Untitled Document

EDEMA, EMBOLISM, INFARCTION AND PULMONARY HYPERTENSION

[ CATS Home | About CATS | CATS Teaching Modules | Course Outline | Pulmonary | UVM Department of Pathology | Other Pathology Sites | UVM College of Medicine | UVM ]

I. PULMONARY EDEMA
II. PULMONARY EMBOLI AND INFARCTION
III. PULMONARY HYPERTENSION

I. PULMONARY EDEMA

Pulmonary edema occurs when the amount of extravascular water present in the alveolar wall interstitium exceeds the lymphatic system's ability to pump it dry.
Two major opposing physiologic forces are at work at the capillary level.
- Intravascular pressure wants to push water out of vessels, oncotic pressure, mainly from protein in the blood, wants to hold water in the vessels.
- If pressure goes up or protein content of the blood goes down, water tends to leak out.
- Also, if you damage the endothelial cell barrier (like some micro-organisms tend to do) you will make the capillary leaky.
Pulmonary edema can result from a large number diseases. The single most common cause is left heart failure. This is a pressure phenomenon since blood is being "backed up" at the lung capillary level.
The gross appearance of the lungs in acute pulmonary edema is that of an over-saturated sponge with frothy hemorrhagic fluid pouring from cut sections.
Microscopic exam of the lung in pulmonary edema shows light pink material filling alveolar spaces.
The chest X-ray appearance of pulmonary edema is that of a butterfly infiltrate, with the "body" of the butterfly centered over the sternum. Lesser degrees of edema cause the prominence of lymph channels at the lung periphery known as "Curly B" lines, with or without pleural effusions.

II. PULMONARY EMBOLI AND INFARCTION

Most pulmonary emboli are made of blood that clots in a systemic vein and then dislodges and shoots off to the lung circulation. Blood that clots in a vein is called thrombus. Therefore, most pulmonary emboli are thromboembolic.
Any condition that predisposes to thrombosis in veins, predisposes the patient to thromboembolism to the lungs.
The 3 most common causes of venous thrombosis are: immobilization, trauma, and coagulopathy.
A large thromboembolus that lodges at the bifurcation of the main pulmonary artery and obstructs lung blood flow is called a saddle embolus. Saddle embolus can cause almost instantaneous death.
Most pulmonary emboli (90%) DO NOT cause lung infarction because the lung has a dual blood supply. Collateral channels between bronchial and pulmonary arteries open immediately after embolic occlusion of a small pulmonary artery and flood the lung distal to the obstruction with oxygenated blood.
Lung infarction occurs when the quality of the bronchial arterial blood is less than optimal-like in patients with severe anemia or lung and heart diseases that cause hypoxia.
A patient who develops one pulmonary embolism is at high risk for more. These patients must be immediately anticoagulated!
Lung thromboembolism causes sudden shortness of breath, usually without local chest wall pain.
Lung infarction may cause shortness of breath, hemoptysis, localized chest wall pain, and a pleural friction rub. Lung infarcts tend to be wedge shaped with one angle of the wedge pointing toward the heart.
Pulmonary embolism is the sole or major cause of about 10% of all hospital deaths.
A pulmonary artery branch occluded by thromboembolism may become patent again by a process known as recanalization.
The most common microscopic finding in the lung after pulmonary embolism is alveolar hemorrhage.
A paradoxical embolus can occur when there is a patent ductus arteriosus.
Other substances can embolize through the blood and lodge in the lung. Three additional important embolic sources are fat, air, and septic material from infected wounds abutting veins and septic phlebitis.

III. PULMONARY HYPERTENSION

QUESTIONS TO CONSIDER AS LEARNING OBJECTIVES:

Fragments of coagulated blood that embolize to the lungs are derived most commonly from this pathologic process.
This is the most common microscopic change in the lung tissue after a pulmonary embolism.
Pulmonary artery branches may be reusable after embolism thanks to this process.
With one leg in the right pulmonary artery and one leg in the left, this cowboy is a real killer.
These specific structures allow survival of the lung in a healthy individual after pulmonary embolism.
This sound may be heard through the chest after a pulmonary infarct.
This term best defines thegeometrical appearance of a lung infarct.
Patients at risk for infarction after pulmonary embolism usually have this kind of disease (not looking for a specific disease).
Patients with pre-existing heart or lung disease may develop this after pulmonary embolism.
These three conditions are the major risk factors for pulmonary embolism.

Go Back to Course Outline

Go Back to Pulmonary

[ CATS Home | About CATS | CATS Teaching Modules | UVM Department of Pathology | Other Pathology Sites | UVM College of Medicine | UVM ]

Questions? Comments? Send a message to the CATS guru: jkessler@salus.uvm.edu