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A 65-year-old woman comes to the emergency department because of hemoptysis and chest pain which worsens upon inspiration for the past 2 hours. She says that she has felt increasingly fatigued over the past 4 months and reports a 13.6-kg (30-lb) weight loss during this period. Physical examination shows scleral icterus and right upper quadrant tenderness. There is a palpable and tender nodule felt over her anterior left leg. A similar tender nodule is palpable on the right leg. A spiral computed tomography scan is done and confirms the diagnosis of pulmonary embolism. After stabilization of this patients condition, which of the following is the next best step in management?
Content Reviewers:Rishi Desai, MD, MPH
Normally, blood makes it back to the heart from all of the tissues and organs through a network of veins that merge over and over.
Superficial veins drain blood into deep veins, which rely on the skeletal muscle pump to move blood forward. The way it works is that the surrounding skeletal muscles compress the vein and propel blood forward, and the veins prevent blood from moving backwards by using one-way valves.
The majority of the time, this blockage is caused by a broken off piece of a blood clot commonly associated with deep vein thrombosis.
Normally, the process starts with damage to the endothelium, or inner lining of blood vessel walls, after which there’s an immediate vasoconstriction or narrowing of the blood vessel which limits the amount of blood flow.
After that, some platelets adhere to the damaged vessel wall, and become activated by collagen and tissue factor, which are proteins that are normally kept separated from the blood by an intact endothelium.
After that, the coagulation cascade is activated.
First off in the blood there’s a set of clotting factors, most of which are proteins synthesized by the liver, and usually these are inactive and just floating around in the blood.
The coagulation cascade starts when one of these proteins gets proteolytically cleaved.
This active protein then proteolytically cleaves and activates the next clotting factor, and so on.
The final step is activation of the protein fibrinogen to fibrin, which deposits and polymerizes to form a mesh around the platelets.
So the activation of the cascade is carefully controlled by anticoagulation proteins that target and inactivate key clotting factors.
For example, antithrombin inactivates Factors IXa, Xa, XIa, XIIa, VIIa and thrombin while protein C inactivates Factors Va and VIIIa.
As the clot grows in size, it limits the amount of blood able to pass by, and pressure in the vein increases.
Usually the clot might start naturally breaking down, for example, enzymes like plasmin break down fibrin into fragments called D-dimers.
But sometimes, the increased pressure in the vein can cause a part of the main clot to break free, becoming a thromboembolus which can travel downstream towards the heart.
When that happens, a thromboemobolus - which is a blood clot on the move - can move from the spot of clot formation and get into the right atrium, and then into the right ventricle and get pumped into the lungs where it can get lodged some place - causing a pulmonary thromboembolism. This is a life-threatening situation because it literally blocks blood from getting into the lungs to pick up oxygen.
If there’s no blood flowing past an alveoli, then that means there are alveoli that are getting ventilated with fresh air but not getting perfused with blood. We call this a ventilation perfusion mismatch or a V/Q mismatch.
A physiologic response to all of this is hyperventilation.
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "CURRENT Medical Diagnosis and Treatment 2020" McGraw-Hill Education / Medical (2019)
- "Thrombosis" Arteriosclerosis, Thrombosis, and Vascular Biology (2014)
- "Acute pulmonary embolism: An update on diagnosis and management" Current Problems in Cardiology (2005)
- "Epidemiology, Pathophysiology, and Natural History of Pulmonary Embolism" Seminars in Interventional Radiology (2018)