Tissue Structure
Layers
Epicardium
The epicardium is the outermost layer. It is composed of a single sheet of squamous epithelial cells overlying delicate connective tissue. The epicardium is the visceral portion of the serous pericardium and folds back on itself to form the parietal portion of the serous pericardium.
This layer contains fibroelastic connective tissue, blood vessels, lymphatics and adipose tissue.
The myocardium is specialized striated muscle in a connective tissue skeleton.
Cardiac muscle can be divided into atrial, ventricular, and specialized pacemaker and conducting cells.
The self-excitatory nature of cardiac muscle cells and their unique organization allow the heart to function as a highly efficient pump. Serial low-resistance connections (intercalated disks) between individual myocardial cells allow the rapid and orderly spread of depolarization in each pumping chamber.
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Electrical activity readily spreads from one atrium to another and from one ventricle to another via specialized conduction pathways. The normal absence of direct connections between the atria and ventricles except through the atrioventricular (AV) node delays conduction and enables atrial contraction to prime the ventricle.
Myocardial cells contains myofibrils, which are specialized organelles consisting of long chains of sarcomeres, the fundamental contractile units of muscle cells. Cardiomyocytes show striations similar to those on skeletal muscle cells. Unlike multinucleated skeletal cells, the majority of cardiomyocytes contain only one nucleus, although they may have as many as four. Cardiomyocytes have a high mitochondrial density, which allows them to produce adenosine triphosphate (ATP) quickly, making them highly resistant to fatigue.
The cardiomyocytes are about 100 to 150 micrometers long and 15 to 20 micrometers in diameter.[
Note: Humans are born with a set number of heart muscle cells, or cardiomyocytes, which increase in size as our heart grows larger during childhood development. Recent evidence suggests that cardiomyocytes are actually slowly turned over as we age, but that less than 50% of the cardiomyocytes we are born with are replaced during a normal life span.[8]The growth of individual cardiomyocytes not only occurs during normal heart development, it also occurs in response to extensive exercise (athletic heart syndrome), heart disease, or heart muscle injury such as after a myocardial infarction. A healthy adult cardiomyocyte has a cylindrical shape that is approximately 100μm long and 10-25μm in diameter. Cardiomyocyte hypertrophy occurs through sarcomerogenesis, the creation of new sarcomere units in the cell. During heart volume overload, cardiomyocytes grow through eccentric hypertrophy.[9] The cardiomyocytes extend lengthwise but have the same diameter, resulting in ventricular dilation. During heart pressure overload, cardiomyocytes grow through concentric hypertrophy.[9] The cardiomyocytes grow larger in diameter but have the same length, resulting in heart wall thickening.
the inner endocardium of endothelium and subendothelial connective tissue;
The cardiac conducting system stimulates rhythmic contractions and consists of modified cardiac muscle fibers forming the sinoatrial (SA) and atrioventricular (AV) nodes, the atrioventricular bundle (of His), left and right bundle branches, and Purkinje fibers.
Sinoarrial
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Purkinje fibers, located just beneath the endocardium of both ventricles, are distinguished from contractile fibers by their greater diameter, abundant glycogen, and more sparse bundles of myofibrils.
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The bundle of His divides in the interventricular septum into the right and left bundle branches. Initially, the right bundle branch off of the bundle of His travels down the interventricular septum near the endocardium. It then dives deeper into the muscular layer before re-emerging near the endocardium again. The right bundle branch receives most of its blood supply from the anterior descending coronary artery. It also receives collateral circulation from the right or left circumflex coronary arteries, depending on the dominance of the heart.[1]
[They are distributed throughout the heart and are responsible for several functions. First, they are responsible for being able to spontaneously generate and send out electrical impulses. They also must be able to receive and respond to electrical impulses from the brain. Lastly, they must be able to transfer electrical impulses from cell to cell.[5]
All of these cells are connected by cellular bridges. Porous junctions called intercalated discs form junctions between the cells. They permit sodium, potassium and calcium to easily diffuse from cell to cell. This makes it easier for depolarization and repolarization in the myocardium. Because of these junctions and bridges the heart muscle is able to act as a single coordinated unit.
The conducting system consists of the sinoatrial (SA) and atrioventricular (AV) nodes, the atrioventricular bundle (of His), and Purkinje fibers. It stimulates rhythmic contraction.
Purkinje fibers, located just beneath the endocardium of both ventricles, are distinguished from contractile fibers by their greater diameter, abundant glycogen, and more sparse bundles of myofibrils.
The normal absence of direct connections between the atria and ventricles except through the atrioventricular (AV) node delays ventricular depolarization, enabling the atria to prime the ventricles.
Masses of dense irregular connective tissue make up the cardiac skeleton, which surrounds the bases of all heart valves, separates the atria from the ventricles, and provides insertions for cardiac muscle.
Histologically, the pericardium is composed predominantly of compactcollagen layers interspersed with elastin fibers. The abundance and orientation of the collagen fibers are responsible for the characteristic viscoelastic mechanical properties of the pericardium. For example, the pressure-volume relation of the pericardium is nonlinear; that is, the relation is initially flat (producing little to no change in pressure for large changes in volume) and develops a "bend" or "knee" at a critical pressure, which terminates in a steep slope (producing large changes in pressure for small changes in volume) (Fig. 85–2)
Pericardial pressure-volume relation in a dog.1
In addition, the pericardium is anisotropic; that is, it stretches more in the short axis than in the long axis.
Physiology of the Pericardium
The pericardium is not essential for life; no adverse consequences follow congenital absence or surgical removal of the pericardium. However, the pericardium serves many important (although subtle) functions
Table. Functions of the Pericardium
| Mechanical |
| Effects on chambers |
| Limits short-term cardiac distention |
| Facilitates cardiac chamber coupling and interaction |
| Maintains pressure-volume relation of the cardiac chambers and output from them |
| Maintains geometry of left ventricle |
| Effects on whole heart |
| Lubricates, minimizes friction |
| Equalizes gravitation and inertial hydrostatic forces |
| Mechanical barrier to infection |
| Immunologic |
| Vasomotor |
| Fibrinolytic |
| Modulation of myocyte structure and function and gene expression |
| Vehicle for drug delivery and gene therapy |
It limits distension of the cardiac chambers and facilitates interaction and coupling of the ventricles and atria.1 Thus, changes in pressure and volume on one side of the heart can influence pressure and volume on the other side. Limitation of cardiac filling volumes by the pericardium may also limit cardiac output and oxygen delivery during exercise.1 The pericardium also influences quantitative and qualitative aspects of ventricular filling; the thin-walled right ventricle (RV) and atrium are more subject to the influence of the pericardium than is the more resistant, thick-walled left ventricle (LV).