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In the setting of circumflex right aortic arch with the ductus arteriosus connecting the left descending aorta and left pulmonary artery, a vascular ring is present and can cause compressive symptoms of the aerodigestive tract. Fetal echocardiogram provides a unique opportunity to assess the aortic arch as the trachea is filled with fluid.
This case was posted on the [link] ultrasound site, of which this ECG blog is a part. I refer you to the video case presentation by one of my colleagues, Dr. Rob Reardon (who has, by the way, a fantastic collection of ED ultrasound cases). However, only the first ECG was shown, and it was recorded before the patient became ill.
She had acute pulmonary edema on exam. On arrival, lung ultrasound confirmed pulmonary edema (B lines). A 49 year old woman with h/o COPD only presented with sudden dyspnea. There is STE and hyperacute T-waves in V2 and V3, with significant STE in I and aVL, and inferior reciprocal STD.
He was started on a heparin drip and CTA of the chest was ordered to rule out pulmonary embolism. Echocardiogram showed severe RV dilation with McConnell’s sign and an elevated RVSP. Electrocardiographic Differentiation Between Acute Pulmonary Embolism and Acute Coronary Syndromes on the Basis of Negative T Waves - ScienceDirect.
He was requiring supplemental oxygen and an initial bedside cardiac ultrasound was unremarkable. Despite his large clot burden, there was absence of obstructive shock.Transthoracic Echocardiogram and bilateral duplex venous ultrasound were obtained to evaluate for right heart strain and clot burden. Cardiology was consulted.
Bedside cardiac ultrasound showed moderately decreased LV function. CT of the chest showed no pulmonary embolism but bibasilar infiltrates. EKG with paced complexes shown below shows much narrower QRS complex and echocardiogram showed improved LV systolic function primarily due to improvement in LV dyssynchrony. (J
He was in acute distress from pulmonary edema, with a BP of 180/110, pulse 110. He had diffuse crackles on exam and B-lines on chest ultrasound, and chest x-ray also confirmed pulmonary edema. The hypertension alone is the likely etiology of the pulmonary edema. He had no chest pain. The cath lab was activated.
This comprehensive evaluation included the use of ultrasoundechocardiograms, computed tomography (CT) scans, electrocardiograms, mutagenesis analysis, and structural analysis to gain insights into the patient's condition and the underlying mechanisms of PD. Further genetic testing identified a homozygous mutation c.2662G>T
Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock. If detected early by ultrasound, the patient can be saved. 3) Oliva et al. (3) Not much change, except a slightly faster ventricular response at 110 bpm.
The patient underwent an emergent formal echocardiogram to look for wall motion abnormality: The estimated left ventricular ejection fraction is 63 %. Exclusion criteria were age less than 18, SBP less than 100 mmHg, echocardiogram with EF less than 50%, STEMI, pregnancy, and trauma. No wall motion abnormality.
An echocardiogram showed no hemopericardium, but D oppler showed a new small ventricular septal defect with left to right shunting. Rupture can be either free wall rupture (causing tamonade) or septal rupture, causing ventricular septal defect with left to right flow and resulting pulmonary edema and shock. 3) Oliva et al. (4)
During echocardiography, a transducer transmits the ultrasound beam towards the heart. The image shown here is an animated 2 dimensional echocardiogram. This one is an older mode known as time-motion mode or M-Mode echocardiogram. Colour flow shows the flow in pulmonary artery.
Smith comment: This patient did not have a bedside ultrasound. Had one been done, it would have shown a feature that is apparent on this ultrasound (however, this patient's LV function would not be as good as in this clip): This is recorded with the LV on the right. In fact, bedside ultrasound might even find severe aortic stenosis.
The next morning the patient went for his routine echocardiogram, where the operator noticed a dilated aortic root at 5.47 Patients with pulmonary embolism or aortic dissection who have normal variant ST elevation are at high risk of being diagnosed with pericarditis when what they have is far more serious!! Pericarditis?
Check : [vitals, SOB, Chest Pain, Ultrasound] If the patient has Abdominal Pain, Chest Pain, Dyspnea or Hypoxemia, Headache, Hypotension , then these should be considered the primary chief complaint (not syncope). Serious outcomes included death, arrhythmia, myocardial infarction, structural heart disease, pulmonary embolism, and hemorrhage.
I suspect pulmonary edema, but we are not given information on presence of B-lines on bedside ultrasound, or CXR findings. Anything that causes pulmonary edema: poor LV function, fluid overload, previous heart failure (HFrEF or HFpEF), valvular disease. Acute coronary occlusion and acute pulmonary edema can coexist.
Transthoracic echocardiogram, bilateral carotid Doppler ultrasound, and electrocardiogram were normal. No previous history of hypertension or diabetes. There was no abnormality in physical examination. Cranial magnetic resonance imaging and magnetic resonance angiography showed no abnormalities.
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