![]() ![]() ![]() Given the patient's persistent elevations despite thrombolytic therapy, interventional cardiology was consulted, and the patient was transferred to a tertiary care facility for cardiac catheterization revealing a thrombotic occlusion in the proximal left anterior descending coronary artery.Īfter transfer to the tertiary care facility for cardiac catheterization, the patient developed cardiogenic shock. STEMI: ST-elevation myocardial infarction Rate 114, sinus tachycardia, left axis deviation, PR 156, QRS 116, QTc 391, ST-segment elevations in aVR, V1, V2, V3, and V4 with reciprocal depressions in II, III, and aVF. Another ECG was repeated which revealed sinus tachycardia, at a rate of 114, now with ST-segment elevations present in aVR, V1, V2, V3, and V4 with depressions in leads II, III, and aVF (Figure (Figure4 4). Hundred milligram of tPA was administered (50 mg as a bolus and 50 mg as a drip given over 60 minutes) with an apparent reperfusion rhythm followed by a "normal" appearing sinus tachycardia. Due to the morphology of the QRS complexes and length of resuscitation time from initial arrest (nearing 90 minutes), tissue plasminogen activator (tPA) was used as a thrombolytic for what was presumed to be a large vessel occlusion myocardial infarction. The CT scan did not reveal any evidence of aortic dissection or pulmonary embolism and a repeat ECG was performed which showed a persistent wide complex tachycardia with no obvious ST-segment changes. CPR was again started, the patient was given atropine, and return of spontaneous circulation (ROSC) was achieved shortly after. In the CT room, he developed bradycardia and subsequently lost his pulse. ![]() Once the patient was stabilized, he was taken for computed tomography (CT) imaging to further evaluate for the possibility of a pulmonary embolism. An improvement was noted after the use of Lidocaine, and a Lidocaine drip was started.Įlectrocardiogram, wide complex tachycardia. The patient was additionally given Lidocaine, 100 mg, due to a wide-complex tachycardia and apparent non-responsiveness to the previously given amiodarone (Figure 3). The patient had a second set of pads applied in the anterior-posterior orientation in addition to the conventional right upper chest and left lateral chest with successful conversion of the ventricular fibrillation. The patient continued with ventricular fibrillation throughout the ACLS algorithm, and the decision was made to attempt DSD. The ACLS algorithm was followed for pulseless ventricular fibrillation, and the patient received multiple rounds of epinephrine, 450 mg of amiodarone (300 mg and then 150 mg), and three conventional defibrillations with increasing joules at 150 J, 200 J, and 200 J (the departmental defibrillators are biphasic and have a maximum output of 200 J). Point-of-care ultrasound (POCUS), phased-array probe, subxiphoid view. ![]()
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