1. Cardiovascular System Heart
Cardiovascular System Heart

2. Much of the text material is from, “Principles of Anatomy and Physiology (12th edition)” by Gerald J. Tortora and Bryan Derrickson (2009). I don’t claim authorship. Other sources are noted when they are used.
Mapping of the lecture slides to the 13th edition is provided in the supplement.

3. Outline Structure Blood circulation
Cardiac muscle tissue and conduction system
Electrocardiography
Cardiac cycle
Cardiac output
Physical exercise and the heart

4. Some Statistics
The heart beats about 100,000 times each day, and about 2.5 billion times in a lifetime.
It pumps about 5 liters of blood per minute, and about 10 million liters in a year.
An even greater volume of blood is pumped to meet tissue demands during physical activity.
Chapter 20, page 717

5. Cardiology
The scientific study of the normal heart and its associated diseases is known as cardiology.
It is becoming an increasing more needed specialty as the population ages.
Chapter 20, page 717

6. Structure

7. Postnatal = after birth.
Circulation
Postnatally, the heart pumps blood into two closed circuits known as systemic circulation and pulmonary circulation.
The circuits are arranged in series so that the output of one becomes the input to the other.
Postnatal = after birth.
Chapter 20, page 728
Figure 20.7

8. Size
The heart is fairly small, measuring about the size, but not the shape, of a closed fist.
It has a mass of about 250 grams in adult females and about 300 grams in adult males.
Chapter 20, page 717
Figure 20.1

9. Location
The heart rests on the diaphragm near the midline of the thoracic cavity, with about two-thirds of the heart usually to the left of the body’s midline.
The heart is located in the mediastinum, the region extending from the sternum to the vertebral column, from the first rib to the diaphragm, and between the lungs.
Chapter 20, page 717
Figure 20.1

10. Pericardium
The pericardium is a membrane that surrounds and protects the heart.
The membrane confines the heart to the mediastinum, while allowing space for movement during rapid and forceful cardiac contractions.
The membrane is a fibrous tissue to prevent overstretching of the heart.
The pericardial cavity located between the pericardium and heart con-tains a small amount of pericardial fluid.
The fluid reduces the friction between the two tissues during contraction of the heart.
Chapter 20, page 719
Figure 20.2

11. Pericardium

12. Heart Wall
The heart wall has three layers—epicardium, myocardium, and endo-cardium.
The epicardium is a thin, transparent outer layer.
The myocardium is muscle tissue—it is about 95 percent of the mass of the heart (much more will be said about the myocardium in this lec-ture).
Chapter 20, page 720
Figure 20.2

13. Heart Wall (continued)
The endocardium, the inner layer, provides a smooth lining for the heart chambers and its valves.
The layer is continuous with the endothelial lining of the large blood ves-sels to minimize surface friction and turbulent blood flow.
The surface of the heart has grooves, or sulci, that contain the coronary arteries along with some fatty tissue.
Chapter 20, page 720
Figure 20.2

14. Heart Chambers The heart has four chambers:
The atria are the two superior receiving chambers for blood.
The ventricles are the two inferior pumping chambers for blood.
Each atrium has a pouch-like structure on its anterior surface that slightly increases its volume.
Chapter 20, page 720
Figure 20.3

15. Heart Chambers (continued)

16. Deoxygenated = oxygen-poor.
Right Chambers
The right atrium receives deoxygenated blood from three major veins— superior vena cava, inferior vena cava, and coronary sinus.
Blood passes from the right atrium into the right ventricle through the tri-cuspid valve.
Blood is ejected from the right ventricle through the pulmonary valve into pulmonary circulation.
Deoxygenated = oxygen-poor.
Pulmonary circulation = the circulation of blood through the lungs for the purpose of oxygenation and the release of carbon dioxide. (
Chapter 20, page 722
Figure 20.4

17. Left Chambers
The left atrium receives oxygenated blood from the lungs via the pul-monary veins.
Blood passes from the left atrium to left ventricle through the biscuspid, or mitral, valve.
Blood is ejected from the left ventricle through the aortic valve into sys-temic circulation.
Systemic circulation = circulation of blood throughout the body through the arteries, capillaries, and veins, which carry oxygen-ated blood from the left ventricle to various tissues and return venous blood to the right atrium. (
Chapter 20, page 722
Figure 20.4

18. Left Chambers (continued)
A small amount of aortic blood flows into the coronary arteries to supply the heart wall.
Most of the aortic blood, however, is distributed to other organs and tis-sues.
Chapter 20, page 722
Figure 20.4

19. Fetal Circulation
During the fetal period, a temporary blood vessel known as the ductus arteriosus shunts blood from the pulmonary trunk into the aorta.
Therefore, very little blood enters into the non-functioning fetal lungs— the notes on bloods vessels covered in Chapter 21 contain more detail.
Chapter 20, page 724
Figure 21.30

20. Pressure Demands
The right and left ventricles are two separate pumps that eject equal volumes of blood.
The right ventricle pumps blood to the lungs at relatively low pres-sure since flow resistance in pulmonary circulation is relatively low.
The left ventricle pumps blood to all other parts of the body at higher pressure since flow resistance in systemic circulation is much higher than in pulmonary circulation.
The mechanisms of flow resistance in blood vessels will be described in the lecture notes for Chapter 21.
Chapter 20, page 724
Figure 20.4

21. Myocardial Thickness
The thickness of the myocardium of each chamber is related to the pres-sure demands.
The thin-walled right and left atria deliver blood under low-pressure to the ventricles.
The walls of the ventricles are thicker since they pump blood at higher pressures into systemic and pulmonary circulations.
The left ventricle has the thickest wall (10-to-15 mm) for the high pres-sure of systemic circulation.
Chapter 20, page 724
Figure 20.4

22. Fibrous Skeleton
The heart wall contains a dense connective tissue that forms its fibrous skeleton.
The fibrous skeleton has four rings of connective tissue that surround the heart valves and merge with the intraventricular septum.
The rings provide a structural framework for the heart valves to prevent overstretching as blood passes through them.
The fibrous skeleton is also an electrical insulator between the atria and ventricles, which is important during the propagation of action potentials generated by the heart.
Chapter 20, page 725
Figure 20.5

23. Valve Operation
The valves open and close in response to pressure changes as the heart contracts and relaxes.
They ensure the one-way flow of blood by opening to enable blood to flow through, and then closing to prevent backflow into each chamber.
Chapter 20, page 725

24. Tricuspid and Bicuspid Valves
The tricuspid and bicuspid (mitral) valves are found on the right and left sides of the heart, respectively.
They are located between the atria and ventricles, and are also known as the atrioventricular (AV) valves.
Chapter 20, page 725
Figure 20.6

25. Tricuspid and Bicuspid Valves (continued)
Bicuspid (mitral) valve
Tricuspid valve

26. Tricuspid and Bicuspid Valves (continued)
The rounded edges of the cusps extend into the ventricle when the AV valve is open to permit blood flow.
When the ventricle contracts, the increased blood pressure in the cham-ber closes the cusps.
Papillary muscles help to assure that the valves cannot open under high ventricular pressure.
Chapter 20, page 725
Figure 20.6

27. Semilunar Valves
The aortic and pulmonary valves in the ventricles are also known as the semilunar valves due to their crescent shapes.
The semilunar valves enable the ejection of blood into the systemic and pulmonary arteries, while preventing backflow into the left and right ven-tricles.
The two valves open when ventricular pressure exceeds the pressures in the aorta and pulmonary artery.
Chapter 20, page 725
Figure 20.6
Crescent shape

28. Semilunar Valves (continued)
Aortic valve
Pulmonary valve

29. Semilunar Valves (continued)
Some of the blood ejected into the aorta and pulmonary artery will flow toward the heart when the ventricles relax.
This blood fills the cusps of the semilunar valves, and closes the valves to prevent backflow into the ventricles.
Chapter 20, page 725
Figure 20.6

30. Where Valves Are Absent
No valves exist between the vena cavae and the right atrium, and the pulmonary veins and the left atrium.
When the atria contract, a small amount of blood flows from the atrial chambers into these veins.
These venous entry points almost collapse to minimize backflow into the veins.
Chapter 20, page 727

31. Blood Circulation

32. Circulatory System
The left side of the heart serves as the pump for systemic circulation— it receives oxygenated blood from the lungs.
The right side of the heart serves as the pump for pulmonary circula-tion—it receives deoxygenated blood from the organs and other body tissues.
Chapter 20, page 728
Figure 20.7

33. Circulatory System (continued)

34. Systemic Circulation
The left ventricle pumps oxygenated blood into the aorta for systemic circulation.
Blood enters progressively smaller arteries as it travels to organs and other tissues.
The smallest arteries branch into even smaller-diameter arterioles that lead to extensive beds of capillaries in body tissues.
Chapter 20, page 728
Figure 20.7

35. Systemic Circulation (continued)
The exchange of gases (O2 and CO2), nutrients, and waste products occurs across the thin capillary walls.
The blood then flows into a venule and progressively larger veins on its return to the heart.
Chapter 20, page 728
Figure 20.7

36. Pulmonary Circulation
The right atrium receives deoxygenated blood from the veins of the systemic circulatory system and pumps it into pulmonary circulation.
Blood pumped from the right ventricle flows into the pulmonary trunk, which branches into pulmonary arteries.
Each pulmonary artery carries blood to either the left lung or right lung.
Chapter 20, page 728
Figure 20.7

37. Pulmonary Circulation (continued)
Progressively smaller-diameter arteries eventually branch into beds of capillaries in the lungs.
The capillaries exchange O2 and CO2 with air sacs known as aveoli.
The freshly-oxygenated blood flows into the pulmonary veins and into the left atrium.
Chapter 20, page 728
Figure 20.7

38. Coronary Circulation
Oxygen and nutrients cannot diffuse from the blood within the heart cham-bers to supply the needs of cardiac tissues.
The myocardium has a network of blood vessels for coronary, or cardiac, circulation.
The coronary arteries branch from the ascending aorta to form a crown-like shape around the heart.
Chapter 20, page 728
Figure 20.8

39. Coronary Circulation (continued)
Aorta
Right coronary
artery
Left coronary
Right pulmonary

40. Coronary Circulation (continued)
When the heart contracts, very little blood can flow into the coronary arteries because they are squeezed shut.
When the heart relaxes, the pressure in the aorta propels oxygen-ated blood into the coronary arteries.
The blood enters beds of capillaries in the wall of the heart to supply the needs of heart tissue.
Chapter 20, page 728
Figure 20.8

41. Coronary Circulation (continued)
The capillaries deliver oxygen and nutrients to heart tissue, and remove carbon dioxide and waste products.
Most of the blood drains into the coronary sinus, a thin-walled vessel that has no smooth muscle to alter its diameter.
The blood in the coronary sinus empties into the right atrium of the heart.
Chapter 20, page 730
Figure 20.8

42. Atherosclerosis
“The development of arterial atherosclerosis may occur when deposits of cholesterol and plaque accumulate at a tear in the inner lining of an artery. As the deposits harden and occlude the arterial lumen, blood flow to distant tissues decreases and a clot may become lodged, completely blocking the artery.” (

43. Angiogram and Angioplasty

44. Cardiac Muscle Tissue and Conduction System

45. Cardiac Muscle Tissue
Cardiac muscle fibers are shorter in length and less circular in cross-section than skeletal muscle fibers.
A typical fiber is m long, and has a diameter of about 14 m.
Cardiac muscle fibers have extensive branching that give them a stair-step appearance (see Table 4.5B).
Usually only one centrally-located nucleus is found in a cardiac muscle fiber, unlike skeletal muscle fibers which have many nuclei at their peri-phery.
Chapter 20, page 731
Figure 20.9
Table 4.5B

46. Myocardium

47. Cardiac Muscle Tissue (continued)
Chapter 20, page 732
Figure 20.9
Each end of a cardiac muscle fiber has thickenings of the sarcolemma known as intercalated discs.
The discs have desmosomes that hold the fibers together to form gap junctions.
Action potentials rapidly ‘jump’ from muscle fiber-to-muscle fiber via these gap junctions.
Gap junctions enable the myocardium of the atria or ventricles to contract as a single, coordinated unit.
Desmosome = a structure that forms the site of adhesion between two cells.

48. Fiber Comparisons Chapter 20, page 732 Figure 20.9
Mitochondria are larger and more numerous in cardiac muscle fibers than in skeletal muscle fibers—about 25 percent versus 2 percent of the cytosolic space.
Cardiac muscle fibers have the same arrangement of actin and myo-sin, and same bands, zones, and Z discs as found in skeletal muscle fibers.
Cytosolic space = the cellular space occupied by cytosol.

49. Fiber Comparisons (continued)
Although the transverse tubules are wider in cardiac muscle fibers, they are less abundant than in skeletal muscle fibers.
The sarcoplasmic reticulum is less extensive than in skeletal muscle.
This difference indicates that cardiac muscle has a smaller intracellu-lar reserve of calcium ions (Ca2+).
Chapter 20, page 732
Figure 20.9

50. Autorhythmic Fibers
Cardiac contractions result from electrical activity generated in heart tissue.
A specialized network of cardiac muscle fibers—known as autorhyth-mic fibers—are self-excitable and the source of this electrical activity.
The autorhythmic fibers generate action potentials to trigger cardiac contractions.
These fibers can continue to stimulate the heartbeat after the heart is removed from the body in transplant surgery.
Chapter 20, page 732

51. Autorhythmic Fibers (continued)
About one percent of the cardiac muscle fibers become autorhythmic during embryonic development.
The autorhythmic fibers serve as the “pacemaker” in establishing the rhythm of electrical excitation (action potentials) for cardiac contrac-tion.
They also form the conduction system so that action potentials prop-agate through the myocardium to enable the chambers to contract in a coordinated manner.
Propagate = loosely defined: to travel along or spread.
Chapter 20, page 732

52. Propagation of Action Potentials
Cardiac excitation normally begins in the sinoatrial (SA) node in the right atrial wall.
The SA node cells spontaneously depolarize and produce a pacemaker potential that triggers the generation of an action potential.
The action potential propagates through the atria via gap junctions of the cardiac muscle fibers.
Chapter 20, page 732
Figure 20.10

53. Propagation (continued)
The action potential reaches the atrioventricular (AV) node in the inter-atrial septum of the heart.
It then enters the atrioventricular bundle (axons) for propagation into the ventricles.
The action potential then enters the left and right AV bundles of the ven-tricles.
Chapter 20, page 732
Figure 20.10

54. Propagation (continued)
In the left and right AV bundles, large-diameter Purkinje fibers rapidly conduct the action potential to the rest of the ventricular myocardium.
The ventricles contract, and blood is ejected from the heart through the semilunar valves.
Chapter 20, page 732
Figure 20.10

55. Fundamental Rhythm
Autorhythmic fibers in the SA node trigger action potentials at a rate of about 100 per minute (fundamental rhythm).
The ANS and hormones (such as epinephrine) can modify the timing and strength of each heartbeat.
Neither the ANS nor hormones, however, establish the fundamental rhythm.
Chapter 20, page 733
Figure 20.10

56. Contractile Fibers
Action potentials generated in the contractile fibers have three phases: depolarization, plateau, and repolarization.
The sequence of the three phases is shown in Figure 20.11—there are similarities and differences with the action potentials in skeletal muscle fibers.
Some of the similarities and differences will be discussed during the lecture.
Chapter 20, page 734
Figure 20.11

57. Mechanisms of Contraction
The mechanism of contraction is similar in cardiac muscle and skeletal muscle.
In cardiac muscle fibers, an action potential from the conduction sys-tem stimulates the release of Ca2+ from the sarcoplasmic reticulum.
Ca2+ binds to the regulatory protein, troponin, to act on tropomyosin.
The thin and thick filaments slide past one another to develop muscle tension.
Chapter 20, page 735

58. Mechanisms of Contraction (continued)
Substances that alter the flow of Ca2+ through the calcium channels can affect the strength of heart contractions.
For example, the hormone epinephrine increases force of contraction by enhancing Ca2+ flow.
Chapter 20, page 735

59. Refractory Period
The refractory period is the time interval when a second action potential cannot be triggered.
The refractory period of a cardiac muscle is longer than the contraction itself.
Therefore, another contraction cannot occur until relaxation is underway.
Chapter 20, page 735
Figure 20.11

60. Refractory Period and Tetanus
Tetanus—a sustained contraction in skeletal muscle—cannot occur in cardiac muscle.
If the heart muscle could undergo tetanus, blood flow would cease since the heart’s pumping action depends on alternating contractions and relax-ations.
Chapter 20, page 735

61. ATP Production
Unlike skeletal muscle, cardiac muscle produces very little ATP for its contractions through anaerobic respiration (glycolysis)
Cardiac muscle relies almost exclusively on aerobic cellular respiration in its many mitochondria.
The oxygen for ATP production diffuses from the blood in the coronary capillaries into the myoglobin in muscle tissue
Chapter 20, page 735
Figure 10.11

62. Creatine Phosphate and Creatine Kinase
Cardiac muscle, like skeletal muscle, produces some ATP from creatine phosphate.
Creatine kinase (CK) is an enzyme that catalyzes the transfer of a phos-phate group from creatine phosphate to ADP to form ATP.
Chapter 20, page 735

63. Creatine Kinase (continued)
One sign that a myocardial infarction (heart attack) has occurred is the presence of creatine kinase in the blood.
While CK and other enzymes are normally confined within cells, they are released from dying or dead muscle fibers.
Myocardial infarction = an occlusion or blockage of arteries supplying the muscles of the heart, resulting in injury or necrosis of the heart muscle.
Chapter 20, page 735

64. Electrocardiography

65. Electrocardiogram
As action potentials propagate through cardiac tissue, they generate electrical voltages that can be detected on the surface of the body.
An electrocardiogram (ECG or EKG) is a recording of these electrical signals.
Two limb leads and six chest leads are attached in standard locations for ECG recording.
An electronic device known as the electrocardiograph amplifies the electrical signals, and produces 12 traces from various combinations of limb and chest leads.
Chapter 20, page 735

66. Electrocardiogram (continued)

67. Diagnostic Value
By comparing ECG traces with standard ECG traces, it is possible to determine:
If the conducting pathway is abnormal
If the heart is enlarged
If specific regions of the heart are damaged
The possible cause of chest pain
Chapter 20, page 735

68. ECG Trace—Waveforms

69. P Wave Three waves appear in an ECG trace with each heartbeat.
The first, known as the P wave, is a small upward deflection in the trace.
The P wave represents atrial depolarization of an action potential propagating from the SA node through the cardiac muscle fibers in right and left atria.
Chapter 20, page 735
Figure 20.12

70. QRS Complex
The waveform second, called the QRS complex, begins as a downward deflection.
It continues as a large, upward, triangular wave, and ends as a second downward deflection.
The QRS complex represents ventricular depolarization as the action potential propagates through the cardiac muscle fibers of the right and left ventricles.
Chapter 20, page 736
Figure 20.12

71. T Wave
The third, known as the T wave, is a dome-shaped upward deflection.
The T wave represents ventricular repolarization when the ventricles are just starting to relax.
The T wave is of smaller amplitude but wider than the QRS complex since repolarization lasts longer than depolarization.
Prior to the T wave and after the QRS complex, the ECG is flat due to a steady period of depolarization.
Chapter 20, page 736
Figure 20.12

72. ECG Indicators
The amplitudes of ECG waves can serve as indicators of some types of cardiac abnormalities:
Large P waves—possible enlargement of one or both of the atria.
Large Q waves—possible myocardial infarction.
Large R waves—possible ventricular enlargement.
Flatter-than-normal T waves—possible insufficient oxygen supply to the heart.
Larger-than-normal T waves—possible hyperkalemia, high blood level of potassium (K+).
Chapter 20, page 736
Figure 20.12

73. ECG Trace—Intervals and Segments

74. P-Q Interval
Analysis of ECG records also involve measuring the time spans be-tween waves—these spans are known as intervals.
The P-Q interval represents the conduction time from the beginning of atrial excitation to the beginning of ventricular excitation.
The P-Q interval can lengthen if action potentials must detour around scar tissue resulting from disorders such as coronary heart disease and rheumatic fever.
Rheumatic fever = an inflammatory disease that can develop as a complication of untreated or poorly treated strep throat. Strep throat is caused by infection with group A streptococcus bacteria. Rheumatic fever can cause permanent damage to the heart that may result in serious harm to the heart valves and heart failure. (
Chapter 20, page 736
Figure 20.12

75. S-T Interval
The S-T interval is the time period when the ventricular muscle fibers are depolarized during the plateau phase of the action potential.
The S-T interval is elevated above baseline in acute myocardial infarc-tion.
It is depressed below baseline when the heart receives insufficient oxy-gen.
Chapter 20, page 736
Figure 20.12

76. Q-T Interval
The Q-T interval is the time period from the beginning of ventricular depolarization to the end of ventricular repolarization.
The interval can lengthen due to myocardial damage, ischemia, or conduction abnormalities.
Ischemia = decreased blood flow to an organ or tissue.
Chapter 20, page 736
Figure 20.12

77. Stress Testing
Stress testing involves evaluating cardiac activity during physical exer-cise.
Narrowed coronary arteries may still carry an adequate amount of oxy-gen when a person is at rest.
They may not, however, meet the heart’s oxygen needs during physical activity.
The ECG and stress testing are used in diagnosing these types of prob-lems.
Chapter 20, page 736

78. Transient Events
Abnormal heart rhythms and inadequate coronary blood supply can be transient.
Ambulatory electrocardiograms are sometimes used to detect such problems.
A portable, battery-powered heart monitor is worn to record the ECG continuously for 24 hours.
The ECG record can be telemetered or downloaded and evaluated by medical personnel.
Transient = not lasting, enduring, or permanent.
Ambulatory = literally, while walking around.
Chapter 20, page 736

79. Systole and Diastole
The atria and ventricles depolarize and contract at different times to enable effective pumping.
Systole refers to the period of contraction, and diastole refers to the period of relaxation.
An ECG can measure the timing of atrial and ventricular systole and diastole.
The details of the timings of each cardiac event are described in the textbook.
Chapter 20, page 736
Figure 20.13

80. Cardiac Cycle

81. Cardiac Cycle
A single cardiac cycle consists of all of the events associated with one heartbeat.
The atria and ventricles alternately contract and relax in each cardiac cycle.
The cardiac cycle measures about 0.8 seconds when the heart rate is 75 beats per minute (bpm).
Chapter 20, page 738

82. Cardiac Cycle (continued)
Atrial systole
Atrial diastole
Ventricular systole
Ventricular diastole
Isvolumetric relaxation (all four chambers)
Chapter 20, page 738

83. Pressure Differentials
As a chamber of the heart contracts, the fluid pressure in the chamber increases.
Cardiac contraction forces blood from areas of relatively high pressure to areas of lower pressure.
Chapter 20, page 738

84. Pressure and Volume Changes
The relationships between the ECG and changes in the heart during a single cardiac cycle are shown in Figure
The changes include:
Atrial pressure
Ventricular pressure
Aortic pressure
Ventricular volume
Chapter 20, page 738
Figure 20.14

85. Pressure and Volume Changes (continued)
The pressures shown in Figure are for the left side of the heart for systemic circulation.
They are considerably lower on the right side for pulmonary circulation.
The left and right ventricles pump an equal volume of blood during one heartbeat regardless of the pressure differences between the left and right sides.
This also holds true for the volume of blood returned to the left and right atria.
Pressure and Volume Changes (continued)
Chapter 20, page 738
Figure 20.14

86. Atrial Systole
During atrial systole, which lasts about 0.1 seconds, the atria contract while the ventricles are relaxed.
As the atria contract, they put pressure on the blood within their cham-bers to force blood through the AV valves into the ventricles.
At the end of atrial systole (also the end of ventricular diastole), the ventricles each contain about 130 ml of blood (known as end-diastolic volume).
The ECG, pressure, and volumes for atrial systole are shown in Figure
mmHg = millimeters of mercury.
Chapter 20, page 738
Figure 20.14

87. Ventricular Systole
During ventricular systole, which lasts about 0.3 seconds, the ventricles contract while the atria are relaxed.
Contraction causes the pressure to increase steeply in the left and right ventricles.
The semilunar valve for the left ventricle opens when ventricular pres-sure exceeds aortic pressure (about 80 mmHg).
The SL valve for the right ventricle opens when ventricular pressure ex-ceeds the pressure in the pulmonary trunk (about 20 mmHg).
Chapter 20, page 738
Figure 20.14

88. Ventricular Systole (continued)
Each ventricle ejects about 70 mL of blood—about 60 mL of the 130 mL of the end-diastolic volume remains in each ventricle.
The blood volume that remains is known as the end-systolic volume.
The blood that is ejected is known as stroke volume.
Therefore, end-diastolic volume minus end-systolic volume equals stroke volume.
The calculation is: 130 mL - 60 mL = 70 mL for a person typically at rest.
Chapter 20, page 738
Figure 20.14

89. Relaxation Period
During the relaxation period, lasting about 0.4 seconds, all four cham-bers (atria and both ventricles) are relaxed.
The relaxation period shortens when the heart beats faster (atrial sys-tole and ventricular systole shorten only slightly).
Chapter 20, page 738
Figure 20.14

90. Relaxation Period (continued)
During ventricular relaxation, blood flows toward the heart from the aorta and pulmonary trunk.
The SL valves close due to the backflow and prevent blood from reenter-ing the ventricles—the aortic SL valve closes at a pressure of about 100 mmHg.
Ventricular blood volumes do not change for a brief period since all four valves (SL and AV) are closed.
This period is known as isovolumetric relaxation.
Isovolumetric = relating to, or characterized by unchanging volume.
Chapter 20, page 738
Figure 20.14

91. Relaxation Period (continued)
Ventricular pressure decreases rapidly as the ventricles continue to relax.
When ventricular pressure falls below atrial pressure, the blood that filled the atria during ventricular systole rushes rapidly into the ventri-cles.
Chapter 20, page 740
Figure 20.14

92. Relaxation Period (continued)
The ventricles are almost three-quarters full at the end of the ven-tricular relaxation period.
The P wave appears in the ECG, and a new cardiac cycle begins.
Chapter 20, page 740
Figure 20.14

93. Heart Sounds
Detecting sounds in the body is often performed with a stethoscope.
This act of listening is known as auscultation.
Heart sounds are the result of turbulent flow of blood due to the closing of heart valves.
Smooth-flowing blood, or laminar flow, is silent and is not detected with a stethoscope.
Although there are four heart sounds, only S1 and S2 are loud enough to be heard from a healthy heart (the other two sounds are S3 and S4).
Chapter 20, page 740
Figure 20.14

94. Stethoscope

95. Heart Sounds (continued)
The first heart sound (S1) is a ‘lub’, which is louder and slightly longer in duration than the second sound (S2).
S1 is due to the closure of the AV valves soon after ventricular systole begins.
S2 is due to closure of the SL valves at the start of ventricular diastole.
S2 is described as a ‘dup.’
Chapter 20, page 740
Figure 20.14

96. Heart Sounds (continued)

97. Heart Sounds (continued)
S1 and S2 are best heard in chest locations slightly away from the valves since the sound waves are carried by blood flow through the arteries.
Although normally not loud enough to be heard, S3 is due to blood turbulence during ventricular filling, and S4 is due to blood turbulence during atrial systole.
Chapter 20, page 740
Figure 20.15

98. Cardiac Output

99. Cardiac Output
Cardiac output (CO) is the volume of blood ejected by the left ventricle into the aorta each minute.
CO equals stroke volume (SV) in milliliters (mL) times the heart rate (HR):
CO = SV x HR
In a resting adult male, SV is about 70 mL and heart rate is about 75 beats per minute.
By working through the formula, cardiac output would be 5.25 liters per minute.
Chapter 20, page 740

100. Cardiac Output (continued)
Cardiac output at rest is very close to total blood volume of about 5 liters in an adult male.
Thus, the total blood volume flows through the systemic and pulmonary circulations about once every minute.
Factors such as physical exercise increase CO by increasing stroke vol-ume and heart rate.
If SV increases to 100 mL/beat and HR to 100 beats/min, CO increases to 10 liters per minute.
Chapter 20, page 741

101. Cardiac Reserve
Cardiac reserve is the difference between a person’s maximum car-diac output and cardiac output at rest.
Many people have an average cardiac reserve of 4-to-5 times the resting value.
Well-conditioned, endurance athletes may have a cardiac reserve of 7-to-8 times the resting value.
People with cardiac disease may have little or no cardiac reserve, which limits their ability to perform simple, routine, everyday tasks.
Chapter 20, page 741

102. Stroke Volume
A healthy heart will pump the amount of blood that was delivered to it during the previous diastole.
The more blood delivered to the heart during diastole, the more blood can be ejected during the next systole.
At rest, the stroke volume is 50-to-60 percent of end-diastolic volume.
This is because 40-to-50 percent of the blood remains in the ventricles after each contraction.
Chapter 20, page 741

103. Regulation of Stroke Volume
Three factors regulate stroke volume and ensure the left and right ventricles pump equal volumes of blood.
They are:
Preload—the degree of stretch of the heart before it contracts.
Contractility—the forcefulness of contraction of individual ventri-cular muscle fibers.
Afterload—the pressure that must be exceeded before ejection of blood from the ventricles can occur.
Detailed descriptions of the factors can be found in Chapter 20 of the textbook.
Chapter 20, page 741

104. Regulation of Heart Rate
Heart rate, as we have discussed, is one of two factors in determining cardiac output—the other is stroke volume.
During physical exercise, cardiac output increases to supply the working organs and other tissues with oxygen and nutrients, and remove waste products.
The ANS and several hormones regulate heart rate and therefore car-diac output.
Chapter 20, page 742

105. ANS Control
Autonomic nervous system regulation of heart rate originates in the cardiovascular (CV) center in the medulla oblongata of the brainstem.
The CV center receives input from sensory systems, hypothalamus, limbic system, and cerebral hemispheres.
The CV center modifies heart rate via the sympathetic and parasym-pathetic divisions.
Chapter 20, page 742
Figure 20.16

106. ANS Control (continued)
The cardiac accelerator nerves of the sympathetic division innervate the SA node, AV node, and most of the myocardium.
Nerve impulses (action potentials) trigger the release of norepineph-rine from the postganglionic neurons, which stimulate the 1 recep-tors in cardiac muscle.
The increased depolarization rates increase pacemaker firing, which increases heartrate.
Norepinephrine also promotes entry of Ca2+ into cardiac muscle to increase the force of contraction.
Chapter 20, page 742
Figure 20.16

107. ANS Control (continued)
Parasympathetic nerve impulses reach the heart via the left and right branches of the vagus (X) nerve.
The vagal fibers (axons) terminate in the SA node, AV node, and atrial myocardium.
The terminal buttons of the fibers release acetylcholine from their syn-aptic vesicles.
Acetylcholine decreases heart rate by slowing the rate of spontaneous depolarization in the pacemaker cells and other autorhythmic fibers.
Chapter 20, page 742
Figure 20.16

108. ANS Control (continued)
A continually-shifting balance exists between sympathetic and para-sympathetic stimulation of the heart.
The parasympathetic division dominates when the body is at rest.
The sympathetic division dominates during physical exercise and emotional arousal.
Chapter 20, page 742

109. Other Factors
Other factors influence the physiology of cardiac muscle and heart rate.
Hypoxia (low oxygen level), acidosis (low pH), and alkalosis (high pH) all depress cardiac activity.
Several hormones and cations (ions with positive charges) also have major cardiac effects.
Chapter 20, page 743
Figure 20.17

110. Catecholamines
Epinephrine and norepinephrine secreted by the adrenal medulla can enhance cardiac output.
These hormones affect cardiac muscle fibers in much the same way as does norepinephrine released by the cardiac accelerator nerves.
Physical exercise, stress, and emotional excitement, through the ANS, stimulate the adrenal medulla to increase its secretion of the catechol-amines.
Chapter 20, page 743
Figure 20.17

111. Thyroid Hormones
Thyroid hormones (T3 and T4) increase cardiac contractility and heart rate.
An indicator of hyperthyroidism is tachycardia, an elevated heart rate.
Chapter 20, page 743

112. Cations
The generation of action potentials in cardiac muscle fibers is depen-dent upon the intracellular and extracellular concentrations of cations, in particular Na+ and K+.
Ionic balances can compromise the heart’s pumping effectiveness.
Elevated levels of Na+ or K+ can decrease heart rate and contractility.
A moderate increase in Ca2+ can increase the heart rate and force of cardiac contraction.
Chapter 20, page 743
Figure 20.17

113. Additional Factors
Additional factors that can affect the regulation of resting heart rate include age, gender, physical fitness, and body temperature.
Some of the details are described in Chapter 20 of the textbook.
Chapter 20, page 743
Figure 20.17

114. Physical Exercise and the Heart

115. Physical Fitness

116. Physical Fitness
With at least a modest level of health, a person’s level of physical fitness can be improved at any age with regular physical exercise.
Aerobics, an activity that works the large skeletal muscles for at least 20 minutes, elevates cardiac output and increases metabolic rate of the body.
From 3-to-5 aerobic sessions per week can improve the health of the cardiovascular system.
Aerobic activities include brisk walking, running, bicycling, swimming, and dancing.
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117. Examples of Aerobic Activities

118. Physiological Effects
Sustained exercise increases the oxygen demands of cardiac and skel-etal muscles.
In a healthy person, the maximum rate of oxygen delivery to the body’s tissues increases after several weeks of physical training.
O2 delivery increases to skeletal muscles since more capillary beds are formed.
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119. Benefits
A well-trained athlete can achieve a cardiac output about twice that of a sedentary person, in part due to hypertrophy of the heart.
The resting cardiac output is about the same as in a healthy, untrained person because the stroke volume has increased while the heart rate has decreased.
Regular physical exercise in most people can have other physical and mental benefits too.
Sedentary = characterized by or requiring much sitting: a sedentary job. Accustomed to sitting or to taking little exercise. (
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