Fluctuations in intrapleural pressure.
The cyclical variations in intrapleural pressure which normally accompany ventilation of the lungs are directly transmitted to the heart and great vessels.

Because intravascular pressure measurements are commonly referenced to atmospheric, rather than the theoretically correct intrapericardial pressure, there is an artifactual component in the normally observed 'respiratory swing' of the intravascular pressures.

The effects of this artifact are more pronounced if lung compliance is low or airway resistance is high - because the excursions in intrapleural pressure are greater under these circumstances.

This 'respiratory swing' is also generally more marked in patients who are mechanically ventilated, but can also be observed in those breathing spontaneously - particularly if they are suffering respiratory distress.

It is technically possible to continuously reference the intravascular pressures to the intrapericardial pressure. Under these circumstances, true measurements of the transmural pressures of the heart are made and the phenomenon of 'respiratory swing' is greatly modified, but not eliminated.

Fluctuations in alveolar pressure.
During IPPV or other forms of assisted ventilation, the airway pressure may also have an important impact on the accuracy of a PAC pressure measurement. Depending on the lung compliance, a variable proportion of the applied airway pressure (Typically 50-60%) will be transmitted to the intrapleural space and hence to the heart and great vessels. This variably transmitted proportion constitutes an effective pressure bias on the measured PAC pressure as described above.

More subtle effects of alveolar (airway) pressure can also occur. The lung has been divided into 'zones' on the basis of the interrelationship between pulmonary arterial, pulmonary venous and alveolar pressures ¹ ('West's zones' Figure 1). - If a PAOP measurement is being made, and the catheter tip is in a West zone I or II arterial branch, then the measured pressure will reflect the alveolar rather than the 'wedge' pressure. This circumstance is particularly likely to produce large errors in patients who are being treated by IPPV with PEEP.

In addition to producing what might be termed an 'artifactual' fluctuation in the measured pressures, changes in alveolar pressure also produce real changes in preload, ventricular interdependence and afterload - all of which lead to secondary (cyclical) changes in right and left ventricular performance. During IPPV, the increase in the intrathoracic pressure during inspiration reduces venous return to the right heart and increases right ventricular afterload ². Simultaneously, the filling of the left ventricle is enhanced as blood is squeezed out of the pulmonary vasculature into the left atrium. This enhanced left atrial return results in a transient increase in LV output and pressure. After a few heartbeats, the decreased right ventricular output reaches the left heart, leading to a decline in left ventricular output and systolic blood pressure. These phenomena are well demonstrated by echocardiography ³. The variation in pulse amplitude ('Pulse - Amplitude Ratio') which occurs during sustained chest inflation has been correlated with the pulmonary artery occlusion pressure ⁴.

Unless the fluctuations in intrapleural and intrathoracic pressure are small, pressure measurements should always be timed to the end-expiratory point of the respiratory cycle. (In this context, it is worth remembering that the nadir of intrathoracic pressure during IPPV is during expiration whereas the reverse is true during spontaneous respiration.) The peak of the 'A' wave of the wedged pressure trace is the most representative measure of LVEDP (Figure 2).

Withdrawal of PEEP and temporary suspension of ventilation prior to measurement of PAC pressures has been advocated by some authors. This practice is now generally frowned upon. - Removal of PEEP can precipitate cardiovascular and respiratory responses which may be acutely deleterious to the patient and anyway, the resulting measurements will reflect the 'unsteady state' of 'Falling PEEP and Transient Apnoea' rather than the 'steady state' of 'PEEP and IPPV'. It is far more appropriate to time all PAC measurements to the end of expiration without altering ventilatory management.

1. West JB, Dollery CT, Naimark A. Distribution of blood flow in isolated lung: relation to vascular and alveolar pressures. J. Appl. Physiol. 19: 713 (1964)

2. Theres H, Binkau J, Laule M et al Phase-related changes in right ventricular cardiac output under volume-controlled mechanical ventilation with positive end-expiratory pressure. Crit Care Med 1999 May;27(5):953-8

3. Coriat P. Vrillon M, Perel A, Baron JF, Le Bret F. Saada M, Viars P. A Comparison of Systolic Blood Pressure Variations and Echocardiophic Estimation of End-Diastolic Left Ventricular Size in Patients after Aortic Surgery. Anesth Analg 1994, 78:46-53.

4. McIntyre KM Vita JA Lambrew CT Freeman J Loscalzo J A noninvasive method of predicting pulmonary- capillary wedge pressure. N Engl J Med 1992 Dec 10, 327 [24]: 1715- 20.

Last edited on: 14/11/2000