We get to the end of the physiology of fluid. Hydrostatic pressure is the pressure that opposes oncotic pressure and added osmolarity. Hydrostatic pressure and oncotic pressure are the two main parts of the Starling equation and help ensure fluid equilibrium within the body.
There is not a lot to add to the explanation of hydrostatic pressure that has not been mentioned in previous posts. As explained before, hydrostatic pressure is like a balloon with a small hole in it. When it is only partially filled with fluid there would be little to no leak from the small hole. The balloon is not completed distended and there is not a lot of pressure on the walls. When the balloon is filled completely, the pressure builds up, and the water will stream out of the hole until the volume decreases to a point where the pressure drops below a critical point. This pressure that wants to push the fluid out is hydrostatic pressure. The osmotic and oncotic pressure draw in the fluid until it reaches a critical point and then the hydrostatic pressure pushes it back out.
Figure 1: Hydrostatic Pressure
Figure 2: Starling Forces
Relooking at the Starling equation we can see that if the hydrostatic pressure in the intravascular space increases without increasing the other variables, the fluid will more likely want to leave the intravascular space. Whereas, increasing oncotic pressure only with make the equation more negative and the fluid movement will be into the intravascular space.
Starling equation:
Jv = LpS [(Pc - Pi] - σ(πc-πi)]
Jv = Rate of fluid entering or leaving the intravascular space
Lp = Hydraulic permeability coefficient
S = Surface area of membrane
Pc = Capillary hydrostatic pressure
Pi = Interstitial hydrostatic pressure (small)
Ï€c = Capillary oncotic pressure
Ï€i = Interstitial oncotic pressure (negligible)
σ = reflection coefficient for protein
How does this affect patients clinically?
I think that this is clinically very interesting. Two patients, similar in age, height, and weight, were next door to each other, and both had been treated for septic shock. Unfortunately, they were both over-resuscitated and, as per the fluid balance in the electronic medical record, they both had a positive fluid balance of 18 liters (This happens more than you think, just keep an eye on the fluid balance in the more traditional ICUs). The interesting part of these two patients is that one was extubated on 2L nasal cannula and the other was intubated with bilateral infiltrates and had a consult for potential ECMO due to ARDS. This patient would not actually qualify as ARDS, as per the Berlin Criteria, due to the volume overload, but the end result of severe hypoxia due to bilateral infiltrates is the same.
So how could two patients with the same disease process and same fluid balance have such different outcomes? The major difference was their oncotic pressures. The patient on 2L NC had an albumin of 1.6 g/dL, while the hypoxic patient had an albumin of 3.2 g/dL.
Low oncotic pressure will have low hydrostatic pressure but fluid will leave due to 3rd spacing, whereas high oncotic pressure leads to high hydrostatic pressure which will push fluid into different areas like the lung interstitium leading to pulmonary edema.
SCAPE, or flash pulmonary edema, is due to increased left ventricular pressures and left atrial pressures (LAP) due to decreased lusitropy. When the LAP pressure increases above 18 mmHg the increased hydrostatic pressure will lead to pulmonary edema.
The same is true for our hypoxic patient. The higher albumin level caused severe pulmonary edema and the significant difference in clinical outcomes.
Why is the lung so sensitive to increased hydrostatic pressure compared to other areas of the body?
We again look at the Starling equation and reflection coefficient. The reflection coefficient takes into account that some areas of the body do have interstitial proteins and the gradient between the intravascular and interstitial space changes based on this. The reflection coefficient ranges from 0 to 1. 1 is when there is negligible proteins on the interstitial side. This coefficient is used with CSF and glomerular filtrate. The liver sinusoids have much higher levels of protein and the coefficient is close to 0. This is why the liver is so prone to congestion with decompensated heart failure. The lung is closer to 0.5 and much more sensitive to increases in hydrostatic pressure.
Using this knowledge clinically:
When I am ensuring that a patient has appropriate oncotic pressure so they will not have third-spacing, they can get too much albumin supplement and it can cause pulmonary edema. This is more common than people realize. For this reason, I do not try to normalize the albumin, especially in volume overloaded patients, unless they have excellent urine output. Keeping the value above 2.5 g/dL will help with third-spacing but should not increase hydrostatic pressure enough to cause severe pulmonary edema.
Putting it all together:
This is the last of the three determinants of intravascular volume in terms of fluid dynamics. You should now be able to keep fluid intravascularly using physiology.
References:
1. "Fluid Physiology" by Kerry Brandis, LibreTexts licensed under CC BY-NC-SA.
2. Starling forces and fluid exchange in the microcirculation: Deranged Physiology. https://derangedphysiology.com/main/cicm-primary-exam/required-reading/cardiovascular-system/Chapter%20471/starling-forces-and-fluid-exchange-microcirculation. Accessed 7/12/21.
3. Tobias A, Ballard BD, Mohiuddin SS. Physiology, Water Balance. [Updated 2020 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK541059/