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A 66-yr-old female, initially admitted to hospital with anorexia, malaise, weakness, shortness of breath, developed urosepsis and acute renal failure. Appropriate treatment, including transient dialysis, was started and her renal function improved. One week later, she complained of bilateral leg weakness and lower extremity swelling that was followed 2 d later by acute dyspnea. She reported no chest pains or hemoptysis.

On examination she was tachypneic (respiratory rate >28/min), tachycardic (heart rate 110 bpm). Significant findings included bilateral leg swelling with tenderness on deep palpation. Distal pulses in both lower extremities were normal. Jugular venous pressure was 13 cm. Heart sounds were normal and no murmurs were heard. Crackles were heard bilaterally in basal lung fields.

Initial echocardiogram showed sinus tachycardia with no signs of acute ischemia. Q-waves were seen in the inferior leads, but no S1Q3T3 pattern observed. Platelet count fell during admission, dropping from 118 K/dL to 18 K/dL and the diagnosis or heparin-induced thrombocytopenia entertained; platelet factor four (PF4) antibodies were requested. Plasma D-dimer enzyme-linked immu-nosorbent assay test (ELISA) and serum troponin I levels were both mildly elevated. Arterial blood gases were reported at the lower limits of normal.

Transthoracic echocardiography (TTE) showed preserved left ventricular function with estimated ejection fraction of 60%. Marked right ventricular dilation with lateral wall hypokinesis with apical sparing was noted. No right ventricular hypertrophy was apparent. Mild tricuspid regurgitation (TR) was present with peak velocity measuring approx 3.1 m/s and pulmonary artery systolic pressure (PASP) measuring 39 mmHg + right atrial pressure (RAP). A relatively mobile echo-dense structure was seen at the bifurcation of the main pulmonary artery (Figs. 1 and 2; please see companion DVD for corresponding video). Ventilation-perfusion scan confirmed the diagnosis. Bilateral deep vein thrombosis was diagnosed by venous ultrasonogra-phy of the lower extremities.

From: Contemporary Cardiology: Essential Echocardiography: A Practical Handbook With DVD Edited by: S. D. Solomon © Humana Press, Totowa, NJ

Fig. 1. Parasternal short axis (PSAX) view at the aortic valve level shows the right ventricular outflow tract (RVOT), main pulmonary artery, and right and left pulmonary artery. An echo-dense structure is seen in at the bifurcation of the main pulmonary artery, consistent with a pulmonary saddle embolus (arrow). (Please see companion DVD for corresponding video.)

Rvot View Echo

Fig. 1. Parasternal short axis (PSAX) view at the aortic valve level shows the right ventricular outflow tract (RVOT), main pulmonary artery, and right and left pulmonary artery. An echo-dense structure is seen in at the bifurcation of the main pulmonary artery, consistent with a pulmonary saddle embolus (arrow). (Please see companion DVD for corresponding video.)

Acute pulmonary embolism (PE) is a common problem with high morbidity and a 30-d mortality rate of 15-20%. Because of the scope and severity of the problem, the accurate diagnosis and management of acute PE is crucial. Echocardiography has increasing applications in the diagnosis, the risk assessment, and the management of PE. As a first-line tool, echocardiography allows for the preliminary differentiation of major life-threatening cardiovascular complications. Additionally, bedside echocardiography affords the opportunity to establish a prompt diagnosis and to identify patients with high-risk features, thus identifying a subset of patients that may benefit from more aggressive therapy, such as thrombolytic therapy. The use of echocardiogra-phy in the evaluation and management of PE is increasingly common as demonstrated in two recent registries, in which approx 50-75% of patients with PE underwent echocardiography.

Pathophysiology

Thrombi can form anywhere within the venous system and travel to the lungs to form a pulmonary embo-lus. Most typically, thrombi form within the deep veins of the legs and then travel through the venous system to the pulmonary circulation. When lodged in the pulmonary circulation, often at the bifurcation of the pulmonary arteries or within the proximal branches of the pulmonary arterioles, the effect of a PE is an acute increase in pulmonary vascular resistance. This increase in pulmonary vascular resistance is responsible for many of the echocardiographic findings seen in patients with acute severe PE. It is important to recognize that pulmonary pressure does not rise acutely in the setting of acute PE, just pulmonary resistance. Because the normal right ventricle (RV) is accustomed to relatively low pulmonary pressures, the maximal systolic right ventricular pressure is generally around 25 mmHg. A previously normal RV cannot acutely handle the increased load associated with a marked increase in pulmonary resistance. Pressure in the pulmonary artery, therefore, does not rise despite acute increase in pulmonary resistance.

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