- Pulmonary capillary hydrostatic pressure (Pcap or Pcp):
- This is the intravascular pressure in the pulmonary capillaries
- It is usually about 8-10mmHg
- It is usually a little higher in the arterial (pre-alveolar) capillaries
- This pressure is one of the determinants of fluid flux through the capillary wall, and represents the vascular hydrostatic force behind the formation of pulmonary oedema
- Measurement of the pulmonary capillary hydrostatic pressure:
- It can be estimated qualitatively from the shape of the curve seen following PA wedging
- It can be calculated from the fast and slow decay components of that curve
- It can be calculated from the Gaar equation:
PPC = LAP + 0.4 × (mPAP - LAP)
- Interpretation of the value
- One way of using this is to determine a threshold value (individual for each patient) at which pulmonary oedema develops, and then to titrate one's fluid management in a way which does not exceed this value.
- Another is to use it as a diagnostic tool to exclude cardiac causes of pulmonary oedema (in cardiogenic pulmonary oedema, Pcap is elevated)
In slightly more detail,
The pulmonary capillary pressure can, therefore, be determined from this graph by three main means:
As you can see, the visual method and the extrapolated curve method tend to give slightly different values:
That Gaar equation is:
PPC = LAP + 0.4 × (mPAP - LAP)
- PPC = pulmonary capillary pressure
- LAP = left atrial pressure
- mPAP = mean pulmonary artery pressure
In other words, Gaar and co. determined that the capillary pressure was under most circumstances about 40% of the total fall from mean PA pressure down to left atrial pressure (which is your occlusion pressure):
Is this empirically derived shortcut accurate? Of course not. In fact, of these methods, none are particularly reliable, and so one must conclude the discussion of pulmonary capillary pressure with the statement that truly, the only thing we can safely say about it is that it is somewhere between pulmonary arterial diastolic and pulmonary venous pressure. In fact, generally speaking, in ICU capillary leakiness is rarely a purely hydrostatic thing. What of sepsis, DIC etc?...
In short, what you are measuring might be pulmonary capillary hydrostatic pressure, but it is not always going to be relevant to your decisionmaking.
Let's assume that you have overcome all the practical and intellectual barriers, and somehow managed to measure a pressure which is the 100% accurate pulmonary capillary hydrostatic pressure. You now have in your hands a value which describes a major determinant of fluid flux across the pulmonary capillary wall. Put in a different way, this is the pressure wot you oedem with. In more formal explanations of this concepts, it is integrated into the Starling equation, like so:
Fluid efflux = Kfc(Pcap -Pint) - Kd(πcap - πcap)
- Kfc is the capillary filtration coefficient (product of capillary wall hydraulic conductivity and capillary surface area),
- Pcap is the capillary hydrostatic pressure,
- Pint is the pulmonary interstitial hydrostatic pressure,
- Kd is the reflection coefficient (where 0 = freely permeable to proteins, and 1 = completely impermeable),
- πcap is the capillary oncotic pressure, and
- πcap is the pulmonary interstitial oncotic pressure.
So, basically, when one has a patient with pulmonary oedema, one may measure this variable, and - if it ends up being low - one should be able to say with some conviction that the oedema is clearly not the consequence of increased pulmonary capillary pressure, i.e. no cardiogenic cause, but some kind of capillary leakiness, as in ARDS.
Alternatively, one can observe a threshold value (individual for each patient) at which pulmonary oedema develops, and then resolve to limit one's fluid management below that threshold, i.e. serially measuring this parameter and witholding further fluid boluses if it is met or exceeded.