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Pulmonary edema



Respiratory system


Upper respiratory tract disorders
Lower respiratory tract disorders
Pleura and pleural space disorders
Pulmonary vascular disorders
Apnea and hypoventilation
Respiratory system pathology review

Pulmonary edema


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High Yield Notes
11 pages

Pulmonary edema

10 flashcards

USMLE® Step 1 style questions USMLE

1 questions

A 66-year-old nonbinary individual presents to the emergency department for evaluation of shortness of breath with exertion. The patient reports increasing shortness of breath over the past several weeks to the point where they can no longer climb a flight of stairs without becoming winded. Past medical history includes hypertension, hyperlipidemia, and deep vein thrombosis following a knee replacement surgery ten years ago. The patient has not seen a physician in years and is currently not on any medications. They currently smoke one pack of cigarettes daily. Temperature is 36.1°C (97.0°F), pulse is 78/min, respirations are 22/min, blood pressure is 188/92 mmHg, and O2 saturation is 91% on room air. Physical examination demonstrates an additional heart sound heard just after S2, and diffuse rales on lung auscultation. Jugular venous distension, pitting edema, and hepatomegaly are absent. A chest X-ray is obtained and demonstrated below. Which of the following best describes the pathophysiology of this patient’s pulmonary findings?  

Image reproduced from Wikimedia Commons

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Content Reviewers:

Rishi Desai, MD, MPH

Pulmonary edema refers to the buildup of fluid in the lungs including the airways like the alveoli - which are the tiny air sacs - as well as in the interstitium, which is the lung tissue that’s sandwiched between the alveoli and the capillaries.

This space is mostly full of proteins, and when it starts filling up with fluid, it can make it hard for oxygen to cross over from the alveoli into the capillary, leaving the body hypoxic - or deprived of oxygen.

To understand pulmonary edema, let’s first talk about the three main factors that determine how fluid moves between the capillaries and interstitial fluid, which are the hydrostatic pressure, oncotic pressure and capillary permeability.

Hydrostatic pressure refers to the pressure felt by fluid in a confined space, pushing the fluid out of that space.

In the interstitial space, it’s the same thing as the blood pressure in the pulmonary capillaries, and because the pulmonary circulation is a low pressure system, the hydrostatic pressure is pretty low. But it’s still higher than the hydrostatic pressure exerted by the interstitial fluid of the lungs - which is almost zero.

So, to be clear, if hydrostatic pressure was the only factor involved, a lot of fluid would be continuously leaking out of the pulmonary capillaries into the lung’s interstitial space.

The next factor, though, is oncotic pressure; which is a type of osmotic pressure exerted by cells and proteins that can’t cross the capillary membrane and therefore tend to attract fluid.

The oncotic pressure is higher in the pulmonary capillaries than in the interstitial fluid, so it opposes the hydrostatic pressure.

Finally, there’s capillary permeability or leakiness which affects how easily fluid is actually able to get through.

When taking these three factors together, the net result is that a very small amount of fluid leaks into the interstitial space, and that fluid is normally whisked away by the lymphatic channels in the lungs, which keeps the lungs free of excess fluid.

Now, the underlying cause of pulmonary edema can be cardiogenic - meaning that it develops as a result of a heart disease, or can be non-cardiogenic which typically involves damage to the pulmonary capillaries or alveoli.

The most common cardiogenic cause is left-sided heart-failure, and in left-sided heart failure, the left ventricle becomes unhealthy and can’t pump effectively, which means that blood starts to backup in the left atrium, and then the pulmonary veins and pulmonary capillaries.

The extra blood in the pulmonary capillaries causes pulmonary hypertension - which is an increase in the hydrostatic pressure of the pulmonary blood vessels, and this pushes more fluid into the interstitial space of the lungs which leads to pulmonary edema.

Another cardiogenic cause is severe systemic hypertension - specifically a blood pressure that is greater than 180 systolic or 110 diastolic. In this situation, the left ventricle is healthy but simply can’t effectively pump blood in a system with such high afterload - in other words, under conditions with such high systemic pressures.

Once again, blood starts to back up in the left atrium, pulmonary veins, and pulmonary capillaries, ultimately leading to pulmonary hypertension and pulmonary edema.

Noncardiogenic causes of pulmonary edema include things like pulmonary infections, inhalation of toxic substances, and trauma to the chest.

All of these can cause direct injury to the alveoli, and when this happens there is usually an inflammatory process that makes nearby capillaries more permeable. As a result, proteins and fluid enter the interstitial space.

Another cause is sepsis, and the key difference is that in sepsis the inflammatory process happens throughout the body rather than just in the lungs, so in addition to pulmonary edema, sepsis can cause extra fluid in the interstitial space of tissues throughout the body.

Another category of non-cardiogenic causes is having low oncotic pressure.


Pulmonary edema is a condition in which fluid accumulates in the lungs, making it difficult for oxygen to pass through the alveoli and into the bloodstream. It is often due to the left ventricular heart failure to adequately remove blood from the pulmonary circulation, which is known as cardiogenic pulmonary edema. It can also be due to an injury to the lung parenchyma or vasculature of the lung - known as noncardiogenic pulmonary edema.

If not treated, pulmonary edema can lead to respiratory failure or cardiac arrest due to hypoxia. Treatment focuses on improving respiratory function, treating the underlying cause, and preventing and avoiding further damage to the lung.

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