Red Flags: The ABCs of acute PE
Kelly Drumright BS, BSN, RN, CCRN-CMC, CSC
Stephanie Julkenbeck BSN, RN
Chris Judd BSN, RN

$3.95
Nursing Made Incredibly Easy!
April 2013 
Volume 11  Number 2
Pages 45 - 49
 
  PDF Version Available!

ABSTRACT
Pulmonary embolism (PE) is the most common preventable cause of death in the hospital setting, claiming between 150,000 and 200,000 lives in the United States each year. PE occurs when a material from another part of the body (such as a thrombus, tumor, air, or fat embolus) forms a blockage of the pulmonary artery or one of its branches (see Picturing pulmonary emboli).Saddle PE denotes an obstruction of the right and left pulmonary arteries at the bifurcation, or split, of the main pulmonary artery. Venous thrombi are typical sources of PE that often form at valve cusps or bifurcations of the veins as a result of decreased blood flow. Thrombi from lower extremities, especially the iliofemoral veins, are frequently the culprits. Thrombi may also originate from the upper extremity venous system, right heart, pelvic, and renal system.PE may be acute or chronic. Patients with chronic PE have progressive symptoms that can span over a period of years, whereas patients with acute PE usually have a sudden onset of symptoms that start with vessel obstruction. Acute PE is categorized as either massive or submassive. Massive PE is often catastrophic, causing hypotension and an elevated central venous pressure (CVP) that typically leads to acute right ventricular (RV) failure and death within 1 to 2 hours of the initial event. Submassive PE includes all acute PE that doesn't fall into the category of massive PE. Although frequently seen as a submassive PE, saddle PE can present as both a submassive PE and a massive PE.There are several risk factors associated with PE. The most common risk factor of PE is deep vein thrombosis (DVT), with PE occurring in more than 50% of patients with a confirmed DVT.Venous thromboembolism (VTE) includes both DVT and PE. Virchow's triad is a theory that highlights the three primary pathogenic causes of VTE, including alterations in blood flow, such as stasis, vascular endothelial injury, and changes in blood constituents such as in hypercoagulopathy

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