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.

Lymphatic Vessels: Lymphatic vessels are thin walled, endothelial-lined channels that originate near the capillary beds and serve as a drainage system for returning interstitial tissue fluid and inflammatory cells to the blood. Afferent lymphatic vessels drain lymph into regional lymph nodes, which then filter and provide immunologic surveillance of the lymph, its cells, and the foreign matter it contains. The filtered lymph continues into larger efferent lymphatic vessels, which eventually drain into the caval blood via the thoracic duct. Both lymphatic vessels and veins have valves to prevent backflow of fluid. A more complete description can be found in Chapter 2.

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.

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 Left-Sided Heart Failure: Acute left-sided heart failure is manifested by pulmonary congestion and edema, whereas chronic left-sided heart failure is manifested by chronic passive pulmonary congestion, chronic pulmonary edema, hemosiderosis (“heart failure cells”; see Fig. 9-39), and fibrosis. The most common causes are (1) myocardial contractility loss associated with myocarditis, myocardial necrosis, or cardiomyopathy; (2) dysfunction of the mitral or aortic valves; and (3) several congenital heart diseases.

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.)

Clinical Diagnostic Procedures:

Information on this topic including Web Appendix 10-3 is available at evolve.elsevier.com/Zachary/McGavin/.