Pulmonary Embolism




Abstract


Pulmonary embolism remains a cause of substantial morbidity and mortality. Echocardiography can be used for diagnosis, management, and assessment of prognosis in pulmonary embolism. Echocardiographic features of pulmonary embolisms include presence of thrombus in the right side of the heart through the pulmonary arteries, and right ventricular dilation and dysfunction. This chapter will review the echocardiographic features present in pulmonary embolism.




Keywords

Pulmonary embolism, pulmonary vascular resistance, right ventricle, thrombolysis, thrombus

 




Introduction


Pulmonary embolism (PE) is associated with substantial morbidity and mortality, accounting for over 50,000 deaths per year in the United States. PE coexists with other cardiac and pulmonary diseases and remains a diagnosis that continues to elude clinicians. Indeed, PE has been called “the great masquerader” because the signs and symptoms of PE mimic that of other diseases. The emergence of interventional strategies that remove or dissolve thrombus, including thrombolysis and surgical or suction embolectomy, makes accurate diagnosis and risk stratification in PE essential. PE is generally a consequence of thrombi that form in the deep veins, which have the potential to migrate to the right side of the heart and lodge in the pulmonary vasculature. Thus, PE is a subset of thromboembolic disease and venous thromboembolism disease, and PEs need to be viewed as a continuum.




Utility of Echocardiography in Pulmonary Embolism


Echocardiography can be extremely helpful in the diagnosis and management of acute PE, and there are several characteristic echocardiographic features in acute PE ( Box 35.1 ). While generally not used as the primary method to diagnose PE—a role reserved for spiral computed tomography (CT) and ventilation/perfusion scanning—echocardiography provides supportive information to complement other diagnostic tests in this disorder. Nevertheless, echocardiography can often be the first imaging test obtained in patients with acute PE, as it is commonly used as a screening test to determine the etiology of nonspecific signs and symptoms. Indeed, echocardiography can be used to distinguish PE from other causes of chest pain, shortness of breath, and hypotension, such as myocardial infarction, tamponade, and aortic dissection.



BOX 35.1





  • Right ventricular dilatation



  • Right ventricular dysfunction (global and regional)



  • Normal or hyperdynamic left ventricular function



  • Paradoxic septal motion, interventricular septal flattening



  • Tricuspid regurgitation



  • Pulmonary artery dilatation



  • Attenuation of normal inspiratory collapse of inferior vena cava



  • Decrease in right ventricular fractional area change



Echocardiographic Features in Pulmonary Embolism


Identification of Thrombus by Echocardiography


Thrombi that result in PE generally arise from the deep venous system in the legs ( Fig. 35.1 ), although they can form de novo in the right side of the heart. Echocardiography can visualize thrombus in the venous system anywhere from the vena cava through the proximal pulmonary arteries. All masses in the heart that might represent potential thrombi need to be distinguished from other cardiac masses, including myxomas, fibroelastomas, and other cardiac tumors (see Chapter 39 ). Thrombi in the pulmonary arteries ( Fig. 35.2 ) can generally be visualized to approximately just past the bifurcation with transthoracic echocardiography (TTE), and somewhat further with transesophageal echocardiography (TEE). Thrombi from the deep venous system of the legs tend to be linear in appearance, although can dissociate and become more rounded, and can be visualized extending from the inferior vena cava ( Fig. 35.3 and ), in the right atrium ( Fig. 35.4 and ), right ventricle (RV) ( Fig. 35.5 and ), or pulmonary outflow tract ( Figs. 35.6–35.8 and ). It is not uncommon for so-called saddle emboli to become lodged at the bifurcation (see Figs. 35.6–35.8 and ), and the pulmonary artery bifurcation should be carefully assessed from the short-axis views in patients with suspected PE.




FIG. 35.1


Thrombi arising from the deep veins of the legs after extraction from pulmonary artery.



FIG. 35.2


Thrombi in pulmonary artery at autopsy.

From Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation . 2011;123(16):1788–1830.



FIG. 35.3


Linear embolus (arrow) in the inferior vena cava (IVC).



FIG. 35.4


Transesophageal echocardiography demonstrating a thrombus (arrow) passing through a patent foramen ovale between the right atrium (RA) and left atrium (LA) in a patient who had both a pulmonary embolism and a stroke.



FIG. 35.5


Round thrombus (arrow) in the right ventricle (RV). LV, Left ventricle.



FIG. 35.6


Saddle embolus (arrow) in the right ventricular outflow tract (RVOT) at the bifurcation of the pulmonary arteries in a parasternal short-axis view.



FIG. 35.7


Close-up view of pulmonary bifurcation saddle embolism (arrow) seen in Fig. 35.6 . RVOT , Right ventricular outflow tract.



FIG. 35.8


Linear thrombus (arrow) at the bifurcation of the pulmonary arteries. RVOT , Right ventricular outflow tract.


Assessment of the Right Ventricle in Pulmonary Embolism


Beyond identification of thrombus in the right side of the heart, echocardiography is particular useful in assessing the effect of PE on cardiac function, particularly right ventricular function. The unique physiology of the RV (see Chapter 16 ) contributes to the characteristic echocardiographic findings in PE. The normal RV, generally accustomed to low pulmonary vascular resistance, and hence very low afterload, needs only to generate relatively low pressures (normal right ventricular systolic pressures are generally no higher than about 25 mm Hg; Fig. 35.9 , left panel ). In the setting of acute PE, pulmonary vascular resistance rises abruptly and substantially, resulting in RV dilatation and, in severe cases, RV failure (see Fig. 35.9 , right panel ). The right ventricular dilatation and dysfunction that can occur in this setting can result in reduced right ventricular cardiac output, which can in turn lead to a reduction in left ventricular preload, and ultimately a reduction in cardiac output, with resultant hypotension. Hypotension can lead to reduced coronary perfusion, which can contribute to ischemia or even infarction of the RV. Moreover, increased right ventricular afterload can lead to an increase in right ventricular wall stress, which can increase RV myocardial oxygen demand. The combination of increased oxygen demand and reduced oxygen supply can lead to further RV dysfunction ( Fig. 35.10 ).




FIG. 35.9


Schematic of normal right ventricle (left panel) and right ventricle after pulmonary embolism (right panel) . Notice the severe right ventricular dilatation. LA , Left atrium; LV , left ventricle; RA , right atrium; RV , right ventricle.



FIG. 35.10


Pathophysiology of acute pulmonary embolism. See text. LV , Left ventricle; O 2 , oxygen; RV , right ventricle.

Adapted from Lualdi JC, Goldhaber SZ. Right ventricular dysfunction after acute pulmonary embolism: pathophysiologic factors, detection, and therapeutic implications. Am Heart J . 1995;130(6):1276–1282.


RV dilatation is the echocardiographic hallmark of PE. This is best visualized from the apical four-chamber view where classic findings include RV diameter greater than left ventricle (LV) diameter, relatively normal LV function, with a small underfilled LV. While right ventricular diameter in the apical four-chamber view is rarely greater than 2.7 cm in normal individuals, these measures can vary widely, and a good rule of thumb is to compare right ventricular diameter to left ventricular diameter in the mid-ventricular regions and the apical four-chamber views.


Regional Right Ventricular Dysfunction: The “Mcconnell” Sign


A distinctive regional wall motion abnormality has been recognized in acute PE in which the RV mid free wall becomes dyskinetic, with relative sparing of the apex and the base. This pattern, alternatively known as the right ventricular strain pattern or McConnell sign ( Figs. 35.11–35.13 ; ), is visually quite characteristic and recognizable. It is highly specific for acute PE, although can be seen rarely in other conditions in which pulmonary vascular resistance increases abruptly, such as acute pneumonia or interstitial lung disease. Nevertheless, acute PE remains the predominant condition in which the “McConnell sign” is seen.




FIG. 35.11


Regional right ventricular dysfunction in acute pulmonary embolism (McConnell sign). Note dyskinesis of mid right ventricular free wall (blue arrows) and relative sparing of the apex and the base (green arrows) . LA , Left atrium; LV , left ventricle; RA , right atrium; RV , right ventricle.



FIG. 35.12


End-diastolic and end-systolic views of a patient with “McConnell sign.” Note that the right ventricle is dilated in both diastole and systole. See videos.

Sep 15, 2018 | Posted by in CARDIOLOGY | Comments Off on Pulmonary Embolism
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