Hypotension and shock can be classified as hypotension caused by reduced or maintained left ventricular (LV) ejection. Reduced left ventricular ejection can result from intrinsic left ventricular, aortic valve, or mitral valve failure, which includes dilated or ischemic cardiomyopathy, left main trunk disease, acute myocarditis, and others. Acute and subacute severe aortic regurgitation can also cause shock. Echocardiography allows noninvasive diagnosis of infective endocarditis and Takayasu′s arteritis to cause severe arotic regurgitation and can also be used to diagnose obstruction of the left ventricular outflow tract. Reduced left ventricular preload can be caused by pericardial effusion and right ventricular ejection failure, which can result from pulmonary embolism, tricuspid regurgitation, right ventricular infarction, tension pneumothorax, hypovolemia, and others characterized by small left ventricle with good ejection fraction. Normal left ventricular ejection may be associated with hypotension. Sepsis, anaphylactic shock, and neural disorder are associated with normal cardiac output. Pseudohypotension may result from aortic dissection, Takayasu′s arteritis, arteriosclerosis obliterans, and aortic coarctation. A right parasternal approach enables better visualization of the ascending aortic dissection. Fundamental echochocardiographic scanning allows approximate yet useful diagnosis of hypotension and shock.

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Purpose: To evaluate the effect of anesthesia on cardiac function. Mitral inflow pattern, especially E/A ratio, is very useful in evaluating diastolic function; however, it is not easy to measure E/A in small animals like mice and rats because of the summations induced by their high heart rate. E/A can generally be measured by administering an anesthetic agent to reduce heart rate, although the effect of anesthesia on cardiac function is unclear. Methods: Sprague Dawley rats were studied by ViVid 7 (GE Healthcare, USA) with a high-frequency transducer (11.5 MHz, 234 FPS) to evaluate fractional area changes (FAC) and mitral flow pattern after step-wise increase in anesthesia. Results: The A wave gradually separated from the E wave as heart rate decreased, and E/A could be measured in all the rats when heart rate was reduced to 300 bpm. Change in fractional area decreased slightly, from 71.4 ± 4.6% to 67.6 ± 3.9%, with reduction in heart rate. Conclusion: The E/A ratio in rats could be measured after heart-rate reduction with little decrease in fractional area changes. The measure of E/A after heart rate reduction may be acceptable except in the special case of evaluating microscopic changes.

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A 72-year-old man came to our hospital complaining of left hemiplegia. Acute ischemic stroke and occlusion of right middle cerebral artery were diagnosed, and conservative medical management was initiated. On the 13th day of hospitalization, echocardiographic examination showed a 0.8 × 0.8 × 3.5 cm mobile hyperechoic mass attached to right ventricular outflow tract (RVOT), but no chest symptoms were presented. While MRI also showed two stalks attaching the mass to the right ventricular outflow tract, we found it difficult to decide between thrombus and tumor. Because the mass was large enough to cause pulmonary embolism, we started administering unfractionated heparin and oral anticoagulant while considering surgical removal of the mass. Perfusion lung scintigraphy showed small defects in right lung fields. Subsequent transesophageal echocardiography showed disappearance of the tumor to be vanishing. The patient had no chest symptoms or thromboembolic complications. Lower leg venous echocardiography showed dilated veins in his left musculus soleus. We considered thrombus with a netlike structure moved from the left musculus soleus to the right ventricular outflow tract. In this patient, echocardiography was useful in making a differential diagnosis and in observing its clinical course.

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The patient was a 20-year-old woman who had undergone medical treatment for essential thrombocythemia for 5 years. She had complained of abdominal distension and jaundice of uncertain etiology when she was thoroughly examined in February 2006. As late as July 2006, the needle biopsy specimen showed congestive liver damage; the abdominal enhanced CT scan, complete hepatic venous obstruction; and the pulsed Doppler ultrasonogram, reverse flow in the right branch of the portal vein with recanalization of the paraumbilical vein. Accordingly, our diagnosis was hepatic venous thrombosis-type Budd-Chiari syndrome (BCS). Follow-up ultrasonography revealed multiple nodules up to 2 cm in diameter in the enlarged liver and showed a heterogeneous solid echoic pattern with a halo. Contrast-enhanced ultrasonography with Sonazoid® was carried out. The imaged nodules demonstrated a spoke-wheel pattern after blood had flowed directly to the center of the liver in the early phase. In the late phase, the stained nodules were more echogenic than the background liver tissue. Liver transplantation was carried out at the request of the patient and her family in March 2007 because of progression of liver failure. Pathologically, the liver explant showed congestive cirrhosis resulting from hepatic venous obstruction. Most of the nodules contained central satellite scar and radial dilated vessels, consistent with the histologic indication of focal nodular hyperplasia (FNH). Ultrasonography using a contrast agent appears to be the method of choice for evaluating dynamic state of liver circulation in BCS and proved invaluable in diagnosing the nodules associated with it in this case.

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