Previous models combining the human cardiovascular and pulmonary systems have not addressed their strong dynamic interaction. They are primarily cardiovascular or pulmonary in their orientation and do not permit a full exploration of how the combined cardiopulmonary system responds to large amplitude forcing (e.g., by the Valsalva maneuver). To address this issue, we developed a new model that represents the important components of the cardiopulmonary system and their coupled interaction. Included in the model are descriptions of atrial and ventricular mechanics, hemodynamics of the systemic and pulmonic circulations, baroreflex control of arterial pressure, airway and lung mechanics, and gas transport at the alveolar-capillary membrane. Parameters of this combined model were adjusted to fit nominal data, yielding accurate and realistic pressure, volume, and flow waveforms. With the same set of parameters, the nominal model predicted the hemodynamic responses to the markedly increased intrathoracic (pleural) pressures during the Valsalva maneuver. In summary, this model accurately represents the cardiopulmonary system and can explain how the heart, lung, and autonomic tone interact during the Valsalva maneuver. It is likely that with further refinement it could describe various physiological states and help investigators to better understand the biophysics of cardiopulmonary disease.
Information regarding the electrical behavior of cells in the sinoatrial (SA) node of the heart is by no means complete; yet sufficiently detailed information is available in the literature to allow the formulation of a reasonably quantitative model of the membrane of the primary pacemaker cell (P-cell) and its parasympathetic innervation. In a previous study [Am. J. Physiol. 243 (Heart Circ. Physiol. 12): H207-H218, 1982], the well-known McAllister-Noble-Tsien model of the cardiac Purkinje fiber is modified to account for the electrical activity of the SA node. In the present study, the effects of vagal activity on sinus rhythm are considered by adding a special acetylcholine-sensitive "muscarinic channel" to the membrane model for the P-cell. The resulting model mimics published data quite well and is capable of characterizing the free-running SA node cell as well as its responses to electrotonic and vagal stimulation.
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