Although many intravascular objects can occlude the lung vasculature, this
chapter considers pulmonary embolism (PE) to occur from clotted blood.
Most PEs originate as clots in large veins, as deep venous thromboses
(DVTs). This chapter henceforth employs the term venous
thromboembolism (VTE) to include PE, DVT, or both.
PE represents the second leading cause of sudden, unexpected,
nontraumatic death in outpatients.1–3 Longitudinal
epidemiologic studies have consistently found that PE has an incidence
of approximately 1 in 1500 per year; the incidence increases geometrically
with age to a maximum of 1 in 300 per year at age 80.4,5 The
incidence is slightly higher in women and blacks than in males and
whites; the incidence is lowest in Asians and Latinos.6 The
rate of PE diagnosis does vary slightly with geography, with an
increase in the South, and the frequency appears to increase in cold
Pulmonary emboli occur when a proximal portion of a venous clot breaks
off, travels through the veins, traverses the right ventricle, and lodges
in the precapillary pulmonary arteries. Patients without prior heart
or lung disease begin to experience symptoms from PE when approximately
20% to 30% of lung vasculature becomes occluded.
Venous thrombi large enough to cause clinically important PE can
form in the popliteal, common femoral, superficial femoral, pelvic,
axillary, jugular, and great veins. These thrombi usually form in
the proximal recesses of venous valves, where blood flow is slowest.
Although 75% to 80% of hospitalized patients with
PE have image-demonstrated DVT, only 40% of ambulatory
ED patients with PE have concomitant DVT.9
Blood plasma exists in equilibrium between liquid and solid phases.
The balance between clot formation and clot removal depends upon
multiple influences. Rudolph Virchow in 1846 succinctly described
three conditions that promote the formation of dangerous blood clots
in the veins: stasis of venous blood flow, tissue damage, and increased
tendency for the blood to clot, referred to variously as either hypercoagulability or thrombophilia (“the
love of clotting”).
PE alters the patient’s intrapulmonary blood flow, but
measuring lung perfusion in the ED is not possible (techniques are
seldom available outside of a research laboratory). Hypoxemia is
one consequence of ventilation–perfusion (V̇/Q̇)
abnormality that can be measured. Most conditions that cause difficulty
breathing and hypoxia in ED populations do so by limiting ventilation,
and the severity of hypoxemia correlates with the proportion of
airways obstructed. In contrast, PE obstructs blood flow, leading
to segments of lung with high ventilation relative to perfusion—a
condition termed alveolar dead space. Hypoxemia
from PE results from redistribution of blood away from the blocked
pulmonary arteries and into patent arteries. If PE diverts a large
volume of blood into areas of lung with a previously low V̇/Q̇ ratio,
then hypoxemia will result. If PE diverts blood into areas of lung
with a previously high ventilation–perfusion ratio, then
the sum of venous–to–fresh air mixing will increase,
and in ...