Journal of Postgraduate Medicine
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Year : 2003  |  Volume : 49  |  Issue : 3  |  Page : 282-284  

The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump

KS Kishore 
 Department of Anatomy, Seth G. S. Medical College & K. E. M. Hospital, Parel, Mumbai - 400012, India

Correspondence Address:
K S Kishore
Department of Anatomy, Seth G. S. Medical College & K. E. M. Hospital, Parel, Mumbai - 400012

How to cite this article:
Kishore K S. The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump .J Postgrad Med 2003;49:282-284

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Kishore K S. The Heart of Structural Development: The Functional Basis of the Location and Morphology of the Human Vascular Pump . J Postgrad Med [serial online] 2003 [cited 2023 May 28 ];49:282-284
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A famous surgeon once proclaimed: “There can be a structure with no function; but there cannot be a function with no structure.” Surgeons can be excused for their bias towards Anatomy, but what the dramatic statement conceals is that, it is the demands of function that designs a structure. Nature in its infinite wisdom, has a functional basis for the morphology as well as the location of every organ - some known, and others waiting to be understood.


   The need for the heart

The circulatory system appears in the middle of the third week of the intra-uterine life when the embryo is no longer able to satisfy its nutritional requirements by diffusion alone.[1] The fundamental purpose of this circulatory system is to carry nutrients and oxygen to the various tissues of the body. In fishes, there are three sets of capillaries in series, in this circulatory system - one at the gut absorbing nutrients, one at the gills absorbing oxygen, and one at the tissues distributing the above two. In any passage of liquid through tubes, the friction of liquid on the walls tend to lessen the pressure. The resistance to the blood flow is inversely proportional to the fourth power of the diameter of the blood vessel's lumen.[2] Thus, the fall in pressure is maximum at the capillaries; hence the need of a pump to maintain tissue perfusion.


   Location of the heart

The earliest vessel to develop in the embryo is the subintestinal vein running from the gut to the gill arches. The pump forms along the course of this vessel. Thus the pericardial cavity which lodges the heart lies at the most cranial and ventral part of the embryonic coelom, primitively in the floor of the throat, below the gills. This makes the heart lie most advantageously to generate sufficient pressure to pump the de-oxygenated blood received from the caudal part of the body, get oxygenated at the gills, and course further cranially to the brain.


   Relations of the heart to other vital organs

In higher vertebrates, the developing lungs are formed dorsal to the heart, on either side of the oesophagus in the pleural cavity. The pericardial cavity is separated from the liver by the septum transversum, while the pleural cavity is continuous with the peritoneal cavity. Only in the viviparous mammals, do the pleuroperitoneal membranes along with the septum transversum form the diaphragm, completely sealing off the thorax from the abdomen.[3]

Incidentally, it is no coincidence that the heart and the lungs are packaged in the incollapsible thoracic cage because these are the only two organs that require negative pressure for their functioning - venous return and inspiration, respectively. The abdominal organs work on positive pressure - the stomach, the intestines, the bladder and especially the uterus, during parturition.

The alimentary tract is co-extensive to the body from the oral end to the aboral end in the primitive annelid, the earthworm. When the animal enlarges, since the surface area of the absorptive part of the alimentary tract increases by only the square of its dimensions, while the nutritional requirements, which depends on the volume, increases by its cube, the alimentary tract enlarges and gets coiled. The stomach and the intestines working under positive pressure are packaged in the compartment caudal to the respiratory diaphragm.

Since the liver and the pancreas are developed as off-shoots from the necessarily fixed (to avoid twisting and kinking of their ducts) parts of the intestine, the duodenum becomes the only part of small intestine to become retro-peritoneal by zygosis. After this, the solid organ, the liver, rotates and goes to the right so that the stomach comes relatively to the left. This not only ensures that the venous blood from the entire gut via the hepatic portal system enters the right atrium directly, but also allows the air-filled fundus of the stomach to cushion the left sided apex of the heart.

While the gonads, developing in the thoracolumbar regions, descend caudally to reach closer to the internal genital tracts, developed in the cloaca, to liberate the gametes, the kidneys developing in the pelvis ascend. The kidneys weigh approximately two-hundredth the body weight but receive one-fifth of the cardiac output - a forty-fold extra vascularity than an average tissue. This high vascularity can be achieved only by ascending and reaching close to the heart, as much as the diaphragm would allow.


   Phylogeny of the heart

The piscean heart consists of a series of four successive chambers - from back to front: sinus venosus, atrium, ventricle and conus (truncus) arteriosus. The avian and the mammalian heart also has four chambers; but it is a double pump, with two chambers in each part, in parallel. When the gills are replaced by the lungs, the heart receives oxygenated and deoxygenated blood. In order to keep the two streams separate, the atrium is divided in the amphibians. Simultaneously, the sinus venosus gets incorporated into the right atrium.

The atrial separation would be in vain, if the two streams were to mingle in the single ventricle. These two streams move around spirally in the ventricle and the truncus to minimise their mixing. With the difference in the systemic and pulmonary pressures not being much in the amphibians and the reptiles, a need for a (complete) ventricular septum is unwarranted.

The warm blooded animals have a high metabolic rate and this is possible only if a good supply of oxygen is available at all times in the systemic circulation.[4] This high metabolic rate causes a significant rise of pressure in the systemic circulation over pulmonary. The conus gets incorporated into the ventricle and a complete septum is seen in the aves and the mammals.


   The pericardial sinuses

The primitive heart tube is initially suspended in the pericardial cavity by a dorsal mesocardium formed from the foregut splanchnopleuric mesoderm. This dorsal mesocardium ruptures forming the transverse pericardial sinus, leaving the heart suspended in the pericardial cavity only by its attached vasculature. The heart needs to be free to change its shape readily in powerful pumping movements.

Though the transverse pericardial sinus may be used by the cardiac surgeons to pass a surgical clamp or placing a ligature around the great arteries,[5] its functional purpose is to allow the intrapericardial portion of the two great elastic arteries to expand posteriorly during cardiac systole. No role has been assigned to the oblique pericardial sinus.

The sinus venosus gets incorporated into the right atrium while the trunk of pulmonary vein and its tributaries get incorporated into the left atrium. The latter produces a blind cul-de-sac behind the left atrium producing the oblique pericardial sinus to allow the expansion of the left atrium. The former does not produce any sinus.

The right atrium requires no such sinus because the increased venous return causing the right atrium to expand occurs when there is negative intra-thoracic pressure during inspiration, when the whole chest wall increases its dimensions. Expiration, in contrast, produces a squeezing effect on the lungs causing increased venous return to the left atrium. The oblique sinus is the only true “friend” of the left atrium allowing it to expand when the rest of the thorax (chest wall, pleural cavity, lungs) “collapse”.


   Folding of the heart tube

On day 23 of intra-uterine life, the heart tube begins to elongate and simultaneously to loop and fold. The bulboventricular portion of the cardiac tube grows more rapidly than the surrounding cavity and doubles its length. As the venous and arterial ends are fixed by the pericardium, the cardiac tube necessarily becomes bent.[6] However, heart excised from experimental animals and grown in culture medium demonstrated an intrinsic ability to loop.[7]

Another theory suggested that the state of hydration of the cardiac jelly controls looping. However, when the jelly was removed enzymatically, looping was unaffected.[7] Still others believed that looping is induced by the haemodynamic forces of the circulating blood. Cultured hearts loop correctly even in the absence of blood flow.[7]

The purpose of the looping is to convert a weak peristaltic force of a straight tube into a powerful pump. The greater the bend, the more powerful is the force. Since the sites of auscultation of the valves depend on the geometry of the associated column of blood from the oscillator (valves) which carries the acoustic waveforms to the chest wall, the direction of the blood flow can be assessed by joining the surface projection of the valves with the site for its optimal auscultation.

The blood flowing through the right ventricle changes direction by 125º in passing the free edge of the anterior tricuspid leaflet while that flowing through the left ventricle changes direction by nearly 180º in passing the free edge of the anterior mitral leaflet.[8] This potentiates a greater pressure in the left chambers.


   Remodelling of the chambers

Initially the chambers of the heart are somewhat cylindrical. The cells of the myocardial mantle invade the subendothelial reticulum and form a complex network of inter-communicating trabeculae. This trabeculated pattern of primitive vertebrates constitutes a lesser volume of propulsive tissue in higher vertebrates. With the incorporation of the great vessels into the chambers, the cavities rapidly become spherical. This evolution from a trabecular heart to an organ with rounder chambers and compacted myocardium is an expression of increased efficiency.[9] This is further emphasized by the fact that whereas the trabeculated pattern constitutes at least the inner two-thirds of the right ventricle, it contributes to less than one-fourth of the left ventricle.[8]



After discussing at length the development of the heart, the 38th edition of Gray's Anatomy concludes on this apologetic note: “In considering the many factors governing cardiac development - phylogenetic, ontogenetic and physiological - the last is usually underestimated and the first is perhaps stated too dogmatically. Ontogenetic mechanisms must conform to the early demand for a functioning heart, and cardiogenesis is not necessarily a mere repetition of the phylogenetic steps, which are themselves uncertain, however plausible they may seem.”

Thus, functional necessity is the mother of structural innovation.


1In: Sadler TW, editor. Langman's Medical Embryology. 8th edn. Philadelphia: Lippincott Williams & Wilkins; 2000. pp. 208.
2Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology. 10th edn. New York: John Wiley and Sons Inc; 2003. pp. 706.
3Romer AS, Parsons TS. The Vertebrate Body. 5th edn. Philadelphia: W B Saunders Company; 1978. pp. 233.
4Taylor DJ, Green NPO, Stout GW, Soper R. Biological Science. 3rd edn. Cambridge: Cambridge University Press; 1997. pp. 463.
5Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th edn. Philadelphia: Lippincott Williams & Wilkins; 1999. pp. 119.
6In: Hamilton WJ, Mossman HW, editors. Hamilton, Boyd and Mossman's Human Embryology. 4th edn. London: The MacMillan Press Ltd; 1978. pp. 232.
7Larsen WJ. Human Embryology. 2nd edn. New York: Churchill Livingstone; 1997. pp. 159.
8Silver MD. Cardiovascular Pathology. 1st edn. New York: Churchill Livingstone; 1983. Vol 1. pp. 16,19.
9In: Williams PL, et al, editors. Gray's Anatomy. 38th edn. Edinburgh: Churchill Livingstone; 2000. pp. 301.

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