Cardiac Anatomy and Physiology



Cardiac Anatomy and Physiology


Eleanor F. Bond*


*The material in this chapter was originally co-authored with Carol Jean Halpenny.



An understanding of cardiac anatomy is helpful for understanding cardiac physiology and the functional consequences of disease. This chapter describes normal human adult cardiac anatomy, cellular structure, and ultrastructure. The chapter also discusses electrical, mechanical, and metabolic activities that underlie cardiac pump performance. The coronary circulation is described and discussed in the context of its linkage to changing demands of cardiac tissue for nutrient delivery and waste removal. Finally, integrated cardiac performance is discussed.


GENERAL ANATOMIC DESCRIPTION

The heart is a hollow muscular organ encased and cushioned in its own serous membrane, the pericardium. It lies in the middle mediastinal compartment of the thorax between the two pleural cavities. Two thirds of the heart extends to the left of the body’s midline (Fig. 1-1).

The heart consists of four muscular chambers, two atria and two ventricles, and associated structures. The right heart (right atrium and ventricle) receives blood from the body and pumps it into the low-pressure pulmonary arterial system. The left heart (left atrium and ventricle) receives oxygenated blood from the lungs and pumps it into the high-pressure systemic arterial system. Interatrial and interventricular septa separate the right from the left atrium and the right from the left ventricle.

The long axis of the heart is directed obliquely, leftward, downward, and forward. Any factor changing the shape of the thorax changes the position of the heart and modifies its directional axis. Respiratory alterations in the diaphragm and the rib cage constantly cause small changes in the cardiac axis. With a deep inspiration, the heart descends and becomes more vertical. Factors that may cause long-term axis variations in healthy people include age, weight, pregnancy, body shape, and thorax shape. A tall, thin person usually has a more vertical heart, whereas a short, obese person usually has a more horizontal heart. Pathologic conditions of the heart, lungs, abdominal organs, and other structures influence the cardiac axis.

The surfaces of the heart are used to reference its position in relation to other structures and to describe the location of damage, as in a myocardial infarction. The right ventricle and parts of the right atrium and the left ventricle form the anterior (or sternocostal) cardiac surface (Figs. 1-1 and 1-2). The right atrium and ventricle lie anteriorly and to the right of the left atrium and ventricle in the frontal plane. Thus, when viewed from the front of the body, the heart appears to be lying sideways, directed forward and leftward, with the right heart foremost.

The small portion of the lower left ventricle that extends anteriorly forms a blunt tip composed of the apical part of the interventricular septum and the left ventricular free wall. Because of the forward tilt of the heart, movement of this apex portion of the left ventricle during cardiac contraction usually forms the point of maximal impulse, which can be observed in healthy people in the fifth intercostal space at the left midclavicular line, 7 to 9 cm from midline. The sternum, costal cartilages of the third to sixth ribs, part of the lungs, and, in children, the thymus, overlie the anterior cardiac surface.

The left atrium and a small section of the right atrium and ventricle comprise the base of the heart, which is directed backward and forms the posterior surface of the heart (Fig. 1-3). The thoracic aorta, esophagus, and vertebrae are posterior to the heart. The inferior or diaphragmatic surface of the heart, composed chiefly of the left ventricle, lies almost horizontally on the upper surface of the diaphragm (Fig. 1-4). The right ventricle forms a portion of the inferior cardiac surface.

The right atrium forms the lateral right heart border; therefore, the right atrium and right lung lie close together. The entire right margin of the heart extends laterally from the superior vena cava along the right atrium and then toward the diaphragm to the cardiac apex. The lateral wall of the left ventricle and a small part of the left atrium form most of the left heart border. This portion of the left ventricle is next to the left lung and sometimes is referred to as the pulmonary surface.

The coronary [or atrioventricular (AV)] sulcus (groove) is the external landmark denoting the separation of the atria from the ventricles. The AV sulcus encircles the heart obliquely and contains coronary blood vessels, cardiac nerves, and epicardial fat. The aorta and pulmonary artery interrupt the AV sulcus anteriorly. The anterior and posterior interventricular sulci separate the right and left ventricles on the external heart surface. The crux of the heart is the point on the external posterior heart surface where
the posterior interventricular sulcus intersects the coronary (AV) sulcus externally and where the interatrial septum joins the interventricular septum internally.






Figure 1-1 Location of the heart and pericardium. This dissection exposes the pericardialsac posterior to the body of the sternum from just superior to the sterna angel to the level of the xiphisternal joint. The pericardial sac is approximately one third to the right of the midsternal line and two thirds to the left. (From Moore, K. L., & Dalley, A. F. [2005]. Clinically oriented anatomy [5th ed., p. 145]. Philadelphia: Lippincott Williams & Wilkins.)

The average adult heart is approximately 12 cm long from its base at the beginning of the root of the aorta to the left ventricular apex. It is 8 to 9 cm transversely at its greatest width, and 6 cm thick anteroposteriorly. Tables have been derived to indicate normal ranges of heart size for various body weights and heights.1

The adult male heart comprises approximately 0.43% of body weight, typically 280 to 350 g, with an average weight of 300 g. The adult female heart comprises approximately 0.40% of body weight, 230 to 300 g, with an average weight of 250 g.2,3 Age, body build, frequency of physical exercise, and heart disease influence heart size and weight.






Figure 1-2 Anterior view of the heart, illustrating the cardiac structures. The pericardial sac has been cut open. (From Anatomical Chart Company, General Anatomy, 2008-05-14 0614, 2008-07-13 1449.)


CARDIAC STRUCTURES


Fibrous Skeleton

Four adjacent, dense, fibrous connective tissue rings, the annuli fibrosi, surround the cardiac valves and provide an internal supporting structure for the heart. The annuli are attached together and connected by a central fibrous core (Fig. 1-5). Each annulus and valve has a slightly different orientation, but the entire
connective tissue structure, termed the fibrous skeleton, is oriented obliquely within the mediastinum.






Figure 1-3 Posterior view of the heart. (From Anatomical Chart Company, General Anatomy, 2008-05-14 0614, 2008-07-13 1449.)

The fibrous skeleton divides the atria from the ventricles. It provides the attachment site for some of the atrial and ventricular cardiac muscle fibers. A portion of the fibrous skeleton extends downward between the right atrium and left ventricle, forming the upper or membranous part of the interventricular septum.






Figure 1-4 Inferior or diaphragmatic heart surface.






Figure 1-5 Schematic view of the fibrous skeleton, illustrating the attachment of the cardiac valves and chambers. The four annuli and their extensions lie in different planes, so it is impossible to depict them accurately on a plane surface. T, tricuspid valve; M, mitral valve; A, aortic valve; P, pulmonic valve. (Adapted from Rushmer, R. F. [1976]. Cardiovascular Dynamics [p. 77]. Philadelphia: WB Saunders.)



Chambers

The wall thickness of each of the four cardiac chambers reflects the amount of force generated by that chamber. The two thin-walled atria serve functionally as reservoirs and conduits for blood that is being funneled into the ventricles; they add a small amount of force to the moving blood. The left ventricle, which adds the greatest amount of energy to the flowing blood, is two to three times as thick as the right ventricle. The approximate normal wall thicknesses of the chambers are as follows: right atrium, 2 mm; right ventricle, 3 to 5 mm; left atrium, 3 mm; and left ventricle, 13 to 15 mm.

The interatrial septum between right and left atria extends obliquely forward from right to left. The interatrial septum includes the fossa ovalis, a remnant of a fetal structure, the foramen ovale. The lower portion of the interatrial septum is formed by the lower medial right atrial wall on one side and the aortic outflow tract of the left ventricular wall on the other side. The lower muscular portion of the interventricular septum extends downward from the upper membranous part of the interventricular septum. The clinical significance of these structures has recently received much attention. A pooled analysis of autopsy studies found that the prevalence of patent foramen ovale in adults is approximately 26%.4 This is clinically significant, providing a potential conduit for a shunt from the right atrium to the left atrium and possibly accounting for increased risk of stroke5 and migraine headache.6

In considering the internal surfaces of the cardiac chambers, it is useful to remember that blood flows more smoothly and with less turbulence across walls that are smooth rather than ridged. Blood pools in appendages or other areas out of the direct blood flow path.






Figure 1-6 Schematic diagram of the right interior view of the heart. (From Anatomical Chart Company, General Anatomy, 2008-05-14 0614, 2008-07-16 2010.)


Right Heart

The posterior and septal right atrial walls are smooth, whereas the lateral wall and the right atrial appendage (auricle) have parallel muscular ridges, termed pectinate muscles. The right auricle extends over the aortic root externally.

The inferior wall of the right atrium and part of the superior wall of the right ventricle are formed by the tricuspid valve (Fig. 1-6). The anterior and inferior walls of the right ventricle are lined by muscle bundles, the trabeculae carneae, which form a roughwalled inflow tract for blood. One muscle group, the septomarginal trabecula or moderator band, extends from the lower interventricular septum to the anterior right ventricular papillary muscle.

Another thick muscle bundle, the christa supraventricularis, extends from the septal wall to the anterolateral wall of the right ventricle. The christa supraventricularis helps to divide the right ventricle into an inflow and outflow tract. The smooth-walled outflow tract, called the conus arteriosus or infundibulum, extends to the pulmonary artery.

The concave free wall of the right ventricle is attached to the slightly convex septal wall. The internal right ventricular cavity is crescent or triangle shaped. The right ventricle also forms a crescent laterally around the left ventricle. Right ventricular contraction causes the right ventricular free wall to move toward the interventricular septum. This bellows-like action is effective in ejecting large and variable volumes into a low-pressure system (Fig. 1-7).

Venous blood enters the right atrium from the upper and the lower posterior parts of the atrium through the superior and
inferior venae cavae. Most of the venous drainage from the heart enters the right atrium through the coronary sinus, which is located between the entrance of the inferior vena cava into the right atrium and the orifice of the tricuspid valve. Blood flows medially and anteriorly from the right atrium through the tricuspid orifice into the right ventricle.






Figure 1-7 Right and left ventricular contraction. (A) Right ventricular contraction. Right ventricular ejection of blood is accomplished primarily by shortening and movement of the free wall toward the interventricular septum. Note the crescent shape of the right ventricle. (B) Blood is ejected from the left ventricle primarily by a reduction in the diameter of the chamber. There is some ventricular shortening. (Adapted from Rushmer, R. [1976]. Cardiovascular dynamics [p. 92]. Philadelphia: WB Saunders.)

Blood enters the right ventricle in an almost horizontal but slightly leftward, anterior, and inferior direction. It is ejected superiorly and posteriorly through the pulmonary valve (Fig. 1-8).


Left Heart

The left atrium is a cuboid structure that lies between the aortic root and the esophagus. The left atrial appendage, or auricle, extends along the border of the pulmonary artery. The walls of the left atrium are smooth except for pectinate muscle bundles in the atrial appendage.

The left ventricle has a cone-like or oval shape, bordered by the generally concave left ventricular free wall and interventricular septum. The mitral valve and its attachments form the left ventricular inflow tract. The outflow tract is formed by the anterior surface of the anterior mitral valve cusp, the septum, and the aortic vestibule. The lower muscular interventricular septum and free walls of the left ventricle are deeply ridged with trabeculae carneae muscle bundles, so most of the interior surface of the ventricle is rough. The upper membranous septum and aortic vestibule region have smooth walls. The interventricular septum is functionally and anatomically a more integral part of the left ventricle than the right ventricle. The septum is triangular, with its base at the aortic area. The upper septum separates the right atrium from the left ventricle and is often called the AV septum.

Blood is ejected from the left ventricle mainly by circumferential contraction of the muscular wall, that is, by decreasing the diameter of the cylinder (see Fig. 1-7). There is some longitudinal shortening. The ventricular cavity has a small surface area in relation to the volume contained, but high pressure can be developed because of the amount of ventricular muscle, the shape of the cavity, and the way the muscles contract.

Four pulmonary veins return blood from the lungs to openings in the posterolateral wall of the left atrium. Blood is directed obliquely forward out of the left atrium and enters the left ventricle
in an anterior, leftward, and inferior direction. Blood flows out of the ventricle from the apex toward the aorta in a superior and rightward direction (Fig. 1-8).






Figure 1-8 Blood flow through cardiac chambers and valves.

Thus, blood flows from posterior orifices into both ventricles in a leftward direction and is ejected superiorly toward the center of the heart. The right ventricular outflow tract is more tubular; the left ventricular outflow tract more conical (Fig. 1-8).


Valves


Atrioventricular Valves

The AV tricuspid and bicuspid (mitral) valve complexes are composed of six components that function as a unit: the atria, the valve rings or annuli fibrosi of the fibrous skeleton, the valve cusps or leaflets, the chordae tendineae, the papillary muscles, and the ventricular walls (Fig. 1-6). The mitral and tricuspid valve cusps are composed of fibrous connective tissue covered by endothelium. They attach to the fibrous skeleton valve rings. Fibrous cords called chordae tendineae connect the free valve margins and ventricular surfaces of the valve cusps to papillary muscles and ventricular walls. The papillary muscles are trabeculae carneae muscle bundles oriented parallel to the ventricular walls, extending from the walls to the chordae tendineae (Fig. 1-6). The chordae tendineae provide many cross-connections from one papillary muscle to the valve cusps or from trabeculae carneae in the ventricular wall directly to valves.

In the adult, the tricuspid orifice is larger (approximately 11 cm in circumference, or capable of admitting three fingers) than the mitral orifice (approximately 9 cm in circumference, or capable of admitting two fingers). The combined surface area of the AV valve cusps is larger than the surface area of the valvular orifice because the cusps resemble curtain-like, billowing flaps.

Most commonly, there are three tricuspid valve cusps: the large anterior, the septal, and the posterior (inferior). There are usually two principal right ventricular papillary muscles, the anterior and the posterior (inferior), and a smaller set of accessory papillary muscles attached to the ventricular septum.

The arrangement of the two triangular bicuspid valve cusps has been compared to a bishop’s hat, or miter; hence the structure is called the “mitral” valve. The smaller, less mobile posterior cusp is situated posterolaterally, behind, and to the left of the aortic opening. The larger, more mobile anterior cusp extends from the anterior papillary muscle to the ventricular septum.

The left ventricle most commonly has two major papillary muscles: the posterior papillary muscle attached to the diaphragmatic ventricular wall and the anterior papillary muscle attached to the sternocostal ventricular wall. Thus, the posteromedial papillary muscle extends to the posterolateral valve leaflet, and the anterolateral papillary muscle extends to the anteromedial valve leaflet. Chordae tendineae from each papillary muscle go to both mitral cusps.

During diastole, the AV valves open passively when pressure in the atria exceeds that in the ventricles. The papillary muscles are relaxed. The valve cusps part and project into the ventricle, forming a funnel and thus promoting blood flow into the ventricles (Fig. 1-8). Toward the end of diastole, the deceleration of blood flowing into the ventricles, the movement of blood in a circular motion behind the cusps, and the increasing pressures in the ventricle compared with lessening pressures in the atria, help to close each valve. During systole, the free edges of the valve cusps are prevented from being everted into the atria by contraction of the papillary muscles and tension in the chordae tendineae. Thus, in the normal heart, blood is prevented from flowing backward into the atria despite the high systolic ventricular pressures.


Semilunar Valves

The two semilunar (pulmonary [or pulmonic] and aortic) valves are each composed of three cup-shaped cusps of approximately equal size that attach at their base to the fibrous skeleton. The valve cusps are convex from below, with thickened nodules at the center of the free margins.

The cusps are composed of fibrous connective tissue lined with endothelium. The endothelial lining on the nonventricular side of the valves closely resembles and merges with that of the intima of the arteries beyond the valves. The aortic cusps are thicker than the pulmonic; both are thicker than the AV cusps.

The pulmonary valve orifice is approximately 8.5 cm in circumference. The pulmonic valve cusps are termed right anterior (right), left anterior (anterior), and posterior (left). The aortic valve is approximately 7.5 cm in circumference. The sinuses of Valsalva are pouch-like structures immediately behind each semilunar cusp. The coronary arteries branch from the aorta from two of the pouches or sinuses of Valsalva. The aortic cusps are designated by the name of the nearby coronary artery: right coronary (right or anterior) aortic cusp, left coronary (left or left posterior) aortic cusp, and noncoronary (posterior or right posterior) aortic cusp.

The aortic and pulmonic semilunar valves are approximately at right angles to each other in the closed position. The pulmonic valve is anterior and superior to the other three cardiac valves. When closed, the semilunar valve cusps contact each other at the nodules and along crescent arcs, called lunulae, below the free margins. During systole, the cusps are thrust upward as blood flows from an area of greater pressure in the ventricle to an area of lesser pressure in the aorta or the pulmonary artery. The effect of the deceleration of blood in the aorta during late systole on small circular currents of blood in the sinuses of Valsalva helps passively to close the semilunar valve cusps. Backflow into the ventricles during diastole is prevented because of the cusps’ fibrous strength, their close approximation, and their shape.


CARDIAC TISSUE

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. [2006]. 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.


Myocardium

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.7,8 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. [1969]. 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.


Endocardium

The endocardium is composed of a layer of endothelial cells and a few layers of collagen and elastic fibers. The endocardium is continuous with the tunica intima of the blood vessels.


Conduction Tissues

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 1907.9,10 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.

Bachmann11 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.13,14 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

Tarawa16 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.19,20

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.23,24 Tracts from the His bundle to upper interventricular septum (termed paraspecific fibers of Mahaim) sometimes occur and are also abnormal.25,26 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

Purkinje fibers, 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.


CORONARY CIRCULATION

The heart is continuously active. Like all tissues, it must receive oxygen and metabolic substrates; carbon dioxide and other wastes must be removed to maintain aerobic metabolism and contractile activity. However, unlike other tissues, it must generate the force to power its own perfusion. The heart requires continuous perfusion.


Coronary Arteries

The major coronary arteries in humans are the right coronary artery and the left coronary artery, sometimes called the left main coronary artery. These arteries branch from the aorta in the region of the sinus of Valsalva (Figs. 1-12 and 1-13). They extend over the epicardial surface of the heart and branch several times. The branches usually emerge at right angles from the parent artery.30 The arteries plunge inward through the myocardial wall and undergo further branching. The epicardial branches exit first. The more distal branches supply the endocardial (internal) myocardium. The arteries continue branching and eventually become arterioles, then capillaries. Partially because the blood supply originates more distally, the endocardium is more vulnerable to compromised blood supply than is the epicardial surface.

There is much individual variation in the pattern of coronary artery branching. In general, the right coronary artery supplies the right atrium and ventricle. The left coronary artery supplies much of the left atrium and ventricle. The following discussion describes the most common arterial pattern. Table 1-1 lists the major cardiac structures, their usual arterial supply, and some common variations (e.g., either the right or the left coronary artery may supply the AV node).









Table 1-1 ▪ AREA SUPPLIED BY COMMON ARTERIES*















































































































Structure


Usual Arterial Supply


Common Variants


Right atrium


Sinus node artery, branch of RCA (55%)


Sinus node artery, branch of L circumflex (45%)


Left atrium


Major L circumflex


Sinus node artery, branch of L circumflex (45%)


Right ventricle



Anterior


Major RCA




Minor LAD



Posterior


Major RCA; posterior descending branch of RCA


Posterior descending may branch from L circumflex (10%)




Minor LAD (ascending portion)


LAD terminates at apex (40%)


Left Ventricle



Posterior (diaphragmatic)


Major L circumflex, posterior descending branch of RCA


Posterior descending may branch from L circumflex (10%)




Minor LAD (ascending portion)


LAD terminates at apex (40%)



Anterior


L coronary artery; L circumflex and LAD



Apex


Major LAD


Intraventricular septum


Major septal branches of LAD


Minor posterior descending may branch from L circumflex, AV nodal may branch from L circumflex




Minor posterior descending branch of RCA and AV nodal branch of RCA


Left ventricular papillary muscles



Anterior


Diagonal branch of LAD; other branches of LAD, other branches of L circumflex


Diagonal may branch from circumflex



Posterior


RCA and L circumflex


RCA and LAD


Sinus node


Nodal artery from RCA (55%)


Nodal artery from L circumflex (45%)


AV node


RCA (90%)


L circumflex (10%)


Bundle of His


RCA (90%)


L circumflex (10%)


Right bundle


Major LAD septal branches




Minor AV nodal artery


Left anterior bundle


Major LAD septal branches




Minor AV nodal artery


Left posterior bundle


LAD septal branches and AV nodal artery



*Percentages in parentheses denote frequency of occurrence in autopsy studies.

Major and minor refer to degree of predominance of an artery in perfusing a structure.


RCA, right coronary artery; LAD, left anterior descending artery; L, left; LV, left ventricle; AV, atrioventricular.


Data from James, T. N. (1961). Anatomy of the coronary arteries. New York: Paul B. Hoeber; James, T. N. (1978). Anatomy of the coronary arteries and veins. In J. W. Hurst (Ed.), The heart (4th ed., pp. 32-47). New York: McGraw-Hill.


Individual anatomic variation should be considered in analyzing patient data. For example, angiographic visualization of the left circumflex artery might show severe stenosis. Although it is not likely that AV node and His bundle perfusion would be affected (because the right coronary artery typically perfuses these structures), in approximately 10% of cases the structures would be at risk. Thus, angiographic information is validated with clinical data. Also, apparently attenuated or narrowed vessels may be normal anatomic variants.






Figure 1-12 Principal arteries and veins on the anterior surface of the heart. Part of the right atrial appendage has been resected. The left coronary artery arises from the left coronary aortic sinus behind the pulmonary trunk. RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle. (Adapted from Walmsley, R., & Watson, H. [1978]. Clinical anatomy of the heart [p. 203]. New York: Churchill Livingston.)


Vessel Dominance

Dominance (or preponderance), a term commonly used in describing coronary vasculature, refers to the distribution of the terminal portion of the arteries. The artery that reaches and crosses the crux
(where the right and left AV grooves cross the posterior interatrial and interventricular grooves) is said to be dominant. In approximately 85% of cases, the right coronary artery crosses the crux and this is “dominant.” The term can be confusing because in most human hearts, the left coronary artery is of wider caliber and perfuses the largest proportion of myocardium. Thus, the dominant artery usually does not perfuse the largest percentage of myocardial mass. The dominant artery supplies the posterior diaphragmatic interventricular septum and diaphragmatic surface of the left ventricle.






Figure 1-13 Principal arteries and veins on the inferoposterior surfaces of the heart. This schematic drawing illustrates the heart tilted upward at a nonphysiological angle; normally, little of the inferior cardiac surface is visible posteriorly. The right coronary artery is shown to cross the crux and to supply the atrioventricular node. The artery to the sinus node in this figure arises from the right coronary artery. FA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle. (Adapted from Wamsley, R., & Watson, H. [1978]. Clinical anatomy of the heart [p. 205]. New York: Churchill Livingston.)


Right Coronary Artery

The right coronary artery supplies the right atrium, right ventricle, and a portion of the posterior and inferior surfaces of the left ventricle. It supplies the AV node and bundle of His in 90% of hearts, and the sinus node in 55% of hearts.30 It originates behind the right aortic cusp and passes behind the pulmonary artery, coursing in the right AV groove laterally to the right margin of the heart and then posteriorly. The major branches of the right coronary artery, in order of origin, are as follows:



  • Conus branch


  • Sinus node artery


  • Right ventricular branches


  • Right atrial branch


  • Acute marginal branch


  • AV nodal branch


  • Posterior descending branch


  • Left ventricular branch


  • Left atrial branch

The conus branch is small; in 60% of cases it exits within the first 2 cm of the right coronary artery. It sometimes originates as a separate vessel with an ostium within a millimeter of the right coronary artery.31 The branch proceeds centrally to the left of the pulmonic valve. It supplies the upper part of the right ventricle, near the outflow tract at the level of the pulmonic valve. When the conus branch anastomoses with a right ventricular branch of the left anterior descending artery, the resulting structure is called the circle of Vieussens, an important collateral link between left and right coronary arteries.

The sinus node artery arises from the right coronary artery in 55% of cases.31 It proceeds in the opposite direction from the conus branch, coursing cranially and to the right, encircling the superior vena cava. It usually has two branches: one supplies the sinus node and parts of the right atrium and the other branches to the left atrium.

The right coronary artery courses along the AV groove, giving rise next to one or more right ventricular branches that vary in length and distribute to the right ventricular wall. The right atrial branch proceeds cranially toward the right heart border and it perfuses the right atrium.

The acute marginal branch is a fairly large branch of the right coronary artery. It originates at the acute margin of the heart near the right atrial artery and courses in the opposite direction, toward the apex. It perfuses the inferior and diaphragmatic surfaces of the right ventricle and occasionally the posterior apical portion of the interventricular septum.

The AV nodal branch is slender and straight. It originates at the crux and is directed inward toward the center of the heart. It perfuses the AV node and the lower portion of the interatrial septum.

The posterior descending branch is an important branch of the right coronary artery. It supplies the posterosuperior portion of the interventricular septum. It exits at the crux and courses in the posterior interventricular sulcus.

The left ventricular branch originates just beyond the crux. It runs centrally in the angle formed by the left posterior AV groove and the posterior interventricular sulcus. It perfuses the diaphragmatic aspect of the left ventricle.

A left atrial branch may course in the posterior left AV groove, perfusing the left atrium.


Left Coronary Artery

The left main coronary artery arises from the aorta in the ostium behind the left cusp of the aortic valve. This artery passes between the left atrial appendage and the pulmonary artery. Typically, it then divides into two major branches: the left anterior descending artery and left circumflex artery.


Left Anterior Descending Artery.

The left anterior descending artery supplies portions of the left and right ventricular
myocardium and much of the interventricular septum. The left anterior descending artery appears to be a continuation of the left main coronary artery. It passes to the left of the pulmonic valve region, courses in the anterior interventricular sulcus to the apex, and then courses around the apex to terminate in the inferior portion of the posterior interventricular sulcus. Occasionally, the posterior descending branch of the right coronary artery extends around the apex from the posterior surface and the left anterior descending artery ends short of the apex. The major branches of the left anterior descending artery, in the order in which they branch, are the following:



  • First diagonal branch


  • First septal branch


  • Right ventricular branch


  • Minor septal branches


  • Second diagonal branch


  • Apical branches

The first diagonal branch is usually a large artery. It originates close to the bifurcation of the left main coronary artery and passes diagonally over the free wall of the left ventricle. It perfuses the high lateral portion of the left ventricular free wall. Several smaller diagonal branches may exit from the left side of the left anterior descending artery and run parallel to the first diagonal branch. The one referred to as the second diagonal branch takes its origin approximately two thirds of the way from the origin to the termination of the left anterior descending artery. This second diagonal branch perfuses the lower lateral portion of the free wall to the apex.

The number of septal branches varies. The first septal branch is the first to exit the left anterior descending artery. The others are referred to as minor septal branches. The septal branches exit at a 90-degree angle. They then course into the septum from front to the back and caudally. Together, the septal branches perfuse two thirds of the upper portion of the septum and most of the inferior portion of the septum. The remaining superoposterior section of the septum is supplied by branches from the posterior descending artery, which usually derives from the right coronary artery.

There can be one or more right ventricular branches. One branch runs toward the conus branch of the right coronary artery; it can anastomose into the circle of Vieussens.

The final branches are the apical branches. These branches perfuse the anterior and diaphragmatic aspects of the left ventricular free wall and apex.


Circumflex Artery.

The circumflex artery supplies blood to parts of the left atrium and left ventricle. In 45% of cases, the circumflex artery supplies the major perfusion of the sinus node; in 10% of cases, it supplies the AV node.31 The circumflex artery exits from the left main coronary artery at a near-right angle and courses posteriorly in the AV groove toward, but usually not reaching, the crux. If the circumflex reaches the crux, it gives rise to the posterior descending artery. In the 15% of cases in which this occurs, the left coronary artery supplies the entire septum and possibly the AV node.31 The branches of the circumflex artery, in order of origin, are as follows:



  • Atrial circumflex branch


  • Sinus node artery


  • Obtuse marginal branches


  • Posterolateral branches

The atrial circumflex branch is usually small in caliber but sometimes is as wide as the remaining portion of the circumflex. It runs along the left AV groove, perfusing the left atrial wall.

In 45% of cases, the sinus node artery originates from the initial portion of the circumflex; it runs cranially and dorsally, to the base of the superior vena cava in the region of the sinus node.31 This artery perfuses portions of the left and right atria as well as the sinus node.

There are between one and four obtuse marginal branches. These branches vary greatly in size. They run along the ventricular wall laterally and posteriorly, toward the apex, along the obtuse margin of the heart. The marginal branches supply the obtuse margin of the heart and the adjacent posterior wall of the left ventricle above the diaphragmatic surface.

The posterolateral branches arise from the circumflex artery in 80% of cases.31 These branches originate in the terminal portion of the circumflex artery and course caudally and to the left on the posterior left ventricular wall, supplying the posterior and diaphragmatic wall of the left ventricle.

The posterior descending and AV nodal arteries occasionally arise from the circumflex. When they do, the entire septum is supplied by branches of the left coronary artery.


Coronary Capillaries

Blood passes from arteries into arterioles, then into capillaries, where exchange of oxygen, carbon dioxide, metabolic compounds, and waste materials takes place. The heart has a dense capillary network with approximately 3,300 capillaries per mm2 or approximately 1 capillary per muscle fiber.32 Blood flow through coronary capillaries is regulated according to myocardial metabolic needs.

When myocardial cells hypertrophy, the cell radius increases. The capillary network; however, does not appear to proliferate.33 The same capillaries must perfuse a larger tissue mass. The diffusion distance is increased. Thus, with hypertrophy, the mass of tissue to be perfused is increased but the efficiency of exchange is diminished.


Coronary Veins

Most of the venous drainage of the heart is through epicardial veins. The large veins course close to the coronary arteries. Two veins sometimes accompany an artery.30 The major veins feed into the great cardiac vein, which runs alongside the circumflex artery, becomes the coronary sinus, and then empties into the right atrium (Fig. 1-13). An incompetent (incompletely shut) semilunar valve, called the valve of Vieussens, marks the junction between the great cardiac vein and the coronary sinus. A similar structure, the Thebesian valve, is also incompetent and is found at the entry of the coronary sinus into the right atrium. Venous blood from the right ventricular muscle is drained primarily by two to four anterior cardiac veins that empty directly into the right atrium, bypassing the coronary sinus (Fig. 1-12).

The Thebesian veins empty directly into the ventricles (Fig. 1-14). These are more common on the right side of the heart, where the pressure gradient is favorable for such flow. Only a small amount of venous blood is returned directly to the left ventricle. When blood is returned to the left ventricle, this flow is a component of physiologic shunt, or unoxygenated blood entering the systemic circulation. Many collateral channels are found in the venous drainage system.







Figure 1-14 Schematic model of coronary circulation. As in other circulatory beds, the coronary circulation includes arteries, capillaries, and veins. Some veins drain directly into the ventricles. Collateral channels may link arterial vessels. Art, arterial. (Adapted from Ruch, T. C., & Patton, H. D. [1974]. Physiology and biophysics [20th ed., Vol 2, p. 249]. Philadelphia: WB Saunders.)


Lymph Drainage

Cardiac contraction promotes lymphatic drainage in the myocardium through an abundant system of lymphatic vessels, most of which eventually converge into the principal left anterior lymphatic vessel. Lymph from this vessel empties into the pretracheal lymph node and then proceeds by way of two channels to the cardiac lymph node, the right lymphatic duct, and then into the superior vena cava.34

The importance of a normally functioning lymphatic system in maintaining an appropriate environment for cardiac cell function is frequently overlooked. Although complete cardiac lymph obstruction is rarely observed, experimental acute and chronic lymphatic impairment causes myocardial and endocardial cellular changes, particularly when occurring in conjunction with venous congestion.34 Experimentally induced myocardial infarction in animals with chronically impaired lymphatic drainage causes more extensive cellular necrosis, an increased and prolonged inflammatory response, and a greater amount of fibrosis than infarction in animals without lymphatic obstruction.34


CARDIAC INNERVATION

Sensory nerve fibers from ventricular walls, the pericardium, coronary blood vessels, and other tissues transmit impulses by way of the cardiac nerves to the central nervous system. Motor nerve fibers to the heart are autonomic. Sympathetic stimulation accelerates firing of the sinus node, enhances conduction through the AV node, and increases the force of cardiac contraction. Parasympathetic stimulation slows the heart rate, slows conduction through the AV node, and may decrease ventricular contractile force.

Sympathetic preganglionic cardiac nerves arise from the first four or five thoracic spinal cord segments. The nerves synapse with long postganglionic fibers in the superior, middle, and cervicothoracic or stellate ganglia adjacent to the spinal cord. Most postganglionic sympathetic nerves to the heart travel through the superior, middle, and inferior cardiac nerves. However, several cardiac nerves with variable origins have been identified.33,35 Parasympathetic preganglionic cardiac nerves arise from the right and left vagus nerves and synapse with postganglionic nerves close to their target cardiac cells.

Both vagal and sympathetic cardiac nerves converge in the cardiac plexus. The cardiac plexus is situated superior to the bifurcation of the pulmonary artery, behind the aortic arch, and anterior to the trachea at the level of tracheal bifurcation. From the cardiac plexus, the cardiac nerves course in two coronary plexuses along with the right and left coronary blood vessels.

Sympathetic fibers are richly distributed throughout the heart. Right sympathetic ganglia fibers most commonly innervate the sinus node, the right atrium, the anterior ventricular walls, and to some extent the AV node. Most commonly, left sympathetic ganglia fibers extensively innervate the AV junctional area and the posterior and inferior left ventricle.35

A dense supply of vagal fibers innervates the sinus node, AV node, and ventricular conducting system. Consequently, many parasympathetic ganglia are found in the region of the sinus and AV nodes. Vagal fibers also innervate both atria and, to a lesser extent, both ventricles.35 Right vagal fibers have more effect on the sinus node; left vagal fibers have more effect on the AV node and ventricular conduction system. However, there is overlap. The clinical importance of vagal stimulation for ventricular function continues to be debated. Although neurotransmitters from cardiac nerves are important modulators of cardiac activity, the success of cardiac transplantation illustrates the capacity of the heart to function without nervous innervation.


MYOCARDIAL CELL STRUCTURE

Myocardial cells are long, narrow, and often branched. A limiting membrane, the sarcolemma, surrounds each cell. Specialized surface membrane structures include the intercalated disc, nexus, and transverse tubules (T-tubules). Major intracellular components are contractile protein filaments (called myofibrils), mitochondria, sarcoplasmic recticulum (SR), and nucleus. There is a small amount of cytoplasm, called sarcoplasm (Fig. 1-15).

The cell membrane or sarcolemma separates the intracellular and extracellular spaces. The sarcolemma is a thin phospholipid bilayer studded with proteins. Across the barrier of the sarcolemma are marked differences in ionic composition and electrical charge. The embedded proteins serve multiple functions. Embedded receptors bind extracellular substances; this binding in turn activates or inhibits cell electrical, contractile, metabolic, or other functions. Embedded ion channels regulate membrane ion permeability and electrical function. Various carrier proteins facilitate uptake of metabolic substrates such as glucose. Some sarcolemma proteins add structural stability, anchoring the cell’s internal and external structural elements.

Structurally, each myocardial cell is distinct. An intercalated disc forms a junction between adjacent cells. A specialized type of cell-to-cell connection, the nexus (sometimes called the gap junction), is present in the intercalated disc. The nexus is the site of direct exchange of small molecules. The nexus also provides a low-resistance electrical path between cells, thus facilitating rapid impulse conduction. Physiologic conditions alter the permeability of the nexus. For example, two substances that vary with physiological state are adenosine triphosphate (ATP)-dependent and cyclic adenosine monophosphate (cAMP)-dependent protein kinases. Both alter nexus permeability.36,37 Because of these
junctions, the heart functions as a syncytium of electrically coordinated cells, although anatomically the cells are discrete.






Figure 1-15 The microscopic structure of working myocardial cells. (A) Working myocardial cells as seen under the light microscope. Note the branching network of fibers and intercalated discs. (B) Schematic illustration of the internal structure of the working myocardial cell. Note the striated appearance of the myofibrils, the intimate association of the sarcoplasmic reticulum (SR) with the myofibrils, the presence of T-tubules, and the large number of mitochondria. (C) Structure of the sarcomere, illustrating alignment of thick and thin filaments. Cross sections taken at three different positions along the sarcomere illustrate a region with only thick filaments, a region with only thin filaments, and a region of overlap where the thick and the thin filaments interdigitate. (Adapted from Braunwald, E., Ross, J., & Sonneblick, E. [1976]. Mechanisms of contraction of the normal and failing heart [2nd ed., p. 3]. Boston: Little, Brown.)

Another specialized membrane structure, the T-tubule system, is an extensive network of membrane-lined tubes systematically tunneling inward through each cell. T-tubules are formed by sarcolemma invaginations and are continuous with the surface membrane. The T-tubule lumen contains extracellular fluid. The T-tubular network carries electrical excitation to the central portions of myocardial cells, allowing near-simultaneous activation of deep and superficial parts of cells.

Myofibrils are long, rod-like structures that extend the length of the cell. They contain the contractile proteins, which convert the chemical energy of ATP into mechanical energy and heat. Muscle contraction involves generation of force, shortening, or both. The orderly alignment of contractile proteins into myofilaments gives the myocardial cell its striated (striped) appearance.

Mitochondria are small, rod-shaped membranous structures located within the cell. Substrate breakdown and high-energy compound synthesis occurs within the mitochondria. The relative abundance of mitochondria in cardiac muscle cells reflects the high level of biochemical activity required to support the heart’s continuous contractile activity.

The SR is an extensive, self-contained internal membrane system. The T-tubules and SR link membrane depolarization to the mechanical activity of the contractile protein filaments. This functional coordination is called excitation-contraction coupling. The SR is the major storage depot for calcium ion, which releases then takes up calcium ions with each contraction of the heart.

The nucleus contains the genetic material of the cell. The nucleus is the site where new proteins are synthesized.


MYOCARDIAL CELL ELECTRICAL CHARACTERISTICS

There is an electrical potential difference across the sarcolemma; it is measured in millivolts (mV). During the interim between excitations, the intracellular space is negative compared with the extracellular space. This potential difference is called the membrane resting potential. During excitation, the potential difference changes: the inside of the cell becomes less negative or slightly positive compared with the extracellular space. This type of potential difference change is called depolarization. After depolarization, the cell membrane repolarizes, or returns to the resting potential value. The normal depolarization-repolarization cycle is known as the action potential. The action potential is the signal evoking contraction. Until the cell repolarizes sufficiently, there can be no action potential. If the potential difference becomes more negative than the usual resting potential, the membrane is said to be hyperpolarized. The more hyperpolarized the membrane, the more current is required to evoke an action potential.

Some myocardial cells have automaticity, that is, an intrinsic ability to depolarize spontaneously and initiate an action potential. The action potential generated in such a cell is then propagated throughout cardiac tissue. Depolarization of one cardiac cell initiates depolarization of adjacent cells and evokes contraction.

There are approximately 19 billion cells in the adult heart; these cells must depolarize in an orderly sequence if the heart is to undergo a coordinated contraction that is able to add force to moving blood. Impulses generated in ectopic sites in the heart are less likely to depolarize in an orderly sequence and less likely to contract in an orderly fashion that effectively pumps blood.


Basis for Myocardial Excitation: Characteristics of Biologic Membranes

Intracellular and extracellular spaces are separated by a thin insulating membrane, the sarcolemma. These spaces have very different ionic compositions. The intracellular space contains high concentrations of potassium ion (positively charged) and protein (negatively charged) and has low concentration of sodium ion (positively charged). The extracellular space consists of high concentrations of sodium ion and chloride ion (negatively charged); extracellular potassium ion concentration is low.









Table 1-2 ▪ APPROXIMATE INTRACELLULAR AND EXTRACELLULAR ION CONCENTRATIONS AND ACTIVITIES IN CARDIAC MUSCLE*








































Ion


Extracellular Concentration


Intracellular Concentration§11


Ratio of Extracellular to Intracellular Concentration


E1


Intracellular Activity#


Na+


145 mM


15 mM


9.7


+60 mV


7.0 mM


K+


4 mM


150 mM


0.027


−94 mV


125 mM


Cl


120 mM


5 mM


24


−83 mV


15 mM


Ca2+


2 mM


10−4M


2 × 104


+129 mV


8 × 10−6 mM


*Values given are approximations and vary according to the cardiac tissue, species, and method used for measurement.

Na+, sodium; K+, potassium; Cl, chloride; Ca2+, calcium.

mM, millimolar.

§11 Most of the intracellular calcium is bound to proteins or sequestered in intracellular organelles; thus, total intracellular calcium content approximates 1 to 2 mm. During contraction, measurable intracellular calcium concentration approximates 10−5 mm.

E1, equilibrium potential; mV, millivolt.

# Median values from summarized data; these values should be considered as subject to revision. Concentrations and equilibrium potentials from Sperelakis, N. (1979). Origin of the cardiac resting potential. In R. M. Berne (Ed.), Handbook of physiology, section 2: The cardiovascular system, vol 1, the heart (p. 193). Bethesda: American Physiological Society. Activities are approximations from Lee, C. O. (1981). Ionic activities in cardiac muscle cells and application of ion-sensitive microelectrodes, American Journal of Physiology, 10, H461, H464 and Fozzard, H. A., & Wasserstrom, J. A. (1985). Voltage dependence of intracellular sodium and control of contraction. In P. P. Zipes, & J. Jalife. Cardiac electrophysiology and arrhythmias (p. 52.). Orlando: Grune & Tratton.

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Jan 10, 2021 | Posted by in NURSING | Comments Off on Cardiac Anatomy and Physiology

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