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Chapter 12

Vanders

Human Physiology
The Mechanisms of Body Function
Tenth Edition
by

Widmaier Raff Strang


The McGraw-Hill Companies, Inc.

Figures and tables from the book, with additional comments by: John J. Lepri, Ph. D., The University of North Carolina at Greensboro

Chapter 12: Cardiovascular Physiology


CO = HR x SV, as follows. The heart is the pump that moves the blood. Its activity can be expressed as cardiac output (CO) in reference to the amount of blood moved per unit of time.

Chapter 12: Cardiovascular Physiology (cont.)

A small fraction of cardiac muscle cells, called the

autorhythmic cells, determine the heart rate (HR).


A much larger group, making up 99% of the total cells in the heart, constitutes the contractile cells. Their activity determines the stroke volume (SV).

Chapter 12: Cardiovascular Physiology (cont.)


Mean arterial pressure, which drives the blood, is the sum of
the diastolic pressure plus one-third of the difference between the systolic and diastolic pressures.

The autonomic system dynamically adjusts CO and MAP.

Blood composition and hemostasis are described.

Figure 12-1

Plasma includes water, ions, proteins, nutrients, hormones, wastes, etc.

The hematocrit is a rapid assessment of blood composition. It is the percent of the blood volume that is composed of RBCs (red blood cells).

Figure 12-2 The heart is the pump that propels the blood through the systemic and pulmonary circuits.

Red color indicates blood that is fully oxygenated. Blue color represents blood that is only partially oxygenated.

Figure 12-3
The distribution of blood in a comfortable, resting person is shown here. Dynamic adjustments in blood delivery allow a person to respond to widely varying circumstances, including emergencies.

Figure 12-4

Though pressure is higher in the lower tube, the flow rates in the pair of tubes is identical because they both have the same pressure difference (90 mm Hg) between points P1 and P2.

Figure 12-6

The major external and internal parts of the heart are shown in this diagram. The black arrows indicate the route taken by the blood as it is pumped along.

Figure 12-8

The general route of the blood through the body is shown, including passage through the heart (colored box).

Figure 12-10

Figure 12-11

The sinoatrial node is the hearts pacemaker because it initiates each wave of excitation with atrial contraction.

The Bundle of His and other parts of the conducting system deliver the excitation to the apex of the heart so that ventricular contraction occurs in an upward sweep.

Click here to play the Conducting System of the Heart Flash Animation

The action potential of a myocardial pumping cell.


The rapid opening of voltagegated sodium channels is responsible for the rapid depolarization phase.

Figure 12-13

The action potential of a myocardial pumping cell.

The prolonged plateau of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUS closure of potassium channels.

Figure 12-12

The action potential of a myocardial pumping cell.

Opening of potassium channels results in the repolarization phase.

Figure 12-12

The action potential of a myocardial pumping cell.


The rapid opening of voltage-gated sodium channels is responsible for the rapid depolarization phase. The prolonged plateau of depolarization is due to the slow but prolonged opening of voltage-gated calcium channels PLUS closure of potassium channels.

Opening of potassium channels results in the repolarization phase.

Figure 12-12

The action potential of an autorhythmic cardiac cell.


Sodium ions leaking in through the F-type [funny] channels PLUS calcium ions moving in through the T [calcium]channels cause a threshold graded depolarization.

Figure 12-13

The rapid opening of voltage-gated calcium channels is responsible for the rapid depolarization phase.
Reopening of potassium channels PLUS closing of calcium channels are responsible for the repolarization phase.

Figure 12-14
The relationship between the electrocardiogram (ECG), recorded as the difference between currents at the left and right wrists, and

an action potential typical of ventricular myocardial cells.

Figure 12-16

Click here to play the Mechanical Events of the Cardiac Cycle Flash Animation

Figure 12-17

Calcium ions regulate the contraction of cardiac muscle: the entry of extracellular calcium ions causes the release of calcium from the sarcoplasmic reticulum, the source of about 95% of the calcium in the cytosol.

Figure 12-18

The prolonged refractory period of cardiac muscle prevents tetanus, and allows time for ventricles to fill with blood prior to pumping.

Figure 12-19

Systole: ventricles contracting

Diastole: ventricles relaxed

Figure 12-20

Pressure and volume changes in the left heart during a contraction cycle.

Figure 12-21

Pressure changes in the right heart during a contraction cycle.

Figure 12-23

Figure 12-24

To speed up the heart rate: deliver the sympathetic hormone, epinephrine, and/or release more sympathetic neurotransmitter (norepinephrine), and/or reduce release of parasympathetic neurotransmitter (acetylcholine).

Figure 12-25

To increase the hearts stroke volume: fill it more fully with blood. The increased stretch of the ventricle will align its actin and myosin in a more optimal pattern of overlap.

Figure 12-26

To further increase the stroke volume: fill it more fully with blood AND deliver sympathetic signals (norepinephrine and epinephrine); it will also relax more rapidly, allowing more time to refill.

Figure 12-27

Sympathetic signals (norepinephrine and epinephrine) cause a stronger and more rapid contraction and a more rapid relaxation.

To increase SV, increase: end-diastolic volume, norepinephrine delivery from sympathetic neurons, and epinephrine delivery from the adrenal medulla.

To increase HR, increase: norepinephrine delivery from sympathetic neurons, and epinephrine delivery from adrenal medulla (reduce parasympathetic).

Figure 12-28

It is not possible, under normal circumstances, to increase one but not the other of these determinants of cardiac output.

In response to the pulsatile contraction of the heart: pulses of pressure move throughout the vasculature, decreasing in amplitude with distance

Figure 12-29

Figure 12-30

The blood moved in a single heart contraction stretches out the arteries, so that their recoil continues to push on the blood, keeping it moving during diastole.

Figure 12-31

Figure 12-32

To estimate systolic and diastolic pressures, pressure is released from an inflatable cuff on the upper arm while listening as blood flow returns to the lower arm.

Click here to play the Sphygmomanometry Flash Animation

Figure 12-33

Dynamic adjustments in the blood distribution to the organs is accomplished by relaxation and contraction of circular smooth muscle in the arterioles.

Figure 12-34

Active hyperemia and flow autoregulation differ in their cause but both result in the production of the same local signals that provoke vasodilation.

Figure 12-35

Sympathetic stimulation of alpha-adrenergic receptors cause vasoconstriction to decrease blood flow to that location. Sympathetic stimulation of beta-adrenergic receptors lead to vasodilation to cause an increase in blood flow to that location.

Figure 12-36

Diversity among signals that influence contraction/relaxation in vascular circular smooth muscle implies a diversity of receptors and transduction mechanisms.

Figure 12-37

Capillary walls are a single endothelial cell in thickness.

The capillary is the primary point exchange between the blood and the interstitial fluid (ISF). Intercellular clefts assist the exchange.

Figure 12-38

Capillaries lack smooth muscle, but contraction/relaxation of circular smooth muscle in upstream metarterioles and precapillary sphincters determine the volume of blood each capillary receives.

Figure 12-39

Six balls in per minute mandates six balls out per minute. Therefore, the velocity of the balls in the smaller tubes is slower.

There are many, many capillaries, each with slow-moving blood in it, resulting in adequate time and surface area for exchange between the capillary blood and the ISF.

Figure 12-41
Movement of fluid and solutes out of the blood is called filtration.

Filtration Absorption

Movement of fluid and solutes into the blood is called absorption.

Figure 12-43

Dynamic changes in vasodilation/vasoconstriction in the arterioles regulate downstream pressures and flow rates.

Figure 12-44

At rest, approx. 60% of the total blood volume is in the veins. Sympathetically mediated venoconstriction can substantially increase venous return to the heart.

Figure 12-45

Venous flow is assisted by the skeletal muscle pump mechanism working in combination with one-way valves.

Figure 12-46

Alterations in venous return alter end-diastolic volume (EDV); increased EDV directly increases stroke volume and cardiac output.

Figure 12-47

Lymphatic fluid, formed by the slight mismatch between filtration and absorption in the capillaries, returns to the blood in the veins.

Figure 12-49

Dynamic changes in vasodilation/vasoconstriction due to changes in the resistance of arterioles can alter the mean arterial pressure (represented as P).

Figure 12-50

Compensatory changes in arteriolar resistance occur to protect the maintenance of mean arterial pressure (represented as P).

Figure 12-51

A summary of dynamic changes in MAP and TPR.

Figure 12-52

Blood loss causes a reduction in MAP, which, if left unchecked, would result in rapid and irreversible damage to the brain and the heart.

Figure 12-53

Baroreceptor neurons function as sensors in the homeostatic maintenance of MAP by constantly monitoring pressure in the aortic arch and carotid sinuses.

Figure 12-54

The action potential frequency in baroreceptor neurons is represented here as being directly proportional to MAP.

Click here to play the Baroreceptor Reflex Control of Blood Pressure Flash Animation

Figure 12-55
i.e., MAP is above homeostatic set point

i.e., reduce cardiac output

Baroreceptor neurons deliver MAP information to the medulla oblongatas cardiovascular control center (CVCC); the CVCC determines autonomic output to the heart.

Click here to play the Chemoreceptor Reflex Control of Blood Pressure Flash Animation

Figure 12-56

The information reported by baroreceptor neurons sets in motion autonomic responses not only to the heart, but also to arterioles and veins.

MAP is more readily moved back closer to the set point by this combined approach.

Figure 12-57

Whatever the cause, an abnormal increase in MAP squeezes more fluid out of the blood and into the urine, leading to a reduction in blood volume, which then reduces MAP back closer to the set point value.

Figure 12-58

Loss of blood causes immediate reductions in MAP, but compensatory responses in cardiac output and total peripheral resistance act quickly to restore MAP.

Figure 12-59

At capillaries, reduced MAP increases absorption and reduces filtration to help protect blood volume.

Figure 12-60

By assisting the return of venous blood to the heart the skeletal muscle pump mechanism on veins opposes the buildup of excessive lymphatic fluid.

Figure 12-61

Dynamic adjustments in blood-flow distribution during exercise result from changes in cardiac output and from changes in regional vasodilation/vasoconstriction.

Figure 12-63

Using stored knowledge, along with information from the periphery (afferent input), the CNS coordinates changes in cardiac output and blood-flow distribution during exercise.

Figure 12-64

The benefits of training include increased cardiovascular capacity during subsequent exercise.

Figure 12-65

Heart failure leads to increased fluid retention, leading to increased blood volume and greater stroke volume; however, the failing heart is less able to handle a large EDV.

An example of angiographic visualization and treatment of blocked blood flow in an impaired heart.

Figure 12-68

The availability of dietary iron can be a limiting factor in erythropoiesis, so storage and recycling mechanisms are highly developed in humans, as protection from anemia.

Figure 12-69

Erythropoiesis is hormonally regulated:

decreased oxygen delivery to the kidney causes the secretion of erythropoietin, which activates receptors in bone marrow, leading to an increase in the rate of erythropoiesis.

Figure 12-70

The major forms of cells in the blood. Among these, only the leukocytes are true cells with nuclei.

Figure 12-71

Stem cells in the bone marrow constitute an important precursor of many of the formed components in the blood.

Figure 12-72
Signaling mediates responses to damage in a blood vessel: collagen is a magnet for platelets, which then become one of the sources of signals that alter blood flow and initiate the steps of clot formation at the affected site.

Figure 12-73

Signaling mediates responses to damage in a blood vessel:


adjacent endothelial cells are a source of signals that influence platelet aggregation and alter blood flow and clot formation at the affected site.

Figure 12-74

Exploration of the details of the clotting pathway has yielded detailed information about the sequence, only a portion of which is represented here. Note thrombins influence in three different directions.

Figure 12-76

Knowledge that thrombin plays a central role in clotting has generated detailed studies of the possible pathways resulting in its formation: the extrinsic pathway is the more important of the two under most circumstances.

Figure 12-77

The liver plays a critical role in producing and modifying blood-borne proteins, including those used in the clotting pathway. Moreover, bile salts from the liver facilitate the absorption of lipids in the diet, including vitamin K, which is required for the synthesis of prothrombin.

Figure 12-78

In an uninjured vessel, thrombin bound to thrombomodulin activates protein C, which blocks the clotting response.

Figure 12-79

Following tissue repair, fibrin clots are dissolved in a process mediated by plasmin; synthetic plasminogen activators can be used immediately after a stroke or heart attack to help dissolve clots and restore blood flow.

The End.