Chapter Nineteen - The Circulatory System: The Heart
I. Gross Anatomy (p. 674)
A. Overview of the Cardiovascular System (p. 674; Fig. 19.1; Transp. 359)
1. The heart and blood vessels make up the cardiovascular system, which transports blood throughout the body.
2. The cardiovascular system has two major divisions: a pulmonary circuit, which serves the lungs, and a systemic circuit, which supplies blood to the remainder of the body. The right side of the heart sends blood to the pulmonary circuit. The left side of the heart sends blood to the systemic circuit.
3. The major arteries and veins close to the heart are called the great vessels because of their relatively large diameters.
B. Size, Shape, and Position of the Heart (p. 674; Figs. 19.2, 19.3)
1. The heart lies at the center of the thoracic cavity in the mediastinum. Its broad, superior portion (the base) is the point of attachment for the great vessels.
2. The heart weighs about 300 g (10 oz).
C. The Pericardium (p. 675; Fig. 19.4; Transp. 360)
1. The heart is enclosed in a double-walled sac called the pericardium.
2. The parietal pericardium consists of a tough, fibrous layer of dense connective tissue with a thin, smooth, moist serous layer.
3. The serous layer turns in at the base of the heart, forming the visceral pericardium covering the heart surface.
4. Between the parietal and visceral pericardia is a space called the pericardial cavity. It contains pericardial fluid that lubricates the membranes and allows the heart to beat almost without friction.
D. The Heart Wall (p. 677)
1. The heart consists of three layers: the epicardium, myocardium, and endocardium.
2. The epicardium is a serous membrane overlying a thin layer of areolar tissue. In many areas, it has thick deposits of adipose tissue.
3. The myocardium is composed of cardiac muscle and forms the bulk of the heart. It performs the work of the heart. Muscle fibers are bound together by a fibrous skeleton that serves to provide support for the heart, gives the muscle something to pull against, and limits the routes by which electrical activity can travel through the heart.
4. The endocardium is made up of a layer of endothelium overlying a thin layer of areolar tissue. It forms the smooth inner lining of the chambers and valves and is continuous with the endothelium of the blood vessels.
E. The Chambers (p. 677; Fig. 19.5; Transp. 361)
1. The heart has four chambers.
2. The right and left atria receive blood flowing to the heart. Each atrium has a small ear-like extension called an auricle that slightly increases its volume.
3. The two inferior chambers, the left and right ventricles, pump the blood into the arteries for distribution elsewhere.
4. Other features of the heart include the atrioventricular sulcus, the anterior and posterior interventricular sulci, the interatrial septum, and the interventricular septum.
F. The Valves (p. 677; Figs. 19.5 - 19.7; Transps. 361-363)
1. Valves prevent the back flow of blood into the heart. The pulmonary valve guards the opening from the right ventricle to the pulmonary trunk. The aortic valve guards the opening from the left ventricle to the aorta. Both these valves are called semilunar valves because of the moonlike shape of their three cusps.
2. An atrioventricular (AV) valve guards the opening between each atrium and ventricle. The right AV valve is also known as the tricuspid valve, the left is also called the bicuspid or mitral valve. String-like chordae tendineae attach the valve cusps to papillary muscles.
3. The opening a closing of the heart valves is the result of pressure gradients from one side of the valve cusps to the other.
G. Blood Flow Through the Heart Chambers (p. 679; Fig. 19.8; Transp. 364)
1. The path that blood takes on its journey through the heart is depicted in Fig. 19.8, p. 681; Transp. 364.
H. Blood Flow Through the Myocardium (p. 681)
1. Although the heart accounts for a tiny fraction of the body weight, it uses 5% of its output to supply its own needs. The myocardium has an extensive network of coronary arteries to ensure an adequate blood supply to itself.
2. Arterial Supply (p. 681; Fig. 19.9; Transp. 365)
a. The first branches off the aorta are the right and left coronary arteries.
b. The left coronary artery supplies blood to the left side of the heart and divides into the anterior interventricular and circumflex arteries.
c. The right coronary artery supplies blood to the right side of the heart and divides into the marginal and posterior interventricular arteries.
d. A myocardial infarction occurs when any of the coronary arteries become occluded with plaque, and a portion of the heart muscle dies from lack of blood flow.
3. Venous Drainage (p. 682)
a. Venous drainage refers to the route by which blood leaves an organ. Blood leaving capillaries collects in small veins that merge to form larger veins. These lead to the great cardiac veins that drains the anterior aspect of the heart, and the middle cardiac vein that collects blood from the posterior aspect of the heart.
b. The great and middle cardiac veins drain into the cardiac sinus that empties into the right atrium.
4. Perfusion in Relation to the Cardiac Cycle (p. 682)
a. In most of the body, arterial blood flow is greater when the ventricles are contracting than it is when they relax. In the coronary arteries, however, flow is greater when the ventricles relax.
I. Development of the Heart (p. 682; Fig. 19.10)
1. A four-chambered heart with complete separation of the pulmonary and systemic circuits is achieved only in birds, mammals, and a few reptiles. This ensures that the organs of the systemic circuit receive only "fresh" fully oxygenated blood has not mixed with the "stale" deoxygenated blood.
2. The four chambers of the human heart are essential for the support of our high metabolic rate.
3. The evolutionary history of the human heart is somewhat replayed in its embryonic development.
II. Cardiac Muscle and the Cardiac Conduction System (p. 683)
A. Structure of Cardiac Muscle (p. 683; Fig. 19.11; Transp. 366)
1. Cardiac muscle cells (myocytes) are different from skeletal muscle fibers in that they are relatively short, thick, branching cells that have one nucleus. The sarcoplasmic reticulum (SR) is less developed, lacks terminal cisternae, but T tubules are larger than in skeletal muscle.
2. Each myocyte is surrounded by a connective tissue endomysium, which allows access to blood capillaries.
3. The myocytes are joined end to end by intercalated disks, which have three distinct features: the plasma membranes of the adjacent cells display interdigitating folds; the cells are tightly joined by desmosomes; and there are gap junctions between the cells.
4. The muscle of a given heart chamber is sometimes described as a functional syncytium.
B. Metabolism of Cardiac Muscle (p. 684)
1. At rest, the heart gets 60% of its energy from fatty acids, 35% from glucose, and 5% from other fuels. Cardiac muscle is more vulnerable to oxygen deficiency than it is to a lack of fuel.
2. Heart muscle is not prone to fatigue because it makes little use of anaerobic fermentation or the oxygen debt mechanism.
C. The Cardiac Conduction System (p. 685; Fig. 19.12; Transp. 367)
1. Vertebrate hearts are myogenic because the pacemaker is in the heart itself, and the autonomic nervous system can only modify heart rate.
2. Cardiac myocytes are autorhythmic. Some of them lose their ability to contract and become specialized for generating and transmitting action potentials. These make up the cardiac conduction system.
3. The cardiac conduction system begins with the sinoatrial (SA) node, which serves as the pacemaker. Signals from the SA node spread throughout the atria and on to the atrioventricular (AV) node near the lower interatrial septum. The AV node is an electrical gateway to the ventricles. The AV bundle leaves the AV node and divides into right and left bundle branches leading into the interventricular septum. Next, the impulse is spread to the Purkinje fibers.
4. In addition to setting heart rate, the cardiac conduction system controls the route and timing of electrical conduction. The four chambers must contract in a coordinated fashion.
5. Failure of any part of the cardiac conduction system to transmit signals is called a heart block.
III. Electrical and Contractile Activity of the Heart (p. 686)
A. The Cardiac Rhythm (p. 686)
1. The normal heartbeat generated by the SA node is called the sinus rhythm, and shows a resting rate of 70-80 bpm. The SA node tends to speed up, and the vagus nerve keeps a brake of heart rate.
2. Sometimes regions other than the SA node fire spontaneously; these are called ectopic foci.
3. An abnormal cardiac rhythm is called arrhythmia.
B. Physiology of the SA Node (p. 686; Fig. 19.13; Transp. 368)
1. The autorhythmic cells of the SA node have a resting potential that starts at -60mV and then drifts spontaneously upward. This gradual depolarization is called the pacemaker potential. The reason for it is uncertain.
2. When the pacemaker potential reaches -40mV (threshold), fast calcium channels open and calcium rushes in. This produces a rising phase of action potential.
3. Next, potassium channels open, potassium rushes out of the cell, and the cytosol becomes more negative, creating a falling phase of action potential.
4. When repolarization is complete, potassium channels close again and the pacemaker potential begins anew. One depolarization of the SA node sets off one heartbeat, and also triggers depolarization in the remainder of the cardiac conduction system.
C. Impulse Conduction to the Myocardium (p. 687)
1. Firing of the SA node stimulates the two atria to contract together almost immediately.
2. Next, impulses travel to the AV node where thinner myocytes slow the impulse momentarily. This gives the ventricles time to fill with blood before contracting.
3. The signal reaches the AV bundle and spreads rapidly through fast Purkinje fibers, causing the entire ventricular myocardium to depolarize and ventricles to contract in unison.
4. The impulse reaches the papillary muscle slightly before it spreads throughout the ventricles, allowing the papillary muscles to tighten chordae tendineae on the AV valves first.
D. Electrical Behavior of the Myocardium (p. 687; Fig. 19.14; Transp. 369)
1. Contractile myocytes exhibit action potentials that are different than neurons or skeletal muscle. They have a stable RMP of -90 mV and depolarize only when stimulated. The influx of sodium ions and depolarization of the myocytes is similar to that seen in neurons.
2. Depolarization of a myocyte, with its sparse SR, causes release of supplemental calcium ions from the ECF. Unlike cardiac muscle, the SR of skeletal muscle contains sufficient calcium.
3. In skeletal muscle and neurons, an action potential falls back to RMP within 2 msec, but in cardiac muscle, slow calcium channels remain open longer (after sodium channels close) prolonging the depolarization of the cell. As long as the action potential is in its plateau and calcium is entering the myocytes, the myocytes contract. These plateaus are more pronounced in the ventricles.
4. Cardiac muscle has an absolute refractory period of 250 msec, compared with 1-2 msec of skeletal muscle.
E. The Electrocardiogram (p. 688; Figs. 19.15 - 19.17; Transps. 370, 371; Table 19.1)
1. Electrical currents generated in the heart can be detected by recording electrodes on the skin. An electrocardiograph amplifies these signals and produces an electrocardiogram (ECG).
2. An ECG shows three principal deflections: the P wave, the QRS complex, and the T wave.
a. The P wave corresponds with depolarization of the atria.
b. The QRS wave marks ventricular depolarization. Atrial repolarization also occurs at the same time, but the signal is hidden by the strong wave of depolarization seen in the ventricles.
c. The T wave is generated by ventricular repolarization immediately before diastole.
d. The ECG affords a wealth of information about the normal electrical activity of the heart. Deviations from the norm are invaluable to the clinician.
IV. Blood Flow, Heart Sounds, and the Cardiac Cycle (p. 691)
A. The cardiac cycle consists of one complete cycle of contraction and relaxation. Its major events, in order of occurrence, are atrial systole, ventricular systole (with simultaneous atrial diastole), ventricular diastole, and a quiescent period.
B. Principles of Pressure and Flow (p. 691)
1. Measurement of Pressure (p. 691)
a. Pressure is often measured by observing how high it can push a column of mercury (Hg) up a manometer.
b. Blood pressure is usually measured with a sphygmomanometer.
2. Pressure Gradients and Flow (p. 691; Fig. 19.18; Transp. 372)
a. Any change in the volume of a container creates a pressure gradient. Pressure gradients cause the alternate opening and closing of heart valves.
b. There is always a positive blood pressure in the aorta, and if it is greater than the pressure in the ventricle, it holds the aortic valve closed and prevents the back flow of blood. When continuing ventricular contraction causes its internal pressure to rise above aortic pressure, the valve is forced open, and blood enters the aorta.
C. Heart Sounds (p. 691)
1. Heart sounds, as heard through a stethoscope, result from the closing of the valve and the turbulence of the blood against the inner heart wall.
2. Heart sounds are described as a "lubb-dupp", or first and second heart sounds (S1 and S2). S1 is louder and longer, while S2 is softer and sharper.
D. Phases of the Cardiac Cycle (p. 692; Fig. 19.19; Transp. 373)
1. Refer to Fig. 19.19, p. 693 (Transp. 373) to examine the phases of the cardiac cycle, pressure changes, and how the pressure changes and valves govern the flow of blood.
2. The cycle begins with the quiescent period in which the heart is at rest, blood is flowing into the atria, and AV valves are open, allowing blood to passively flow through to the ventricles.
3. The SA nodes fire, and atrial systole results.
4. Third, isovolumetric contraction of the ventricles occurs after the ventricles depolarize. The AV valves close as ventricular blood surges back against the cusps. This phase is called isovolumetric because the ventricles do not yet eject blood and there is no change in their volume even though they are contracting.
5. Next comes ventricular ejection, in which the amount known as stroke volume passes into the major vessels on top of the heart.
6. Isovolumetric relaxation and ventricular filling follow, completing one cardiac cycle. Pressure changes that occur coincident with these events are best viewed in Fig. 19.19; Transp. 373.
E. Overview of Volume Changes (p. 694; Fig. 19.20; Transp. 374)
1. Viewing the balance sheet, p. 694, it is evident that the ventricle pumps out as much blood as it received during diastole. The two ventricles eject the same amount of blood, but pressure is less in the right ventricle than it is in the left. The left ventricle contracts with greater force to overcome the arterial pressure of the systemic circuit.
V. Cardiac Output (p. 696)
A. Heart Rate (p. 696)
1. Cardiac output (CO) is the volume pumped by each ventricle per minute. A person's cardiac reserve is the difference between maximum and resting cardiac output. Agents that raise and lower the heart rate are called positive and negative chronotropic agents; agents that alter stroke volume of the ventricles are inotropic agents.
2. The resting heart rate of an adult is 64-72 in males, and 72-80 in females. In infants, it is 120 bpm or more.
3. Tachycardia is a persistent, resting heart rate above 100 bpm. This can be caused by anxiety, drugs, heart disease, or elevated body temperature. The opposite condition, bradycardia, is a persistent resting adult heart rate of less than 60 bpm. This can be seen in well-conditioned athletes, but can also indicate hypothermia and occurs with immersion of the face in water.
4. Chronotropic Effects of the Autonomic Nervous System (p. 696)
a. The cardiac center of the medulla oblongata receives input from the cerebral cortex, limbic system, and hypothalamus; many sensory and emotional stimuli can alter heart rate. The cardiac center also monitors the condition of the body through input received from proprioceptors, chemoreceptors, and baroreceptors, and can adjust heart rate accordingly.
b. The cardiac center is divided into a cardioacceleratory center and a cardioinhibitory center that connect by nerves to the SA node.
5. Chronotropic Effects of Chemicals (p. 697)
a. Sympathetic neurotransmitters and adrenal gland hormones can accelerate heart rate, as can arousal, and stress.
b. Chemicals that lower heart rate include sodium (in hypernatremia), and potassium (hyperkalemia), the latter of which can kill. Hypercalcemia increases heart rate and can lead to cardiac arrest.
B. Stroke Volume (p. 697)
1. Preload (p. 697)
a. Stroke volume is governed mainly by preload, contractility, and afterload.
b. The amount of tension in the ventricular myocardium immediately before it begins to contract is called preload.
c. As more blood enters the heart, it stretches the myocardium. Due to the length-tension relationship, moderate stretch enables myocytes to generate more tension during contraction. If the ventricles contract more forcefully, they expel more blood, thus adjusting cardiac output to the increase in venous return.
d. This relationship is summarized by the Frank-Starling law of the heart, which states, in essence, that the ventricles tend to pump out all the blood that entered them.
2. Contractility (p. 698; Table 19.2)
a. The contractility of the myocardium refers to its strength of contraction for a given preload. It can increase as a result of inotropic factors that make the myocytes more responsive to stimulation, such as calcium, epinephrine, norepinephrine, and glucagon.
b. Negative inotropic agents include myocardial hypoxia, hypercapnia, acidosis, and barbiturates.
3. Afterload (p. 698)
a. The blood pressure in the arteries just outside the semilunar valves, called the afterload, opposes the opening of these valves. An increased afterload, then, reduces stroke volume. Anything that impedes arterial circulation (scar tissue in the lungs, for example) can increase the afterload.
b. As the ventricle works harder to overcome the overload, it hypertophies. Stress and hypertrophy of a ventricle can eventually cause it to weaken and fail.
C. Exercise and Cardiac Output (p. 698)
1. The act of exercise increases cardiac output because proprioceptors signify the cardiac center that the muscles are active and need more oxygen delivery and carbon dioxide removal. During exercise, venous return to the heart increases, which increases preload on the heart.
2. A sustained program of exercise causes hypertrophy of the ventricles, which increases their stroke volume, and lowers heart rate. Athletes have greater cardiac reserve, so they can tolerate more exertion than a sedentary person can.
CHAPTER ESSAY: Coronary Atherosclerosis (p. 699; Fig. E.1)
i. Atherosclerosis is a disorder in which fatty plaque is deposited in arteries, causing damage to the arterial wall and blocking the lumen.
ii. The cause of atherosclerosis is high low-density lipoproteins in the blood plasma; arterial cells dysfunction by taking up too much of these plasma lipids and building up cholesterol.
iii. Risk factors for coronary atherosclerosis are hereditary hypercholesterolemia, diet, cigarette smoking, dietary fat, and dietary fiber intake.
iv. Treatments for atherosclerosis include coronary artery bypass surgery, balloon angioplasty, laser angioplasty, and, the best, prevention.
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