Background: The pulmonary venous pressure waveform is typically described by the downstream events in the left atrium and ventricle. These downstream events create waves that contribute to the overall waveform.

Methods: In anesthetised open-chest dogs, measurements of pressure and flow were made in the pulmonary artery and vein. Experiments involved increases to blood volume and the application of 10 cm H₂O positive end-expiratory pressure (PEEP). The reservoir-wave model describes the reservoir pressure, which is subtracted from measured pressure, to result in the excess pressure (P_excess). Excess velocity (U_excess) is similarly formulated. P_excess and U_excess are used in wave intensity analysis to calculate wave speed and separate the contributions of waves originating upstream (forward waves) and downstream (backward waves).

Results: Separated waves are shown in the bottom panel of Figure 1. The effect of PEEP resulted in larger decreases to P_backward (p < 0.001) after the mitral valve opened. As a result, y was lower than x by ∼2.0 mmHg. With PEEP, the delay between arterial and venous forward waves increased from 155 ± 4 ms to 183 ± 4 ms (mean ± SE, p < 0.001).

Figure 1

Common venous markers related to measured pressures (top panel) and the separation of P_excess into forward and backward components (bottom panel) at control conditions.

Conclusion: The majority of pulmonary venous pressure landmarks can be attributed to the actions of the left atrium and ventricle but the v wave has substantial contributions from waves originating in the pulmonary artery. Diastolic suction has a larger effect with PEEP, presumably from some external constraint applied to the heart and consequently lowered end-systolic left ventricular volume.