So, you got the balloon inflated.
Remember, that with an inflated balloon the flow (Q) in the pulmonary artery is zero. In the absence of flow, the resistance of the pulmonary circulation becomes irrelevant, and the only pressure measured here should be the pressure of the left atrium.
PC - PLA = Q ×X
PC = capillary pressure
PLA = left atrial pressure
Q = pulmonary artery flow
R = resistance
Thus, when flow is zero:
PC - PLA = 0 ×X
PC - PLA = 0
PC = PLA
Thus, the PAWP should be equivalent to the LA pressure when pulmonary arterial flow is zero. The left atrial pressure at end-diastole (LAP) should in turn be a reflection of the left ventricular end-diastolic pressure (LVEDP) while the mitral valve is still open. So, if everything is equal and the mitral valve is competent and the measurement is taken at the end of expiration, PAWP = LAP = LVEDP. And the LVEDP is then interpreted as a surrogate marker of LV preload. The limitations of this relationship are discussed below (in summary, LVEDP and preload are only loosely associated).
Relationship to catheter tip position
PAWP is equivalent to left atrial pressure ONLY in the most dependent portion of the lung (Wests Zone 3), where pulmonary arterial pressure is greater than alveolar air pressure.
The bottom line is, you need to have some blood around the catheter to measure any sort of blood pressure; and you can only guarantee this in Zone 3, where respiration does not squish blood out of the capillaries.
The pulmonary artery wedge waveform
- The PAWP waveform has 3 distinct waves:
- a wave: left atrial contraction
- c wave: mitral valve closure (with the resulting prolapse of valve leaflets back into the atrium, increasing the pressure therein)
- v wave: left ventricular contraction
You would be right to say that this is very similar to the CVP waveform; indeed it is a central venous pressure you are measuring.
This means, you can make certain inferences about left atrial (and mitral) function from the shape of the waveform. For instance, an abnormally large cv wave (a fusion of c and v waves) suggests mitral regurgitation- a direct analogy to the large cv wave of tricuspid regurgitation seen on a CVP trace. If this happens suddenly in the context of mitral valve replacement (i.e when a previously normal PAWP waveform develops huge cv waves) one can make the diagnosis of prosthetic valve failure.
What the PAWP is NOT:
Bloody preload, that’s what its not. Like CVP, PAWP does not estimate left ventricular preload very well. In a perfect situation, it tells you what pressure the left ventricle is being filled with, and this has some vague relationship to the volume which will be generated - but not to Preload, which can be defined more formally as "all of the factors that contribute to passive ventricular wall stress (or tension) at the end of diastole" or as "initial myocardial fibre length prior to contraction", i.e. sarcomere stretch. In fact, there is some fierce disagreement as to what exactly the definition of preload is anyway.
For the purposes of this PAWP-themed discussion, preload can be defined as the LV volume at the end of diastole, as this is the thing which is closest to the sarcomere stretch. This definition was suggested by Carl Rothe (2003) specifically because he wanted something which he could measure, or relate to measurable parameters. LVEDV is a measurable parameter, and is to some extent determined by the LV filling pressure, as well as LV compliance and a whole host of other factors. So long as those other factors do not interfere too much, LV filling pressure is a reasonable surrogate for LV preload.
PAWP as a predictor of fluid responsiveness
In 2004, Kumar et al published an influential paper which laid waste to the concept of PAWP as a predictor of fluid response. Indeed, they found that neither PAWP nor CVP correlated even slightly with end-diastolic volume or stroke volume variation. Nor did PAWP or CVP change appreciably after a fluid bolus (Whereas LVEDI and SVI certainly changed, suggesting that these derived variables probably do mean something). This lack of relationship between PAWP and preload was consistently observed among both critically ill patients and in the normal population.
In short, PAWP is not a very good predictor of fluid responsiveness. The ICU public have come to appreciate this fact after perhaps three decades of waxing and waning enthusiasm. The precise details of how this came about are discussed in the Fluid Resuscitation section. The uselessness of the PAWP should not deter people from using the PA catheter to guide resuscitation in other situations where it is indicated.