Edema - Osmosis Transcript PDF

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Assignment 2 notes about edema from OSMOSIS...

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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. And this could result from not making enough proteins like albumin due to malnutrition or from liver failure. Alternatively it could be due to losing protein too quickly like in nephrotic syndrome. Regardless of the cause, low oncotic pressure leads to fluid moving from the capillary and into the interstitial space throughout the body, and in the lungs that results in pulmonary edema. Pulmonary edema can develop in a few ways and often develops through a combination of mechanisms. Pulmonary edema makes gas exchange difficult because oxygen and carbon dioxide have to diffuse through a wide layer of interstitial fluid, to get from the alveoli to the pulmonary capillary and vice versa. That journey can take too long relative to how quickly blood moves through the lungs, and that makes it hard to fully oxygenate the blood. Pulmonary edema can lead to severe shortness of breath, and in left-sided heart failure, it can lead to orthopnea which is when there’s worse shortness of breath while lying flat. This happens because there’s increased pulmonary congestion while lying down, and in leftsided ventricular heart failure, the pulmonary circulation is already overloaded. As a result, the extra blood can’t be pumped out efficiently, and it causes shortness of breath. This pulmonary congestion and shortness of breath decreases when a person sits up. The diagnosis of pulmonary edema is usually made with a chest x-ray or chest CT scan that shows fluid in the interstitial space. Treatment for pulmonary edema typically involves giving supplemental oxygen. Other treatments are dependent on the underlying cause - if the cause is cardiogenic in nature, medications aimed at boosting the heart’s performance or lowering the blood pressure can be helpful. If the cause is related to inflammation or low oncotic pressure, then managing that illness will help resolve the pulmonary edema.

Summary Alright, as a quick recap, pulmonary edema refers to fluid accumulation in the interstitial space of the lungs which can be seen on a chest Xray or chest CT scan.

Common cardiogenic causes include left sided heart failure and hypertension, both of which lead to increased hydrostatic pressure in the pulmonary capillaries. Common non-cardiogenic causes include inflammation in the lungs or systemwidinflammation which causes the pulmonary capillaries to be more permeable. Other causes include a low oncotic pressure which can be from malnutrition, liver failure, and nephrotic syndrome. Regardless of the cause, pulmonary edema interferes with gas exchange and results in shortness of breath....