Pericardium. 

The heart and the origins of the great vessels are surrounded and enclosed by the pericardium. The outermost fibrous pericardium is a thick envelope that is tough and inelastic. Ligaments anchor the outer pericardium to the diaphragm and the great vessels such that the heart is maintained in a fixed position within the thoracic cavity. The pericardium also provides a physical barrier to infection. Inside the fibrous layer is an inner, double-walled membrane described as the serous pericardium.⁴ The two layers are labeled “parietal” and “visceral.” The parietal pericardium adheres to the tough, outer pericardium. The visceral pericardium is flexible, adheres directly to the heart, and folds with the surface contours of the heart. The pericardial cavity is the potential space between the visceral and parietal layers.^4,5 The space between these two layers normally contains a small amount of pericardial fluid, which is secreted, resorbed, and serves as a lubricant between the layers so that the heart can move without friction.⁵ The fibrous, outer pericardial sac is noncompliant and unable to adapt to rapid increases in pericardial fluid.⁵ For example, blood can collect in this sac in cardiac tamponade, or serum can collect in pericardial effusion. If the fluid collection in the sac impinges on ventricular filling, ventricular ejection, or coronary artery perfusion, removal of the excess pericardial fluid may be necessary, a procedure known as pericardiocentesis.⁵ The phrenic nerve provides sensory fibers to the pericardium. The pain that accompanies pericardial effusion and cardiac tamponade is sensed via phrenic nerve innervation.⁵

Epicardial Fat. 

In adults, a layer of adipose tissue is typically present beneath the visceral pericardium and may surround the heart. This epicardial fat accumulates along the routes of the major coronary arteries and veins. Autopsy data indicate that epicardial fat increases until age 20 to 40 years, but thereafter, the quantity does not depend on age.⁶ Epicardial fat covers 80% of the surface of the heart and constitutes about 20% of the total weight of the heart, with the largest quantity positioned over the right ventricle.⁶ If a person is overweight or obese with a large quantity of visceral and subcutaneous adipose tissue, usually more epicardial fat is present.⁷ Because obesity is endemic in modern society, epicardial fat is receiving more attention. Epicardial fat is hypothesized to increase the risk of coronary artery disease (CAD) because it contains smaller adipocytes compared with other fat deposits, has a different fatty acid composition, and has a higher protein content. This composition facilitates the infiltration of free fatty acids and adipokines into coronary arteries.⁸ The fibrous, outer pericardium does not contain any fat deposits.

Epicardium. 

The epicardium is tightly adhered to the heart and the base of the great vessels as described earlier. The coronary arteries lie on the top of the visceral epicardium.

Myocardium. 

The next layer of the heart is the myocardium, a thick, muscular layer. This layer includes all of the atrial and ventricular muscle fibers necessary for contraction. The fibers of the myocardium do not have the same thickness throughout the ventricular walls. The left ventricle is much thicker than the right ventricle or the atria. The fibers are organized in such a manner that the force of contraction is most efficient in ejecting blood toward the outflow tracts in a wringing motion from the apex toward the base (Fig. 12-2).⁹ The myocardium is the muscle that is damaged by a “heart attack” or transmural myocardial infarction (MI).

Endocardium. 

The innermost layer is the endocardium, which is a thin layer of endothelium and connective tissue lining the inside of the heart. This layer is continuous with the endothelium of the great vessels to provide a continuous closed system. Disruption in the endothelium as a result of surgery, trauma, or congenital abnormality can predispose the endocardium to infection. This infective endocarditis is a devastating disease, which, if left untreated, can lead to massive valve damage or sepsis and death.

Atrioventricular Valves. 

The two atrioventricular (AV) valves are named for their location between the atria and the ventricles. These are the tricuspid valve on the right and the mitral valve on the left. The mitral valve is described as having two leaflets, although the “leaflets” are a continuous, noninterrupted structure.¹¹ The AV valves are open during ventricular diastole (filling) and prevent backflow of blood into the atria during ventricular systole (contraction). The chordae tendineae and papillary muscles, which attach to the tricuspid and mitral valves, give the valves stability and prevent valve leaflet eversion during systole (Fig. 12-5). Papillary muscles arise from the ventricular myocardium and derive their blood supply from the coronary arteries. Each papillary muscle gives rise to approximately 4 to 10 main chordae tendineae, which divide into increasingly finer cords as they approach and attach to the valve leaflets. The chordae tendineae are fibrous, avascular structures covered by a thin layer of endocardium. Dysfunction of the chordae tendineae or of a papillary muscle may cause incomplete closure of an AV valve, which results in backflow of blood into the atrium. Degenerative disease of the valve leaflets is another cause of regurgitation of blood into the atrium.¹² Valvular regurgitation produces a murmur that can be auscultated with a stethoscope.

Semilunar Valves. 

The semilunar valves are pulmonic and aortic valves. Each valve has three cuplike leaflets (Fig. 12-6). These valves separate the ventricles from their respective outflow arteries (Table 12-1). During ventricular systole (contraction), semilunar valves open, allowing blood to flow out of the ventricles. As systole ends and the pressure in the outflow arteries exceeds that of the ventricles, the semilunar valves close, preventing blood regurgitation back into the ventricles. In most individuals, the aortic valve has three leaflets. In less than 1% of the population, it is bicuspid (a two-leaflet valve), which increases susceptibility to aortic valve failure over time.^13,14 Aortic valve dysfunction, from any cause, not only affects the valve leaflets but also pathologically alters the shape of the left ventricle.

Sinoatrial Node. 

The SA node is considered the natural pacemaker of the heart because it has the highest degree of automaticity, producing the fastest intrinsic heart rate (Table 12-2). The node is a spindle-shaped structure located near the entrance of the superior vena cava, on the posterior aspect of the right atrium. Some normal variability in the position and shape of the node exists. The SA node is supplied from the right coronary system in 63% of people and from the left coronary system in 37%.¹⁶ The SA node contains two types of cells, the specialized pacemaker cells found in the node center and the border zone cells. Both cell types have inherent pacemaker properties (they automatically depolarize 60 to 100 times per minute). The cells in the nodal center are responsible for the pace making of the heart, whereas the intrinsic depolarization capability of the fibers in the border zone is depressed by surrounding atrial tissue.

Once the center nodal cells depolarize, the impulse is conducted through the nodal border zone toward the atrium. Atrial depolarization occurs cell to cell. Some anatomists postulate that specialized conduction pathways exit the SA node (Fig. 12-7A). These internodal pathways are directed to the AV node.¹⁷ An intra-atrial conduction pathway, known as Bachmann’s bundle, travels from the right atrium to the left atrium.^18,19

Atrioventricular Node. 

The AV node is located posteriorly on the right side of the interatrial septum, on the floor of the right atrium.²⁰ The AV node receives its blood supply from the first posterior septal branch of the right (90%) or left (10%) coronary artery.¹⁶ Because the atria and ventricles are separated by nonconductive tissue, electrical impulses initiated in the atria are conducted to the ventricles only via the AV node. The AV node performs four essential functions to support cardiac conduction:

Bundle of His, Bundle Branches, and Purkinje Fibers. 

Electrical impulses are conducted in the ventricles through the bundle of His, the bundle branches, and the Purkinje fibers (see Fig. 12-7C). These structures run through the subendocardium, down the right side of the interventricular septum. About 12 mm from the AV node, the bundle of His divides into the right and left bundle branches. The right bundle branch continues down the right side of the interventricular septum toward the right apex. The left bundle branch is thicker than the right and takes off from the bundle of His at an almost right angle. It traverses the septum to the subendocardial surface of the left interventricular wall, where it divides into a thin anterior branch and a thick posterior branch. Functionally, when one of the left branches is blocked, it is referred to as a hemiblock. All of the bundle branches are subject to conduction defects (bundle branch blocks) that give rise to characteristic changes in the 12-lead electrocardiogram (ECG).

The right bundle branch and the two divisions of the left bundle branch eventually divide into the Purkinje fibers, which have the fastest conduction velocity of all heart tissue. Purkinje fibers divide many times, terminating in the subendocardial surface of both ventricles. This is followed by ventricular muscle depolarization (see Fig. 12-7D).

Coronary Veins. 

The cardiac (coronary) veins, which carry deoxygenated blood, are adjacent to the paths of the coronary arteries, with one significant difference. The coronary veins ultimately join together to become the coronary sinus (the largest cardiac vein), which primarily empties into the back of the right atrium. The coronary venous blood then mixes with the systemic venous blood in the right atrium.²²

Physiologic Cardiac Shunts. 

A shunt occurs when deoxygenated blood (usually venous blood with reduced oxygen content) mixes with arterial oxygenated blood. In the heart in a specific situation, this is a normal physiologic process. The thebesian veins are small vessels that connect the capillary beds directly with the cardiac chambers via irregular endothelium-lined sinuses within the myocardium. The thebesian veins add a small quantity of deoxygenated blood to the oxygenated blood in the left ventricle.

An example of an abnormal, or pathologic, intracardiac shunt is an opening in the ventricular septum, between the left and right sides of the heart. In the ventricle, this septal opening, called a ventricular septal defect (VSD), allows mixing of blood from both ventricles. The clinical impact depends on the size of the intracardiac shunt. A VSD is a congenital opening between the ventricles; a ventricular septal rupture (VSR) can occur as a complication of a large anterior-wall MI, as shown in Figure 15-15.

Arterial System. 

Arteries are constructed of three layers (Fig. 12-11): 1) The adventitia, the outermost layer, is composed largely of a connective tissue coat to provide strength and shape to the vessel; 2) the media, or muscular middle layer, is made up of smooth muscle and elastic tissue. The muscular layer changes the lumen diameter when necessary; and 3) the innermost layer, or intima, consists of a thin lining of endothelium and a small amount of elastic tissue. The smooth endothelial lining decreases resistance to blood flow and minimizes opportunity for platelet aggregation.

The intimal and the adventitial layers remain relatively constant in the vascular system, whereas the elastin and smooth muscle in the media vary in proportion, depending on the size and type of the vessel. The aorta contains the greatest amount of elastic tissue. This is necessary because of the sudden shifts in pressure created by the left ventricle. The arterioles, or smaller arteries, and precapillary sphincters have more smooth muscle than do the larger arteries and aorta because they function to change the luminal diameter when regulating blood pressure and blood flow to tissues (Fig. 12-12).

Blood Flow and Blood Pressure. 

The pulsatile nature of arterial flow is caused by intermittent cardiac ejection and the stretch of the ascending aorta. The pressure wave initiated by left ventricular ejection (Fig. 12-13) travels considerably faster than does blood itself. When an examiner palpates a pulse, it is the propagation of the pressure wave that is perceived.

In the normal arterial system, blood flow is described as laminar, or streamlined, because the fluid moves in one direction. However, differences exist in the linear velocities within a blood vessel. The layer of blood immediately adjacent to the vessel wall moves relatively slowly because of the friction created as it comes in contact with the motionless vessel wall. In contrast, the more central blood in the lumen travels more rapidly (Fig. 12-14).

Stay updated, free articles. Join our Telegram channel

Join