DB-2 Questions

STUDENT LEARNING OBJECTIVES

At the completion of this chapter, you should be able to do the following:

1.List the basic components of the cardiovascular system.

2.Describe the structures of the heart and how they serve to pump blood.

3.Discuss the deflection waves of a normal ECG and explain their significance.

4.Outline the basic steps of the cardiac cycle.

5.Discuss the primary principle of circulation and the significance of high arterial blood pressure.

6.Describe factors that affect stroke volume and heart rate.

7.Discuss the significance of peripheral resistance in the cardiovascular system.

8.Discuss the significance of the vasomotor control mechanism.

9.Discuss how the respiratory pump and skeletal muscle pump work to assist the venous return of blood to the heart.

10.Outline the hormonal mechanisms that regulate blood volume.

11.Discuss the significance of the pulse mechanism.

12.List several major pulse points in the body.

LANGUAGE OF SCIENCE AND MEDICINE

Before reading the chapter, say each of these terms out loud. This will help you avoid stumbling over them as you read.

ADH mechanism (A-D-H MEK-ah-nih-zem)

[ADH antidiuretic hormone, mechan- machine, -ism state]

ANH mechanism (A-N-H MEK-ah-nih-zem)

[ANH atrial natriuretic hormone, mechan- machine, -ism state]

atrioventricular (AV) bundle (ay-tree-oh-ven-TRIK-yoo-lar BUN-del)

[atrio- entrance courtyard, -ventr- belly, -icul- little, -ar relating to]

atrioventricular (AV) node (ay-tree-oh-ven-TRIK-yoo-lar)

[atrio- entrance courtyard, -ventr- belly, -icul- little, -ar relating to, nod- knot]

baroreceptor (bar-oh-ree-SEP-tor)

[baro- pressure, -recept- receive, -or agent]

cardiac cycle (KAR-dee-ak SYE-kul)

[cardi- heart, -ac relating to, cycle circle]

cardiac output (CO) (KAR-dee-ak)

[cardi- heart, -ac relating to]

conduction system of the heart (kon-DUK-shen SIS-tem)

[conduct- lead, -tion process, system organized whole]

contractility (kon-trak-TIL-ih-tee)

[con- together, -tract- drag or draw, -il- of or like, -ity quality of]

diastole (dye-ASS-toh-lee)

[dia- through, -stole contraction]

diastolic blood pressure (dye-ah-STOL-ik PRESH-ur)

[dia- apart or through, -stol- contraction, -ic relating to]

ectopic pacemaker (ek-TOP-ik PAYS-may-ker)

[ec- out of, -top- place, -ic relating to]

electrocardiogram (ECG or EKG) (eh-lek-troh-KAR-dee-oh-gram)

[electro- electricity, -cardio- heart, -gram drawing]

heart murmur

[murmur hum]

heart rate (HR)

hemodynamics (hee-moh-dye-NAM-iks)

[hemo- blood, -dynami- force, -ic relating to]

peripheral resistance (peh-RIF-er-al)

[peri- around, -phera- boundary, -al relating to]

primary principle of circulation (PRY-mair-ee PRIN-sip-al of ser-kyoo-LAY-shun)

[prim- first, -ary relating to, princip- foundation, circulat- go around, -tion process]

pulse

[pulse beat]

pulse pressure (PRESH-ur)

[pulse beat]

pulse wave

[pulse beat]

P wave

[named for letter of Roman alphabet]

QRS complex (Q R S KOM-pleks)

[named for letters of Roman alphabet]

renin-angiotensin-aldosterone system (RAAS) (REE-nin-an-jee-oh-TEN-sin-al-DAH-stair-ohn SIS-tem)

[ren- kidney, -in substance, angio- vessel, -tens- pressure or stretch, -in substance, aldo- aldehyde, -stero- solid or steroid derivative, -one chemical, system organized whole]

residual volume (ree-ZID-yoo-al)

[residu- remainder, -al relating to]

sinoatrial (SA) node (sye-no-AY-tree-al)

[sin- hollow (sinus), -atri- entrance courtyard, -al relating to, nod- knot]

sphygmomanometer (sfig-moh-mah-NOM-eh-ter)

[sphygmo- pulse, -mano- thin, -meter measure]

stroke volume (SV)

subendocardial branch (sub-en-doh-KAR-dee-al)

[sub- under, -endo- within, -cardi- heart, -al relating to]

systole (SIS-toh-lee)

[systole contraction]

systolic blood pressure (sis-TOL-ik PRESH-ur)

[systole- contraction, -ic relating to]

T wave

[named for letter of Roman alphabet]

vasoconstriction (vay-soh-kon-STRIK-shun)

[vaso- vessel, -constrict- draw tight, -tion state]

vasodilation (vay-soh-dye-LAY-shun)

[vaso- vessel, -dilat- widen, -tion state]

vasomotor center (vay-so-MOH-tor)

[vaso- vessel, -motor move]

vasomotor mechanism (vay-so-MOH-tor MEK-ah-nih-zem)

[vaso- vessel, -motor move, mechan- machine, -ism state]

venous pump (VEE-nus pump)

[ven- vein, -ous relating to]

venous return (VEE-nus)

[ven- vein, -ous relating to]

BOBBY was in a hurry to finish the last job of the day. He had been called in to help complete and inspect the wiring in a museum that was due to open the next week. Bobby called to his coworker, Jerry, to confirm the current was off to the electrical box on which he was working. When he heard a positive response, he climbed the ladder and reached up to tighten a few loose screws. As he was tightening the screws with his right hand, he lost his balance and reached up with his left hand to catch hold of the ladder…but instead caught a live wire that sent a jolt of electricity through his body.

Jerry came running and knocked the ladder out from under Bobby so he would fall to the floor, breaking the electric arc. “Are you okay?” he asked Bobby, who appeared dazed, but was conscious. “I don't feel so great,” he replied, smiling weakly. Then he collapsed. Jerry yelled at the other workers in the room to call 911, checked Bobby's pulse, and started CPR. The foreman rushed in with an automated external defibrillator (AED) and attached the electrodes to Bobby's chest. The AED's mechanical voice said, “Press button when clear.”

As you read through this chapter, you'll understand the electrical mechanism that operates your heart.

Now that you have read this chapter, see if you can answer these questions about the shock Bobby received in the Introductory Story.

When activated, the AED shocks the heart—the intended purpose being electrical stimulation of the cardiac muscle cells to elicit a response from the heart's pacemaker that will cause the cells to contract in unison to effectively pump blood.

1.What bundle of cells in Bobby's heart (and yours) is known as the pacemaker?

a.SV node

b.SA node

c.AV node

d.AV bundle

When the paramedics arrive, they rush Bobby to the hospital. “Let's get an EKG!” the attending physician calls out.

2.What is an EKG?

a.Electrocardiogram

b.Electrocirculogram

c.Encephalocardiogram

d.Enhancercardiogram

3.Ventricular depolarization is shown as which part of the EKG?

a.V wave

b.P wave

c.T wave

d.QRS complex

To solve a case study, you may have to refer to the glossary or index, other chapters in this textbook, A&P Connect, Mechanisms of Disease, and other resources.

FUNCTION OF THE HEART AND BLOOD VESSELS

Our bodies are never at rest. In fact, a continuous supply of energy is required to maintain a relatively constant internal environment. This homeostatic maintenance of our body is due in large part to the continuous and controlled movement of blood throughout our circulatory system. Blood carries out most of its important transport functions in the thousands of miles of capillaries that comprise much of this system. As you might suspect, however, the body's total blood volume is not evenly distributed. The regulation of blood pressure and blood flow must therefore change in response to cellular activity.

There are many control mechanisms that help to regulate and integrate the diverse functions and component parts of our cardiovascular system. This system must work to supply blood to specific body areas according to their immediate needs. These mechanisms ensure a relatively constant internal environment surrounding each body cell. In this chapter we will explore the control mechanisms that regulate the pumping action of the heart. We will also see how these mechanisms ensure the smooth and directed flow of blood throughout our circulatory system.

HEMODYNAMICS

Hemodynamics refers to the various mechanisms that influence the movement of blood. This is vital, of course, because different organs may need vastly different amounts of blood flow, depending on their metabolic activity. For example, working muscles need a far greater blood supply than do resting muscles. This is because tissues and organs (such as working muscles) with a greater metabolic rate obviously need more oxygen. And that oxygen is delivered by the RBCs of flowing blood in the capillaries. Because the amount of blood in our bodies is relatively constant, this means that the flow of blood to specific areas must be managed according to their activities. We will begin with a discussion of the physiology of the heart and then examine blood flow throughout the cardiovascular system.

A&P CONNECT

Whether blood flows straight through vessels or in a swirling, turbulent pattern has great clinical significance. For example, turbulent flow may signal a partially blocked artery and may promote the formation of dangerous blood clots. Learn more about this concept in Focus on Turbulent Blood Flow online at A&P Connect.

THE HEART AS A PUMP

Recall from Chapter 17 that the left side of the heart services the systemic circulatory route, which supplies blood flow to the entire body, except to the lungs. The right side of the heart services the pulmonary circulatory route, which supplies blood flow to and from the lungs. Both routes require coordination so that they function as a single pumping structure. To do this, the impulses (action potentials) that trigger contraction must be coordinated. The heart must have a system to generate rhythmic impulses. It must then distribute these impulses to the different regions of the myocardium. This distribution is accomplished by the impulse-conducting pathway. Four structures make up the core of the conduction system of the heart:

1.Sinoatrial (SA) node

2.Atrioventricular (AV) node

3.AV bundle (bundle of His)

4.Subendocardial branches (Purkinje fibers)

You can see these structures represented in Figure 18-1. Please refer to this figure as you read through the following discussion.

The structures that make up the heart's conduction system are composed of cells that differ in function from those of ordinary cardiac muscle: The heart conduction cells cannot contract strongly. Instead, they permit the generation or rapid conduction of an action potential throughout the myocardium.

Normally, the cardiac impulses that control heart contraction begin in the sinoatrial (SA) node. This node, also called the “pacemaker,” is located just below the atrial epicardium at its junction with the superior vena cava (Figure 18-1, A). The pacemaker cells in the SA node have an intrinsic rhythm. This means that they do not require nervous input from the brain or spinal cord. They themselves initiate impulses at regular intervals. In fact, if you remove pacemaker cells and put them in a nutrient solution, they will continue to beat! They do not require nervous or hormonal stimulation to contract.

FIGURE 18-1 Conduction system of the heart. Specialized cardiac muscle cells (boldface type) in the wall of the heart rapidly initiate or conduct an electrical impulse throughout the myocardium. Both the sketch of the conduction system (A) and the flowchart (B) show the origin and path of conduction. The signal is initiated by the SA node (pacemaker) and spreads directly to the rest of the right atrial myocardium. From there, it travels to the left atrial myocardium by way of a bundle of interatrial conducting fibers, and then to the AV node by way of three internodal bundles. The AV node then initiates a signal that is conducted through the ventricular myocardium by way of the AV bundle (of His) and subendocardial branches (Purkinje fibers).

However, in a living heart, there are nervous and hormonal components that influence the cells of the pacemaker.

Here's an overview of how the heart's conduction system works (Figure 18-1, B). Each impulse generated at the sinoatrial (SA) node travels swiftly throughout the muscle fibers of both atria. (An interatrial bundle of conducting fibers provides rapid conduction to the left atrium.) Thus, the atria begin to contract. The action potential next enters the atrioventricular (AV) node via three internodal bundles. These bundles are also composed of conducting fibers. Here the conduction of the impulse slows considerably. This allows the atria to contract completely before the conduction reaches the ventricles below.

After passing slowly through the AV node, the conduction velocity increases again as the impulse is relayed through the atrioventricular (AV) bundle (also called the bundle of His). At this point, the right and left bundle branches and the subendocardial branches (also called the Purkinje fibers) in which they terminate conduct the impulses throughout the muscle of both ventricles. This impulse stimulates the ventricular muscle fibers to contract almost simultaneously.

Thus the SA node initiates each heartbeat and sets the basic pace—it is the heart's own natural pacemaker. Under the influence of autonomic and endocrine controls, the SA node will normally “fire” at an intrinsic rhythmical rate of 70 to 75 beats per minute under resting conditions. However, if for any reason the SA node loses its ability to generate an impulse, pacemaker activity will shift to another excitable component of the conduction system. These might include the AV node or the subendocardial branches. Pacemakers other than the SA node are abnormal. They are called ectopic pacemakers. Unfortunately, such ancillary pacemakers usually set a much slower rhythm—only 40 to 60 beats per minute. If the heart's own pacemaker fails to maintain a healthy heart rhythm, an artificial pacemaker can be implanted to restore normal function.

A&P CONNECT

Artificial pacemakers can help keep individuals with damaged hearts alive for many years. Check out Artificial Cardiac Pacemakers online at A&P Connect to see how these devices work and how they are implanted.

Electrocardiogram (ECG)

Electrocardiography

Impulse conduction in the heart generates tiny electrical currents that spread through surrounding tissues to the surface of the body. This fact has great clinical importance because these currents can be measured with an electrocardiograph. An electrocardiogram (ECG) is produced by attaching electrodes of a recording voltmeter (the electrocardiograph) to the chest and/or limbs of the subject (Figure 18-2, A).

FIGURE 18-2 Electrocardiogram. A, A nurse monitors a patient's ECG as he exercises on a treadmill. B, Idealized ECG deflections represent depolarization and repolarization of cardiac muscle tissue. C, Principal ECG intervals between P, QRS, and T waves. Note that the P-R interval is measured from the start of the P wave to the start of the Q wave.

FIGURE 18-3 The basic theory of electrocardiography.

FIGURE 18-4 Events represented by the electrocardiogram (ECG). It is impossible to illustrate the invisible, dynamic events of heart conduction in a few cartoon panels or “snapshots.” However, the sketches here give you an idea of what is happening in the heart as an ECG is recorded. Note that depolarization triggers contraction in the affected muscle tissue. Thus cardiac muscle contraction occurs after depolarization begins.

(The abbreviation for an electrocardiogram is ECG when it is written and EKG when it is spoken.) The ECG is not a record of the heart's contractions but of the electrical events that precede the contractions.

You can see changes in voltage (which represent changes in the heart's electrical activity) as deflections of the line in a recording voltmeter (Figure 18-3). We've simplified the situation somewhat by showing only a single cardiac muscle fiber with the two electrodes of a recording voltmeter nearby.

Before the action potential reaches either electrode, there is no difference in charge between them. Thus, no change in voltage is recorded on the voltmeter graph (Figure 18-3, step 1).

As an action potential reaches the first electrode, the external surface of the sarcolemma becomes relatively negative. This results in an upward deflection of the pen of the recording chart (Figure 18-3, step 2). (Note that the voltmeter records the difference in charge between the two electrodes.) When the action potential also reaches the second electrode, the pen returns to the zero baseline. This happens because there is no difference in charge once again between the two electrodes (Figure 18-3, step 3).

As the end of the action potential passes the first electrode, the sarcolemma is again relatively positive on its outer surface. This causes the pen to again deflect away from the baseline. This time, however, because the direction of the negative and positive electrodes is reversed, the pen deflects downward (Figure 18-3, step 4). After the end of the action potential also passes the second electrode, the pen again returns to the zero baseline (Figure 18-3, step 5).

In short, when ECG electrodes are set up this way, depolarization of the cardiac muscle causes a deflection upward; repolarization causes a deflection downward. However, depending on the location of electrodes relative to heart muscle, the direction of ECG waves can vary. It is this activity that is detected in an electrocardiogram. Many ECG setups in use today show these voltage fluctuations in real time on a video monitor and at the same time records them in a computer file and on a paper chart (like the one represented in Figure 18-3).

ECG Waves

We will limit our discussion of electrocardiography to normal ECG deflection waves and the ECG intervals between them. As we do so, please refer to Figure 18-2 and the sequence of events presented in Figure 18-4.

As you can see in Figures 18-2 and 18-4, the normal ECG is composed of deflection waves called the P wave, QRS complex, and T wave. (The letters do not represent any words; they were simply chosen as an arbitrary sequence of letters!)

The P wave represents depolarization of the atria. It measures the deflection caused by the passage of an electrical impulse from the SA node through the musculature of the atria.

The QRS complex represents the depolarization of the ventricles. This is a multi-step process. First there is the depolarization of the interventricular septum. This is followed by the spread of depolarization by the subendocardial branches (Purkinje fibers) through the lateral ventricular walls. All three deflections, then—Q, R, and S together—represent the entire process of depolarization of the ventricles.

There is a slight catch. At the same time that the ventricles are depolarizing, the atria are repolarizing. You might expect to see some indication of this in the ECG tracing. However, the massive ventricular depolarization that is occurring at the same time literally “drowns out” the relatively small voltage fluctuation produced by atrial repolarization. For this reason, the QRS complex represents the net deflection due to both ventricular depolarization and atrial repolarization.

The T wave reflects repolarization of the ventricles. Depending on exactly where the electrodes are placed relative to the direction of electrical activity in the ventricular myocardium, this repolarization wave may deflect the ECG trace in the same direction as in depolarization.

ECG Intervals

The principal ECG intervals between P, QRS, and T waves are illustrated for you in Figure 18-2, C. Measurement of these intervals can provide important information concerning the rate of conduction of an action potential through the heart.

1. What is meant by hemodynamics?

2. Briefly outline the conduction system of the heart.

3. How does an electrocardiograph work?

4. What are the major deflections in an ECG?

5. What conduction event does each type of ECG wave represent?

Cardiac Cycle

The cardiac cycle describes a complete heartbeat or a single pumping cycle. It consists of contraction (systole) and relaxation (diastole) of both atria and both ventricles. First, the two atria contract simultaneously. Then, as the atria relax, the two ventricles contract and relax. As a result, all the chambers of the heart do not contract as a single unit. This alternation of contraction and relaxation imparts a pumping rhythm to the heart.

During the following discussion, please refer often to Figure 18-5, which shows the major phases of the cardiac cycle.

Atrial Systole

The contracting myocardium of the atria forces the blood into the ventricles below. The atrioventricular (cuspid) valves are opened during this phase to allow for the passage of blood into the relaxed ventricles. The semilunar valves are closed, preventing blood return from the aorta or the pulmonary trunk. This part of the cycle is represented by the P wave on an ECG. Passage of the electrical wave of depolarization is then followed almost immediately by actual contraction of the atrial musculature.

Ventricular Contraction

During the brief period of ventricular contraction (between the start of ventricular systole and the opening of the semilunar valves), the volume of blood in the ventricles remains constant (isovolumetric). However, the pressure inside the ventricles increases rapidly. The ventricular systole is marked by the R wave on the ECG. At this time, the first audible heart sound (often described as a “lubb”) is produced.

Ejection

The semilunar valves open and blood is ejected under great force from the ventricles. At this point, the pressure in the ventricles exceeds the pressure in the pulmonary artery and aorta, and blood is pushed into these vessels. This rapid ejection is characterized by a marked increase in ventricular and aortic pressure. The T wave of the ECG appears during the later, long phase of reduced ejection. You might think of this as the tail end of the contraction. However, a considerable quantity of blood, called the residual volume, remains in the ventricles even at the end of the ejection period. In heart failure, the residual volume remaining in the ventricles may greatly exceed the volume ejected into the aorta and pulmonary trunk.

Ventricular Relaxation

Diastole—the relaxation of the ventricles—begins with this period between closing of the semilunar valves and the opening of the atrioventricular valves. At the end of ventricular contraction, the semilunar valves close so that blood cannot re-enter back into the ventricles from the great vessels. The second heart sound (described as a “dupp”) is now heard.

The atrioventricular valves do not open until the pressure in the atrial chambers exceeds the pressure in the relaxed ventricles. The result is a dramatic fall in intraventricular pressure—but no change in blood volume. This is an isovolumetric phase—both sets of valves are closed.

Passive Ventricular Filling

The continuing return of venous blood from the venae cavae and the pulmonary veins increases pressure within both atria until the atrioventricular valves are forced open. When this happens, blood rushes into the relaxed ventricles. This rapid influx of blood lasts only about 0.1 second but results in a

FIGURE 18-5 The cardiac cycle. The five steps of the heart's pumping cycle described in the text are shown as a series of changes in the heart wall and valves. The term isovolumetric means that the volume remains constant.

dramatic increase in the volume of blood in the ventricle. The abrupt inflow of blood that occurs immediately after opening of the AV valves is followed by a slow and continuous flow of venous blood into the atria. This blood then flows through the open AV valves and into the ventricles, slowly building up the blood pressure and volume within the ventricles.

Heart Sounds

The first “lubb” or systolic sound is caused largely by the contraction of the ventricles and by the closing atrioventricular valves. It is longer and lower than the second or diastolic sound, which is short and sharp. Vibrations of the closing semilunar valves cause this second “dupp” sound.

Heart sounds have clinical significance and can provide information about the valves. Any variation from normal “lubb-dupp” sounds may suggest imperfect valve function. A heart murmur is one commonly heard type of abnormal heart sound. Sometimes it is described as a “swishing” sound. This may indicate an incomplete closing of the valves or stenosis (constriction or narrowing) of the valves.

6. Briefly outline the steps of the cardiac cycle.

7. When are heart sounds of medical importance?

PRIMARY PRINCIPLE OF CIRCULATION

In order for blood to flow within the circulatory system, there must be a gradient from high pressure to low pressure (Figure 18-6). This is sometimes called the primary principle of circulation. For example, blood enters an arteriole at 85 mm Hg and leaves at 35 mm Hg. The blood thus moves down a pressure gradient (from 85 mm Hg to 35 mm Hg) as it flows through the arteriole. The pressure difference drives the flow of blood.

ARTERIAL BLOOD PRESSURE

High pressure in the arteries must be maintained to keep blood flowing through the circulatory system. The volume of blood within the arteries largely determines arterial blood pressure. Thus, an increase in arterial blood volume tends to increase arterial pressure. Likewise, a decrease in arterial volume tends to decrease arterial pressure. However, many factors determine arterial pressure through their influence on arterial volume. Two of the most important, cardiac output and peripheral resistance, are directly proportional to blood volume, as we will see below.

FIGURE 18-6 The primary principle of circulation. Fluid always travels from an area of high pressure to an area of low pressure. Water flows from an area of high pressure in the tank (100 mm Hg) toward the area of low pressure above the bucket (0 mm Hg). Blood tends to move from an area of high average pressure at the beginning of the aorta (100 mm Hg) toward the area of lowest pressure at the end of the venae cavae (0 mm Hg). Blood flow between any two points in the circulatory system can always be predicted by the pressure gradient.

Cardiac Output

Cardiac output (CO) is the amount of blood that flows out of a ventricle per unit of time. For example, the resting cardiac output from the left ventricle into the systemic arteries is about 5,000 ml/min. The cardiac output influences the flow rate to the various organs of the body. For the sake of our discussion, we will focus on the cardiac output from the left ventricle into the systemic loop.

Cardiac output is determined by the volume of blood pumped out of a ventricle by each beat (stroke volume or SV) and by heart rate (HR). Because contraction of the heart is called systole, sometimes the volume of blood pumped by one contraction is called the systolic discharge. Stroke volume, or volume pumped per heartbeat, is one of two major factors that determine cardiac output. CO can be determined by the following equation:

SV

(

volume

/

beat

)

×

HR

(

beats

/

min

)

=

CO

(

volume

/

min

)

Thus the greater the stroke volume, the greater the CO (but only if the heart rate remains constant). Anything that changes the rate of the heartbeat or its stroke volume tends to change CO. This means that anything that makes the heart beat faster or stronger (increases its stroke volume) tends to increase CO and therefore arterial blood volume and pressure. Conversely, anything that causes the heart to beat more slowly or more weakly (decreases its stroke volume) tends to decrease CO, arterial volume, and blood pressure.

The following sections, and Figure 18-7, summarize a few of the major factors that affect cardiac output.

Factors that Affect Stroke Volume

Mechanical, neural, and chemical factors regulate the strength of the heartbeat and therefore its stroke volume.

One mechanical factor that helps determine stroke volume is the length of the myocardial fibers at the beginning of ventricular contraction. According to the Frank-Starling mechanism, the longer or more stretched the heart fibers are at the beginning of contraction (up to a critical limit), the stronger is their contraction. The more blood returned to the heart per minute, the more stretched will be their fibers. This will lead to stronger contractions and a larger volume of blood ejected with each contraction.

However, if too much blood stretches the heart beyond a certain critical limit, the myocardial muscle seems to lose its elasticity. As a result the heart contracts less vigorously.

We can now see that the heart pumps out what it receives. That is, within certain limits, the strength of myocardial contraction matches the pumping load. This is contrary to most mechanical pumps that do not adjust themselves to their input with every stroke. In the case of a human heart, under ordinary conditions, it automatically adjusts output (stroke volume) to input (venous return to the heart).

Other factors that influence stroke volume are neural and endocrine chemical factors. Norepinephrine (released by sympathetic fibers in the cardiac nerve) and epinephrine (released into the blood by the adrenal medulla) can both increase the strength of contraction, or contractility, of the myocardium. This increased contractility of the heart muscle forces more blood volume out of the heart per cardiac stroke, thus increasing the stroke volume.

Factors that Affect Heart Rate

Although the sinoatrial node normally initiates each heartbeat, the heart rate it sets can be altered. In fact, various factors can and do change the rate of the heartbeat. One major modifier is the ratio of sympathetic and parasympathetic impulses conducted to the node per minute. This is because autonomic control of heart rate is the result of opposing influences between the parasympathetic (chiefly vagus) and sympathetic (cardiac nerve) stimulation. The parasympathetic stimulation is inhibitory—mediated by acetylcholine released by the vagus nerve. The sympathetic stimulation is stimulatory—mediated by the release of norepinephrine at the distal end of the cardiac nerve.

Cardiac Pressoreflexes

Receptors sensitive to changes in pressure (baroreceptors) are located in two places near the heart. The aortic baroreceptors and the carotid baroreceptors send afferent nerve fibers to cardiac control centers in the medulla oblongata. These stretch

FIGURE 18-7 Factors affecting cardiac output.

receptors, located in the aorta and carotid sinus, respectively, are vitally important to controlling heart rate. Baroreceptors operate with integrators in the cardiac control centers in negative feedback loops called pressoreflexes. These oppose changes in pressure by adjusting heart rate.

Other Reflexes that Influence Heart Rate

Reflexes involving important factors such as emotions, exercise, hormones, blood temperature, pain, and stimulation of various exteroceptors also influence heart rate. Anxiety, fear, and anger often make the heart beat faster to the point where it seems to pound within the chest. Interestingly, grief tends to slow heart rate. Emotions produce changes in the heart rate through the influence of impulses from the “higher centers” (in the cerebrum and hypothalamus) on the cardiac control centers in the brainstem.

As you know, heart rate accelerates during intense exercise. Amazing as it may sound, the mechanism for this acceleration is still not completely understood. However, it certainly involves mechanisms that influence the brainstem's cardiac control centers. The hormone epinephrine is also believed to be an important cardiac accelerator.

Increased blood temperature or stimulation of skin heat receptors also tends to increase the heart rate. Decreased blood temperature or stimulation of skin cold receptors tends to slow it. Sudden, intense stimulation of pain receptors in visceral structures such as the gallbladder, ureters, or intestines can result in slowing of the heart rate to such an extent that fainting can result.

Finally, reflexive increases in heart rate often result from an increase in sympathetic stimulation of the heart. Sympathetic impulses originate in the cardiac control center of the medulla and reach the heart by way of sympathetic fibers. Norepinephrine released as a result of sympathetic stimulation increases heart rate and the strength of cardiac muscle contraction.

8. Discuss the role of pressure gradient and the flow of blood.

9. What factors determine cardiac output?

10. List some factors that affect stroke volume.

11. List some factors that affect heart rate.

12. How can emotions affect heart rate and stroke volume?

Peripheral Resistance

How Resistance Influences Blood Pressure

Peripheral resistance—the resistance to blood flow caused by the friction of blood striking the walls of the vessels—helps maintain arterial blood pressure. The friction that produces peripheral resistance develops partly because of the viscosity (resistance to flow) of blood and partly from the small diameter of arterioles and capillaries. The resistance created by arterioles, in particular, accounts for almost one half of the total resistance in the systemic circulation. An increase in the number of blood cells can increase viscosity of blood and therefore resistance. Under certain abnormal conditions, such as severe anemia or hemorrhage, a decrease in blood viscosity may lower peripheral resistance and arterial pressure dangerously, even to the point of circulatory failure.

The muscular layer of the arterioles allows them to constrict or dilate and thus change the amount of resistance to blood flow. This muscular mechanism in the vessels is called the vasomotor mechanism. Reducing the vessel diameter by increasing the contraction of the muscular layer is called vasoconstriction. This process increases resistance to blood flow, and thus blood flow into tissues also decreases. Vasodilation, the relaxation of vascular muscles, decreases resistance to blood flow. As a result, blood flow increases to the tissues. As Figure 18-8 shows, even small changes in

FIGURE 18-8 Vessel diameter. The effect of changing diameter of arterioles on peripheral resistance and blood flow. The cross sections show vasodilation (top), normal diameter (center), and vasoconstriction (bottom) as tension in smooth muscle fibers changes. Note that reducing the diameter of a blood vessel to one half of normal does not reduce blood flow by half—it reduces blood flow to 1/16 of normal. Likewise, doubling the vessel diameter does not double the blood flow—it increases blood flow to 16 times over that of normal flow!

diameter can cause relatively large changes in resistance, and therefore large changes in local blood flow. As you can see, the vasomotor mechanism is well suited for quickly and dramatically changing blood flow under a variety of conditions.

Vasomotor Control Mechanism

Our blood pressure and even the amount of blood distributed to different organs can be influenced by the diameter of arterioles. The control center for this complex system lies in the vasomotor center of the medulla. When stimulated, the control system sends out impulses via sympathetic fibers, causing the constriction of smooth muscles surrounding some vessels. These include both resistance vessels (such as arterioles) and capacitance vessels (such as the venous networks of the spleen and liver and the veins surrounding blood reservoirs).

A relatively large volume of blood resides in the systemic veins and venules of a resting adult, compared to the volume of blood residing in other vessels of the body. This is why we call systemic veins and venules “reservoirs.” Blood can be quickly moved out of blood reservoirs and shunted to arteries when skeletal muscles demand.

A sudden increase in arterial blood pressure stimulates aortic and carotid baroreceptors—the same ones that initiate cardiac reflexes. Not only does this stimulate the cardiac control center to reduce heart rate, but it also inhibits the vasomotor center. The parasympathetic fibers fire more impulses per second to the heart and blood vessels. As a result, the heartbeat slows and arterioles and venules of the blood reservoirs dilate. The nervous pathways involved in this mechanism are outlined for you in Figure 18-9.

You can readily see how interconnected these feedback systems are. A decrease in arterial pressure causes the aortic and carotid baroreceptors to send more impulses to the medulla's vasoconstrictor centers. The centers are stimulated and send out impulses via the sympathetic fibers to stimulate vascular smooth muscle and cause vasoconstriction. This squeezes more blood out of the blood reservoirs, increasing the amount of venous blood return to the heart. Ultimately, this “extra blood” from the reservoirs flows to active skeletal muscles and the heart because their arterioles become dilated (by another local mechanism). These mechanisms are especially important during high metabolic activity such as during strenuous exercise (Box 18-1).

There are also similar chemoreceptor reflexes originating in the aorta and carotid arteries that function to alter heart rate and blood flow when excess blood carbon dioxide and low oxygen content endanger the stability of the internal environment.

FIGURE 18-9 Vasomotor pressoreflexes. Carotid sinus and aortic baroreceptors detect changes in blood pressure and feed the information back to the cardiac control center and the vasomotor center in the medulla. In response, these control centers alter the ratio between sympathetic and parasympathetic output. If the pressure is too high, a dominance of parasympathetic impulses will reduce it by slowing heart rate, reducing stroke volume, and dilating blood “reservoir” vessels. If the pressure is too low, a dominance of sympathetic impulses will increase it by increasing heart rate and stroke volume and constricting reservoir vessels.

BOX 18-1 Sports & Fitness

The Cardiovascular System and Exercise

Exercise produces short-term and long-term changes in the cardiovascular system. Short-term changes involve negative feedback mechanisms that maintain set-point levels of blood oxygen, glucose, and other physiological variables. Because moderate to strenuous use of skeletal muscles greatly increases the body's overall rate of metabolism, oxygen and glucose are used up at a faster rate. This requires an increase in transport of oxygen and glucose by the cardiovascular system to maintain normal set-point levels of these substances. One response by the cardiovascular system is to increase the cardiac output (CO) from 5 to 6 L/min at rest to as much as 30 to 40 L/min during strenuous exercise. This represents a fivefold to eightfold increase in the blood output of the heart! Such an increase is accomplished by a reflexive increase in heart rate coupled with an increase in stroke volume. Exercise can also trigger a reflexive change in local distribution of blood flow to various tissues, as the figure shows. This results in a larger share of blood flow going to the skeletal muscles than to some other tissues. We've summarized a number of central and local regulatory effects that operate during exercise in the figure.

Long-term changes in the cardiovascular system come only when moderate to strenuous exercise occurs regularly over a long period.

Evidence indicates that 20 to 30 minutes of moderate aerobic exercise (such as cycling or running) three times per week produce profound, healthful changes in the cardiovascular system. Among these long-term cardiovascular changes are (1) an increase in the mass and contractility of the myocardial tissue, (2) an increase in the number of capillaries in the myocardium, (3) a lower resting heart rate, and (4) a decrease in peripheral resistance during rest. The lower resting heart rate coupled with an increase in stroke volume and increased myocardial mass and contractility produce a greater range of CO. Coupled with the other listed effects, a greater maximum CO is achieved. Perhaps you can see why exercise is also known to decrease the risk of various cardiovascular disorders, including arteriosclerosis, hypertension, and heart failure.

Regulation of blood flow during exercise. A summary of some important central and local regulatory mechanisms. GI, Gastrointestinal.

Local Control of Arterioles

There are several kinds of local mechanisms that produce vasodilation in localized areas. They are not completely understood but we know that they function in times of increased tissue activity. They may account for increased blood flow into skeletal muscles during exercise, and also operate in oxygen-deprived tissues—serving as homeostatic mechanisms that restore normal blood flow.

13. What two major factors affect peripheral resistance of blood flow?

14. If the diameter of an artery decreases, what effect does it have on peripheral resistance?

15. How do vasomotor pressoreflexes affect the flow of blood to different organs?

16. Explain briefly what is meant by “local control” of arterioles.

VENOUS RETURN TO THE HEART

Venous return refers to the amount of blood returned to the heart via the veins. A number of factors influence venous return, including the reservoir functions of veins. Whenever blood pressure drops, the elasticity of the venous walls adapts the diameter of veins to the lower pressure. In this manner, blood flow and venous return to the heart is maintained at a relatively steady state. Likewise, when overall blood pressure rises, the elastic nature of blood vessels allows them to expand, thus maintaining normal blood flow. This effect, which occurs in all blood vessels to a greater or lesser degree, is sometimes called the stress-relaxation effect.

The force of gravity works against venous return of blood to the heart. As a result, there is a tendency for some blood to remain pooled in the veins of the extremities—especially when standing or sitting. Venous pumps maintain the pressure gradient necessary to keep blood moving to the venae cavae and from there to the atria of the heart. Changes in the total volume of blood in the vessels can also alter venous blood return to the heart.

Venous Pumps

An important factor promoting the return of blood is the blood-pumping action of respirations and skeletal muscle contraction. Both actions increase the pressure gradient between the peripheral veins and the venae cavae. Each time the diaphragm contracts, the thoracic cavity becomes larger and the abdominal cavity smaller. Therefore, the pressure in the thoracic cavity (and in the thoracic portion of the venae cavae and the atria) decreases. This change in pressure, between expiration and inspiration, acts as a sort of “respiratory pump” that helps move blood along the

FIGURE 18-10 Respiratory pump. This venous pumping mechanism operates by alternately decreasing thoracic pressure during inspiration (thus pulling venous blood into the central veins) and increasing pressure in the thorax during expiration (thus pushing central venous blood into the heart). As in the skeletal muscle pump (see Figure 18-11), one-way valves prevent backflow and thus keep blood pumping toward the heart.

venous route back to the heart (Figure 18-10). Deeper respirations intensify these effects. When you exercise, increasing ventilation and rate of ventilation increase circulation.

Likewise, the contractions of skeletal muscles serve as “booster pumps” for the heart. As each skeletal muscle contracts, it squeezes the soft veins scattered throughout its interior. This contraction pushes blood upward, toward the heart. The one-way valves of the veins prevent blood from flowing back as the muscle relaxes—as you can see in Figure 18-11. This nullifies the effect of gravity as it pulls back on the blood pushed forward. The net effect of muscle contraction, then, is to increase the push of blood back to the heart. This explains why just standing is so much more uncomfortable than sitting. After standing even for just a few minutes, blood pools in the extremities. The repeated contraction of the muscles when walking, or doing any other exercise, keeps the blood moving forward in the veins.

Total Blood Volume

It's easy to see that the greater the volume of blood in your body, the greater the volume of blood returned to the heart. There are several mechanisms that can increase or decrease the total volume of blood. One such mechanism involves moving water into the plasma (increasing blood volume) or removing water from the blood (decreasing blood volume). It is the balance between the movement of water into and out of the plasma that affects the homeostasis of blood flow.

FIGURE 18-11 Skeletal muscle pump. This venous pumping mechanism operates by the alternate increase and decrease in peripheral venous pressure that normally occurs when the skeletal muscles are used for the activities of daily living. One-way valves aid pumping by preventing backflow of venous blood when pressure in a local area is low. A, Local high blood pressure pushes the flaps of the valve to the side of the vessel, allowing easy flow. B, When pressure below the valve drops, blood begins to flow backward but fills the “pockets” formed by the valve flaps, pushing the flaps together and thus blocking further backward flow.

Osmotic pressure tends to promote diffusion of fluid into the plasma. Increasing osmotic pressure of plasma, generated by increasing the number of large solute particles such as plasma proteins, can draw water into the plasma. Where arterioles join capillaries, there tends to be a net loss of blood volume to the surrounding interstitial fluid. However, this fluid is recaptured where the ends of capillaries join to create venules. As a result, the capillaries recover much of the fluid they have lost (Figure 18-12).

In actuality, there is a 10% loss of blood volume along the network of capillaries. However, this is recovered by the lymphatic system and returned to the venous blood before it returns to the heart. We will study this fluid recovery in greater detail in the following chapter.

Changes in Total Blood Volume

In Chapter 15, we studied the endocrine reflexes that help control water retention in the body. In particular, antidiuretic hormone (ADH) is released by the posterior pituitary and acts on the kidneys to reduce the amount of water loss. ADH does this by increasing the amount of water that the kidneys reabsorb from urine before it is excreted. The more ADH, the more water retention, and the greater the volume of the blood. Receptors in the body that detect the balance between water and solutes trigger the ADH mechanism.

Another endocrine reflex mechanism is the renin-angiotensin-aldosterone system (RAAS). The enzyme renin is released when blood pressure in the kidney is low. This triggers a series of events that leads to the secretion of aldosterone from the adrenal cortex. Aldosterone in turn promotes sodium retention by the kidneys, which stimulates the osmotic flow of water from kidney tubules back into the blood plasma. But this only occurs when ADH is present to allow the movement of water. Thus, low blood pressure increases the secretion of aldosterone. This in turn stimulates retention of water and an increase in blood volume back toward normal.

Yet another mechanism that can change blood plasma volume (and thus venous return of blood to the heart) is the ANH mechanism. ANH (atrial natriuretic hormone) is secreted by heart muscle cells located in the atrial wall. This takes place in response to overstretching of the atrial wall (such as when venous return to the heart is abnormally high). ANH adjusts venous return back down to its normal set point by promoting the loss of water from the plasma. As a result, there is a decrease in blood volume. ANH does this by increasing sodium loss from the blood into the urine, which causes water to follow by osmosis. The ANH mechanism opposes the effects of ADH and

FIGURE 18-12 Starling's law of the capillaries. At the arterial end of a capillary, the outward driving force of blood pressure (hydrostatic pressure of blood) is larger than the inwardly directed force of osmosis—thus fluid moves out of the vessel. At the venous end of a capillary, the inward driving force of osmosis is greater than the outwardly directed force of hydrostatic pressure—thus fluid enters the vessel. About 90% of the fluid leaving the capillary at the arterial end is recovered by the blood before it leaves the venous end. The remaining 10% is recovered by the venous blood eventually, by way of the lymphatic vessels (see Chapter 19).

FIGURE 18-13 Three mechanisms that influence total plasma volume. The antidiuretic hormone (ADH) mechanism and renin-angiotensin-aldosterone system (RAAS) tend to increase water retention and thus increase total plasma volume. The atrial natriuretic hormone (ANH) mechanism opposes these mechanisms by promoting water loss and thus promoting a decrease in total plasma volume.

aldosterone. These actions and counteractions produce a balanced, precise control of blood volume. Figure 18-13 summarizes these mechanisms.

17. What is meant by venous return?

18. In general, how do venous pumps operate to promote the return of venous blood to the heart?

19. Discuss the several venous pumping mechanisms (the respiratory pump and the contraction/relaxation of skeletal muscles).

20. How does capillary exchange affect total blood volume?

21. Discuss several ways in which endocrine reflexes affect changes in total blood volume.

MEASURING ARTERIAL BLOOD PRESSURE

Blood pressure is measured with a sphygmomanometer. This makes it possible to measure the amount of air pressure equal to the blood pressure in an artery. The measurement is made in terms of how many millimeters (mm) high the air pressure raises a column of mercury (Hg) in an enclosed glass tube (Figure 18-14, A). The result is expressed as millimeters of mercury (mm Hg). Most sphygmomanometers today have mercury-free mechanical or electronic pressure sensors that are still calibrated to the mercury scale.

The cuff of the sphygmomanometer is wrapped around the arm over the brachial artery. Air is then pumped into the cuff by means of the bulb. In this way, air pressure in the cuff is exerted against the outside of the artery. Air is pumped in until the air pressure in the cuff exceeds the pressure within the artery. This compression of the artery by the air pressure in the cuff stops the flow of blood through the artery. This can be determined by a stethoscope placed over the brachial artery at the bend of the elbow, along the inner margin of the biceps muscle. No sounds can be heard.

Then the air is slowly released from the cuff as the examiner listens carefully for the first return of blood. This is the point at which blood flow in the artery first overcomes the pressure from the external cuff. The sharp “tapping” sound heard becomes increasingly louder as the pressure in the cuff is lowered even further. Finally the sounds become muffled and disappear altogether. Health professionals train themselves to hear these different sounds (Korotkoff sounds) and read the column of mercury at the same time (Figure 18-14, B).

The first tapping sounds when blood begins to return are a measure of the systolic blood pressure. This is the force with which the blood is pushing against the artery walls when the ventricles are contracting. The lowest point at which the sounds finally disappear is approximately equal to the diastolic blood pressure. This is the force of the blood when the ventricles are relaxing. Systolic pressure gives us valuable information about the force of the left ventricular contraction. Diastolic pressure gives valuable information about the resistance of the blood vessels.

Blood in the arteries of an adult with a blood pressure reading at the high end of the normal range exerts a pressure equal to that required to raise a column of mercury about 120 mm high in the glass tube during systole of the ventricles and 80 mm high in a glass tube during diastole. This is expressed as a systolic/diastolic pressure of “120 over 80” or 120/80. The first number indicates the systolic pressure and the second the diastolic pressure. The difference between systole and diastole is called pulse pressure. The pulse pressure typically increases in arteriosclerosis. This is because systolic pressure increases more than diastolic pressure.

As you've seen, blood exerts a comparatively high pressure in arteries but a very low pressure in veins. For this

FIGURE 18-14 Sphygmomanometer. This mercury-filled pressure sensor is used in clinical and research settings to quickly and accurately measure arterial blood pressure. A, The pressure cuff is pumped with air until the pressure inside the cuff exceeds the expected systolic pressure of the large arteries of the arm. No sound caused by pulsing of blood in the arteries can then be heard with a stethoscope. As the pressure inside the cuff is slowly released from a valve, the air pressure equals the maximum pressure of the pulse waves in the artery—thus the pulsing sounds can then be heard. B, The sounds of pulsing (Korotkoff sounds) continue as long as the cuff pressure is equal to pressures of the pulse wave. The sounds disappear at the point that cuff pressure drops below the minimum pulse pressure in the arteries.

reason, it gushes forth with considerable force from a cut artery, but seeps in a slow steady stream from a vein. As the ventricles contract, blood spurts forth forcefully, but when the ventricles relax, the flow ebbs to almost nothing because of the fall in pressure. In contrast, a steady pressure exists in the capillaries and veins.

PULSE AND PULSE WAVE

Pulse Wave

Pulse is defined as the alternating expansion and recoil of an artery. Two factors are responsible for a pulse that you can actually feel: (1) pulses of blood injected from the heart's left ventricle into the aorta (see Figure 18-6, p. 411), and (2) the elasticity of the arterial wall. If blood flowed steadily from the heart into the aorta, you would feel no pulse because the flow would be constant. Likewise, if our vessels were made from some inelastic material such as copper pipe, there might still be an alternating raising and lowering of pressure within the vessels, but the walls could not expand and recoil. Thus there would be no palpable pulse.

Each ventricular systole starts a new pulse that proceeds as a wave of expansion throughout the arteries. This is called the pulse wave. It gradually dissipates as it travels through the circulatory system, disappearing entirely in the capillaries. The pulse wave felt at the common carotid artery in the neck is large and powerful. Figure 18-15 shows that the carotid pulse wave begins during ventricular systole. Note that the closure of the aortic valve produces a detectable notch (a dicrotic notch) in the pulse wave. However, the pulse felt in the radial artery at the wrist does not coincide with the contraction of the ventricles. Instead, it follows the carotid pulse but with a detectable time lag because of its distance from the heart. The pulse reveals important information about the cardiovascular system, heart action, blood vessels, and circulation.

FIGURE 18-15 Normal carotid pulse wave. This series of pulse waves shows rhythmic increases and decreases in pressure as measured at the common carotid artery in the neck. The dicrotic notch represents the pressure fluctuation generated by closure of the aortic valve.

FIGURE 18-16 Functional role of the pulse wave. The arterial pulse conserves energy by absorbing and storing force from the ventricular contraction. Force is stored by the elastic expansion of the arterial wall. The energy is used to maintain continued blood flow during ventricular relaxation by elastic recoil of the arterial wall—thus producing enough arterial pressure to keep blood flowing.

The pulse wave actually conserves energy produced by the pumping action of the heart (Figure 18-16). When the pressure of blood is ejected from the ventricle into the aorta, the walls of the aorta store part of this effort as potential energy, like a stretched rubber band. During ventricular diastole, the elastic nature of the aortic wall allows it to recoil. This recoil exerts pressure on the blood and thus keeps it moving. If the wall of the aorta were inelastic, it would not alternately expand and recoil. Thus, the blood would not move continuously. Instead, you'd see arterial blood as alternating as spurting then stopping, spurting then stopping. This would not be a good plan for continuous blood flow needed by the entire body!

Feeling Your Pulse

You can feel your pulse whenever an artery comes close to the surface and passes over a bone or other firm background (Figure 18-17). Here are some specific areas you can feel (and sometimes see) your pulse.

Radial artery: at the anterior, lateral surface of your wrist

Temporal artery: in front of your ear and above and to the outer side of your eye

Common carotid artery: along the anterior edge of the sternocleidomastoid muscle

Brachial artery: at the bend of your elbow, along the inner margin of the biceps

Posterior tibial artery: behind the medial malleolus (inner “ankle bone”)

Femoral artery: in the middle of groin, where artery passes over pelvic bone; pulse can also be felt there

Dorsalis pedis artery: on the dorsal (upper) surface of your foot

22. How is blood pressure measured?

23. What is the difference between systolic blood pressure and diastolic blood pressure?

24. What is the pulse wave? Where can it be measured?

Cycle of LIFE

As we've seen in the previous chapter, enormous changes occur in our circulatory system immediately after birth. Of course, there are physiological changes as well. For example, changes at the time of birth adapt the circulatory system from an aquatic environment to a terrestrial environment. As a result, changes in the blood pressure gradients take place that alter blood flow throughout much of our bodies.

FIGURE 18-17 Pulse points. Each pulse point is named after the artery with which it is associated. (Some arteries in the figure have been enlarged to clarify the location of pulse points.)

Likewise, there are degenerative changes in our circulatory system that take place as we age. The heart has a reduced ability to maintain cardiac output and the arteries are less able to withstand high blood pressure.

Changes in arterial blood pressure are easily measured. In a newborn, normal arterial blood pressure is only about 90/55 mm Hg—much lower than values approaching 120/80 seen in many healthy adults. In older adults, arterial blood pressures commonly reach 150/90, so you can imagine the wear and tear on the elasticity of the vessels because of this dramatically increased blood pressure.

Another commonly observed change as we age is in the heart rate. A newborn may have heart rates ranging from 120 to 170 beats per minute. The resting heart rate of a preschooler can range from 80 to 160 beats per minute. The typical resting heart rate for adults is about 72 beats per minute, but in older adults, resting heart rates range from 40 to 100 beats per minute. These ranges vary according to body weight and the degree to which a person is in good cardiovascular shape. A young cross-country runner may have a resting heart rate in the mid-40s. This rate may not change much as the person ages, depending on his or her aerobic fitness.

The BIG Picture

One of the basic and most important concepts of homeostasis is that renewable fluid comprises our internal environment. If we were not able to maintain the chemical nature and other physical characteristics of our internal fluid environment, we could not survive. To maintain this constancy, we must be able to shift and exchange nutrients, gases, hormones, waste products, agents of immunity, and other materials such as solutes around the body. As certain materials are depleted in one tissue and new materials enter the internal environment in another, redistribution must occur and continue to take place. As we have seen, the circulatory is the system by which the constancy of the internal environment is maintained.

Recall also from our earlier study of the integumentary and muscular systems that shifting the flow of blood to or away from warm tissues is essential to maintaining homeostasis of the body temperature. And, as we will see in Chapter 23, the ability of our blood to increase or decrease blood pressure in the kidney has a great impact on that organ's vital function of filtering the internal blood fluid. Understanding how blood flows and some of the basic physical parameters behind that flow is required for us to understand the fluid dynamics of our body.

MECHANISMS OF DISEASE

As you might expect, cardiovascular disease is a major health issue in North America—affecting millions across the continent. Sometimes, the heart loses its normal rhythm—a type of condition called dysrhythmia. Dysrhythmia, or damage to the myocardium caused by blocked coronary blood flow, can lead to partial or full heart failure. Mechanisms that cause a sudden drop in blood pressure can produce circulatory shock. And factors that cause blood pressure to increase may result in chronic hypertension (HTN) (high blood pressure).

To understand the heart better by exploring what can go wrong, check out Mechanisms of Disease: Physiology of the Cardiovascular System online.

CHAPTER SUMMARY

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FUNCTION OF THE HEART AND BLOOD VESSELS

A. Homeostatic maintenance of our body is due to the continuous and controlled movement of blood throughout our circulatory system

B. Many control mechanisms help to regulate and integrate the diverse functions and component parts of our cardiovascular system

HEMODYNAMICS

A. Hemodynamics—refers to the various mechanisms that influence the movement of blood

B. Different organs may need vastly different amounts of blood flow, depending on their metabolic activity

THE HEART AS A PUMP

A. Heart must have a system to generate rhythmic impulses and distribute them to different regions of the myocardium

1. Distribution is accomplished by the impulse-conducting pathway

2. Four structures make up the core of the conduction system of the heart (Figure 18-1):

a. Sinoatrial (SA) valve

b. Atrioventricular (AV) node

c. AV bundle (bundle of His)

d. Subendocardial branches (Purkinje fibers)

3. SA node—“pacemaker”; has own intrinsic rhythm

a. Impulse generated travels swiftly throughout the muscle fibers of both atria

b. Action potential next enters the atrioventricular (AV) node

c. Impulse is relayed through the atrioventricular (AV) bundle

d. Right and left bundle branches and the subendocardial branches in which they terminate conduct the impulses throughout the muscle of both ventricles

B. Electrocardiogram (ECG)

1. Electrocardiography—impulse currents can be measured with an electrocardiograph

a. Electrocardiogram—record of the electrical events that precede the contractions

b. Produced by attaching electrodes of a recording voltmeter (the electrocardiograph) to the chest and or limbs of the subject (Figure 18-2, A)

c. Changes in the heart's electrical activity can be seen as deflections of the line from a video monitor (Figure 18-3)

2. ECG waves—normal ECG is composed of deflection waves called the P wave, QRS complex, and T wave (Figures 18-2 and 18-4)

a. P wave—represents depolarization of the atria

b. QRS complex—represents depolarization of the ventricles

c. T wave—reflects repolarization of the ventricles

3. ECG intervals—provide important information concerning the rate of conduction of an action potential through the heart

C. Cardiac cycle—a complete heartbeat or a single pumping cycle (Figure 18-5)

1. Atrial systole—contracting myocardium of the atria forces the blood into the ventricles below; represented by the P wave on an ECG

2. Ventricular contraction—brief period between the start of ventricular systole and the opening of the semilunar valves; marked by the R wave on the ECG (isovolumetric)

3. Ejection—semilunar valves open and blood is ejected under great force from the ventricles

a. Rapid ejection—characterized by a marked increase in ventricular and aortic pressure

b. Reduced ejection—coincides with the T wave of the ECG

4. Ventricular relaxation (diastole)—period between closing of the semilunar valves and the opening of the atrioventricular valves (isovolumetric)

5. Passive ventricular filling—continuing return of venous blood from the venae cavae and the pulmonary veins increases pressure within both atria until the atrioventricular valves are forced open

D. Heart sounds

1. First “lubb” or systolic sound is caused largely by the contraction of the ventricles and by the closing atrioventricular valves

2. Vibrations of the closing semilunar valves cause the second “dupp” sound

PRIMARY PRINCIPLE OF CIRCULATION

A. In order for blood to flow within the circulatory system, there must be a gradient from high pressure to low pressure; primary principle of circulation (Figure 18-6)

B. Pressure difference drives the flow of blood

ARTERIAL BLOOD PRESSURE

A. The volume of blood within the arteries largely determines arterial blood pressure

1. Many factors determine arterial pressure through their influence on arterial volume; for example, cardiac output and peripheral resistance (Figure 18-7)

B. Cardiac output (CO)—amount of blood that flows out of a ventricle per unit of time

1. CO influences the flow rate to the various organs of the body

2. CO is determined by the volume of blood pumped out of a ventricle by each beat (stroke volume or SV) and by heart rate (HR)

3. CO (volume/min) = SV(volume/beat) × HR (beats/min)

C. Factors that affect stroke volume—mechanical, neural, and chemical factors regulate the strength of the heartbeat (stroke volume)

D. Factors that affect heart rate—sinoatrial (SA) node normally initiates each heartbeat

1. Various factors can change the rate of the heartbeat

a. Ratio of sympathetic and parasympathetic impulses conducted to the node per minute

E. Cardiac pressoreflexes—receptors sensitive to changes in pressure are located in two places near the heart (Figure 18-9)

1. Aortic baroreceptors

2. Carotid baroreceptors

F. Other reflexes that influence heart rate—emotions, exercise, hormones, blood temperature, pain, and stimulation of various exteroceptors also influence heart rate

G. Peripheral resistance—the resistance to blood flow caused by the friction of blood striking the walls of the vessels

1. Vasomotor mechanism—muscular layer of the arterioles constricting or dilating and thus changing the amount of resistance to blood flow (Figure 18-8)

a. Vasoconstriction—reducing the vessel diameter by increasing the contraction of the muscular layer

b. Vasodilation—relaxation of vascular muscles, decreases resistance to blood flow

H. Vasomotor control mechanism

1. Control center for this complex system lies in the vasomotor center of the medulla

2. Upon stimulation, the control system sends out impulses causing the restriction of smooth muscles surrounding some vessels (Figure 18-9)

3. Sudden increase in arterial blood pressure stimulates aortic and carotid baroreceptors; results in arterioles and venules of the blood reservoirs dilating

4. Decrease in arterial pressure causes the aortic and carotid baroreceptors to send more impulses to the medulla's vasoconstrictor centers; causes the vascular smooth muscles to constrict

5. There are also chemoreceptor reflexes in the aorta and carotid arteries

a. Function when excess blood carbon dioxide and low oxygen content endangers the stability of the internal environment

I. Local control of arterioles—several kinds of local mechanisms that produce vasodilation in localized areas

1. Function in times of increased tissue activity

VENOUS RETURN TO THE HEART

A. Venous return—amount of blood returned to the heart via the veins

1. Stress-relaxation effect—occurs when a change in blood pressure causes a change in vessel diameter

B. Venous pumps—blood-pumping action of respirations and skeletal muscle contractions facilitate venous return by increasing pressure gradient between peripheral veins and venae cavae

1. Change in pressure, between expiration and inspiration, helps move blood along the venous route back to the heart (Figure 18-10)

2. As each skeletal muscle contracts, it squeezes the soft veins scattered throughout its interior; contractions push blood upward, toward the heart (Figure 18-11)

a. Repeated contraction of the muscles when walking or doing any other exercise keeps the blood moving forward in the veins aided by one-way valves (Figure 18-11)

C. Total blood volume—changes in total blood volume change the amount of blood returned to the heart

1. Balance between the movement of water into and out of the plasma that affects the homeostasis of blood flow

D. Changes in total blood volume

1. Receptors in the body that detect the balance between water and solutes trigger the ADH mechanism

a. ADH is released by the posterior pituitary and acts on the kidneys to reduce the amount of water loss

2. Renin-angiotensin-aldosterone system (RAAS)

a. Renin is released when blood pressure in the kidney is low

b. Release of renin triggers a series of events that leads to the secretion of aldosterone from the adrenal cortex

c. Aldosterone promotes sodium retention by the kidneys; stimulates the osmotic flow of water from kidney tubules back into the blood plasma

3. ANH mechanism

a. ANH is secreted by specialized cells in the atria

b. ANH adjusts venous return back down to its normal set point by promoting the loss of water from the plasma

c. ANH increases sodium loss from the urine; causes water to follow by osmosis

MEASURING ARTERIAL BLOOD PRESSURE

A. Blood pressure is measured with a sphygmomanometer (Figure 18-14, A)

B. Systolic blood pressure—force with which the blood is pushing against the artery walls when the ventricles are contracting

C. Diastolic blood pressure—force of the blood when the ventricles are relaxing

D. Pulse pressure—difference between systolic and diastolic blood pressure

PULSE AND PULSE WAVE

A. Pulse—alternating expansion and recoil of an artery

1. Two factors are responsible for a pulse you can actually feel:

a. Pulses of blood injected from the heart's left ventricle into the aorta

b. Elasticity of the arterial wall

2. Pulse wave (Figure 18-16)

a. Each pulse starts with ventricular contraction and proceeds as a wave of expansion throughout the arteries

b. Gradually dissipates as it travels through the circulatory system, disappearing entirely in the capillaries

B. Feeling your pulse—can feel your pulse whenever an artery comes close to the surface and passes over a bone or other firm background