18: The Cardiovascular System:
The Heart
Objectives
Heart Anatomy
1. Describe the size, shape, location, and orientation of the heart in the thorax.
2. Name the coverings of the heart.
3. Describe the structure and function of each of the three layers of the heart wall.
4. Describe the structure and functions of the four heart chambers. Name each chamber and
provide the name and general route of its associated great vessel(s).
5. Trace the pathway of blood through the heart.
6. Name the major branches and describe the distribution of the coronary arteries.
7. Name the heart valves and describe their location, function, and mechanism of operation.
Cardiac Muscle Fibers
8. Describe the structural and functional properties of cardiac muscle, and explain how it differs
from skeletal muscle.
9. Briefly describe the events of cardiac muscle cell contraction.
Heart Physiology
10. Name the components of the conduction system of the heart, and trace the conduction
pathway.
11. Draw a diagram of a normal electrocardiogram tracing. Name the individual waves and
intervals, and indicate what each represents.
12. Name some of the abnormalities that can be detected on an ECG tracing.
13. Describe normal heart sounds, and explain how heart murmurs differ.
14. Describe the timing and events of the cardiac cycle.
15. Name and explain the effects of various factors regulating stroke volume and heart rate.
16. Explain the role of the autonomic nervous system in regulating cardiac output.
Developmental Aspects of the Heart
17. Describe fetal heart formation, and indicate how the fetal heart differs from the adult heart.
18. Provide examples of age-related changes in heart function.
Lecture Outline
I. Heart Anatomy (pp. 662–672; Figs. 18.1–18.10)
A. Size, Location, and Orientation (p. 663; Fig. 18.1)
1.
The heart is the size of a fist and weighs 250–300 grams.
2.
The heart is found in the mediastinum and two-thirds lies left of the midsternal line.
3.
The base is directed toward the right shoulder and the apex points toward the left
hip.
B. Coverings of the Heart (p. 663; Fig. 18.2)
1.
The heart is enclosed in a doubled-walled sac called the pericardium.
2.
Deep to the pericardium is the serous pericardium.
3.
The parietal pericardium lines the inside of the pericardium.
4.
The visceral pericardium, or epicardium, covers the surface of the heart.
C. Layers of the Heart Wall (pp. 663–664; Fig. 18.3)
1.
The myocardium is composed mainly of cardiac muscle and forms the bulk of the
heart.
2.
The endocardium lines the chambers of the heart.
D. Chambers and Associated Great Vessels (pp. 664–668; Fig. 18.4)
1.
The right and left atria are the receiving chambers of the heart.
2.
The right ventricle pumps blood into the pulmonary trunk; the left ventricle pumps
blood into the aorta.
E. Pathway of Blood Through the Heart (pp. 668–669; Fig. 18.5)
1.
F.
The right side of the heart pumps blood into the pulmonary circuit; the left side of
the heart pumps blood into the systemic circuit.
Coronary Circulation (pp. 669–670; Fig. 18.7)
1.
The heart receives no nourishment from the blood as it passes through the chamber.
2.
The coronary circulation provides the blood supply for the heart cells.
3.
In a myocardial infarction, there is prolonged coronary blockage that leads to cell
death.
G. Heart Valves (pp. 670–672; Figs. 18.8–18.10)
1.
The tricuspid and mitral valves prevent backflow into the atria when the ventricles
contract.
2.
When the heart is relaxed the AV valves are open, and when the heart contracts the
AV valves close.
3.
The aortic and pulmonary valves are found in the major arteries leaving the heart.
They prevent backflow of blood into the ventricles.
4.
When the heart is relaxed the aortic and pulmonary valves are closed, and when the
heart contracts they are open.
II. Cardiac Muscle Fibers (pp. 672–676; Figs. 18.11–18.12 )
A. Microscopic Anatomy (pp. 672–673; Fig. 18.11)
1.
Cardiac muscle is striated and contraction occurs via the sliding filament mechanism.
2.
The cells are short, fat, branched, and interconnected by intercalated discs.
B. Mechanism and Events of Contraction (pp. 673–675; Fig. 18.12)
1.
Some cardiac muscle cells are self-excitable.
2.
The heart contracts as a unit or not at all.
3.
The heart’s absolute refractory period is longer than a skeletal muscle’s, preventing
tetanic contractions.
C. Energy Requirements (p. 675)
1.
The heart relies exclusively on aerobic respiration for its energy demands.
2.
Cardiac muscle is capable of switching nutrient pathways to use whatever nutrient
supply is available.
III. Heart Physiology (pp. 676–687; Figs. 18.13–18.23)
A. Electrical Events (pp. 676–680; Figs. 18.13–18.18)
1.
The intrinsic conduction system is made up of specialized cardiac cells that initiate
and distribute impulses, ensuring that the heart depolarizes in an orderly fashion.
2.
The autorhythmic cells have an unstable resting potential, called pacemaker
potentials, that continuously depolarizes.
3.
Impulses pass through the autorhythmic cardiac cells in the following order:
sinoatrial node, atrioventricular node, atrioventricular bundle, right and left bundle
branches, and Purkinje fibers.
4.
The autonomic nervous system modifies the heartbeat: the sympathetic center
increases rate and depth of the heartbeat, and the parasympathetic center slows the
heartbeat.
5.
An electrocardiograph monitors and amplifies the electrical signals of the heart and
records it as an electrocardiogram (ECG).
B. Heart Sounds (p. 681; Fig. 18.19)
1.
Normal
a. The first heart sound, lub, corresponds to closure of the AV valves, and occurs
during ventricular systole.
b. The second heart sound, dup, corresponds to the closure of the aortic and
pulmonary valves, and occurs during ventricular diastole.
2.
Abnormal
a. Heart murmurs are extraneous heart sounds due to turbulent backflow of blood
through a valve that does not close tightly.
C. Mechanical Events: The Cardiac Cycle (p. 682; Fig. 18.20)
1.
Systole is the contractile phase of the cardiac cycle and diastole is the relaxation
phase of the cardiac cycle.
2.
A cardiac cycle consists of a series of pressure and volume changes in the heart
during one heartbeat.
a. Ventricular filling occurs during mid-to-late ventricular diastole, when the AV
valves are open, semilunar valves are closed, and blood is flowing passively into
the ventricles.
b. The atria contract during the end of ventricular diastole, propelling the final
volume of blood into the ventricles.
c. The atria relax and the ventricles contract during ventricular systole, causing
closure of the AV valves and opening of the semilunar valves, as blood is ejected
from the ventricles to the great arteries.
d. Isovolumetric relaxation occurs during early diastole, resulting in a rapid drop in
ventricular pressure, which then causes closure of the semilunar valves and
opening of the AV valves.
D. Cardiac Output (pp. 682–687; Figs. 18.21–18.23)
1.
Cardiac output is defined as the amount of blood pumped out of a ventricle per beat,
and is calculated as the product of stroke volume and heart rate.
2.
Regulation of Stroke Volume
a. Preload: the Frank-Starling law of the heart states that the critical factor
controlling stroke volume is the degree of stretch of cardiac muscle cells
immediately before they contract.
b. Contractility: contractile strength increases if there is an increase in cytoplasmic
calcium ion concentration.
c. Afterload: ventricular pressure that must be overcome before blood can be ejected
from the heart.
3.
Regulation of Heart Rate
a. Sympathetic stimulation of pacemaker cells increases heart rate and contractility,
while parasympathetic inhibition of cardiac pacemaker cells decreases heart rate.
b. Epinephrine, thyroxine, and calcium influence heart rate.
c. Age, gender, exercise, and body temperature all influence heart rate.
4.
Homeostatic Imbalance of Cardiac Output
a. Congestive heart failure occurs when the pumping efficiency of the heart is so low
that blood circulation cannot meet tissue needs.
b. Pulmonary congestion occurs when one side of the heart fails, resulting in
pulmonary edema.
IV. Developmental Aspects of the Heart (pp. 688–690; Figs. 18.24–18.25)
A. Embryological Development (pp. 688–689; Figs. 18.24–18.25)
1.
The heart begins as a pair of endothelial tubes that fuse to make a single heart tube
with four bulges representing the four chambers.
2.
The foramen ovale is an opening in the interatrial septum that allows blood returning
to the pulmonary circuit to be directed into the atrium of the systemic circuit.
3.
The ductus arteriosus is a vessel extending between the pulmonary trunk and the
aortic arch that allows blood in the pulmonary trunk to be shunted to the aorta.
B. Aging Aspects of the Heart (pp. 689–690)
1.
Sclerosis and thickening of the valve flaps occurs over time, in response to constant
pressure of the blood against the valve flaps.
2.
Decline in cardiac reserve occurs due to a decline in efficiency of sympathetic
stimulation.
3.
Fibrosis of cardiac muscle may occur in the nodes of the intrinsic conduction system,
resulting in arrhythmias.
4.
Atherosclerosis is the gradual deposit of fatty plaques in the walls of the systemic
vessels.
19: The Cardiovascular System:
Blood Vessels
Objectives
PART 1: OVERVIEW OF BLOOD VESSEL STRUCTURE AND FUNCTION
Structure of Blood Vessel Walls
1. Describe the three layers that typically form the wall of a blood vessel, and state the function
of each.
2. Define vasoconstriction and vasodilation.
Arterial System
3. Compare and contrast the structure and function of the three types of arteries.
Capillaries
4. Describe the structure and function of a capillary bed.
Venous System
5. Describe the structure and function of veins, and explain how veins differ from arteries.
PART 2: PHYSIOLOGY OF CIRCULATION
Introduction to Blood Flow, Blood Pressure, and Resistance
6. Define blood flow, blood pressure, and resistance, and explain the relationships between
these factors.
Systemic Blood Pressure
7. List and explain the factors that influence blood pressure, and describe how blood pressure is
regulated.
8. Define hypertension. Describe its manifestations and consequences.
Lecture Outline
PART 1: OVERVIEW OF BLOOD VESSEL STRUCTURE AND FUNCTION (pp. 694–
703; Figs. 19.1–19.5; Table 19.1)
I. Structure of Blood Vessel Walls (p. 695; Figs. 19.1–19.2; Table 19.1)
A. The walls of all blood vessels except the smallest consist of three layers: the tunica intima,
tunica media, and tunica externa (p. 695; Fig. 19.1).
B. The tunica intima reduces friction between the vessel walls and blood; the tunica media
controls vasoconstriction and vasodilation of the vessel; and the tunica externa protects,
reinforces, and anchors the vessel to surrounding structures (p. 695; Fig. 19.2; Table 19.1).
II. Arterial System (pp. 695–698; Fig. 19.2; Tables 19.1–19.2)
A. Elastic, or conducting, arteries contain large amounts of elastin, which enables these
vessels to withstand and smooth out pressure fluctuations due to heart action (p. 697; Fig.
19.2; Table 19.1).
B. Muscular, or distributing, arteries deliver blood to specific body organs, and have the
greatest proportion of tunica media of all vessels, making them more active in
vasoconstriction (p. 698; Table 19.1).
C. Arterioles are the smallest arteries and regulate blood flow into capillary beds through
vasoconstriction and vasodilation (p. 698).
III. Capillaries (pp. 698–700; Figs. 19.3–19.4; Table 19.1)
A. Capillaries are the smallest vessels and allow for exchange of substances between the
blood and interstitial fluid (pp. 698–699; Fig. 19.3; Table 19.1).
1.
Continuous capillaries are most common and allow passage of fluids and small
solutes.
2.
Fenestrated capillaries are more permeable to fluids and solutes than continuous
capillaries.
3.
Sinusoidal capillaries are leaky capillaries that allow large molecules to pass between
the blood and surrounding tissues.
B. Capillary beds are microcirculatory networks consisting of a vascular shunt and true
capillaries, which function as the exchange vessels (pp. 699–700; Fig. 19.4).
C. A cuff of smooth muscle, called a precapillary sphincter, surrounds each capillary at the
metarteriole and acts as a valve to regulate blood flow into the capillary (p. 700; Fig. 19.4).
IV. Venous System (pp. 700–701; Fig. 19.5; Table 19.1)
A. Venules are formed where capillaries converge and allow fluid and white blood cells to
move easily between the blood and tissues (p. 700; Table 19.1).
B. Venules join to form veins, which are relatively thin-walled vessels with large lumens
containing about 65% of the total blood volume (pp. 700–701; Fig. 19.5; Table 19.1).
V. Vascular Anastomoses (pp. 701, 703)
A. Vascular anastomoses form where vascular channels unite, allowing blood to be supplied
to and drained from an area even if one channel is blocked (p. 701).
PART 2: PHYSIOLOGY OF CIRCULATION (pp. 703–721; Figs. 19.6–19.18; Table 19.2)
VI. Introduction to Blood Flow, Blood Pressure, and Resistance (pp. 703–704)
A. Blood flow is the volume of blood flowing through a vessel, organ, or the entire
circulation in a given period, and may be expressed as ml/min (p. 703).
B. Blood pressure is the force per unit area exerted by the blood against a vessel wall, and is
expressed in millimeters of mercury (mm Hg) (p. 703).
C. Resistance is a measure of the friction between blood and the vessel wall, and arises from
three sources: blood viscosity, blood vessel length, and blood vessel diameter (p. 704).
D. Relationship Between Flow, Pressure, and Resistance (p. 704)
VII.
1.
If blood pressure increases, blood flow increases; if peripheral resistance increases,
blood flow decreases.
2.
Peripheral resistance is the most important factor influencing local blood flow,
because vasoconstriction or vasodilation can dramatically alter local blood flow,
while systemic blood pressure remains unchanged.
Systemic Blood Pressure (pp. 704–706; Figs. 19.6–19.7)
A. The pumping action of the heart generates blood flow; pressure results when blood flow
is opposed by resistance (p. 704).
B. Systemic blood pressure is highest in the aorta, and declines throughout the pathway
until it reaches 0 mm Hg in the right atrium (p. 705; Fig. 19.6).
C. Arterial blood pressure reflects how much the arteries close to the heart can be stretched
(compliance, or distensibility), and the volume forced into them at a given time (p. 705;
Fig. 19.6).
1.
When the left ventricle contracts, blood is forced into the aorta, producing a peak in
pressure called systolic pressure (120 mm Hg).
2.
Diastolic pressure occurs when blood is prevented from flowing back into the
ventricles by the closed semilunar valve, and the aorta recoils (70–80 mm Hg).
3.
The difference between diastolic and systolic pressure is called the pulse presssure.
4.
The mean arterial pressure (MAP) represents the pressure that propels blood to the
tissues.
D. Capillary blood pressure is low, ranging from 40–20 mm Hg, which protects the
capillaries from rupture, but is still adequate to ensure exchange between blood and
tissues (p. 705; Fig. 19.6).
E. Venous blood pressure changes very little during the cardiac cycle, and is low, reflecting
cumulative effects of peripheral resistance (pp. 705–706; Fig. 19.7).
VIII. Maintaining Blood Pressure (pp. 706–713; Figs. 19.8–19.12; Table 19.2)
A. Blood pressure varies directly with changes in blood volume and cardiac output, which
are determined primarily by venous return and neural and hormonal controls (p. 706; Fig.
19.8).
B. Short-term neural controls of peripheral resistance alter blood distribution to meet
specific tissue demands, and maintain adequate MAP by altering blood vessel diameter
(pp. 706–709; Fig. 19.9).
1.
The vasomotor center is a cluster of sympathetic neurons in the medulla that controls
changes in the diameter of blood vessels.
2.
Baroreceptors detect stretch and send impulses to the vasomotor center, inhibiting its
activity and promoting vasodilation of arterioles and veins.
3.
Chemoreceptors detect a rise in carbon dioxide levels of the blood, and stimulate the
cardioacceleratory and vasomotor centers, which increases cardiac output and
vasoconstriction.
4.
The cortex and hypothalamus can modify arterial pressure by signaling the
medullary centers.
C. Chemical controls influence blood pressure by acting on vascular smooth muscle or the
vasomotor center (p. 709; Table 19.2).
1.
Norepinephrine and epinephrine promote an increase in cardiac output and
generalized vasoconstriction.
2.
Atrial natriuretic peptide acts as a vasodilator and an antagonist to aldosterone,
resulting in a drop in blood volume.
3.
Antidiuretic hormone promotes vasoconstriction and water conservation by the
kidneys, resulting in an increase in blood volume.
4.
Angiotensin II acts as a vasoconstrictor, as well as promoting the release of
aldosterone and antidiuretic hormone.
5.
Endothelium-derived factors promote vasoconstriction, and are released in response
to low blood flow.
6.
Nitric oxide is produced in response to high blood flow or other signaling molecules,
and promotes systemic and localized vasodilation.
7.
Inflammatory chemicals, such as histamine, prostacyclin, and kinins, are potent
vasodilators.
8.
Alcohol inhibits antidiuretic hormone release and the vasomotor center, resulting in
vasodilation.
D. Long-Term Mechanisms (p. 710; Figs. 19.10–19.11)
1.
The direct renal mechanism counteracts an increase in blood pressure by altering
blood volume, which increases the rate of kidney filtration.
2.
The indirect renal mechanism is the renin-angiotensin mechanism, which counteracts
a decline in arterial blood pressure by causing systemic vasoconstriction.