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Bedside ED ultrasound showed exceedingly poor global LV function, and no B lines. Then I always look to see if the initial deflection of the QRS has a lot of voltage change per change in time (seen in tachycardias that are initiated from above the ventricle because the propagate through fast conducting purkinje fiber.
Bedside cardiacultrasound showed moderately decreased LV function. See this post: How a pause can cause cardiacarrest 2. Even with tachycardia and a paced QRS duration of ~0.16 She was intubated. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. The plan: 1. Place temporary pacemaker 3.
He had multiple cardiacarrests with ROSC regained each time. CardiacUltrasound may be a surprisingly easy way to help make the diagnosis Answer: pulmonary embolism. Now another, with ultrasound. Submitted by a Med Student, with Great Commentary on Bias! What is the Diagnosis? This is a quiz. Answer at bottom.
A bedside cardiacultrasound was normal, with no effusion. This sinus tachycardia ( at ~130/minute ) — is consistent with the patient’s worsening clinical condition, with development of cardiogenic shock. He had the following EKG recorded: Low voltage, suggests effusion. There is minimal, probably normal STE in V2-V6.
This progressed to electrical storm , with incessant PolyMorphic Ventricular Tachycardia ( PMVT ) and recurrent episodes of Ventricular Fibrillation ( VFib ). Another approach is sympathetic chain (stellate ganglion) blockade if you have the skills to do it: it requires some expertise and ultrasound guidance.
Bedside ultrasound showed no effusion and moderately decreased LV function, with B-lines of pulmonary edema. See here for management of Polymorphic Ventricular Tachycardia , which includes Torsades. If cardiacarrest from hypokalemia is imminent (i.e., He was managed medically with Clopidogrel. He appeared to be in shock.
Is it ventricular tachycardia (VT) due to hyperK or is it a supraventricular rhythm with hyperK? On arrival, the patient was in shock, was intubated, and had an immediate cardiacultrasound. What does a heart look like on ultrasound when the EKG looks like that? If cardiacarrest from hypokalemia is imminent (i.e.,
I would do bedside ultrasound to look at the RV, look for B lines as a cause of hypoxia (which would support OMI, and argue against PE), and if any doubt persists, a rapid CT pulmonary angiogram. There was 100% proximal LAD occlusion with TIMI 0 flow, and cardiacarrest in the cath lab. There is sinus tachycardia at ~100/minute.
Thirty-six patients (36%) presented with cardiacarrest, and 78% (28/36) underwent emergent angiography. Systematic Assessment of the ECG in Figure-1: My Descriptive Analysis of ECG findings in Figure-1 is as follows: Sinus tachycardia at ~110/minute. A emergent cardiology consult can be helpful for equivocal cases.
The ECG shows sinus tachycardia, a narrow, low voltage QRS with alternating amplitudes, no peaked T waves, no QT prolongation, and some minimal ST elevation in II, III, and aVF (without significant reciprocal STD or T wave inversion in aVL). It is difficult to tell if there is collapse during diastole due to the patient’s tachycardia.
Patients who present with chest pain or cardiacarrest and have an ECG diagnostic of STEMI could have myocardial rupture. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual.
There is sinus tachycardia and also a large R-wave in aVR. Drug toxicity , especially diphenhydramine , which has sodium channel blocking effects, and also anticholinergic effects which may result in sinus tachycardia, hyperthermia, delirium, and dry skin. Her temperature was 106 degrees. As part of the workup, she underwent an ECG.
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