PubMed · 8592562
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W C Shoemaker. 1996-03-21. Goal-oriented hemodynamic therapy.. https://pubmed.ncbi.nlm.nih.gov/8592562/
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To analyse parametrically (in terms of the qualitative theory of dynamical systems) the mechanical influence of inertia, resistance (positive and negative), elasticity and other global properties of the heart-muscle on the left ventricular pressure, an active rheodynamic model based on the Newtons's principles is proposed. The equation of motion of the heart mass centre is derived from an energy conservation law balancing the rate of mechanical (kinetic and potential) energy variation and the power of chemical energy influx and dissipative energy outflux. A corresponding dynamical system of two ordinary differential equations is obtained and parametrically analysed in physiological conditions. As a result, the following main conclusion is made: in physiological norm, because of the heart electrical activity, its equilibrium state is unstable and around it, mechanical self-oscillations emerge. In case the electrical activity ceases, an inverse phase reconstruction occurs during which the unstable equilibrium state of the system becomes stable and the self-oscillations disappear.
Doppler utrasonography has made it possible to record blood flow to the digestive tract (the superior mesenteric artery) directly and continuously in unanaesthetized, healthy humans. Several research groups have demonstrated how blood flow to the tract increases gradually and markedly after a meal, and more so after a big meal than after a small one. The increase in blood flow reaches its maximum after 20-40 minutes and lasts for 1.5-2 hours. In the postprandial period there is a parallel and similar increase in cardiac output; the meal thus imposes an increased work load on the heart. Carbohydrate meals, as well as meals of protein or fat all release increases in local blood flow as well as in cardiac output. Surprisingly, during physical exercise of relatively high intensity, there is no reduction in blood flow to the digestive tract in humans. This is in contrast to the exercise-caused flow reduction observed in several animal species. In the postprandial state the large increase in cardiac output caused by muscular exercise is actually added to the increase already established by the meal. This course of events helps to explain why patients with angina pectoris are more prone to chest pains after a meal.