This chapter has no relevance to any specific Section of the 2017 CICM Primary Syllabus, and is probably irrelevant to most ICU trainees, mainly because pulmonary artery wedge pressure measurement is largely irrelevant to most ICU practitioners. However, in case anybody is curious about why it is irrelevant and how we as a craft group came to this conclusion, there may be some value in reading the rest of this garbage, or at least perusing the peer-reviewed references from which the author tried to borrow some respectability.
 
In summary, 
  • The use of PAWP for patient care rests on the assumption that: 
    • PAWP is equal to the left atrial pressure, and...
    • Left atrial is equal to the left ventricular end-diastolic pressure, and...
    • Left ventricular end-diastolic pressure is a good reflection of LV end-diastolic volume, and...
    • LV end-diastolic volume is a satisfactory surrogate for LV preload, and...
    • LV preload is something we should use as an endpoint for therapy
  • However:
    • PAWP may be higher then LVEDP if:
      • Pulmonary venous resistance may be increased (eg. by a mass in that hilum, or consolidation, or god knows what)
      • The fluid column distal to the wedge is not continuous (eg. it is interrupted, like when the catheter is outside of Wests Zone 3)
      • The fluid distal to the wedge is not static (eg. incompletely wedged)
    • PAWP may be lower then LVEDP if:
      • there is aortic or mitral regurgitation
      • the LV is poorly compliant (eg. LVH)
      • There is excessive positive intrathoracic pressure
    • LVEDP may not predict LV end-diastolic volume (LVEDV) if:
      • the LV is poorly compliant, eg. LVH or MI
      • there is extracardiac compression, eg. tamponade
      • the RV is overdistended and LV compliance is affected through interventricular interdependence
  • Thus: PAWP has limited uses as a diagnostic tool or treatment endpoint:
    • Some society guidelines mention it as a static parameter which can
      • Identify patients who are "fluid-responsive" (low PAWP), though this practice is basically extinct
      • Discriminate between cardiogenic shock (high PAWP) vs. other types of shock
    • It is useful in the diagnosis of pulmonary hypertension
    • The wedged waveform can identify mitral regurgitation

Raper & Sibbald (1986) is probably the best resource for this topic. Nothing else really comes close in terms of detail or clarity.  It is unfortunately paywalled, but if asked nicely I am sure the authors would send you a copy. 

The assumption that PAWP helps guide preload management

Basically, the PA catheter was originally developed as an instrument to determine preload and to help guide fluid resuscitation. Swan and Ganz specifically intended their invention to assist with "the accurate management of fluid-volume control in patients with a wide variety of serious illnesses". In fact, the idea of using PAWP for the purpose of measuring left atrial pressure pre-dates the yellow snake, as others (Connoly et al, 1954Luchsinger et al, 1962) had previously described this practice. The main problem at this early stage was the actual cannulation of the pulmonary artery, which required patience, skill, and the availability of fluoroscopy. The greatest contribution by Swan and Ganz was, therefore, an easier method of obtaining wedge measurements, which allowed the adaptation of this principle into the critical care environment.
The lines of reasoning were (are) as follows:
  • LV preload is an important determinant of cardiac output
  • LV preload can be defined as LV end-diastolic volume
  • An important determinant of LV end-diastolic volume is LV end-diastolic pressure
  • LV end-diastolic pressure should be reasonably close to left atrial end-diastolic pressure, as the ventricles fill from the atria in diastole
  • Left atrial pressure should be approximately the same as PAWP
  • Ergo, PAWP is basically a direct measurement of LV preload, and you should be able to titrate your fluid resuscitation using this parameter, as it should be more accurate than clinical or biochemical markers (which are indirect). 

This had been the series of arguments which made the PAWP a popular instrument of haemodynamic management. Guidelines were drawn up to use this as a resuscitation endpoint.  "As a rough guide to therapy, left ventricular preload should be kept in the range of 15-20 mm. Hg in shock associated with acute myocardial infarction, and at less than 15 mm. in congestive heart failure associated with acute myocardial infarction", wrote Swan et al in May 1970, three months before NEJM published his paper with Ganz. In a couple of years, the use of PAWP for this purpose was widespread; for example Willerson (1972) describes wedge pressure as "the most common way in which LVEDP is measured currently and the one that we employ in the coronary care unit at Parkland Memorial Hospital".

So, there are two main assumptions here:

  • That PAWP predicts LV preload
  • That PAWP is a useful guide for preload-directed therapy

This chapter aims to at least discuss the first. 

The assumption that PAWP is the same as left atrial pressure

As already discussed in the chapter dealing with the relationship of PAWP and left atrial pressure, there are several preconditions which must be met in order for one to resemble the other:

  • The catheter tip must be in a Zone 3 position
  • This means that:
    • The catheter tip should be somewhere below the level of the left atrium, as that is where Wests' Zone 3 usually tends to be found.
    • The positive intrathoracic pressure cannot be too high, else Zones 1 and 2 expand and the catheter tip might end up inside them
    • The patient must be reasonably well-filled, or else the size of Zones 1 and 2 will increase

And, there are several features which should not be present, as they increase the discrepancy between the PAWP and the LA pressure:

  • Where the PAWP is higher than the LA pressure:
    • Poor LA compliance (eg. scarring following radiotherapy or Cox-Maze procedure)
    • Mechanical atrial obstruction (eg atrial myxoma)
    • Pulmonary venous obstruction, by
      • Lung tumour (extrinsic compression or invasion)
      • Consolidation
      • Pulmonary fibrosis
      • Radiation therapy
      • Pulmonary veno-occlusive disease
  • Where the PAWP is lower than the LA pressure:
    • Mitral regurgitation
    • Poor LV compliance

However, usually the magnitude of the difference is relatively small.

The assumption that LA pressure is the same as LVEDP

So, let's say you have actually managed to measure the "true" LA pressure with the PA catheter. The next assumption is that this LA pressure is somehow predictive of LV end-diastolic pressure. That makes some logical sense, because the LV fills out of the LA in diastole, and with the mitral valve open these two chambers should have fairly similar pressure towards the end of diastole. However, this may not be the case, particularly in the setting of valve disease:

  • Mitral stenosis: on the way into the ventricle, blood from the LA needs to overcome a mighty obstacle in the form of a crusty stenotic mitral valve. The pressure in the LA may therefore end up being higher than the LVEDP, as the LA will not be able to empty effectively. 
  • Mitral regurgitation: the massive regurgitant wave in systole will upset the automated measurement of the LA pressure (and PAWP), making it look higher.
  • Aortic regurgitation will continue to fill the LV with aortic-grade pressure during diastole, increasing the LVEDP above the LAP

But let's say that there are none of these issues and you have somehow managed to measure LVEDP. Is this really a useful achievement?

The assumption that LVEDP is a good reflection of preload

As discussed in the chapter on the determinants of preload, it is difficult to define as a concept, and even now the experts appear to be divided into groups who define it in terms of a change in sarcomere dimensions (i.e. volume) and a group who define it in terms of force or load (i.e. pressure). Thus, for some people, to measure LVEDP is to measure preload, whereas others will insist on LVEDV. Reading between the lines of past CICM questions, one can see that the college examiners are in the "volume" group, i.e the preferred definition of the college seems to be  "myocardial sarcomere length just prior to contraction"  which logically leads to LVEDV. Unfortunately, the LVEDV and LVEDP don't really correlate. Observe:

  • LV compliance can change the relationship between LVEDP and LVEDV. A stiff noncompliant ventricle will not increase in volume very much, even at a high filling pressure. 
  • Extracardiac pressure will alter the relationship between LVEDP and LVEDV.  In this scenario, LVEDP will be higher and LVEDV will be lower, giving the impression that the LV has become poorly compliant, whereas in fact there has been no change to the properties of the myocardium.
  • Ventricular interdependence: even if one is able to measure the LVEDP accurately, the LV may be rendered less compliant by the effects of a hugely dilated right ventricle, which may push the septum to the left in diastole, preventing effective diastolic filling. This would not be apparent from PAWP measurements.

In short, the measurement of LVEDP may not be particularly predictive of LVEDV, and if LVEDV is your chosen surrogate for preload, you're not getting preload out of your PA wedge pressure. 

But let's say all these assumptions hold, and you've got one of those unique unicorn-like patients who has the rare combination of a real clinical need for a PA catheter (eg. a mixed shock state) combined with the absolutely none of the features which might invalidate the PAWP measurement.  Surely, under these circumstances, you could use it to guide your management?

Supported uses PAWP as a diagnostic tool or clinical endpoint

Under some circumstances, the PAWP remains useful.

  • Mixed shock states: yes, you can still use the PAWP with a straight face in front of your colleagues. Various societies still recommend its use in heart failure patients with "clinically indeterminate volume status and those refractory to initial therapy, particularly if intracardiac filling pressures and cardiac output are unclear" (ACCF/AHA guidelines, 2013). That doesn't mean that it finds wide acceptance in the intensive care community (because what does?) but at least the support of such scholarly bodies helps paint a veneer of legitimacy over this practice. In summary, a PAWP in excess of 15 mmHg suggests that there is something cardiogenic about the shock state you are experiencing.
  • Predicting fluid responsiveness: a low PAWP (say, 5-ish) probably suggests the patient needs more fluid. However, this use of PAWP has lost a lot of its former popularity.  In 2004, Kumar et al published an influential paper which laid waste to the concept of PAWP as a predictor of fluid response - 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. We are still expected to mention it in an exam answer (i.e. it is still one of the options, even though it's not a very good option).
  • Diagnosis of pulmonary hypertension: PAWP measurement is required to discriminate between patients with Group 1 PAH (pre-capillary pulmonary arterial hypertension) and patients with Group 2 PAH (post-capillary, due to left heart failure). This finds support in the WHO guidelines (Simmoneau et al, 2019).
  • Interpretation of mitral valve function through waveform analysis: though not directly related to the measurement of wedge pressure per se, one can derive much useful information from the shape of the wedged waveform: a sudden failure of a mitral valve repair will be immediately identified by a change in the PAWP waveform pattern. The PAWP will also rise, mainly due to the fact that the automated monitor will dutifully integrate the area under the curve of the huge new waves, reporting a high mean pressure.

The pulmonary artery wedge waveform

PAWP 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.

References

Swan HJ, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D (August 1970). "Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter"N. Engl. J. Med. 283 (9): 447–51.

The PA catheter section from The ICU Book by Paul L Marino (3rd edition, 2007) is the source for most of this information.

Additionally, Ohs Manual (7th ed)  has a Figure 12.2 on page 111 which outlines the abovementioned assumptions, and where they are active.

CONNOLLY, DANIEL C., JOHN W. KIRKLIN, and EARL H. WOOD. "The relationship between pulmonary artery wedge pressure and left atrial pressure in man." Circulation research 2.5 (1954): 434-440.

Swan, H. J. C., et al. "Power failure in acute myocardial infarction." Progress in cardiovascular diseases 12.6 (1970): 568-600.

Willerson, James T. "Cardiogenic shock and its current treatment." (1972).

Calvin, J. E., A. A. Driedger, and W. J. Sibbald. "Does the pulmonary capillary wedge pressure predict left ventricular preload in critically ill patients?." Critical care medicine 9.6 (1981): 437-443.

Luchsinger, Peter C., Harry W. Seipp Jr, and Dali J. Patel. "Relationship of pulmonary artery-wedge pressure to left atrial pressure in man." Circulation Research 11.2 (1962): 315-318.

Raper, R., and William J. Sibbald. "Misled by the wedge?: The Swan-Ganz catheter and left ventricular preload." Chest 89.3 (1986): 427-434.

Lozman, Jeffrey, et al. "Correlation of pulmonary wedge and left atrial pressures: a study in the patient receiving positive end expiratory pressure ventilation." Archives of Surgery 109.2 (1974): 270-277.

Yancy, Clyde W., et al. "2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines." Journal of the American College of Cardiology 62.16 (2013): e147-e239.

Simonneau, Gérald, et al. "Haemodynamic definitions and updated clinical classification of pulmonary hypertension." European Respiratory Journal 53.1 (2019).

Rosenkranz, Stephan, and Ioana R. Preston. "Right heart catheterisation: best practice and pitfalls in pulmonary hypertension." European Respiratory Review 24.138 (2015): 642-652.