The tracing of an electrocardiogram (ECG) is one of the most popular icons displayed whenever referring to the field of medicine. From a clinical point of view, the mea­surement of the ECG is attractive because it involves a noninvasive procedure that can be performed quickly using either portable or fixed equipment. The cardiac system can best be described as a mechanical pump system that is trig­gered and synchromized by electrical signals. Because of its noninvasive nature, the ECG is helpful in providing some preliminary information on cardiac rhythm, electrical con­duction, and its disturbances. Figure 6 shows the preferen­tial pathways for conduction of the excitation wave, which closely follows functional anatomy of the heart, that is, starting at the sinus node in the right atrium, traveling towards the apex of the ventricles, followed by a spread to­wards the outflow tract. This route implies that the blood

Figure 6. A cross-sectional view of the heart, showing the two ventricles and both atria, along with the conduction system for the electrical impulse running from the sinus node towards the apex and then upwards along the muscular walls of the ventricles.

is expelled from the ventricles similar to the optimal direc­tion for squeezing out the contents of a tube of toothpaste, that is, running from the very bottom up towards the open­ing at the opposite site.

The rhythm of the healthy heart is not constant but ex­hibits a certain degree of HRV (20). Many studies have em­ployed advanced mathematical techniques to analyze the cardiac rhythm and estimate the relative contribution of the sympathetic and parasympathetic drives, respectively (21, 22). But the perpetual change of the rhythm has also profound mechanical consequences: An increase in cycle length implies facilitation of ejection both by increased fill­ing (i. e., elevated preload) and reduced opposing pressure at the time of the valve opening (i. e., lower afterload), while during the next beat with a shorter interval the opposite applies. In other words, impeded and facilitated beats ap­pear to alternate, thus possibly improving stability of the complete circulatory system.

The left ventricle has often been modeled as a sphere or prolate ellipsoid, but neither geometry conforms with reality. Independent of geometrical assumptions, Beringer and Kerkhof (23) have shown that a fairly linear relation­ship exists between end-systolic volume (ESV) and end — diastolic volume (EDV). This notion has been verified in human patients and also in their experimental investiga­tions when studying the volume regulation in physiolog­ically operating chronically instrumented dogs (24). The regression coefficients appear to be characteristic of ven­tricular volume regulation and are sensitive to inotropic intervention (i. e., adrenergic agonists and blockers). This relationship implies that a clinically important cardiac per­formance indicator, namely ejection fraction (EF) is in­versely related to ESV (25). Furthermore, using the Suga — model, myocardial oxygen consumption can potentially be predicted from a single noninvasive determination of ESV Quite similar to the description of pulmonary dynamics, the dynamics ofheart and vessels are also characterized by pressure-volume (P-V) relationships. Flow ( Q) equals the time derivative of a changing volume. Another frequently employed derived index is elastance ( E), the reciprocal of compliance, which is defined as the material property that enables resisting deformation. In analytical form,

where V0 is the unstressed volume. This is analogous to Hooke’s law (length-tension relationship), which states that tension (i. e., force per unit area) equals Young’s mod­ulus times the relative change in length.

Spontaneous oscillations of arteries have also been ob­served, with a period ranging from 45 s to 60 s for the ra­dial artery diameter under resting conditions, resulting in an almost twofold change in distensibility (26). A general model of the properties of a muscular blood vessel at vary­ing levels of contraction predicts that the vessel becomes unstable at high levels of contraction (27). A lumped model of the arterial tree can also be considered, similar to the lumped model for the lungs as presented before. Imagine that the arterial bed with all its branches is replaced by a single vessel with a diameter similar to the human aorta and encompassing an identical hemodynamic resistance ( R). How long would this hypothetical noncollapsible aorta be? From Poiseuille’s law we know that R = 8nl/nr4. If the radius r =1 cm, the blood viscosity n = 3 cP, and R is the mean driving pressure divided by mean flow, that is, 100/5 mmHg-min/L, then the length l turns out to be approxi­mately 200 m.

Obviously, the real circulation consists of various vas­cular beds that supply blood to the various organs such as brains, kidneys, skeletal muscles, and intestines. One pow­erful regulatory mechanism used to accommodate varying needs in a single organ is based on the principle of redis­tribution of flow within the body by local vasodilation and constriction of arterioles. Another phenomenon, called au­toregulation, is based on vasoactivity that maintains the flow at a particular level even during acute changes in pres­sure.

Arterial blood pressure is well controlled by several sys­tems. Figure 7 presents a survey with emphasis on time course and gain for each subsystem involved (28). Hyper­tension can then be interpreted as a disorder in which the set point is altered while the control systems continue to regulate towards an erroneously determined set point. This view also explains the chronic nature of a condition in which blood pressure even at rest is elevated. Going back to Fig. 1 this abnormality would be equivalent to a situation in which the heater feedback system continues to maintain a given (wrong) set point.

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