defibrillated and resuscitated. Such cases are classified as MINOCA (Myocardial Infarction with Non-Obstructed Coronary Arteries).
She was never seen to be in ventricular fibrillation and was never defibrillated. Rather it is due to coronary insufficiency due to a tight left main or 3-vessel disease with inadequate coronary flow. Medics found her apneic and pulseless, began CPR, and she was found to be in asystole. BP gradually rose.
It was reportedly a PEA arrest; there was no recorded V Fib and no defibrillation. 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). CPR was initiated immediately.
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.
Recall that, in the setting of ACS symptoms, ST depression that are maximal in leads V1-V4 (as opposed to V5 and V6) not attributable to an abnormal QRS complex is specific for OMI. When the ICD was finally interrogated, the syncopal events and shocks correlated with two VF events that were defibrillated successfully.
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 mmol/L or <_ 70 mg/dL) should be avoided.
Written by Pendell Meyers A woman in her 70s with known prior coronary artery disease experienced acute chest pain and shortness of breath. But thankfully, when the clinical context is clearly and highly concerning for ongoing ischemia from ACS, this distinction doesn't matter much. Vital signs were within normal limits.
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. She was defibrillated perhaps 25 times.
In ACS, chest pain is the warning sign of ongoing ischemia. ONLY give opiates if the pain is intolerable or you will activate the cath lab at the first objective evidence of coronary ischemia. In this case, you should get a second defibrillator and perform double sequential external defibrillation (DSED).
After ruling out for ACS, the patient underwent angiography where he was found to have severe stable disease, which was already known. 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.
Whenever I see PVCs with the morphology and axis seen in todays case I always look for signs of AC ( Arrhythmogenic Cardiomyopathy ). See this case for an in-depth discussion of AC and an example of VT and ECG changes associated with this disorder. CT coronary angiogram showed a hypoplastic RCA and dominant LCx.
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