Pulmonary artery pulsatility is the main cause of cardiogenic oscillations.

The genesis of cardiogenic oscillations, i.e. the small waves in airway pressure (COS(paw)) and flow (COS(flow)) signals recorded at the airway opening is under debate. We hypothesized that these waves are originated from cyclic changes in pulmonary artery (PA) pressure and flow but not from the physical transmission of heartbeats onto the lungs. The aim of this study was to test this hypothesis. In 10 anesthetized pigs, COS were evaluated during expiratory breath-holds at baseline with intact chest and during open chest conditions at: (1) close contact between heart and lungs; (2) no heart-lungs contact by lifting the heart apex outside the thoracic cavity; (3) PA clamping at the main trunk during 10 s; and (4) during manual massage after cardiac arrest maintaining the heart apex outside the thorax, with and without PA clamping. Baseline COS(paw) and COS(flow) amplitude were 0.70 ± 0.08 cmH(2)O and 0.51 ± 0.06 L/min, respectively. Both COS amplitude decreased during open chest conditions in step 1 and 2 (p < 0.05). However, COS(paw) and COS(flow) amplitude did not depend on whether the heart was in contact or isolated from the surrounding lung parenchyma. COS(paw) and COS(flow) disappeared when pulmonary blood flow was stopped after clamping PA in all animals. Manual heart massages reproduced COS but they disappeared when PA was clamped during this maneuver. The transmission of PA pulsatilty across the lungs generates COS(paw) and COS(flow) measured at the airway opening. This information has potential applications for respiratory monitoring.