Textbook of Cardiovascular & Thoracic Nursing P Hariprasath
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1Cardiac Nursing
  • • Anatomy and Physiology of Heart
  • • Assessment and Diagnostic Evaluation
  • • Pharmacology of Heart
  • • Nursing Management of Patients with Hypertension
  • • Nursing Management of Patients with Coronary Artery Disease
  • • Nursing Management of Patients with Dysrhythmia
  • • Nursing Management of Patients with Heart Failure
  • • Nursing Management of Patients with Inflammatory Heart Disease
  • • Nursing Management of Patients with Valvular Disorders
  • • Nursing Management of Patients with Congenital Heart Disease
  • • Interventional Cardiology
  • • Pacemaker
  • • Defibrillators
  • • Mechanical Circulatory Assistive Devices
  • • Nursing Care of Patient Undergoing Cardiac Surgery2

Anatomy and Physiology of Heart1

  • ☞ Embryology of the Heart
  • ☞ Anatomy and Physiology of Heart
  • ☞ Heart and its Location
  • ☞ Cardiac Tissue
  • ☞ Conduction Tissues
  • ☞ Chambers of the Heart
  • ☞ Heart Valves
  • ☞ Coronary Circulation
  • ☞ Physiology of Coronary Circulation
  • ☞ Conduction System
  • ☞ Cardiac Cycle
After fertilization the heart begins develop from mesoderm on 18 or 19 day. In the head end of the embryo, the heart develops from a group of mesodermal cells called the cardiogenic area. In response to signals from the underlying endoderm, the mesoderm in the cardiogenic area forms a pair of elongated strands called cardiogenic cords. Shortly after, these cords develop a hollow center and then become known as endocardial tubes. With lateral folding of the embryo, the paired endocardial tubes approach each other and fuse into a single tube called the primitive heart tube on day 21 following fertilization (Fig. 1.1). On 22 day the primitive heart tube develops into five distinct regions and begins to pump blood. From tail end to head end (the direction of blood flow) they are:
  • Sinus venosus
  • Atrium
  • Ventricle
  • Bulbus cordis
  • Truncus arteriosus
The sinus venosus initially receives blood from all the veins in the embryo; contractions of the heart begin in this region and follow sequentially in the other regions.
Thus, at this stage, the heart consists of a series of unpaired regions. The fates of the regions are as follows:
  • The sinus venosus develops into part of the right atrium, coronary sinus, and sinoatrial (SA) node.
  • The atrium develops into part of the right atrium, right auricle, and the left atrium and left auricle.
  • The ventricle gives rise to the left ventricle.
  • The bulbus cordis develops into the right ventricle.
  • The truncus arteriosus gives rise to the ascending aorta and pulmonary trunk.
On day 23, the primitive heart tube elongates. Because the bulbus cordis and ventricle grow more rapidly than other parts of the tube and because the atrial and venous ends of the tube are confined by the pericardium, the tube begins to loop and fold. At first, the primitive heart tube assumes a U-shape; later it becomes S-shaped. As a result of these movements, which are completed by day 28, the atria and ventricles of the future heart are reoriented to assume their final adult positions. The remainder of heart development consists of reconstruction of the chambers and the formation of septa and valves to form a four-chambered heart. On about day 28, thickenings of mesoderm of the inner lining of the heart wall, called endocardial cushions, appear they grow toward each other, fuse, and divide the single atrioventricular canal (region between atria and ventricles) into smaller, separate left and right atrioventricular canals. Also, the interatrial septum begins its growth toward fused endocardial cushions. Ultimately, the interatrial septum and endocardial cushions unit and an opening in the septum, the foramen ovale, develops. The interatrial septum divides the atrial region into a right atrium and a left atrium. Before birth, the foramen ovale allows most blood entering the right atrium to pass into the left atrium. After birth, it normally closes so that the interatrial septum is a complete partition.
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Figs 1.1A to F: Embryology of heart
The remnant of the foramen ovale is the fossa ovalis. Formation of the interventricular septum partitions the ventricular region into a right ventricle and a left ventricle. Partitioning of the atrioventricular canal, atrial region, and ventricular region is basically complete by the end of the fifth week. The atrioventricular valves form between the fifth and eighth weeks. The semilunar valves form between the fifth and ninth weeks.
Heart is a roughly cone shaped hollow muscular organ. It measures about 12 cm in length, 8 to 9 cm in breadth at the broadest part, and 6 cm in thickness. Its weights is 280 to 340 g in male and 230 to 280 g in female.
The heart lies in the thoracic cavity in the mediastinum (space between the lungs) (Fig. 1.2). It lies obliquely, a little more to left than right and presents a base as above and apex below. The apex is about 9 cm to the left of midline at the level of 5th intercostals space, little below the nipple and slightly nearer the midline. The base extends to the level of 2nd rib.
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 (Fig. 1.3).
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.
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Fig. 1.2: Location of heart
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Fig. 1.3: Cardiac tissue
This continuous membrane thus forms the pericardial sac and encloses a potential space, the pericardial cavity. 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.
The pericardial cavity is usually filled with 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.
Pathophysiologic conditions such as cardiac tamponade 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 be accumulated without serious ventricular impairment. When greater volumes accumulate, ventricular filling is impaired. If this happens slowly, the ventricles may be able to maintain an adequate cardiac output 6by contracting more vigorously. The pericardium is histologically similar to pleural and peritoneal serous membranes, so inflammation of all three membranes may occur with certain systemic conditions such as rheumatoid arthritis.
The myocardial layer is composed of cardiac muscle (Fig. 1.4) cells interspersed with connective tissue and small blood vessels. Some atrial and ventricular myocardial fibers are anchored to the fibrous skeleton. 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-of-eight individual muscle fiber path spirals anchored to the fibrous skeleton. 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. This vortex arrangement allows for the circumferential generation of tension throughout the ventricular wall and thus 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. The orientation of these fibers gradually rotates through the thickness of the wall.
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Fig. 1.4: Cardiac muscle structure
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 owing to the orderly arrays of the abundant contractile protein filaments. Working myocardial cells make-up 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 and AV nodes. 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 conduction of electrical impulses, 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, contributing to these cells resistance to damage during anoxic periods. 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.
The endocardium is composed of a layer of endothelial cells and a few layers of collagen and elastic fibers. The endocardium is in continuation with the tunica intima of the blood vessels.
  • 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. The sequential contraction of the atria and ventricles as coordinated units depends on the anatomic arrangement of the specialized cardiac 7conducting tissue. Small cardiac nerves, arteries, and veins lie close to the specialized conducting cells, providing neurohumoral modulation of cardiac impulse generation and conduction.
  • 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. 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.
The heart has four chambers. The two superior receiving chambers are the atria and the two inferior pumping chambers are the ventricles. On the anterior surface of each atrium is a wrinkled pouchlike structure called an auricle, so named because of its resemblance to a dog's ear. Each auricle slightly increases the capacity of an atrium so that it can hold a series of grooves, called sulci, that contain coronary blood vessels and a variable amount of fat. Each sulcus marks the external boundary between two chambers of the heart. The deep coronary sulcus encircles most of the heart and marks the external boundary between the superior atria and inferior ventricles. The anterior interventricular sulcus is a shallow groove on the anterior surface of the heart that marks the external boundary between the right and left ventricles. This sulcus continues around to the posterior surface of the heart as the posterior interventricular sulcus, which marks the external boundary between the ventricles on the posterior aspect of the heart.
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Fig. 1.5: Chambers of heart
Right Atrium
The right atrium forms the right border of the heart and receives blood from three veins—the superior vena cava, inferior vena cava, and coronary sinus (veins always return blood to the heart). The right atrium is about 2–3 mm (0.08–0.12 in.) in average thickness. The anterior and posterior walls of the right atrium are very different. The posterior wall is smooth; the anterior wall is rough due to the presence of muscular ridges called pectinate muscles which also extend into the auricle. Between the right atrium and left atrium is a thin partition called the interatrial septum. A prominent feature of this septum is an oval depression called the fossa ovalis, the remnant of the foramen ovale, an opening in the interatrial septum of the fetal heart that normally closes soon after. Blood passes from the right atrium into the right ventricle through a valve that is called the tricuspid valve because it consists of three leaflets or cusps. It is also called the right atrioventricular valve. The valves of the heart are composed of dense connective tissue covered by endocardium.
Right Ventricle
The right ventricle is about 4-5 mm (0.16-0.2 in.) in average thickness and forms most of the anterior surface of the heart. The inside of the right ventricle contains a series of ridges formed by raised bundles of cardiac muscle fibers called trabeculae carneae. Some of the trabeculae carneae convey part of the conduction system of the heart. The cusps of the tricuspid valve are connected to tendonlike cords, the chordae tendineae which in turn are connected to cone shaped trabeculae carneae called papillary muscles. Internally, the right ventricle is separated from the left ventricle by a partition called the interventricular septum. Blood passes from the right ventricle through the pulmonary valve (pulmonary semilunar valve) into a large artery called the pulmonary trunk, which divides into right and left pulmonary arteries. Arteries always take blood away from the heart.
Left Atrium
The left atrium is about the same thickness as the right atrium and forms most of the base of the heart. It receives blood from the lungs through four pulmonary veins. Like the right atrium, the inside of the left atrium has a smooth posterior wall. 8Because pectinate muscles are confined to the auricle of the left atrium, the anterior wall of the left atrium also is smooth. Blood passes from the left atrium into the left ventricle through the bicuspid (mitral) valve, which, as its name implies, has two cusps. The term mitral refers to the resemblance of the bicuspid valve to a bishop's miter (hat), which is two-sided. It is also called the left atrioventricular valve.
Left Ventricle
The left ventricle is the thickest chamber of the heart, averaging 10–15 mm (0.4–0.6 in.) and forms the apex of the heart. Like the right ventricle, the left ventricle contains trabeculae carneae and has chordae tendinae that anchor the cusps of the bicuspid valve to papillary muscles. Blood passes from the left ventricle through the aortic valve (aortic semilunar valve) into the ascending aorta. Some of the blood in the aorta flows into the coronary arteries, which branch from the ascending aorta and carry blood to the heart wall. The remainder of the blood passes into the arch of the aorta and descending aorta (thoracic aorta and abdominal aorta). Branches of the arch of the aorta and descending aorta carry blood throughout the body.
Atrioventricular Valves
The tricuspid and bicuspid (mitral) valve (Fig. 1.7) 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. 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. The chordae tendineae provide many cross-connections from one papillary muscle to two valve cusps or from trabeculae carneae in the ventricular wall directly to valves.
  • The adult 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).
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    Fig. 1.6: Cross-section of heart showing tricuspid, mitral, aortic and pulmonary valves
    The combined 9surface 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 principle 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 with a bishop's hat, or miter. 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.
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Fig. 1.7: Mitral valve and its associated structures
  • 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. Pressure in the atria exceeds that in the ventricles. The papillary muscles are relaxed. The valve cusps part, projecting into the ventricle, forming a funnel, which helps to promote blood flow into the ventricles. 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, 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 non-ventricular 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 8.5 cm in circumference, the pulmonic valve cusps are termed right anterior (right), left anterior (anterior), and posterior (left).
  • The aortic valve orifice 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 non-coronary (posterior or right posterior) aortic cusp (Fig. 1.8).
  • The two semilunar valves are approx-imately 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 crescentic 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 10of 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.
Two coronary arteries, the right and left coronary arteries, branch from the ascending aorta and supply oxygenated blood to the myocardium (Figs 1.9 and 1.10).
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 and then typically divides into two major branches: the left anterior descending artery and the left circumflex artery.
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Fig. 1.8: Aortic valve with coronary arteries
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, 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; 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 and second diagonal branch
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.
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Fig. 1.9: Coronary arteries anterior viewAbbreviations: LCA, left coronary artery; RCA, right coronary artery.
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Fig. 1.10: Coronary arteries posterior viewAbbreviations: LCA, left coronary artery; RCA, right coronary artery.
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.
First septal branch and minor septal branches
A variable number of septal branches occur. 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 and course in the septum from the 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.
Right ventricular branch
One or more right ventricular branches may exist. One runs toward the conus branch of the right coronary artery and may anastomose into the circle of Vieussens.
Apical branches
The final branches are the apical branches. These 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, it supplies the major perfusion of the sinus node; in 10% of cases, it supplies the AV node. 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. The branches of the circumflex artery, in order of origin, are as follows:
Atrial circumflex branch
The atrial circumflex branch is usually small in caliber but may be as wide as the remaining portion of the circumflex. It runs along the left AV groove and perfuses the left atrial wall.
Sinus node artery
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. This artery perfuses portions of the left and right atria as well as the sinus node.
Obtuse marginal branches
From one to four obtuse marginal branches may be seen. These 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.
Posterolateral branches
The posterolateral branches arise from the circumflex artery in 80% of cases. 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.
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. 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
The conus branch is small and exits within the first 2 cm of the right coronary artery in 60% of cases. It sometimes originates as a separate vessel with an ostium within a millimeter of the right coronary artery. 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.
Sinus Node Artery
The sinus node artery arises from the right coronary artery in 55% of cases. 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.
Right Ventricular Branches
Right ventricular branch arises from the right coronary artery courses along the AV groove and supplies ventricular wall.
Right Atrial Branch
The right atrial branch proceeds cranially toward the right heart border and perfuses the right atrium.
Acute Marginal Branch
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.
AV Nodal Branch
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.
Posterior Descending Branch
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.
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Fig. 1.11: Coronary veins
Left Ventricular Branch
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.
Left Atrial Branch
A left atrial branch may course along the posterior left AV groove and perfuse the left atrium.
Coronary Veins (Fig. 1.11)
After blood passes through the arteries of the coronary circulation, it flows into capillaries, where it delivers oxygen and nutrients to the heart muscle and collects carbon dioxide and waste, and then moves into coronary veins. Most of the deoxygenated blood from the myocardium drains into a large vascular sinus in the coronary sulcus on the posterior surface of the heart; called vascular sinus. It is a thin walled vein that has no smooth muscle to alter its diameter. The deoxygenated blood in the coronary sinus empties into the right atrium. The principle tributaries carrying blood into the coronary sinuses are the following:
  • Great cardiac vein in the anterior interventricular sulcus, which drains the areas of the heart supplied by the left coronary artery (left and right ventricles and left atrium).
  • Middle cardiac vein in the posterior interventricular sulcus, which drains the areas supplied by the posterior interventricular branch of the right coronary artery (left and right ventricles).
  • Small cardiac vein in the coronary sulcus, which drains the right atrium and right ventricle.
  • Anterior cardiac veins, which drain the right ventricle and open directly into the right atrium.
The resting coronary blood flow in the human being averages about 225 mL/min, which is about 4 to 5 percent of the total cardiac output. During strenuous exercise, the heart in the young adult increases its cardiac output fourfold to sevenfold, and it pumps this blood against a higher than normal arterial pressure. Consequently, the work output of the heart under severe conditions may increase sixfold to ninefold. At the same time, the coronary blood flow increases threefold to fourfold to supply the extra nutrients needed by the heart. This increase is not as much as the increase in workload, which means that the ratio of energy expenditure by the heart to coronary blood flow increases. Thus, the “efficiency” of cardiac utilization of energy increases to make-up for the relative deficiency of coronary blood supply.
Control of Coronary Blood Flow
Local Muscle Metabolism is the Primary Controller of Coronary Flow
Blood flow through the coronary system is regulated mostly by local arteriolar vasodilation in response to cardiac muscle need for nutrition. That is, whenever the vigor of cardiac contraction is increased, regardless of cause, the rate of coronary blood flow also increases. Conversely, decreased heart activity is accompanied by decreased coronary flow. This local regulation of coronary blood flow is almost identical to that occurring in many other tissues of the body, especially in the skeletal muscles all over the body.
Oxygen Demand as a Major Factor in Local Coronary Blood Flow Regulation
Blood flow in the coronaries usually is regulated almost exactly in proportion to the need of the cardiac musculature for oxygen. Normally, about 70 percent of the oxygen in the coronary arterial blood is removed as the blood flows through the heart muscle. Because not much oxygen is left, very little additional oxygen can be supplied to the heart musculature unless the coronary blood flow increases. Fortunately, the coronary blood flow does increase almost in direct proportion to any additional metabolic consumption of oxygen by the heart. However, the exact means by which increased oxygen consumption causes coronary dilation has not been determined. It is speculated by many research workers that a decrease in the oxygen concentration in the heart causes vasodilator substances to be released from the muscle cells and that these dilate the arterioles.
A substance with great vasodilator propensity is adenosine. In the presence of very low concentrations of oxygen in the muscle cells, a large proportion of the cell's ATP degrades to adenosine monophosphate; then small portions of these are further degraded and release adenosine into the tissue fluids of the heart muscle, with resultant increase in local coronary blood flow. After the adenosine causes vasodilation, much of it is reabsorbed into the cardiac cells to be reused. Adenosine is not the only vasodilator product that has been identified. Others include adenosine phosphate compounds, potassium ions, hydrogen ions, carbon dioxide, bradykinin, and possibly, prostaglandins and nitric oxide.
First, pharmacologic agents that block or partially block the vasodilator effect of adenosine do not prevent coronary vasodilation caused by increased heart muscle activity. Second, studies in skeletal muscle have shown that continued infusion of adenosine maintains vascular dilation for only 1 to 3 hours, and yet muscle activity still dilates the local blood vessels even when the adenosine can no longer dilate them.
Nervous Control of Coronary Blood Flow
Stimulation of the autonomic nerves to the heart can affect coronary blood flow both directly and indirectly. The direct effects result from action of the neurotransmitter substances acetylcholine from the vagus nerves and norepinephrine and epinephrine from the sympathetic nerves on the coronary vessels themselves.
The indirect effects result from secondary changes in coronary blood flow caused by increased or decreased activity of the heart. The indirect effects, which are mostly opposite to the direct effects, play a far more important role in normal control of coronary blood flow. Thus, sympathetic stimulation, which releases norepinephrine and epinephrine, increases both heart rate and heart contractility as well as increases the rate of metabolism of the heart. In turn, the increased metabolism of the heart sets off local blood flow regulatory mechanisms for dilating the coronary vessels, and the blood flow increases approximately in proportion to the metabolic needs of the heart muscle. In contrast, vagal stimulation, with its release of acetylcholine, slows the heart and has a slight depressive effect on heart contractility. These effects in turn decrease cardiac oxygen consumption and, therefore, indirectly constrict the coronary arteries.
Direct Effects of Nervous Stimuli on the Coronary Vasculature
The distribution of parasympathetic (vagal) nerve fibers to the ventricular coronary system is not very great. However, the acetylcholine released by parasympathetic stimulation has a direct effect to dilate the coronary arteries. There is much more extensive sympathetic innervations of the coronary vessels. The sympathetic transmitter substances norepinephrine and epinephrine can have either vascular constrictor or vascular dilator effects, depending on the presence or absence of constrictor or dilator receptors in the blood vessel walls. The constrictor receptors are called alpha receptors and the dilator receptors are called beta receptors. Both alpha and beta receptors exist in the coronary vessels. In general, the epicardial coronary vessels have a preponderance of alpha receptors, whereas the intramuscular arteries may have a preponderance of beta receptors. Therefore, sympathetic stimulation can, at least theoretically, cause slight overall coronary constriction or dilation, but usually constriction. In some people, the alpha vasoconstrictor 15effects seem to be disproportionately severe, and these people can have vasospastic myocardial ischemia during periods of excess sympathetic drive, often with resultant anginal pain. Metabolic factors—especially myocardial oxygen.
Consumption are the major controllers of myocardial blood flow. Whenever the direct effects of nervous stimulation alter the coronary blood flow in the wrong direction, the metabolic control of coronary flow usually overrides the direct coronary nervous effects within seconds.
Factors Affecting Blood Flow
  • Blood flow: It is the volume of blood that flows through any tissue in a given time period (in mL/min). Total blood flow is cardiac output (CO), the volume of blood that circulates through systemic (or pulmonary) blood vessels each minute. The cardiac output depends on heart rate and stroke volume—Cardiac output (CO) × Heart rate (HR) × stroke volume (SV). How the cardiac output becomes distributed into circulatory routes that serve various body tissues depends on two more factors:
    1. The pressure difference that drives the blood flow through a tissue
    2. The resistance to blood flow in specific blood vessels. Blood flows from regions of higher pressure to regions of lower pressure; the greater the pressure difference.
  • Blood pressure: Contraction of the ventricles generates blood pressure (BP), the hydrostatic pressure exerted by blood on the walls of a blood vessel. BP is determined by cardiac output blood volume, and vascular resistance. BP is highest in the aorta and large systemic arteries; in a resting, young adult, BP rises to about 110 mm Hg during systole (ventricular contraction) and drops to about 70 mm Hg during diastole (ventricular relaxation).
Systolic blood pressure is the highest pressure attained in arteries during systole, and diastolic blood pressure is the lowest arterial pressure during diastole. As blood leaves the aorta and flows through the systemic circulation, its pressure falls progressively as the distance from the left ventricle increases.
Blood pressure decreases to about 35 mm Hg as blood passes from systemic arteries through systemic arterioles and into capillaries, where the pressure fluctuations disappear. At the venous end of capillaries, blood pressure has dropped to about 16 mm Hg. Blood pressure continues to drop as blood enters systemic venules and then veins because these vessels are farthest from the left ventricle. Finally, blood pressure reaches 0 mm Hg as blood flows into the right ventricle.
Mean arterial pressure (MAP), it is the average blood pressure in arteries and it can be calculated as:
MAP = (SBP+2DBP)/3 or
MAP= DBP+ 1/3 (pulse pressure)
Vascular Resistance
Vascular resistance is the opposition to blood flow due to friction between blood and the walls of blood vessels.
Vascular resistance depends on:
Size of the Blood Vessel Lumen
The smaller the lumen of a blood vessel, the greater its resistance to blood flow. Resistance is inversely proportional to the fourth power of the diameter (d) of the blood vessel's lumen (R=1/d4). The smaller the diameter of the blood vessel, the greater the resistance it offers to blood flow. For example, if the diameter of a blood vessel decreases by one-half, its resistance to blood flow increases 16 times. Vasoconstriction narrows the lumen, and vasodilation widens it. Normally, moment-to-moment fluctuations in blood flow through a given tissues are due to vasoconstriction and vasodilation of the tissue's arterioles. As arterioles dilate, resistance decreases, and blood pressure falls. As arterioles constrict, resistance increases, and blood pressure rises.
Blood Viscosity
The viscosity (thickness) of blood depends mostly on the ratio of red blood cells to plasma (fluid) volume, and to a smaller extent on the concentration of proteins in plasma. The higher the blood's viscosity, the higher the resistance. Any condition that increases the viscosity of blood, such as dehydration or polycythemia (an unusually high number of red blood cells), thus increases blood pressure. A depletion of plasma proteins or red blood cells, due to anemia or hemorrhage, decreases viscosity and thus decreases blood pressure.
Total Blood Vessel Length
Resistance to blood flow through a vessel is directly proportional to the length of the blood vessel. The longer a blood vessel, the greater the resistance.
Obese people often have hypertension (elevated blood pressure) because the additional blood vessels in their adipose tissue increase their total blood vessel length. An estimated 650 km (about 400 miles) of additional blood vessels develop for each extra kilogram (2.2 lb) of fat.
Systemic vascular resistance (SVR), also known as total peripheral resistance (TPR), refers to all the vascular resistances offered by systemic blood vessels. The diameters of arteries and veins are large, so their resistance is very small because most of the blood does not come into physical contact with the walls of the blood vessel. The smallest vessels—arterioles, capillaries, and venules—contribute the most resistance. A major function of arterioles is to control SVR and therefore blood pressure and blood flow to particular tissues by changing their diameters.
Arterioles need to vasodilate or vasoconstrict only slightly to have a large effect on SVR. The main center for regulation of SVR is the vasomotor center in the brainstem.
Venous Return
The volume of blood flowing back to the heart through the systemic veins occurs due to the pressure generated by contractions of the heart's left ventricle. The pressure difference from venules (averaging about 16 mm Hg) to the right ventricle (0 mm Hg), although small, normally is sufficient to cause venous return to the heart. If pressure increases in the right atrium or ventricle, venous return will decrease. One cause of increased pressure in the right atrium is an incompetent (leaky) tricuspid valve, which lets blood regurgitate (flow backward) as the ventricles contract. The result is decreased venous return and build-up of blood on the venous side of the systemic circulation. When you stand-up, for example, the pressure pushing blood up the veins in your lower limbs is barely enough to overcome the force of gravity pushing it back down. Besides the heart, two other mechanisms “pump” blood from the lower body back to the heart— The skeletal muscle pump, the respiratory pump.
Both pumps depend on the presence of valves in veins. The skeletal muscle pump operates as follows:
  • While you are standing at rest, both the venous valve closer to the heart (proximal valve) and the one farther from the heart (distal valve) in this part of the leg are open, and blood flows upward toward the heart.
  • Contraction of leg muscles, such as when you stand on tiptoes or takes a step, compresses the vein. The compression pushes blood through the proximal valve, an action called milking. At the same time, the distal valve in the uncompressed segment of the vein closes as some blood is pushed against it. People who are immobilized through injury or disease lack these contractions of leg muscles. As a result, their venous return is slower and they may develop circulation problems.
  • Just after muscle relaxation, pressure falls in the previously compressed section of vein, which causes the proximal valve to close. The distal valve now opens because blood pressure in the foot is higher than in the leg, and the vein fills with blood from the foot.
  • The respiratory pump is also based on alternating compression and decompression of veins. During inhalation, the diaphragm moves downward, which causes a decrease in pressure in the thoracic cavity and an increase in pressure in the abdominal cavity. As a result, abdominal veins are compressed, and a greater volume of blood moves from the compressed abdominal veins into the decompressed thoracic veins and then into the right atrium. When the pressures reverse during exhalation, the valves in the veins prevent backflow of blood from the thoracic veins to the abdominal veins.
Velocity of Blood Flow
  • The speed or velocity of blood flow (in cm/sec) is inversely related to the cross-sectional area. Velocity is slowest where the total cross-sectional area is large. Each time an artery branches, the total cross-sectional area of all its branches is greater than the cross-sectional area of the original vessel, so blood flow becomes slower and slower as blood moves further away from the heart, and is slowest in the capillaries. Conversely, when venules unite to form veins, the total cross-sectional area becomes smaller and flow becomes faster.
  • In an adult, the cross-sectional area of the aorta is only 3–5 cm2, and the average velocity of the blood there is 40 cm/sec. In capillaries, the total cross-sectional area is 4500–6000 cm2, and the velocity of blood flow is less than 0.1 cm/sec. In the two venae cavae combined, the cross-sectional area is about 14 cm2, and the velocity is about 15 cm/sec. 17Thus, the velocity of blood flow decreases as blood flows from the aorta to arteries to arterioles to capillaries, and increases as it leaves capillaries and returns to the heart. The relatively slow rate of flow through capillaries aids the exchange of materials between blood and interstitial fluid.
  • Circulation time is the time required for a drop of blood to pass from the right atrium, through the pulmonary circulation, back to the left atrium, through the systemic circulation down to the foot, and back again to the right atrium. In a resting person, circulation time normally is about 1 minute.
An inherent and rhythmical electrical activity is the reason for the heart's lifelong beat. The source of this electrical activity is a network of specialized cardiac muscle fibers called autorhythmic fibers because they are self-excitable. Autorhythmic fibers repeatedly generate action potentials that trigger heart contractions. They continue to stimulate a heart to beat even after it is removed from the body for example, to be transplanted into another person and all of its nerves have been cut. Surgeons do not attempt to reattach heart nerves during heart transplant operations. For this reason, it has been said that heart surgeons are better “plumbers” than they are “electricians.” During embryonic development, only about 1% of the cardiac muscle fibers become autorhythmic fibers; these relatively rare fibers have two important functions.
  • They act as a pacemaker, setting the rhythm of electrical excitation that causes contraction of the heart.
  • They form the conduction system, a network of specialized cardiac muscle fibers that provide a path for each cycle of cardiac excitation to progress through the heart. The conduction system ensures that cardiac chambers become stimulated to contract in a coordinated manner, which makes the heart an effective pump.
Cardiac action potentials propagate through the conduction system in the following sequence (Fig. 1.12)
  • Cardiac excitation normally begins in the sinoatrial (SA) node, located in the right atrial wall just inferior and lateral to the opening of the superior vena cava. SA node cells do not have a stable resting potential. Rather, they repeatedly depolarize to threshold spontaneously. The spontaneous depolarization is a pacemaker potential. When the pacemaker potential reaches threshold, it triggers an action potential each action potential from the SA node propagates throughout both atria via gap junctions in the intercalated disks of atrial muscle fibers. Following the action potential, the atria contract.
  • By conducting along atrial muscle fibers, the action potential reaches the atrioventricular (AV) node, located in the interatrial septum, just anterior to the opening of the coronary sinus.
  • From the AV node, the action potential enters the atrioventricular (AV) bundle (also known as the bundle of His). This bundle is the only site where action potentials can conduct from the atria to the ventricles. (Elsewhere, the fibrous skeleton of the heart electrically insulates the atria from the ventricles.)
  • After propagating along the AV bundle, the action potential enters both the right and left bundle branches. The bundle branches extend through the interventricular septum toward the apex of the heart.
  • Finally, the large-diameter Purkinje fibers rapidly conduct the action potential beginning at the apex of the heart upward to the remainder of the ventricular myocardium. Then the ventricles contract, pushing the blood upward toward the semi lunar valves
    • On their own, autorhythmic fibers in the SA node would initiate an action potential about every 0.6 second, or 100 times per minute. This rate is faster than that of any other autorhythmic fibers. Because action potentials from the SA node spread through the conduction system and stimulate other areas before the other areas are able to generate an action potential at their own, slower rate, the SA node acts as the natural pacemaker of the heart. Nerve impulses from the autonomic nervous system (ANS) and blood-borne hormones (such as epinephrine) modify the timing and strength of each heartbeat, but they do not establish the fundamental rhythm. In a person at rest, for example, acetylcholine released by the parasympathetic division of the ANS slows SA node pacing to about every 0.8 second or 75 action Potentials per minute.
Action Potential and Contraction of Contractile Fibers
The action potential initiated by the SA node travels along the conduction system and spreads out to excite the “working” atrial and ventricular muscle fibers, called contractile fibers. An action potential occurs in a contractile fiber as follows:
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Fig. 1.12: Conduction of heart
Unlike autorhythmic fibers, contractile fibers have a stable resting membrane potential that is close to 90 mV. When a contractile fiber is brought to threshold by an action potential from neighboring fibers, its voltage gated fast Na+ channels open. These sodium ion channels are referred to as “fast” because they open very rapidly in response to a threshold-level depolarization. Opening of these channels allows Na+ inflow because the cytosol of contractile fibers is electrically more negative than interstitial fluid and Na+ concentration is higher in interstitial fluid. Inflow of Na+ down the electrochemical gradient produces a rapid depolarization. Within a few milliseconds, the fast Na+ channels automatically inactivate and Na+ inflow decreases.
The next phase of an action potential in a contractile fiber is the plateau, a period of maintained depolarization. It is due in part to opening of voltage-gated slow Ca2+ channels in the sarcolemma. When these channels open, calcium ions move from the interstitial fluid (which has a higher Ca2+ concentration) into the cytosol. This inflow of Ca2+ causes even more Ca2+ to pour out of the sarcoplasmic reticulum into the cytosol through additional Ca2+ channels in the sarcoplasmic reticulum membrane. The increased Ca2+ concentration in the cytosol ultimately triggers contraction.
Several different types of voltage-gated K+ channels are also found in the sarcolemma of a contractile fiber. Just before the plateau phase begins, some of these K+ channels open, allowing potassium ions to leave the contractile fiber. Therefore, depolarization is sustained during the plateau phase because Ca2+ inflow just balances K+ outflow. The plateau phase lasts for about 0.25 sec, and the membrane potential of the contractile fiber is close to 0 mV. By comparison, depolarization in a neuron or skeletal muscle lacks a plateau phase.
The recovery of the resting membrane potential during the repolarization phase of a cardiac action potential resembles that in other excitable cells. After a delay (which is particularly prolonged in cardiac muscle), additional voltage-gated K+ channels open. Outflow of K+ restores the negative resting membrane potential (–90 mV). At the same time, the calcium channels in the sarcolemma and the sarcoplasmic reticulum are closing, which also contributes to repolarization.
The mechanism of contraction is similar in cardiac and skeletal muscle: The electrical activity (action potential) leads to the mechanical response (contraction) after a short delay. As Ca2+ concentration raises inside a contractile fiber, Ca2+ binds to the regulatory protein troponin, which allows the actin and myosin filaments to begin sliding past one another, and tension starts to develop. Substances that alter the movement of Ca2+ through slow Ca2+ channels influence the strength of heart contractions. Epinephrine for example, increases contraction force by enhancing Ca2+ flow into the cytosol.
19In muscle, the refractory period is the time interval during which a second contraction cannot be triggered. The refractory period of a cardiac muscle fiber lasts longer than the contraction itself as a result; another contraction cannot begin until relaxation is well underway. For this reason, tetanus (maintained contraction) cannot occur in cardiac muscle as it can in skeletal muscle. The advantage is apparent if you consider how the ventricles work. Their pumping function depends on alternating contraction (when they eject blood) and relaxation (when they refill). If heart muscle could undergo tetanus, blood flow would cease.
Electrocardiogram (Fig. 1.13)
As action potentials propagate through the heart, they generate electrical currents that can be detected at the surface of the body. An electrocardiogram, abbreviated either ECG or EKG is a recording of electrical signals. The ECG is a composite record of action potentials produced by all the heart muscle fibers during each heartbeat. The instrument used to record the changes is an electrocardiograph.
In a typical record, three clearly recognizable waves appear with each heartbeat.
The first, called the P wave, is a small upward deflection on the ECG. The P wave represents atrial depolarization, which spreads from the SA node through contractile fibers in both atria.
The second wave, called the QRS complex, begins as a downward deflection, continues as a large, upright, triangular wave, and ends as a downward wave. The QRS complex represents rapid ventricular depolarization, as the action potential spreads through ventricular contractile fibers.
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Fig. 1.13: Normal ECG Wave
The third wave is a dome-shaped upward deflection called the T wave. It indicates ventricular repolarization and occurs just as the ventricles are starting to relax. The T wave is smaller and wider than the QRS complex because repolarization occurs more slowly than depolarization. During the plateau period of steady depolarization, the ECG tracing is flat.
Correlation of ECG Waves with Atrial and Ventricular Systole (Fig. 1.14)
The atria and ventricles depolarize and then contract at different times because the conduction system routes cardiac action potentials along a specific pathway. The term systole refers to the phase of contraction; the phase of relaxation is diastole dilation or expansion.
The ECG waves predict the timing of atrial and ventricular systole and diastole. At a heart rate of 75 beats per minute, the timing is as follows:
  • A cardiac action potential arises in the SA node. It propagates throughout the atrial muscle and down to the AV node in about 0.03 sec. As the atrial contractile fibers depolarize, the P wave appears in the ECG.
  • After the P wave begins, the atria contract (atrial systole). Conduction of the action potential slows at the AV node because the fibers there have much smaller diameters and fewer gap junctions. The resulting 0.1 sec delay gives the atria time to contract, thus adding to the volume of blood in the ventricles, before ventricular systole begins.
  • The action potential propagates rapidly again after entering the AV bundle. About 0.2 sec after onset of the P wave, it has propagated through the bundle branches, Purkinje fibers, and the entire ventricular myocardium. Depolarization progresses down the septum, upward from the apex, and outward from the endocardial surface, producing the QRS complex. At the same time, atrial repolarization is occurring, but it is not usually evident in an ECG because the larger QRS complex masks it.
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Fig. 1.14: Electrical events of cardiac cycle
  • Contraction of ventricular contractile fibers (ventricular systole) begins shortly after the QRS complex appears and continues during the S-T segment. As contraction proceeds from the apex toward the base of the heart, blood is squeezed upward toward the semilunar valves.
  • Repolarization of ventricular contractile fibers begins at the apex and spreads throughout the ventricular myocardium. This produces the T wave in the ECG about 0.4 sec after the onset of the P wave.
  • Shortly after the T wave begins, the ventricles start to relax (ventricular diastole). By 0.6 sec, ventricular repolarization is complete and ventricular contractile fibers are relaxed.
  • During the next 0.2 sec, contractile fibers in both the atria and ventricles are relaxed. At 0.8 sec, the P wave appears again in the ECG, the atria begin to contract, and the cycle repeats.
A single cardiac cycle includes all the events associated with one heartbeat. Thus, a cardiac cycle consists of systole and diastole of the atria plus systole and diastole of the ventricles.
Pressure and Volume Changes During the Cardiac Cycle (Fig. 1.16)
In each cardiac cycle, the atria and ventricles alternately contract and relax, forcing blood from areas of higher pressure to areas of lower pressure. As a chamber of the heart contracts, blood pressure within it increases. Each ventricle expels the same volume of blood per beat, and the same pattern exists for both pumping chambers. When heart rate is 75 beats/min, a cardiac cycle lasts 0.8 sec.
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Fig. 1.15: Cardiac cycle
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Fig. 1.16: Pressure and volume changes during cardiac cycle
Atrial Systole
During atrial systole, which lasts about 0.1 sec, the atria are contracting. At the same time, the ventricles are relaxed:
  • Depolarization of the SA node causes atrial depolarization, marked by the P wave in the ECG.
  • Atrial depolarization causes atrial systole. As the atria contract, they exert pressure on the blood within, which forces blood through the open AV valves into the ventricles.
  • Atrial systole contributes a final 25 mL of blood to the volume already in each ventricle (about 105 mL). The end of atrial systole is also the end of ventricular diastole (relaxation). Thus, each ventricle contains about 130 mL at the end of its relaxation period (diastole). This blood volume is called the end diastolic volume (EDV).
  • The QRS complex in the ECG marks the onset of ventricular depolarization.
Ventricular Systole
During ventricular systole, which lasts about 0.3 sec, the ventricles are contracting. At the same time, the atria are relaxed in atrial diastole.
  • Ventricular depolarization causes ventricular systole. As ventricular systole begins, pressure rises inside the ventricles and pushes blood up against the atrioventricular (AV) valves, forcing them shut. For about 0.05 seconds, both the SL (semilunar) and AV valves are closed. This is the period of isovolumetric contraction. During this interval, cardiac muscle fibers are contracting and exerting force but are not yet shortening. Thus, the muscle contraction is isometric (same length). Moreover, because all four valves are closed, ventricular volume remains the same (isovolumic).
  • Continued contraction of the ventricles causes pressure inside the chambers to rise sharply. When left ventricular pressure surpasses aortic pressure at about 80 millimeters of mercury (mm Hg) and right ventricular pressure rises above the pressure in the pulmonary trunk (about 20 mm Hg), both SL valves open. At this point, ejection of blood from the heart begins. The period when the SL valves are open is ventricular ejection and lasts for about 0.25 sec. The pressure in the left ventricle continues to rise to about 120 mm Hg, whereas the pressure in the right ventricle climbs to about 25–30 mm Hg.
  • The left ventricle ejects about 70 mL of blood into the aorta and the right ventricle ejects the same volume of blood into the pulmonary trunk. The volume remaining in each ventricle at the end of systole, about 60 mL, is the end systolic volume (ESV). Stroke volume, the volume of blood ejected per beat from each ventricle, equals end diastolic volume minus end systolic volume (SV= EDV – ESV).
  • The T wave in the ECG marks the onset of ventricular repolarization.
Relaxation Period
During the relaxation period, which lasts about 0.4 sec, the atria and the ventricles are both relaxed. As the heart beats faster and faster, the relaxation period becomes shorter and shorter, whereas the durations of atrial systole and ventricular systole shorten only slightly.
  • Ventricular repolarization causes ventricular diastole. As the ventricles relax, pressure within the chambers falls, and blood in the aorta and pulmonary trunk begins to flow backward toward the regions of lower pressure in the ventricles. Backflowing blood catches in the valve cusps and closes the semilunar valves. The aortic valve closes at a pressure of about 100 mm Hg. Rebound of blood off the closed cusps of the aortic valve produces the dicrotic wave on the aortic pressure curve. After the semilunar valves close, there is a brief interval when ventricular blood volume does not change because all four valves are closed. This is the period of isovolumetric relaxation.
  • As the ventricles continue to relax, the pressure falls quickly. When ventricular pressure drops below atrial pressure, the AV valves open and ventricular filling begins. The major part of ventricular filling occurs just after the AV valves open. Blood that has been flowing into and building up in the atria during ventricular systole then rushes rapidly into the ventricles. At the end of the relaxation period, the ventricles are about three-quarters full. The P wave appears in the ECG, signaling the start of another cardiac cycle.
Heart Sounds
Auscultation the act of listening to sounds within the body is usually done with a stethoscope. The sound of the heartbeat comes primarily from blood turbulence caused by the closing of the heart valves. Smoothly flowing blood is silent. Compare the sounds made by white water rapids or a waterfall with the silence of a smoothly flowing river. During each 23cardiac cycle, there are four heart sounds, but in a normal heart only the first and second heart sounds (S1 and S2) are loud enough to be heard through a stethoscope. The first sound (S1), which can be described as a lubb sound, is louder and a bit longer than the second sound. S1 is caused by blood turbulence associated with closure of the AV valves soon after ventricular systole begins. The second sound (S2), which is shorter and not as loud as the first, can be described as a dupp sound. S2 is caused by blood turbulence associated with closure of the semilunar valves at the beginning of ventricular diastole. Although S1 and S2 are due to blood turbulence associated with the closure of valves, they are best heard at the surface of the chest in locations that are slightly different from the locations of the valves. This is because the sound is carried by the blood flow away from the valves. Normally not loud enough to be heard, S3 is due to blood turbulence during rapid ventricular filling, and S4 is due to blood turbulence during atrial systole.
Cardiac Output
Although the heart has autorhythmic fibers that enable it to beat independently, its operation is governed by events occurring throughout the body. All body cells must receive a certain amount of oxygenated blood each minute to maintain health and life. When cells are metabolically active, as during exercise, they take-up even more oxygen from the blood. During rest periods, cellular metabolic need is reduced, and the workload of the heart decreases.
Cardiac output (CO) is the volume of blood ejected from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute. Cardiac output equals the stroke volume (SV), the volume of blood ejected by the ventricle during each contraction, multiplied by the heart rate (HR), the number of heartbeats per minute.
CO = SV × HR
This volume is close to the total blood volume, which is about 5 liters in a typical adult male. Thus, your entire blood volume flows through your pulmonary and systemic circulations each minute. Factors that increase stroke volume or heart rate normally increase CO. During mild exercise for example, stroke volume may increase to 100 mL/beat, and heart rate to 100 beats/min. Cardiac output then would be 10 L/min. During intense (but still not maximal) exercise, the heart rate may accelerate to 150 beats/min, and stroke volume may rise to 130 mL/beat, resulting in a cardiac output of 19.5 l/min.
Cardiac reserve is the difference between a person's maximum cardiac output and cardiac output at rest. The average person has a cardiac reserve of four or five times the resting value. Top endurance athletes may have a cardiac reserve seven or eight times their resting CO. People with severe heart disease may have little or no cardiac reserve, which limits their ability to carry-out even the simple tasks of daily living.
Regulation of Stroke Volume
A healthy heart will pump out the blood that entered its chambers during the previous diastole. In other words, if more blood returns to the heart during diastole, then more blood is ejected during the next systole. At rest, the stroke volume is 50–60% of the end diastolic volume because 40–50% of the blood remains in the ventricles after each contraction (end systolic volume).
Three factors regulate stroke volume and ensure that the left and right ventricles pump equal volumes of blood:
  • Preload, the degree of stretch on the heart before it contracts
  • Contractility, the forcefulness of contraction of individual ventricular muscle fibers
  • Afterload is the peripheral resistance against which the left ventricle has to pump.
Preload Effect of Stretching
  • A greater preload (stretch) on cardiac muscle fibers prior to contraction increases their force of contraction. Preload can be compared to the stretching of a rubber band. The more the rubber band is stretched, the more forcefully it will snap back. Within limits, the more the heart fills with blood during diastole, the greater the force of contraction during systole. This relationship is known as the Frank-Starling law of the heart. The preload is proportional to the end diastolic volume (EDV) (the volume of blood that fills the ventricles at the end of diastole). Normally, the greater the EDV, the more forceful the next contraction.
  • Two key factors determine EDV: (1) the duration of ventricular diastole and (2) venous return, the volume of blood returning to the right ventricle. When heart rate increases, the duration of diastole is shorter. Less filling time means a smaller EDV, and the ventricles may contract before they are adequately filled. By contrast, when venous return increases, a greater volume of blood flows into the ventricles, and the EDV is increased.
The second factor that influences stroke volume is myocardial contractility, the strength of contraction at any given preload. Substances that increase contractility are positive inotropic agents; those that decrease contractility are negative inotropic agents. Thus, for a constant preload, the stroke volume increases when a positive inotropic substance is present. Positive inotropic agents often promote Ca2+ inflow during cardiac action potentials, which strengthens the force of the next contraction. Stimulation of the sympathetic division of the autonomic nervous system (ANS), hormones such as epinephrine and norepinephrine, increased Ca2+ level in the interstitial fluid, and the drug digitalis all have positive inotropic effects. In contrast, inhibition of the sympathetic division of the ANS, anoxia, acidosis, some anesthetics, and increased K+ level in the interstitial fluid have negative inotropic effects. Calcium channel blockers are drugs that can have a negative inotropic effect by reducing Ca2+ inflow, thereby decreasing the strength of the heartbeat.
Ejection of blood from the heart begins when pressure in the right ventricle exceeds the pressure in the pulmonary trunk (about 20 mm Hg), and when the pressure in the left ventricle exceeds the pressure in the aorta (about 80 mm Hg). At that point, the higher pressure in the ventricles causes blood to push the semilunar valves open. The pressure that must be overcome before a semilunar valve can open is termed the afterload. An increase in afterload causes stroke volume to decrease, so that more blood remains in the ventricles at the end of systole. Conditions that can increase afterload include hypertension (elevated blood pressure) and narrowing of arteries by atherosclerosis.