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Pulmonary embolism

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Pulmonary embolism

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Pulmonary embolism

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Preview

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?

Transcript

Content Reviewers:

Rishi Desai, MD, MPH

A pulmonary embolism happens when an embolus, which is a type of blockage, suddenly gets lodged inside a pulmonary artery.

Depending on which pulmonary artery or arteries are affected by the blockage, that can seriously decrease the amount of oxygenated blood that gets out to the body.

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.

Ultimately, all of the blood ends up in the superior or inferior vena cava and dumps into the right atrium.

From there the blood goes into the right ventricle and gets pumped into pulmonary artery and eventually into the lungs.

The pulmonary artery splits at a spot called the pulmonary saddle, which looks like a bit like a horse saddle, and then the right and left pulmonary arteries enter their respective lungs.

Subsequent branches off the pulmonary artery lead to smaller and smaller arteries, then arterioles, and finally capillaries that form nets around the alveoli, which is where gas exchange occurs.

When a pulmonary embolism happens, a blockage in any of the arteries leads to a decrease in blood flow to lung tissue downstream.

The majority of the time, this blockage is caused by a broken off piece of a blood clot commonly associated with deep vein thrombosis.

A deep vein thrombosis most commonly develops in the lower legs, below the knee, although a blood clot can form in both superficial and deep veins and also in other parts of the body as well.

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.

These platelets then recruit additional platelets to form a platelet plug. This formation of the platelet plug is called primary hemostasis.

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 these steps leading up to fibrin reinforcement of the platelet plug make up the process called secondary hemostasis and results in a hard clot at the site of the injury.

This cascade has a huge degree of amplification and takes only a few minutes from injury to clot formation.

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.

The body needs oxygenated blood to function and can therefore only tolerate a bit of a V/Q mismatch, before the lungs are no longer able to meet the needs of the body.

The amount of V/Q mismatch ultimately depends on the number, size, and location of the pulmonary thromboembolisms, which tells us the amount of lung tissue that’s being denied blood flow.

A physiologic response to all of this is hyperventilation.