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Pulmonary Embolism

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Abstract

Acute pulmonary embolism (aPE) is one of the great masqueraders in medicine. Therefore, a high index of clinical suspicion coupled with a detailed history and physical examination is invaluable when evaluating patients. Acute venous thromboembolism (VTE) that usually originates from the lower extremity deep veins (DVT) is clearly recognized as a significant healthcare problem. In the United States an estimated 900,000 cases of DVT and PE occur per year, causing approximately 300,000 deaths. Clinically, aPE is defined as massive, sub-massive, or non-massive. In the assessment and management of patients presenting with suspected aPE, clinical information is critical not only to the initial assessment of prognosis, but also to guide therapeutic decision-making. Hemodynamic stability and right ventricular (RV) function are found to be critically important in determining morbidity and mortality. Thus, risk stratification algorithms have been proposed to help physicians identify high- versus low-risk aPE patients in order to expedite diagnosis and treatment. Computed tomographic pulmonary angiography (CTPA) has been the imaging of choice in aPE patients not only for its higher sensitivity and specificity, but also for providing alternate diagnosis in patients with nonspecific signs and symptoms of aPE. More recently, echocardiography has been able to provide anatomical, functional, as well as mechanical information regarding RV function and RV-pulmonary unit interaction. This chapter intents to not only summarize the most important pathophysiological processes involved from clot formation to distal pulmonary embolization, but also describe potential hemodynamic implications and associated clinical manifestations. Current diagnostic and therapeutic algorithms are reviewed; available imaging modalities with most typically diagnostic aPE features are described; and mechanical characterization of the anatomical and functional abnormalities with regard to RV function are examined in terms of the hemodynamic derangement caused by acute obstruction to pulmonary flow.

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Abbreviations

aPE:

Acute pulmonary embolism

AUC:

Appropriate use criteria

BP:

Blood pressure

BNP:

Brain natriuretic peptide

CDMT:

Catheter-directed mechanical thrombectomy

CTEPH:

Chronic thromboembolic pulmonary hypertension

CTPA:

Computed tomographic pulmonary angiography

DVT:

Deep venous thrombosis

DOACs:

Direct-acting oral anticoagulants

ECG:

Electrocardiogram

ESLD:

End-stage liver disease

ESC:

European Society of Cardiology

FAC:

Fractional area change

IVS:

Interventricular septum

LV:

Left ventricle

LMWH:

Low-molecular-weight heparin

OR:

Odds ratio

PIOPED:

Prospective investigation of pulmonary embolism diagnosis

PA:

Pulmonary artery

PERC:

Pulmonary Embolism Rule-out Criteria

PH:

Pulmonary hypertension

PVR:

Pulmonary vascular resistance

RHS:

Right-heart strain

RV:

Right ventricle

RVOT:

RV outflow tract

TTE:

Transthoracic echocardiogram

TAPSE:

Tricuspid annular plane systolic excursion

TR:

Tricuspid regurgitation

UFH:

Unfractionated heparin

VTI:

Velocity time integral

VTE:

Venous thromboembolism

V/Q scan:

Ventilation-perfusion scintigraphy

VKA:

Vitamin K antagonist

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López-Candales, A., Vallurupalli, S. (2021). Pulmonary Embolism. In: Gaine, S.P., Naeije, R., Peacock, A.J. (eds) The Right Heart. Springer, Cham. https://doi.org/10.1007/978-3-030-78255-9_14

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