- 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.
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:
This chapter aims to at least discuss the first.
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:
And, there are several features which should not be present, as they increase the discrepancy between the PAWP and the LA pressure:
However, usually the magnitude of the difference is relatively small.
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:
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?
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:
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?
Under some circumstances, the PAWP remains useful.
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.
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.