CARDIAC MECHANICS
Category
The heart is a very efficient hydrodynamic pump
G. Bozzi
The human heart is a muscle of about 300 g surrounding four cavities and equipped with four valves. The human heart is an incredibly powerful engine: in rest conditions, with every pulse, it pushes about 70 ml of blood into the aorta and as many into the pulmonary artery. For a frequency of 70 beats/min, the cardiac output is 4.9 l/min both for the right and left ventricles: in total 9.8 l/min.
Because in a day there are 1,440 minutes: 9.8 * 1,440 = 14,112 liters of blood per day, or more than 14 cubic meters of blood without stopping, and keeping the temperature around 37° centigrade. During exercise, the heart rate can reach a value of (220 - age in years) beats/min, and the stroke volume can increase up to 30%. So the heart can increase the capacity up to 4 times in the event of heavy physical work (at least in the young people). In conclusion, the amount of blood ejected from the heart every 24 hours is higher than the one above, because no reasonable man is sitting at rest night and day.
A second important feature of cardiac activity consists in the fact that the blood in the heart chambers and the vessels accelerates and flows with laminar flux, without vortices that would damage in a short time endothelium and valves.
A third feature, the only exception in the whole body, is the lack of an antagonist muscle lengthening fibers after contraction. This feature serves to keep down the weight of the heart, which is essential for the balance between accelerated and displaced masses, but it seems logical the question of how to face the heart to stretch their fibers. The explanation is quite complicated and starts considering that the heart, obliged to comply with the laws of dynamics, actually uses them to his advantage.
The first observation is that the heart produces a sophisticated elastic system with the ascending aorta and arch. Only two points fix the system: the apex to the diaphragm and the aortic isthmus to the spine. All other structures are free to move, in particular, the valves (Fig 1.1).
I would have liked to prove the hypothesis that the ascending aorta to brachiocephalic artery detachment is structured to lengthen, while the rest of the vessel to widen. The observation suggests this hypothesis that with the wear caused by aging, the ascending aorta tends to expand, while the rest lengthens. Years ago I tried an approach to this problem but didn't find a department of Pathology willing to face this study.
Therefore, the contraction starts from the basal parts of the ventricle, which lead the diameter of the under-aortic portion to a value closer to that of the aorta. The aortic valve is still closed, and the ventricle stretches slightly (see the first sequence of video series). When the pressure in the ventricle exceeds the pressure in the aorta, the valve opens, and left ventricle pushes a blood cylinder without vortices into the aorta. This cylinder has a base area between 5 and 7 square cm and a length of 9 to 13 cm (fig. 1.2).
Fig. 1. 1, left: mechanic representation of system heart-aorta. C1 &C2 are fixing points. V1, V2, V3 are elastic support of aortic arch. L: ascending aorta with elastic lamina favoring lengthening. A: aortic arc with elastic lamina approving widening. Blood cylinder forms with the sliding of blood lamina which velocity decreases from center to periphery (decreasing length arrows). ob: obliterated apex. 2, right: ideal representation of left ventricular blood: B: stroke volume. E: residual volume. D: blood portion is belonging to one or other preceding parts, according to venous return and adrenergic tone.
For the action-reaction phenomenon, the heart lowers into the chest of about 1.5 cm; the ascending aorta stretches and accumulates elastic energy in its walls. When the ejection is exhausted, and the aorta begins its elastic recall, the pressure inside the ventricle rapidly drops, because the tip of the heart is held in place by the vacuum of the pericardial sac and the pericardium by diaphragmatic-pericardial ligaments. When the pressure in the ventricle falls below the value of the pressure in the aorta, the valve closes. At this point, the blood of the atria forms a common mass with the respective ventricular residual volumes, because the leaflets of the atrioventricular valves are irrelevant. These masses, moved down from recoil, tend to stay where they are (dynamics 1° principle), and the ventricles, going up, stretch the walls sideways.
The following calculation suggests the system efficacy: the aortic valve closes about 1.5 cm lower than where it is open: going up, it drags a small blood cylinder (approximately 10.6 ml). It seems little, but it is more than 1,000 liters of blood recovered as cardiac output every day.
Thus, the distension of the ventricle in the longitudinal direction is due to the elastic recall of the aorta, while the distension in the lateral direction depends on the encounter of the heart walls with the blood masses (atrial + residual volume). This mechanism is shown in Figure 3, in which you can see that during rapid filling (y depression of atrial curve), the pressure drops in both atria (from which the blood comes out), but also in the ventricle (the blood instead comes in). In conclusion, the ventricular filling does not depend
by pressures in chambers, but by external forces and must necessarily take place immediately after systole.
Fig. 2 shows the temporal relationship between electrical (ECG) and mechanical activity (pressure curves) of the heart. Note how the pressure falls rapidly in the ventricle with the closure of the aortic valve and how it continues to decline even after the intersection with the atrial curve (v wave), at which time the opening of the mitral valve involves the passage of blood from the atrium to the ventricle (fast fill). The fact that the two curves are parallel, and that the pressure continues to fall in both chambers, confirms that the dilation of the ventricle is not due to blood pressure, but to an external force.
In the following period, said diastasis, the pressure rises slowly in the left ventricle, because of the continuous flow of blood from the venous system, but the amount of blood that passes from the atria to the ventricles is irrelevant. And this is reasonable because the duration of the diastasis varies with the heart rate since to shrink almost to 0 for high frequencies. The atrial contraction also, in normal conditions, does not cause passage of blood from the atria to the ventricles but has the aim of bringing leaflets of the atrioventricular valves between them so that ventricular contraction begins to closed valves.
This description suggests that among cardiac mass, ejected blood, residual volumes and masses acceleration some relationships should not be changed more than absolute values to avoid altering the balance that ensures the smooth functioning of the system over time.
The reduction of the ascending aorta and arch elasticity accounts for the loss of efficiency of the system observed with age.
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