Anatomy of the Heart
Majid Ali, M.D.
The heart is a pump. A water pump functions well if it pumps clean water. An air pump functions well if it pumps clean air. And so it with the heart. It stays healthy as long as it pumps clean blood. So, heart coronary disease is a problem of the circulating blood, which has two guardian angels: the spirit (sun) and the bowel (soil). That simply stated, is my Sun-Soil Model of Heart Health.
The heart is a muscle. What distinguishes the heart muscle from most other types of muscles is its indefatigability. Nature conferred upon the heart the unique ability to regulate its own rhythm for its entire healthful life.
Two Hearts, One Lung
The heart is a single organ only on the surface, though structurally it is encased within a single pericardial sac and its four chambers are strongly enjoined. Functionally, it is a different story. The right and left atria, its upper two chambers, work in unison —as a single neuromuscular entity—while the same holds for the right and left ventricle located below the upper chambers. When the two atria act synergistically —a functional characteristic assured by a structural syncytium of myocardial fibers that make up their wall—the blood flows from the right atrium into the right ventricle through the tricuspid valve and from the left atrium to the left ventricle through the bicuspid (mitral) valve. Functionally, the heart works as two organs in yet other way. The “right heart”—comprising right atrium and right ventricle—pushes venous, deoxygenated blood to the lungs via pulmonary arteries. Similarly, the “left heart”—comprising left atrium and left ventricle— pumps oxygenated blood it receives from the lungs to the arterial tree via the aorta.
In contrast to the heart, the lungs—though structurally distinct and located on either side of the heart —work as a single functional unit. From a pathophysiologic point, the essential functions of ventilation, oxygenation of blood, disposal of carbon dioxide and other volatile waste substances are served in identical fashion and to similar degrees in both lungs. The same holds for “neuro-pulmonary” regulatory functions. Individuals who lose one of the lungs abruptly during surgery—for resection of neoplasm, for instance— rapidly adjust to the loss of that organ without suffering clinically significant long-term consequences. The remaining lung, of course, hypertrophies to compensate for the surgically absent pulmonary parenchyma. Henry Gray’ Gray’s Anatomy10 and Arthur Guyton’s Human Physiology and Mechanisms of Disease11 are two highly recommended texts for detailed study of the anatomy and physiology of the heart.
The cavity of the right atrium can contain up to two ounces of blood and is larger than that of the left atrium. Its walls are thinner than those of the left atrium. The right ventricle can accomodate about three ounces of blood and forms most of the front surface of the heart, located behind the sternum. The left ventricle is larger and has a thicker wall than the right ventricle, the ratio of thickness between the two being 3:1. It forms the apex of the heart and most of the posterior surface. The cusps of the mitral valve are anchored to the wall of the left ventricle through thick muscular structures called chordae tendineae. Uncommonly, infarction of the muscle in those structures leads to rupture of chordae tendineae and acute incompetence of the valve and subsequent acute heart failure.
The weight of the heart varies with the weight, height and skeletal structure of the person. The heart ranges from 300 to 350 gm in adult males and 250 to 300 gm in females. The thickness of the right ventricle varies from 0.3 to 0.5 cm and that of the left ventricle from 1.3 to 1.5 cm. Cardiomegaly is enlargement of the heart and generally includes increased ventricular thickness. Dilatation of the heart means enlargement of the chambers without thickening of the left ventricular wall (or with minimal changes.)
Figure 1. The Anatomy of the Bisected Heart Revealing the Features of the Four Chambers and the Valves Between Them
The openings into the right atrium include: (1) superior vena cava; (2) inferior vena cava; (3) coronary sinus; (4) foramina Thebesii (openings of minute veins draining myocardium); and (5) auriculoventricular opening (tricuspid valve). The openings of the left atrium include those of four pulmonary veins and the atrioventricular channel (bicuspid valve). Semilunar valves, three in number, guard the openings of the pulmonary and aortic valves. Sinuses of Valsalva are three pouch-like areas of dilatation between the pulmonary semilunar valves and the beginning of the pulmonary artery. The corresponding sinuses of Valsalva of the aortic valve are larger than those of the pulmonary artery.
During early fetal life, atria are larger than ventricles. The two atria communicate freely through the foramen ovale. The contents of the right ventricle are ejected into the pulmonary artery and then, through ductus arteriosus—the large channel between that artery and aorta—into the aorta. In this circulation, the lungs are bypassed and the workload on the left ventricle remains very low, thus accounting for the fact that the wall of the right ventricle is thicker than that of the left ventricle during that stage. That pattern of circulation is rapidly altered after birth with the closure of ductus arteriosus, with resulting rapid increase in the thickness of the left ventricle.
The nerves supplying the heart are derived from cardiac plexuses, which comprise both cranial and sympatheic outflows. Those nerves are distributed on the surface of the heart as well as within the myocardial substance. Lymphatics from the heart terminate in the right lymphatic and thoracic ducts.
The heart muscle, the myocardium, is a collection of branching and anastomosing fibers composed of individual cells(cardiac myocytes). The cardiac myocyte is divided into structural and functional subunits, the sarcomeres, that have partially overlapping myosin (thick) and actin (thin) filaments and whose lengths range from 1.6 to 2.2 um, depending on the state of contraction. Cardiac contraction involves collective shortening of sarcomeres by sliding of the actin filaments between the myosin filaments toward the center of each sarcomere. Shorter sarcomeres have considerable overlap of actin filaments in their centers, even during diastole, whereas longer lengths, to a degree, enhance contractility (Frank-Starling mechanism.) Thus moderate ventricular dilation increases the force of contraction. There is a point, however, with progressive dilation at which overlap of the actin and myosin filaments is reduced, and the force of contraction turns sharply downward, as occurs in heart failure.
Histologically, the myocardium is a syncytium of cells. Cardiac myocytes link up with each other to make up fibers that divide, recombine, spread out, and converge to form a remarkably efficient latticework that contracts in harmony, one hundred thousand times a day under physiologic resting condition in an average person. The cardiac myocytes contain actin and myosin myofibrils arranged in a fashion very similar to those in skeletal muscle cells. In regions where the cell membrane of one myocyte meets with that of another within a myocardial fiber is designated as intercalated disc. The critical importance of the highly specialized structure of this disc is that it offers electrical resistance that is only 1/400th of that of the cell membrane in other areas. This quality of high permeability to ions has earned the intercalated disc also the title of communicating junction (or gap junctions), through which ions move at high speeds along the longitudinal axis of myocardial fibers. The expected consequence of that structural design is that action potential travels from one cell to another with impedance that is far less than would exist if cardiac cells were linked up with each other as cells are in other tissues. The syncytial character of the cardiac musculature provides the highly adapted “electrical grid” for efficient transfer of action potential energy.
The pericardium is a conical sac composed of a strong fibro-serous sheath—with an external fibrous and an internal serous layer—that encases the heart as well as the commencement of the great vessels of mediastinum. The smooth internal serous lining provides a smooth surface on which the heart muscle glides over during contraction. The apex is directed upwards and surrounds the vessels, while the base is attached to the central tendon and the adjoining left part of the diaphragm. Laterally, it is covered by the pleura, while posteriorly it rests upon the structures in the roots of the lungs.
Fluid accumulating in the pericardial sac is called pericardial effusion, which may be serous (as in viral pericarditis), purulent (as in bacterial pericarditis), or hemorrhagic (as in involvement with malignant tumors). Hemopericardium is a condition in which blood fills up the pericardial sac, usually after rupture of a myocardial infarct, uncommonly after penetrating injury of the heart. Since the pericardium is an unyielding membranous structure surrounding the heart, accumulation of any type of fluid intereferes with myocardial performance by simple mechanical compression—cardiac temponade is the commonly used clinical term for that. Indeed, rapidly progressive tempnade is fatal condition unless cardiac compression is quickly relieved. This can be as true of rapidly accumulating serous fluid in viral pericarditis as in the developing hemopericardium following penetrating myocardial injuries, though the former usually occurs following some days of clinical neglect of the entity.
Endocardium is a smooth, thin transparent membrane that lines the inside of all chambers of the heart as well as all surfaces of the heart valves, producing the characteristic glistening appearance of myocardium when the sectioned heart is examined at autopsy. It is thicker in the atria than in the ventricles—the left atrial lining being the thickest and somewhat opaque. The endocardial lining the tips of papillary muscles is also thicker than that in regions in close vicinity.
The endocardium is an unsung hero of the oxygen saga. The reason for that—it seems to me—is that its form and function is equated with the endothelial lining of blood vessels, to which it is continuous with. Clearly, endocardium covers only an infinitesmally small fraction of the total inner surface of the cardiovascular system with its vast arterial and venous channels. Thus, it may seem that the lining cells of the endocardium do not amount to much in the overall scheme of things. That is an error. A clear understanding of the enormous contribution to cardiac health can be derived from a consideration of states in which the enodocardium is unable to subserve its otherwise unappreciated roles: bacterial endocarditis, intraventricular thrombus over a segment of infarcted myocardium, and others. Unprotected by the endocardial lining, the damaged heart valves or ventricular surfaces cause churning of blood, formation of thrombotic vegetations, and a variety of embolic phenomena. It is also useful to recall the role endocardium plays during the embyronic development of the heart. The term endocardial cushions is a term for two thickenings—one ventral and the other dorsal—which exist during early embyronic development and grow to divide the short straight auricular canal into the future right and left atrioventricular orifices.
The Excitatory and Conducting System
The heart is a autoregulating muscular organ par excellence. Among its many self-regulatory functions is preservation of its rhythm through a broad range of pathophysiologic stresses and its ability to revert back to its rhythm after periods of having been forced out of it. For that the heart harnesses its own highly specialized system of nerves and fibers collectively designated as the conducting system. The two primary functions of this system are:
1. Rhythmic generation of energy (electrical) pulses to elicit myocardial contraction; and
2. To facilitate prompt and closely monitored transmission (conductance) of the energy impulse throughout the myocardium to assure that the entire myocardium responds in unison, creating a slight—about one sixth of a second —but needed interval between atrial and ventricular contractions to maximize the pump efficiency of the heart muscle.
Here I emphasize a fundamental difference between the prevailing drugs-stents-bypass model and the integrative oxidative-dysoxygenative model of CHD. Consider the following from the second paragraph of the chapter on the rhythmical excitation of the heart in Human Physiology and Mechanisms of Disease by Guyton and Hall (6th edition, 1997):5
Unfortunately, though, this rhythmical and conduction system of the heart is very susceptible to damage by heart disease, especially by ischemia of the heart tissues resulting from poor coronary flow. The consequence is often a very bizarre heart rhythm, even to the extent of death.
Guyton and Hall have written an excellent book. But, they are not clinicians—they uncritically reproduce what appears in the drugs-stents-bypass cardiology textbooks.
Based on extended personal experience, I can categorically state that the vast majority of cardiac arrhythmiasinitially are triggered by hyperglycemic-hyperinsulinemic-hyperadrenergic shifts induced by heavy sugar intake, lifestyle stress, excessive caffeine consumption, environmental chemical triggers, and issues of chronic anger and hostility. The proof of the above statement is the non-drug control of such arrythmias which I have personally observed in the vast majority of patients by addressing the causes of abnormal heart rhythms listed in the preceding sentence of this section.
Specifically, I have controlled many arrhythmias by simply prescribing one to one and one-half tablespoon of suitable proein powders—with 90% or so amino acid content—twice daily, at breakfast and mid-afternoon to prevent sugar roller coasters. Of course, sugar intake has to be severely restricted and relevant triggers—such as environmental mycotoxins and industrial pollutants (such as formaldehyde, perchloroethylene, and others)—have to be addressed effectively as well.
The excitatory and conducting system of the heart is outlined in Figure 2 (the numbers indicate the first four structures listed below). The system has the following major components:
1. Sinus node
2. Internodal pathways
3. Atrioventricular (A-V) node
4. Atrioventricular bundle
5. Right bundle of Purkinje fibers
6. Left bundle of Purkinje fibers
The sinus node (also designated sinoatrial node) is a flattened and ellipsoid strip of highly specialized neural tissue. It is situated in the superior lateral wall of the right atrium, immediately below and somewhat lateral to the opening of the superior vena cava. In adult, it measures approximately 15 x 3 x 1 millimeter. Histologically, the filaments of the node are much thinner (three to five micrometers in diameter) as compared with fibers of surrounding atrial myocardium that measure 10 to 15 micrometers in diameter. The nodal fibrils directly connect with atrial fibrils so that any action potential—propagating wave of electrons—that develops in the node is very rapidly conducted. The bibrils of the sinus node are not the only cardiac fibers capable of self-excitation; however, their activity in health determines the cardiac rhythm.
The potential of the nodal fibrils between discharges is generally between -55 to -60 millivolts (mV). This value is notably lower than that of the ventricular fibers which is generally -85 to -90 mV. The explanation of the reduced negativity in the nodal fibrils is that their cell membranes naturally leak more sodium ions than the ventricular membranes. The term reduced negativity—though traditionally used in medical texts— requires an explanation. In reality, a value of -55mV represents a number of electrons (state of energy) that is lower than that expressed in a value of -90mV. Energetically, both values represent a positive energy states.
Figure 2. The Excitatory and Conduction System of the Heart