| Cardiac Pumping and Beat-to-Beat Circulatory Control |
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There is no need for an outline of the anatomy of the heart itself (cf. [8, 100, 136, 170]).
The heart is completely embedded in other tissues. This implies in a functional sense, that the walls of the chambers of the heart, atria and ventricles, are not merely myocardium and pericardium. They extend farther and include blood and adjacent tissues of the thoracic cage.
They also constitute the medium, in which the heart has to carry out its work. Physical interaction of this medium with the working heart is different from that of a compressible substance, such as air. The air pressure prevailing in the lungs is approximately 760 mm Hg, whereas atrial pressures are a few mm in excess of that. The atrial pressures effect on adjacent tissues will thus be small. The heart then, should not be thought of as doing its work in physical isolation from the rest of the body [71].
The boundaries of the ventricles may be described as follows:
| Right Ventricle: | |
| Ventrally-medially: | muscular wall of right ventricle, pericardium, chest wall |
| Caudally: | muscular wall of right ventricle, pericardium, diaphragm, etc. |
| Dorsally-superiorly: | tricuspid valve, blood in right atrium, etc. |
| Dorsally-laterally: | interventricular septum, blood in left ventricle, etc. |
| Left Ventricle: | |
| Ventrally-medially: | interventricular septum, blood in right ventricle, etc. |
| Caudally: | muscular wall of left ventricle, pericardium, diaphragm, etc. |
| Dorsally-superiorly: | mitral valve, blood in left atrium, etc. |
| Dorsally-laterally: | muscular wall of left ventricle, pericardium, pleura, etc. |
The expansion, or contraction, of the atria will similarly be affected by adjacent tissues. The right atrium and the blood vessels entering the atria are surrounded mainly by pericardium, pleura and the lungs. The left atrium is to a large part squeezed between the spinal column and the rest of the heart. Both atria at their transitional regions near the left and right ventricles have fold-like appendages (the left and right auricles) which have a contour-smoothing function in systole [31].
In contrast to the ventricles, the atria never become separated from the rest of the circulatory system during the cardiac cycle. The tricuspid and mitral valves constitute a border to the ventricles, for the atrial volume. The region of the orifices of vena cava superior and inferior into the right atrium, can be regarded as a part of the atrial volume. The same is valid for the region of the orifices of the pulmonary veins into the left atrium.
A body immersed in a non-compressible fluid (e.g. a liquid, or liquid-like, matter such as living soft tissue) will displace its own volume of this fluid. An increased change in volume of such a body, will result in displacement of additional fluid equivalent to the volume added. This simple principle applied to the human heart means, that a change in its total volume during the cardiac cycle, must correspondingly affect the tissues surrounding it. That is, no change in total heart volume is possible without a corresponding displacement of adjacent tissues.
Pictorial representation of the heart in cross-sectional view in different phases of the cardiac cycle, is rare in monographs. One opinion is, however, evident from the cross-sectional heart images used, to illustrate the pumping of the heart [2, 4848, 119, 166]; that is, that the heart is looked upon as a displacement pump, changing its atrial and ventricular outer contour rhythmically during atrial and ventricular systole.
Brecher [22], referring to Böhme [31], argues for the importance of the expansion of the atria at ventricular systole, for the venous return.
Rushmer [147, 148, 149], Hawthorne [72] and McDonald [35] propose that the systolic descent of the heart base occurs mainly before ejection. That is a result of early activation and shortening of endocardial layers of myocardium, including the papillary muscles. The mitral valve cusps are thought to be drawn downward, with resulting expansion of the left ventricle ("initial systolic expansion"). Ejection is thought to be accomplished by subsequent circumferential contraction, with little further change in left ventricular length. Arguments for the energetic advantage of this pumping mechanism have been delivered.
Others, Katz [91], Braunwald [16], Brobeck [25], Guyton [60], Gauer [49], Ganong [48] and Kenner [94], do not mention the compensation of ventricular shrinking by atrial expansion and vice versa. This does not mean that these authors are arguing against the course of events, but rather that they do not consider it to be of major relevance.
The discussion of the in vivo situation, regarding volume changes during the cardiac cycle, may be simplified by the construction of appropriate theoretical models.
In one such model, the heart is surrounded by soft tissues, which in turn are confined within rigid walls. The only openings arranged in these walls, are those for the major arteries and veins emanating from the heart. In such conditions the effect of the heart pumping by periodic contraction and expansion is quite obvious:
Another model, otherwise identical to the first, can be designed with flexible outer walls. This is approximately the situation we find in the human body. It would certainly allow the heart to exert its pumping function. But the walls would then bulge outward or inward, along with the expansion or contraction of the heart. This implies, that pumping has to be done at the energy cost of moving the mass of tissue between the heart and the compartment walls. Passive diastolic filling would be possible with this model, but its sensitivity to variations in venous pressure will be low. These apparent limitations do not, however, invalidate it.
In the living heart, there are some rigid regions in its confining "walls" (ribs, sternum and spine). There are also parts near the heart, that have a flexible outer wall. Furthermore, bordering the pericardium is lung tissue, which is compressible. The transmission of the movements of the heart to adjacent tissues should primarily affect those complying most easily, i.e. pulmonary tissue. If the heart were pumping in this way, one would thus expect a periodic contraction and expansion of the heart towards the pleura in systole and diastole, respectively. That should approximately correspond to the combined ejection volume of the ventricles. Such a movement, at least to a quantitatively important extent, is not observed. This material is discussed in Chapter 3 and Chapter 4.
Blair and Wedd [13] expressed some of the above views, although they overstressed the importance of intrathoracic pressure changes on venous return. Their idea was corrected by Hamilton and Lombard [67]. Hamilton [66] and Holzlöhner [81] had found earlier, that during the cardiac cycle, intrathoracic blood volume changes by only a small fraction of the stroke volume. This means, a rapid systolic inflow to the chest that nearly equalizes systolic outflow.
The output of the human heart is amazing. Pumping capacity varies from a few liters per minute, to 15-20 l/minute for healthy adults and up to 35 l/minute for some well-trained athletes.
How important are venous pressure (vis a tergo) and active filling through the movement of the valve plane in systole (vis a fronte) for ventricular filling? How big role plays the contribution of elastic forces (diastolic suction cf. [23])? These questions is still a matter of debate.
There is, however, a consensus of opinion concerning diastolic filling being of paramount importance for cardiac output.
For an authoritative view on the role of atrial contraction (atriums as "booster" or "primer" pumps), see Mitchell et al. [116] and Guyton [60]. This view seems to pervade modern cardiophysiological literature.
It is obvious, that current views on the action and control of the human heart need clarification. This can be done by some reconsidering about cardiac pumping, in the context of the specific criteria, described in the first part of this chapter. Our tools for that will be a few basic laws and facts of physics (cf. [29 ,30]) and fresh observations of the living heart, by a number of imaging techniques.
In this analysis, cardiac pumping and physical control functions can be crystallized into two basic concepts.
The first concept defines the actual mode of pumping:
The heart strives to do its pumping, with a fairly constant total volume and outer contour, in an environment conferring a substantial moment of inertia.
The second concept identifies the method of control, by which arterial and venous circulation is balanced:
The interventricular septum regulates ventricular stroke volumes, to maintain proper balance between systemic- and pulmonary circulation.
The pumping mode according to Concept 1 was, at least in a rudimentary way, envisaged by Harvey [70]. It is related to the operating principle of the well-known garden-pump; it consists of a steel tube surrounding a movable receptacle. Two one-way valves allow water flow in an upward direction only. This pump, has an essentially unidirectional force. In one step, it provides in- and out- flowing water with necessary energy, transmitted through the valve (at the bottom of the receptacle) in a closed position. That valve corresponds to the valve plane in the heart; it exerts a "gripping" action on the water column, by moving it stepwise towards the outlet.
A similar view has been expressed by Carlsson [32], based on experiments with tantalum-labelled ventricles in dogs. He noticed that "this emptying mechanism is probably more economical from an energy point of view than the generally accepted squeezing mechanism of the ventricles" (author's emphasis).
Further support for this pumping mechanism has been provided by McDonald [35], and by Slager et al. [164], based on endocardially implanted radio-opaque markers and contrast angiograms.
The active phase of the garden-pump is somewhat similar to ventricular systole and the passive phase to ventricular diastole. Water inflow is, however, discontinuous. When the stroke rate increases, the pumping mode becomes continuous, because of the dynamic forces smoothing the movement of the water column over the entire pumping cycle.
In contrast to the receptacle of the garden-pump, the left ventricle has the form of a paraboloid. The right ventricle (with a much smaller work load) is more complex in form; it is attached to the left ventricle, so as to form a new paraboloid in combination.
The paraboloid muscle mass below the valve plane, may be reduced to a cone; it keeps its fundamental geometric properties, when shrinking in the direction of its axis.
Contraction of the muscle fibres of the ventricular wall is arranged in a complex pattern (cf. [9, 170]). It may be represented by two force vectors:
Their resultant is approximately parallel to the wall, in the direction of the apex. Contraction may result either in the cone base approaching the apex, or vice versa.
The importance of the anatomical setting of the heart, was already obvious to Henke [76] in the end of the 19th century. It is vividly expressed in his criticism, of the determination of outer contour variation on excised hearts by Hesse. Hesse arrived at the result that the ventricles, when shrinking by contraction, definitely do not become shorter, but only more narrow. Henke pointed out that this sort of extension, or contraction, of the heart freely suspended in air or immersed in liquids differ form heart in vivo. It does not prove anything concerning the change in form which it experiences in life.
Henke further stated that "the diastolic form of the ventricles, according to the conclusions of Hesse, would approach the form of a hemisphere. Think of this hemisphere put into the human thorax in the sharp corner between the diaphragm and the anterior thoracical wall. This is the end of all topography".
Henke also clearly conceived the approximately constant volume of the heart, over the cardiac cycle.
It should be noted, that his findings received little attention at that time. The well-known textbook of the physiology of circulation by Tigerstedt [175], published nine years later and otherwise up-to-date, did not mention that work.
Movement of the apex atrially, would necessitate the yielding of the tissues surrounding it, in order to fill the imaginary volume created by its shrinkage. Because of the fixation of the pericardium to the diaphragm, and the rigidity of the thoracic cage, the cone base will approach the apex. A part of the blood volume of the atria, and the great veins, will move apically and fill this imaginary volume.
This mass transfer that occurs in real time, is to a large extent balanced by thoracic systolic blood in- and outflow. The difference will be mainly made up by venous blood, transmitting it's acceleration to the large surface of the major veins. It necessitating a minor acceleration only of their walls, and adjacent tissues in the direction of their lumen.
The pericardium seems to be a stabilizing- and volume-limiting factor [1010, 38, 71, 79, 80, 99, 138, 177], although a different opinion has been expressed recently [111]. Because of its configuration, and the specific properties of the cardiac muscle, the heart thus slides in the pericardial sac. In a similar way the receptacle of the garden -pump slides in its steel tube.
Motion of the ventricular cone apically is preferable to radial contraction, with regard to energy [29].
This pumping mechanism is similar to the valve plane concept by von Spee [167], who 1909 coined the term ventilebene.
He was not aware of the importance of the inertia of tissues, in which the heart is embedded.
Ventricular filling is seen to proceed in two distinct phases at low heart rate: a "fast" and a "slow" phase.
The fast phase is dominated of dynamic forces; the valve plane moving atrially have accelerated the blood in the atrium, under ventricular systole. When the valves into the ventricles opens, the accelerated blood rush into the ventricles.
After a moment the inrush of blood subsides, and the slow phase with low, or no inflow at all, begins (dominance of static forces). During the later stage of the slow phase, influx increases again, due to atrial systole. The contraction of the relatively thin atrial walls does not push blood into the ventricles, by the increase of atrial pressure. The actual role of atrial systole, is instead to move the valve plane further away from the apex, sliding it along the atrial blood mass [4040, 76, 92, 167]. The ventricular volumes increase, by the movement of the valve plane atrially, stretching and thinning the ventricular walls.
At higher heart rates, the fast phase is directly followed by atrial systole, and inflow to the ventricles proceeds at a rapid rate over the entire ventricular diastole.
Experimental proof of this mechanism was provided by Gribbe et al., on anaesthetised intact dogs [57, 58]. Recent non-invasive findings with ventriculography [154, 164], and two-dimensional Doppler echocardiography [46], on the whole agree with this filling sequence. But a substantial part of diastolic filling though, is brought about by the displacement of the ventricular wall relative to the cardiac blood volume, not observable in Doppler echocardography.
The gist of this is, that the importance of the atrial contraction is close to zero at higher heart rates.
The pumping action of the heart is primarily designed for the transport of blood mass by intermittent acceleration, and not for the generation of pressure. But the ventricles also have to do their work against aortic and pulmonary pressures (Hauffe [71]; cf. also [94]). The importance of systolic acceleration of blood in the atria and large veins, by the movement of the AV-plane was (as mentioned earlier) first suggested by Purkinje [137].
Epstein [36] 1904, wrote a thorough survey covering the research of the diastolic filling mechanism of the heart. The major concepts for the filling mechanism were static filling pressure (e.g. [75]) and active diastolic suction (e.g. [107]). That survey seem to have prevented the ideas of Purkinje and his followers, from being seriously considered for a long time.
Once blood is circulating, dynamic forces influence the working of the heart (see especially [20, 22]). This is because the blood mass accelerated in systole on both sides of the valve plane is significant, in comparison with the total mass of the heart. The return of the valve plane at the end of ventricular systole and the ventricles diastolic form and volume, has been the subject of many investigations. It has been explained in terms of elastic and hydraulic [110] intramyocardial forces, by arterial blood pressure straightening the aortic arch, and by the action of atrial systole.
The former mechanisms release energy stored in systole (cf. [4]). The role of elastic components in the heart wall has been much debated. Experiments that support elastic recoil (passive elasticity, or operative chamber stiffness [21, 42, 158]), are in contrast to others that disprove it [11]. Brecher [23] states that the vis a fronte is the force which concerns ventricular filling directly. Others [27] argue for relaxation factors, and that the quantitative significance of ventricular wall elasticity for diastolic filling should be smaller, than that of wall viscosity (.f. [1, 47, 173]).
In Chapter 8, another filling mechanism of the ventricles will be described.
In summary, the "gripping" pumping mode of the heart provides effective output, at a relatively constant volume and form. Ventricular filling requires low energy input. Atria and large vessels make the inflow smooth, and the atria also contribute to ventricular filling, by active displacement of the valve plane in atrial systole.
The circulatory system is basically made up of communicating volumes containing moving blood, in which dynamic conditions maintain pressure gradients and thus locally and temporarily varying pressures.
Total blood volume may vary, through water and solute transfer between intravascular and extravascular space, excretion, water intake, etc. These changes are normally rather slow. In a short time perspective i.e., in time periods of seconds (rather than minutes and hours), these control mechanisms are unimportant.
This short term circulatory control ensures the provision of the different parts of the circulatory system. The different parts will have their proper share of total blood volume, and the maintenance or change of this distribution according to metabolic needs.
An important control mode in this respect, is generally accepted to be the control of arterial pressure. This is controlled by regulation of heart rate, stroke volume, ventricular contraction (inotrop effect) and arteriolar constriction, mediated by the sympathetic nervous system. The afferent signals comes from high pressure baroreceptor areas, in the carotid sinus and arch of aorta. Low pressure baroreceptors in the venous system, indirect affects the high pressure baroreceptors (Lindblad [103103]).
The heart is a double pump:
Diastolic atrial pressure varies in the normal heart between about 3 and 15 mm Hg on both sides, although the pressure in the left atrium (LA), in general exceeds that prevailing in the right atrium (RA).
Atrial systole raises atrial pressure only slightly, between about 2 and 10 mm Hg.
These low pressures have to be compared with systolic left ventricular pressure, which (during physical exertion of healthy subjects) may exceed 200 mm Hg.
Right ventricular systolic pressure (in the absence of disease) seldom rises above 40 mm Hg (Bevegård [12]).
The pressure in the left ventricle (LV) surpasses that prevailing in the right ventricle (RV) both in diastole and systole. That should result in an essentially circular systolic configuration of the left ventricle (LV), in a plane perpendicular to the major LV axis. If the distribution of pressure were the opposite, the right ventricle would adopt this circular configuration.
Changes in resistive- and elastic properties of the circulatory system due to the effects of control mechanisms, cause a redistribution of intravascular volume. That also cause a varying extent of redistribution between pulmonary circulation and systemic circulation. As the reciprocating rate of the ventricles is by nature the same (even LV and RV end-diastolic volumes and ejection fractions are approximately identical [113]), redistribution must be effected through temporary differences in stroke output between LV and RV. The physical cause for this redistribution, and how it is controlled, is not completely understood.
It is commonly assumed that circulatory balance is maintained by the Starling mechanism1 (e.g. [2, 4, 11, 16, 19, 25, 43, 62, 68, 77, 96, 159, 166]). Experiments was designed to test the hypothesis, that balance in ventricular output is maintained or restored in accordance with the Starling mechanism. Franklin et al. [45] and Le Winter et al. [102] arrived at the conclusion, that the Starling mechanism is not the only mechanism that maintains or restores balance.
In connection with criticism of the hypothesis of the Frank-Starling law [129] i.e., that the impact of venous return governs the output of the normal heart, Hamilton delivered his idea. He stated that he could not think of any other explanation for evolution having preserved the Frank-Starling relationship, if not to maintain the circulatory balance.
In this, Hamilton was supported by some [14, 50, 141, 150], and preceded by Reindell and Delius [140] and others.
At present, there is a prevailing controversy reflected in many research papers and the major monographs cited above.
Braunwald [1717, 18], Sonnenblick [16] and others [34, 157] gives support for a major role of the Frank-Starling law (in the control of cardiac output in the normal heart).
This is at least partially questioned by Noble [120], Bassenge [4] and others [37, 88, 104, 124, 145, 182].
Experimental findings supporting the Frank-Starling relationship have been obtained either on isolated heart-muscle preparations or on open-chest animals. In some cases experimental findings have been obtained on excised and denervated animal hearts, often with their pericardia removed. For early criticism of results obtained from models other than intact animals, see Hamilton [66] and Sjöstrand [163].
Experimental work presented in this thesis aims at demonstrating the following; rigid or semi-rigid environment (and thus the natural setting of the heart) has a profound impact on its working mode and on the regulation of its output.
Considering the pumping mode of Concept 1, it is evident that the predominate mechanism for the ventricles to vary their respective volumes, is by displacement of the ventricular septum (VS). It is the only part of their walls which they have in common (the VS is mainly formed by subendocardial RV and LV fibres, Torrent-Guasp [176]). This volume variation is made possible by the process of ventricular polarization/depolarization. In diastole, ventricular depolarization confers plasticity to the septum. That lets it adopt a position determined by the dynamic and static pressure components, of left and right heart blood volumes during ventricular filling.
At the onset of systole, the AV-plane starts its movement towards the apex, the tricuspid and mitral valves close and after a short interval (the "isovolumetric phase") the aortic and pulmonic valves open.
When the left ventricle is put under excessive pressure, its walls will adopt the most stable configuration, which is the circular one in a transverse plane. That position also predetermines the position of the ventricular septum, as a circular segment of systolic LV wall (cf. [33]). If the configuration of the VS at the onset of systole deviates from the "predetermined" circular segment [3], LV pressure rise will displace it and make it adopt that configuration.
In addition to the pumping action by the valve plane moving apically, the septum itself will exert a membrane pump-like function and thereby affect blood volumes ejected from both ventricles.
Diastolic pressure interdependence of LV and RV [7, 28, 38, 55, 78, 93, 95, 115, 127, 155, 171, 177, 178] under a variety of abnormal or pathological conditions, and a dependence of diastolic pressure-volume relationship of LV on RV filling pressure [1, 7, 74, 127] has been noted. No common explanation for these phenomenons has been given. This may be partly due to different, and sometimes contradictory, findings concerning the interaction of ventricular septum (VS).
Some claim that the deflected VS retains its diastolic position in systole [54, 87, 95, 151]. Others believe that LV compliance [7, 122, 171, 179] and contractility [24] changes, and still others that crista supraventricularis [85] is damaged and that the pericardium interferes [162], etc.
The general importance of the VS for the equilibration of pulmonic- and systemic circulation has therefore been emphasized (cf. [126]). Support for the concept that the VS exerts a balancing influence, is provided by the study of VS displacement by echocardiography in cases of heart disease with atrial pressure overload (Chapter 6). The possibility of maintaining circulatory balance by displacement of the intraventricular septum is also illustrated by experiments with a double pump (Chapter 7).
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