Cardiovascular System and Lymphatic Vessels


Cardiovascular System and Lymphatic Vessels


Development of the Heart and Great Vessels

The heart is a conical, muscular organ that in mammals has evolved into a four-chambered pump with four valves. During early fetal development, it is converted from an elongated muscular tube into a C-shaped structure by a process termed looping (Fig. 10-1). Subsequently, septation occurs to produce the right and left atrial and ventricular chambers and separation of the common truncus arteriosus into the aorta and pulmonary artery, respectively. The heart is interposed as a pump into the vascular system, with the right side supplying the pulmonary circulation and the left side the systemic circulation (Web Fig. 10-1; also see Chapter 2). The vascular system is subdivided into arterial, capillary, venous, and lymphatic segments. The arteries are classified into three types: elastic arteries, muscular arteries, and arterioles. The venous vessels are termed venules and veins. The lymphatic vasculature includes lymphatic capillaries and lymphatic vessels. Interposed between the arterial and venous segments are the capillary beds. A vascular segment termed the microcirculation (systemic capillary beds) includes arterioles, capillaries, and venules and is the major area of exchange between the circulating blood and the peripheral tissue (see Web Fig. 10-1; also see Chapter 2).

Macroscopic Structure

The heart lies within a fibroelastic sac called the pericardium, and the wall of the heart is composed of three layers: the epicardium, the myocardium, and the endocardium (Fig. 10-2). Structurally, the heart contains in order of blood flow four major blood vessels (vena cava, pulmonary artery, pulmonary vein, and aorta), four chambers (right atrium/auricle, right ventricle, left atrium/auricle, and left ventricle), and four valves (tricuspid, pulmonic semilunar, mitral, and aortic semilunar) (Fig. 10-3).

Pericardium and Epicardium

The pericardium, which normally contains a small amount of clear, serous fluid (see Fig. 10-2), is composed of an outer fibrous component and an inner serous layer, which form the sac surrounding the heart. The outer component is continuous with the mediastinal pleura. The base of the fibrous pericardium surrounds and blends with the adventitia of the greater arteries and veins exiting and entering the heart. The serous pericardium forms a closed sac surrounding the heart.

The epicardium (also known as visceral pericardium), the outermost layer of the heart, is continuous at the cardiac base with the parietal pericardium. The parietal pericardium is fused with the fibrous pericardium. The entire inner surface of the pericardial cavity is covered by mesothelium. The subepicardial layer is attached to the myocardium and consists of a thin layer of fibrous connective tissue, variable but generally abundant amounts (in well-nourished animals) of adipose tissue, and numerous blood vessels, lymphatic vessels, and nerves.


The myocardium is the muscular layer of the heart. It consists of cardiac muscle cells (cardiac myocytes [also known as cardiac rhabdomyocytes]) arranged in overlapping spiral patterns. These sheets of cells are anchored to the fibrous skeleton of the heart, which surrounds the atrioventricular valves and the origins of the aorta and pulmonary artery. The myocardial thickness is related to the pressure present in each chamber; thus the atria are thin walled and the ventricles are thicker. In adult animals, the thickness of the left ventricular free wall is approximately threefold that of the right ventricle, measured in a transverse section across the middle of the ventricles, because the pressure is greater in the systemic circulation than in the pulmonary circuit.

The arterial supply to the heart is the left and right coronary arteries, which arise from the aorta at the sinus of Valsalva behind the left and right cusps of the aortic valves. The arteries course over the heart in the subepicardium and give off perforating intramyocardial arteries that supply a rich capillary bed throughout the myocardium. Extensive anastomoses occur between the capillaries that tend to run parallel to the elongated cardiac muscle cells. The ratio of the area of capillaries to that of muscle cells is approximately 1 : 1, a fact evident when the myocardium is viewed histologically in cross-section.

Cardiac Conduction System

The heart is a muscular four chamber pump that simultaneously supplies blood to the pulmonary and systemic circulatory beds (see Web Fig. 10-1 and Fig. 2-1). Mechanical pumping is composed of sequential contraction (systole) and relaxation (diastole) that must be preceded by an electrophysiologic process that triggers a coordinated chronologic sequence of electrical events that result in muscle contractions. This electrophysiologic process is made possible by a network of special conducting fibers that are collectively referred to as the cardiac conduction system.

The cardiac conduction system is infrequently examined in animals because it is a labor-intensive process. Exceptions are cases with documented electrocardiographic alterations of undetermined origin. Components include (1) the sinoatrial node (SAN) at the junction of the cranial vena cava and the right atrium, (2) the atrioventricular node (AVN) located above the septal leaflet of the tricuspid valve and the atrioventricular (AV) bundle traversing the lower atrial septum onto the dorsal portion of the muscular interventricular septum, and (3) the right and left bundle branches that descend on each side of the muscular interventricular septum and eventually ramify in the ventricular myocardium as the Purkinje fiber network.

The major pacemaker of the cardiac conduction system is the SAN. This disk-shaped structure lies between the wall of the cranial vena cava and the external wall of the right auricular appendage. Four internodal pathways connect the SAN with the AVN. The AVN is present in the wall of the right atrium dorsal to the septal cusp of the tricuspid valve. For the atria to be electrically insulated from the ventricles, so that an unwarranted ectopic conduction wave will not activate the ventricles (or vice versa) and disrupt the synchronous events of the cardiac cycle, a fibrous cardiac skeleton composed of a layer of dense collagen (central fibrous body [CFB]), as well as occasional plates of chondroid and osseous metaplasia, separates the atrial from the ventricular myocardium. This skeleton forms two fibrous rings around the AV orifices and the aortic and pulmonic orifices. Conduction fibers arising from the AVN, known as the bundle of His or AV bundle, pierce through the CFB into the ventricles and continue along the subendocardium of the interventricular septum. The AV bundle then splits into the right and left bundle branches that further split and ramify into many other smaller branches that blend into the ventricular myocardium. Purkinje fibers constitute the AV bundle and downstream conduction pathways.

Endocardium and Heart Valves

The endocardium is the innermost layer of the heart and lines the chambers and extends over projecting structures such as the valves, chordae tendineae, and papillary muscles. The endocardium of the atria is thicker than that of the ventricles and thus normally appears white to gray on gross examination. The surface of the endocardium is endothelium that lies on a thin layer of vascularized connective tissue; the subendocardial layer contains blood vessels, nerves, and connective tissue. Purkinje fibers are distributed in the subendocardium throughout both ventricles. The heart valves (tricuspid valve [right AV valve], mitral valve [left AV valve], aortic valve, and pulmonary valve) are attached to fibrous rings and have thin avascular cusps. The valves open and close to regulate blood flow through the heart. During embryogenesis, endocardial cushions (mesenchymal tissue covered by endothelium) are precursors of the valve cusps. By remodeling, growth, and elongation, the cushions become thin mature cusps composed of connective tissue with an endothelial covering.

Blood and Lymphatic Vascular Systems

Blood Vessels: The aorta originates from the left ventricle and provides oxygenated blood to the entire body via arteries. In a treelike manner, arteries branch and become smaller arterioles as they approach capillary beds (see Web Fig. 10-1; also see Chapter 2). These beds and postcapillary venules provide the site for exchange of oxygen, carbon dioxide, nutrients, and waste. Small venules return the exchanged fluid and blood to larger veins and eventually the postcava and precava drain into the right atrium. The poorly oxygenated blood enters the pulmonary artery from the right ventricle. Oxygen exchange occurs in the capillaries of the lung, and oxygenated blood is returned to the heart via the pulmonary veins into the left atrium.

Microscopic Structure


The myocardium consists of cardiac muscle cells surrounded by interstitial components that include blood and lymphatic vessels, nerves, and connective tissue cells, such as fibroblasts, histiocytes, mast cells, pericytes, primitive mesenchymal stem cells, and extracellular matrix elements of connective tissue, including collagen fibrils, elastic fibers, and acid mucopolysaccharides. Cardiac muscle cells can be divided into two populations: the contracting myocytes and the specialized fibers of the conduction system. The contracting myocyte is a cross-striated branching fiber of an irregular cylindric shape that measures 60 to 100 µm in length and 10 to 20 µm in diameter, with centrally located, elongated nuclei. Myocytes in young animals are smaller and have small amounts of sarcoplasm. Atrial myocytes are smaller than ventricular myocytes. Adjacent myocytes are joined end-to-end by specialized junctions known as intercalated disks and less frequently by side-to-side connections termed lateral junctions. Multinucleated fibers with nuclei arranged in central rows are frequently seen in hearts of growing pigs (Fig. 10-4). The myocytes of old animals commonly have large polyploid nuclei. The cytoplasm (sarcoplasm) of myocytes is largely occupied by the contractile proteins that are highly organized into sarcomeres, the repeating contractile units of the myofibril (see Figs. 15-3 and 15-8). Myofibrils are formed by end-to-end attachment of many sarcomeres. The cross-striated or banded appearance of myocytes is the result of sarcomere organization into A bands composed of myosin in the form of “thick” filaments (12 to 16 nm in diameter), I bands composed of actin in the form of “thin” filaments (5 to 8 nm in diameter), and dense Z bands at the end of each sarcomere. Thick and thin filaments interdigitate and provide the basis for the sliding mechanism of muscle contraction. Myocytes are enclosed by the sarcolemma, which consists of the plasma membrane and the covering basal lamina (external lamina). Other important components of cardiac muscle cells are generally only apparent in electron micrographs and include abundant mitochondria, a highly organized network of intracellular tubules termed the sarcoplasmic reticulum, cylindric invaginations of the plasma membrane called T tubules, ribosomes, cytoskeletal filaments, glycogen particles, lipid droplets, Golgi complexes, atrial granules (contain atrial natriuretic factor), lysosomes, and residual bodies (Web Fig. 10-2).

Cardiac Conduction System

The morphologic features of the cardiac muscle cells that form specialized conduction tissues, including the SAN, AVN, AV bundle (bundle of His), and bundle branches, vary greatly at different sites and among animal species but generally are thin, branching nodal muscle cells with scarce myofibrils separated by highly vascularized connective tissue (Fig. 10-5; Web Fig. 10-3). Autonomic nerve fibers are contained within the SAN. The Purkinje fibers (cardiac conduction fibers) are distinguished by their large diameters (in horse, ox) and abundant pale eosinophilic sarcoplasm rich in glycogen and poor in myofibrils.


Fig. 10-5 Cardiac conduction system.
A, Sinoatrial (SA) node, foal. The center of the SA node (1) contains a nodal artery (2). H&E stain. A1, Higher magnification. Haphazardly oriented myofibers are embedded within abundant loose collagenous and elastic connective tissue. H&E stain. A2, Higher magnification. Nodal myofibers have discrete cell borders, a moderate amount of wavy sarcoplasm and an elongated nucleus. H&E stain. B, Atrioventricular (AV) node, goat. The AV node (1) is composed of interconnecting nodal myofibers that are supported by loose collagenous and elastic fibrous stroma. The node is embedded in adipose tissue (2). Note that in this illustration the AV node (1) is a poorly demarcated region (see B1 for greater detail) that is elongated (flattened) from top to bottom and that it and its surrounding adipose tissue are positioned adjacent to the cardiac fibrous skeleton (arrows) that has undergone focal chondroid metaplasia (3). The position and overall shape of the AV node in a histologic section is dependent upon the plane of section. Endocardium (arrowhead). H&E stain. B1, AV node, goat. In this higher magnification of B, AV nodal myofibers have a characteristic pale eosinophilic and thin sarcoplasm, with abundance of distinct striations and a short oval to elongated nucleus with dispersed chromatin. An autonomic myelinated nerve is present in the AV node (arrow). H&E stain. C, AV bundle, goat. The AV bundle (1) travels diagonally through the center of the figure from the lower left to the upper right margins. It is formed by an interweaving pseudosyncytium of cardiac myofibers supported by a loose to dense intervening collagenous stroma (see C1 for greater detail) and may be surrounded by adipose tissue (2). Cardiac cartilaginous skeleton (3). H&E stain. C1, Higher magnification. The AV bundle myofibers of the pseudosyncytium have moderate to large, pale eosinophilic sarcoplasm with prominent striations and large nuclei with fine stippled chromatin. H&E stain. (Courtesy Drs. A. Gal and J.F. Zachary, College of Veterinary Medicine, University of Illinois.)

Sinoatrial Node: The SAN is positioned adjacent to the epicardial adipose tissue and is often centered around a branch of the right coronary artery (Fig. 10-5, A). Several large autonomic nervous system ganglions can occasionally be seen clustering in the epicardium adjacent to the node. The SAN lacks discrete structure, and its ill-defined borders merge with the adjacent atrial wall. It structurally consists of a collection of haphazardly oriented myofibers that appear as a pseudosyncytium and are embedded within abundant loose collagenous and elastic connective tissue, with rare cores of epicardially oriented dense collagen fibers (Fig. 10-5, A1). The nodal myofibers have discrete cell borders, a moderate amount of wavy sarcoplasm with sparse myofibrils, and an elongated nucleus that contains clumps of coarse chromatin (Fig. 10-5, A2).

Atrioventricular Node, Atrioventricular Bundle, and Bundle Branches: The AVN lies within the right atrial subendocardium and consists of a discrete, compact to loose mass of interconnecting myofibers that are often embedded within adipose tissue. A small nodal artery, parasympathetic ganglia, and large myelinated autonomic nerves are often present adjacent to the AVN. The nodal myofibers that have characteristic pale eosinophilic and thin sarcoplasm generally run parallel to each other but occasionally have an interweaving pattern with intervening loose collagen fibers. These myofibers contain a moderate amount of sarcoplasm with abundance of distinct striations and a short oval to elongated nucleus with dispersed chromatin.

The AV bundle (Fig. 10-5, B) emerges from the cranial pole of the AVN (Fig. 10-5, B1) and pierces through the CFB, approximately at the level of the annuli of the aortic and mitral valves (Fig. 10-5, B2), to become the left and right bundle branches. The size of an AV bundle myofiber progressively enlarges and its cytomorphology transitions from a pale eosinophilic, small and thin (AVN-like morphology) myofiber to a pale eosinophilic, foamy to waxy, large, and somewhat rectangular myofiber that lacks cross striations (a Purkinje-like cellular morphology) (Fig. 10-5, C).

Autonomic Nervous System: The nerve supply to the heart is autonomic and includes sympathetic, parasympathetic, and nonadrenergic noncholinergic innervation. Histologically, large nerves can be seen in the epicardium and adjacent to the coronary blood vessels, whereas special staining techniques are required for demonstration of neural tissue elsewhere. Electron microscopy and immunohistochemistry allow differentiation between sympathetic and parasympathetic nerves that are otherwise indistinguishable with H&E stain. Preganglionic parasympathetic fibers pass to the heart through the cardiac branch of the vagal nerve and synapse with parasympathetic ganglionic neurons. Postganglionic neurons are distributed to the SAN and AVN, as well as to atrial and, to a much lesser extent, ventricular myocardium (however, the ventricular conduction system is well supplied by cholinergic innervation). Postganglionic sympathetic fibers arising from the cervicothoracic and middle cervical ganglia intensely innervate the SAN and AVN and to lesser extent the AV bundle. The atrial endocardium, myocardium, and epicardium are evenly innervated, whereas the ventricles are considerably less innervated with epicardium more densely populated by neural tissue than the endocardium.

Endocardium and Heart Valves

The endocardium, lining the atrium and ventricles, consists of a continuous endothelium, subendothelium, and subendocardium. The subendothelial layer contains dense irregular fibroblasts intermixed with collagen and elastic fibers and occasional smooth muscle cells. Elastic fibers are abundant within the subendocardium of the atria. The subendocardial layer contains vascular structures, elastic and collagen bands, and fibroblasts and is continuous with the myocardium. Purkinje fibers are located in the subendocardium. The heart valves are poorly vascularized, endocardial folds covered by endothelium. The subendothelial layer is composed of fibroblasts with abundant elastic and collagen fibers. The AV valves (AVVs) consist of a layer of stratum spongiosum and stratum fibrosum. The stratum spongiosum consists of loosely arranged fibroblasts with moderate amounts of collagen and elastin fibers and vascular structures. The stratum fibrosis contains fibroblasts and collagen, which are continuous with the annulus fibrosis and chordae tendineae.

Blood and Lymphatic Vascular Systems

The overall design of the blood and lymphatic vessels is similar, except that luminal diameter, wall thickness, and the presence of other anatomic features, such as valves, vary between the different segments. The luminal surface of all vessels is lined by longitudinally aligned endothelial cells covering a basal lamina. Vessel walls are divided into three layers or tunics: intima, media, and adventitia. However, some of the layers can be absent or all of the layers can be thinned in some segments of the vascular system, depending on the intravascular pressures. The large elastic arteries, such as the aorta, have (1) an intima composed of endothelium and subendothelial connective tissue, (2) a very thick tunica media composed of fenestrated elastic laminae with interposed smooth muscle cells and ground substance and bordered internally by the internal elastic lamina and externally by the external elastic lamina, and (3) an outer tunica adventitia layer composed of collagen and elastic fibers and connective tissue cells with penetrating blood vessels, termed the vasa vasorum, supplying nutrients to the adventitia and the outer half of the media. In muscular arteries and arterioles, the tunica media is composed largely of smooth muscle cells arranged in a circumferential pattern. Arterioles are the smallest arterial channels and are generally less than 100 µm in diameter and with one to three layers of smooth muscle cells in the tunica media.

Capillaries are 5 to 10 µm in diameter, and their endothelium is one of three types: (1) continuous, (2) fenestrated (as in the endocrine glands), or (3) porous (as in renal glomeruli). The endothelium rests on an external lamina surrounded by pericytes. Pericytes are located abluminally to capillaries and postcapillary venules and because of their location, contractility, and cytoskeletal proteins may play a role in regulating capillary and venular blood flow. Lesions of the endothelium might not be evident by light microscopy, and electron microscopy is required for characterization.

Veins have thin walls in relation to their luminal size when compared with those of arteries, in which blood pressure is greater. The adventitia is the thickest layer. Valves are present to prevent retrograde blood flow (i.e., away from the heart).

Lymphatic capillaries lack a basal lamina. Large lymphatic vessels are similar in structure to veins and generally have large lumina, thin walls, and intimal valves but contain lymph.

The morphology of large arteries, veins, microvasculature, and lymphatic vessels is described in Chapter 2 and is not discussed further in this chapter.

Necropsy Assessment of Heart and Vascular Structures

Information on this topic including Web Appendix 10-1 and Web Figs. 10-4 and 10-5 is available at

Examination of the Cardiovascular System and Lymphatic Vessels at Necropsy and Tissue Sampling for Histopathologic Evaluation

Information on this topic including Web Appendix 10-2 and Web Fig. 10-6 is available at


The primary function of the cardiovascular and lymphatic systems is to maintain an adequate and steady supply of nutrients to and facilitate the removal of waste products from all organs and tissues of the body. Cardiac myocytes provide the force of contraction; the conduction system and the nervous system control the flow and volume.


The results of normal cardiac function include the maintenance of adequate blood flow, called cardiac output, to peripheral tissues that provide delivery of oxygen and nutrients, the removal of carbon dioxide and other metabolic waste products, the distribution of hormones and other cellular regulators, and the maintenance of adequate thermoregulation and glomerular filtration pressure (urine output). The normal heart has a threefold to fivefold functional reserve capacity, but this capacity can eventually be lost in cardiac disease and the result is impaired function.

Cardiac Pathophysiology: Myocardial Dysfunction

Cardiovascular dysfunction is the result of one or more of six basic pathophysiologic mechanisms (Box 10-1). Compensatory mechanisms operate in both normal and diseased hearts in an attempt to meet both the short- and long-term demands for adequate cardiac output. These mechanisms include cardiac dilation, myocardial hypertrophy, increase in heart rate, increase in peripheral resistance, increase in blood volume, and redistribution of blood flow. These compensatory mechanisms can maintain cardiac output that is adequate for some time, even in animals with severe cardiac disease sufficient to compromise cardiac function from loss of myocardial contractility, sustained pressure overload, or sustained volume overload. Cardiac dilation can occur as a terminal lesion in many cardiac diseases (Fig. 10-6, A). As a compensatory response to achieve increased cardiac output, dilation allows stretching of cardiac muscle cells to increase contractile force according to the Frank-Starling phenomenon and increased stroke volume is the result. However, stretching beyond certain limits decreases contractile strength. Myocardial hypertrophy is an important long-term compensatory response of the heart to maintain adequate cardiac output in the face of increased pressure or volume overload (see the discussion on the myocardium in the section on Responses to Injury) (Fig. 10-6, B).

Types of Heart Failure

A wide variety of experimental animal models of heart failure exist (see Web Table 10-1). The models have been used to develop an understanding of human cardiac diseases.

Congestive Heart Failure: Congestive heart failure usually develops slowly from gradual loss of cardiac pumping efficiency coupled with either pressure or volume overload or myocardial damage (Figs. 10-7 and 10-8; also see Figs. 8-29, 8-30, and 9-39). Pathophysiologically, congestive heart failure is initiated by development of cardiac disease (e.g., myocardial, valvular, congenital) or increased workload associated with pulmonary, renal, or vascular disease leading to loss of cardiac reserve and development of decreased blood flow to peripheral tissue (forward failure) and accumulation of blood behind the failing chamber (backward failure). Reduced renal blood flow creates hypoxia in the kidneys and increases renin release from the juxtaglomerular apparatus, resulting in stimulation of aldosterone release from the zona glomerulosa of the adrenal cortex. Sodium and water retention are the results of the action of aldosterone on the renal tubules; increased plasma volume follows, as does accumulation of edema fluid (mainly in body cavities). Hypoxia also stimulates increased erythropoiesis in bone marrow and extramedullary organs, such as the spleen, causing polycythemia and thus increased viscosity of the blood. The hypervolemia from aldosterone-induced water retention increases the workload on the already failing heart. Thus a vicious cycle of cardiac decompensation is initiated that eventually leads to death from cardiac failure unless therapeutic intervention occurs. Cardiac dilation, hypertrophy, and increased heart rate can provide some compensation for the increased workload.

Acute and Chronic Right-Sided Heart Failure: Acute right-sided heart failure results in acute passive congestion (see Fig. 2-35) leading to hepatomegaly and splenomegaly (see Figs. 2-35 and 13-50, A), whereas chronic right-sided heart failure (see Fig. 2-36) results in hepatic congestion (nutmeg liver) (see Fig. 8-30) and more severe sodium and water retention than in left-sided heart failure. Edema is evident predominantly as ventral subcutaneous edema in horses and ruminants (see Fig. 10-8), ascites in dogs, and hydrothorax in cats. Causes of right-sided failure include (1) pulmonary hypertension, (2) cardiomyopathy, and (3) disease of the tricuspid and pulmonary valves. (See Chapters 8 and 9 for further details on hepatic and pulmonary lesions, respectively, associated with congestive heart failure.)

Cardiac Conduction System

Cells of the cardiac conduction system are modified cardiac myofibers that are able to spontaneously depolarize, which is also called autoexcitation, and function to (1) coordinate the sequence of events required for efficient ventricular filling during diastole and ejection during systole and (2) maintain the pressure in the pulmonary and systemic circuits (see Web Fig. 10-1).

Depolarization of the membrane of these pacemaker cells is due to a transiently increased rapid permeability to sodium ions and a slightly longer lasting increase in permeability to calcium ions that results in their influx into the myofiber sarcoplasm, thus changing the membrane potential (see Chapter 14). As this transient permeability is lost, membranal potassium channels open, and rapid outward potassium flux results in myofiber membranal hyperpolarization (along with sodium and calcium efflux), ultimately bringing the membrane potential back to a “normal” steady state (resting potential). During this period of time (refractory period), the myocyte cannot depolarize again because of a special conformation of membrane sodium channels that is transiently lost with depolarization and regained only with hyperpolarization. Intrinsically, the resting membrane potential of pacemaker cells is more positive than that of contracting cardiomyocytes and slightly more negative than the membrane threshold potential. This difference is due to leakiness of the pacemaker cell membrane to sodium and calcium ions and a steady low-grade influx of these ions.

Once one pacemaker cell depolarizes, a wave of depolarization propagates through the surrounding myocytes because these cells are connected to each other by special membranal pores (gap junctions), which allow for ionic exchange between adjacent cells. The number of gap junctions between cells of the conduction system is therefore a property that affects conduction velocity. Because the heart cycle must be strictly coordinated so that both atria and both ventricles contract and relax at the same time, and atrial contraction occurs simultaneous to the late ventricular relaxation, the depolarization wave has to be conducted fast at certain points along the conduction pathway and slower at others. Therefore, at different anatomic regions along the conduction pathway, the degree of cell-to-cell interaction dictates a slightly different cellular morphology.

When an electric signal (a propagating depolarization front) is generated in the SAN and spreads throughout the atria from cell to cell and eventually reaches the AVN, it is also conveyed through the specialized internodal conducting fibers. The conduction in these fibers is approximately three times faster than that of the atrial myofibers. By conveying the signal through these fibers, both atria can contract simultaneously and in a coordinated manner that allows the process of pushing of blood into the ventricles. Correlating with their special fast conducting function, these cells have a Purkinje-like morphology. The conduction velocity is then slowed down when propagating through the AVN. The time it takes to conduct the signal through the AVN and penetrating AV bundles is approximately four times longer than the time it takes for it to be conducted from the SAN to the AVN. This delay in conduction serves to empty the atria from blood before the ventricles start to contract. It also contributes to the unidirectional blood flow between the atria and the ventricles, above and beyond the similar role played by the AVVs.

Finally, the signal is delivered through the AV bundle, bundle branches, and Purkinje fibers in a velocity approximately 150 times faster than that of the AVN. The bundle branches run along the subendocardium of the interventricular septum and free ventricular walls and give rise to Purkinje fibers that supply the myocardium in a subendocardial-to-epicardial direction. This organization allows for a rapid and synchronous contraction of both ventricles at an order that ultimately enables blood to be “squeezed” from apex-to-base, toward both outflow tracts.

Cardiac myofibers have a unique property of intrinsic coupling of the electrical stimulation with mechanical contraction, which is fundamental for cardiac function. Diastole starts immediately at the end of ventricular contraction, as the cardiac muscle (myocardium) starts to relax. For a brief moment, relaxation leads to a rapid fall in ventricular pressure, without change in ventricular volume as the AVVs are still sealed off (isovolumetric relaxation). Because of the fall in ventricular pressure, the blood that has pooled in the atria during systole, along with incoming blood that constantly flows from systemic and pulmonary veins through the atria, pushes the AVV open and rapidly and passively fills the ventricles (rapid-filling phase). Next, because of the resultant pressure rise in the ventricles, the flow of blood that continues to enter the ventricles through the atria abruptly ends (diastasis phase). The last phase of diastole is active contraction of the atria, which pushes blood into the (now somewhat less compliant) ventricles and further raises their pressure (“atrial kick”).

In systole, the myocardium contracts, leading to a rapid increase in intraventricular pressure. Since the aortic and pulmonary valves are shut during diastole, the sudden rise in pressure leads to closure of the AVVs. In this brief period, which is termed isovolumetric contraction, the change in ventricular pressure has not led to a change in ventricular volume, since the blood had not yet been ejected into the aorta and pulmonary arteries. When the pressure in the ventricles exceeds the pressure in the great arteries, the aortic and pulmonary valves (semilunar valves) open and the ejection of the blood through the right and left side outflow tracts ensues (ejection phase). Simultaneously with the ejection phase, the atria relax, atrial pressure falls, and blood enters the atria and pools within it passively.

An additional level of complexity is brought about by the innervation of the autonomous nervous system (ANS). In general, the ANS influences heart rate (chronotropy), alters the rate of conduction (dromotropy), and controls myocardial contractility (inotropy) and the rate of mechanical relaxation (lusitropy). Parasympathetic postganglionic nerve terminals secrete acetylcholine that affects muscarinic (M2) receptors, whereas sympathetic postganglionic nerve terminals secrete norepinephrine that predominantly acts on the β1-adrenergic receptors. The latter, when stimulated by catecholamines, lead to a chain of intracellular events that increases calcium influx, increases the magnitude of potassium and chloride repolarization, and shortens the refractory period. Therefore adrenergic agonists are said to be positive chronotropes, inotropes, dromotropes, and lusitropes, whereas parasympathetic agonists have the opposite effects. Heart rate is primarily regulated by opposing effects of adrenergic and cholinergic nerve terminals on the SAN and at the same time by modulation of conduction velocity of the AVN and AV bundle. Physiologically, the force of contraction represents the sum of interactions between myocardial contractility, which is positively modulated by adrenergic nerve terminals that act on β1 receptors on ventricular myocardial myofibers (positive inotropic effect), and by the volume of blood that is present in the ventricles just before contraction (preload), as well as by the resistance in front of which contraction actually takes place (afterload).

Endocardium and Heart Valves

The endocardium lines the myocardium and contains Purkinje nerve fibers, which transmit a rhythmic action potential throughout the myocardium leading to contraction. The endocardium is lined by endothelial cells, which modulate many aspects of normal hemostasis. In normal states, the endothelial cells are antithrombotic preventing circulating cells from attaching and thus allowing normal flow of blood through the heart and blood vessels. The endocardium is continuous with the endothelium of blood and lymphatic vessels. Normal flow of blood through the heart depends on functional valves (see Chapter 2). Properly functioning valves serve as one-way valves, allowing blood to flow either from one chamber to another (AVVs) or exiting from the heart to either the pulmonary circulation (pulmonic valve) or the systemic circulation (aortic valve).

Sep 17, 2016 | Posted by in GENERAL | Comments Off on Cardiovascular System and Lymphatic Vessels
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