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anesthesia monitor, airflow, airway resistance, Bourland, cardiac function, cardiac depression, ejection fraction, formula, Geddes, mechanism, monitor, oscillations, pulse, pumping, respiration, unidirectional valves, ventricles, waveform, Wessale.


This paper presents a new and more complete mechanism for the genesis of the pneumocardiogram—a record of the small oscillations in airflow in the trachea and upper airways accompanying each heartbeat. This signal may be the basis of a simple, inexpensive and noninvasive measure of cardiac stroke volume; however, research into its practical use has languished because of poor understanding of its underlying cause and meaning. This paper explains the genesis of the pneumocardiogram, based upon net changes in intrathoracic blood volume during the cardiac cycle, together with low pass filtering of the volume signal by airway resistance and lung-chest compliance. A novel analytical model of the physics of both blood flow and airflow answers the core question of how the pneumocardiogram is produced, and in turn, how to extract the cardiac output and stroke volume from the pneumocardiographic signal. The approach is tested in a numerical model of the systemic circulation, pulmonary circulation, chest cavity, and lungs. Results show good agreement between predicted and true stroke volume over a wide range of normal and abnormal test conditions, with an average ratio of estimated to true stroke volume of 1.00 in the standard normal model, 0.99 with three times normal airway resistance, 0.82 with one third normal airway resistance, and 0.99 with reduced ventricular contraction time. It is time for the biomedical research community to reconsider practical exploitation of this freely available signal, both in anesthetized or intubated patients, and perhaps even in awake, conscious people using well-sealed face masks.