The heart wall is composed mainly of a muscular layer, the myocardium. The epicardium and the pericardium cover the external surface. Internally, the endocardium covers the surface.
Epicardium and Pericardium
The epicardium is a layer of mesothelial cells that forms the visceral or heart layer of the serous pericardium. Branches of the coronary blood and lymph vessels, nerves, and fat are enclosed in the epicardium and the superficial layers of the myocardium.
The epicardium completely encloses the external surface of the heart and extends several centimeters along each great vessel, encircling the aorta and pulmonary artery together. It merges with the tunica adventitia of the great vessels, at which point it doubles back on itself as the parietal pericardium. This continuous membrane thus forms the pericardial sac and encloses a potential space, the pericardial cavity (Fig. 1-1
). The serous parietal pericardium lines the inner surface of the thicker, tougher fibrous pericardial membrane. The pericardial membrane extends beyond the serous pericardium and is attached by ligaments and loose connections to
the sternum, diaphragm, and structures in the posterior mediastinum.
▪ Figure 1-9 Schematic view of spiral arrangement of ventricular muscle fibers. (From Katz, A. . Physiology of the heart [4th ed., p. 8]. Philadelphia: Lippincott Williams & Wilkins.)
The pericardial cavity usually contains 10 to 30 mL of thin, clear serous fluid. The main function of the pericardium and its fluid is to lubricate the moving surfaces of the heart. The pericardium also helps to retard ventricular dilation, helps to hold the heart in position, and forms a barrier to the spread of infections and neoplasia.
Pathophysiological conditions such as cardiac bleeding or an exudate-producing pericarditis may lead to a sudden or large accumulation of fluid within the pericardial sac. This may impede ventricular filling. From 50 to 300 mL of pericardial fluid may accumulate without serious ventricular impairment. When greater volumes accumulate, ventricular filling is impaired; this condition is known as cardiac tamponade. If the fluid accumulation builds slowly, the ventricles may be able to maintain an adequate cardiac output by contracting more vigorously. The pericardium is histologically similar to pleural and peritoneal serous membranes, so inflammation of all three membranes may occur with certain systemic conditions such as rheumatoid arthritis.
The myocardial layer is composed of cardiac muscle cells interspersed with connective tissue and small blood vessels. Some atrial and ventricular myocardial fibers are anchored to the fibrous skeleton (see Fig. 1-5
). The thin-walled atria are composed of two major muscle systems: one that surrounds both of the atria and another that is arranged at right angles to the first and that is separate for each atrium.
Each ventricle is a single muscle mass of nested figure eights of individual muscle fiber path spirals anchored to the fibrous skeleton.7
Ventricular muscle fibers spiral downward on the epicardial ventricular wall, pass through the wall, spiral up on the endocardial surface, cross the upper part of the ventricle, and go back down through the wall (Fig. 1-9
). This vortex arrangement allows for the circumferential generation of tension throughout the ventricular wall; it is functionally efficient for ventricular contraction. Some fiber paths spiral around both ventricles. The fibers form a fan-like arrangement of interconnecting muscle fibers when dissected horizontally through the ventricular wall.8
The orientation of these fibers gradually rotates through the thickness of the wall (Fig. 1-10
▪ Figure 1-10 Changing ventricular muscle fiber angles at different depths. Reconstructed from a series of microphotographs. (From Streeter, D. D., Jr, Spotnitz, H. M., & Patel, D. P., et al. . Fiber orientation in the canine left ventricle during diastole and systole. Circulation Research, 24, 342-347, with permission of the American Heart Association, Inc.)
▪ Figure 1-11 Schematic illustration of the human cardiac conducting system. (From LifeART image © 2007 Lippincott Williams & Wilkins.)
The myocardial tissue consists of several functionally specialized cell types.
Working myocardial cells generate the contractile force of the heart. These cells have a markedly striated appearance caused by the orderly arrays of the abundant contractile protein filaments. Working myocardial cells comprise the bulk of the walls of both atrial and both ventricular chambers.
Nodal cells are specialized for pacemaker function. They are found in clusters in the sinus node and AV node. These cells contain few contractile filaments, little sarcoplasmic reticulum (SR), and no transverse tubules. They are the smallest myocardial cells.
Purkinje cells are specialized for rapid electrical impulse conduction, especially through the thick ventricular wall. The large size, elongated shape, and sparse contractile protein composition reflect this specialization. These cells are found in the common His bundle and in the left and right bundle branches as well as in a diffuse network throughout the ventricles. Purkinje cell cytoplasm is rich in glycogen granules; thus, making these cells more resistant to damage during anoxia. A secondary function of the Purkinje cells is to serve as a potential pacemaker locus. In the absence of an overriding impulse from the sinus node, Purkinje cells initiate electrical impulses.
In areas of contact between diverse cell types, there is usually an area of gradual transition in which the cells are intermediate in appearance.
In the normal sequence of events, the specialized nodal myocardial cells depolarize spontaneously, generating electrical impulses that are conducted to the larger mass of working myocardial cells (Fig. 1-11
). The sequential contraction of the atria and ventricles as coordinated units depends on the anatomic arrangement of the specialized cardiac conducting tissue. Small cardiac nerves, arteries, and veins lie close to the specialized conducting cells, providing neurohumoral modulation of cardiac impulse generation and conduction.
Keith and Flack9
first described the sinus node in 1907.9
The sinus node lies close to the epicardial surface of the heart, above the tricuspid valve, near the anterior entrance of the superior vena cava into the right atrium. The sinus node is also referred to as the sinoatrial node.
It is approximately 10 to 15 mm long, 3 to 5 mm wide, and 1 mm thick. Small nodal cells are surrounded by and interspersed with connective tissue. They merge with the larger working atrial muscle cells.
originally described an interatrial myocardial bundle conducting impulses from the right atrium to the left atrium. James12
presented evidence for three internodal conduction pathways
from the sinus node to the AV node. It is unclear whether the pathways have functional significance.13
It is generally believed that the cardiac impulse spreads from the sinus node to the AV node via cell-to-cell conduction through the atrial working myocardial cells.15
initially described the AV node in 1906. It is located subendocardially on the right atrial side of the central fibrous body, in the lower interatrial septal wall. The AV node is close to the septal leaflet of the tricuspid valve and anterior to the coronary sinus. A group of fibers connects the AV node to working myocardial cells in the left atrium.17
The AV node is approximately 7 mm long, 3 mm wide, and 1 mm thick.18
Nodal fibers are interspersed with normal working myocardial fibers; it is difficult to precisely identify the AV node boundaries. There are several zones of specialized conducting tissue in the AV junction area: the compact AV node, a transition zone containing small nodal and larger
working atrial myocardial cells, the penetrating AV bundle, and the branching AV bundle.19
Fibers from the AV node converge into a shaft termed the bundle of His
(also called the penetrating AV bundle
or common bundle
). It is approximately 10 mm long and 2 mm in diameter.18
The bundle of His passes from the lower right atrial wall anteriorly and laterally through the central fibrous body, which is part of the fibrous skeleton.
As first noted by His in 1893,21
the His bundle provides the only cellular connection between the atria and ventricles and is of pivotal functional importance. Cardiac impulse transmission is slowed at this site, providing time for atrial contraction to dispel blood from the atria into the ventricles. This slowing boosts ventricular volume and increases the cardiac output during subsequent ventricular contraction. At the membranous septal region of the heart, the right atrium and left ventricle are opposite each other across the septum, with the right ventricle in close proximity. Three of the four cardiac valves are nearby.22
Thus, pathology of the fibrous skeleton, tricuspid, mitral, or aortic valves can affect functioning of one or more of the other valves or may affect cardiac impulse conduction. Dysfunction of the AV conducting tissue may affect the coordinated functioning of the atria and ventricles.
Abnormal accessory pathways, termed Kent bundles,
occasionally join the atria and ventricles through connections outside the main AV node and His bundle.23
Tracts from the His bundle to upper interventricular septum (termed paraspecific fibers of Mahaim
) sometimes occur and are also abnormal.25
AV conduction is accelerated when impulses bypass the delay-producing AV junction and travel instead through these abnormal connections. When accelerated AV conduction occurs, cardiac output often decreases because there is inadequate time for atrial contraction to boost ventricular filling.27
The His bundle begins branching in the region of the crest of the muscular septum (Fig. 1-11
). The right bundle branch typically continues as a direct extension of the His bundle. The right bundle branch is a well-defined, single, slender group of fibers approximately 45 to 50 mm long and 1 mm thick. It initially courses downward along the right side of the interventricular septum, continues through the moderator band of muscular tissue near the right ventricular apex, and then continues to the base of the anterior papillary muscle. If a small segment of the bundle is damaged, the entire distal distribution is affected because of the right bundle’s thinness, length, and relative lack of arborization.
The left bundle branch arises almost perpendicularly from the His bundle as the common left bundle branch. This common left bundle, approximately 10 mm long and 4 to 10 mm wide, then divides into two discrete divisions, the left anterior bundle branch and the left posterior bundle branch. The left anterior bundle branch, or left anterior fascicle, is approximately 25 mm long and 3 mm thick. It usually arises directly from the common left bundle after the origin of the posterior fascicle and close to the origin of the right bundle. It branches to the anterior septum and courses over the left ventricular anterior (superior) wall to the anterior papillary muscle, crossing the aortic outflow tract. Anterior and septal myocardial infarctions and aortic valve dysfunction often affect the left anterior bundle branch.
The large, thick, left posterior bundle branch, or left posterior fascicle, arises either from the first portion of the common left bundle or from the His bundle directly. The left posterior fascicle goes inferiorly and posteriorly across the left ventricular inflow tract to the base of the posterior papillary muscle; it then spreads diffusely through the posterior inferior left ventricular free wall. It is approximately 20 mm long and 6 mm thick. This fascicle is often the least vulnerable segment of the ventricular conducting system because of its diffuseness, its location in a relatively protected nonturbulent portion of the ventricle, and its dual blood supply (Table 1-1
Three, rather than two, major divisions of the left bundle branch are sometimes found, with a group of fibers ramifying from the left posterior fascicle and terminating in the lower septum and apical ventricular wall.20
This trifascicular configuration of the bundles explains some conduction defects involving partial bundle-branch block. Sometimes instead of three discrete bundles the common left bundle fans out diffusely along the septum and the free ventricular wall.28
first described in 1845, form a complex network of conducting tissue ramifications that provide a continuation of the bundle branches in each ventricle.29
The Purkinje fibers course down toward the ventricular apex and then up toward the fibrous rings at the ventricular bases. They spread over the subendocardial ventricular surfaces and then spread from the endocardium through the myocardium; thus, spreading from inside outward, providing extensive contacts with working myocardial cells, and coupling myocardial excitation with muscular contraction.