final study guide

Intermediate Human Physiology (PCB3702L) Dr. Lisa Brinn Respiratory and Hematology Lab Supplemental Resource

I. Your body's cells continually use oxygen (O2) for the metabolic reactions that generate ATP

from the breakdown of nutrient molecules. At the same time, these reactions release carbon

dioxide (CO2) as a waste product. Because an excessive amount of CO2 produces acidity that

can be toxic to cells, excess CO2 must be eliminated quickly and efficiently. You inhale needed

O2 and exhale the waste product CO2 because of the respiratory system. In addition, the

respiratory system helps regulate blood pH, contains receptors for the sense of smell, filters

inspired air, produces sounds, and rids the body of some water and heat in exhaled air. In this

chapter, you will learn about the various functions of the respiratory system.

II. Overview of the Respiratory System

A. The process of supplying the body with O2 and removing CO2 is known as respiration, which

has five basic steps:

1. Ventilation (breathing). Air flows into and out of the

lungs. Movement of air into the lungs is called

inspiration (inhalation). Movement of air out of the

lungs is referred to as expiration (exhalation).

Inspiration allows O2 to enter the lungs and expiration

permits CO2 to leave the lungs.

2. Pulmonary gas exchange. Gases are exchanged

between the alveoli (air sacs) of lungs and blood in

pulmonary capillaries. In this step, pulmonary capillary

blood gains O2 and loses CO2.

3. Transport of O2 and CO2 by the blood. The blood carries

O2 from the lungs to tissue cells and CO2 from tissue

cells to the lungs.

4. Systemic gas exchange. Gases are exchanged between

blood in systemic capillaries and tissue cells of the body.

In this step, systemic capillary blood loses O2 and gains

CO2.

5. Cellular respiration. Cells consume O2 and give off CO2 as metabolic reactions break down

nutrient molecules to produce ATP.

III. Components of the Respiratory System

A. Respiratory tract - consists of nose, pharynx,

larynx, trachea, primary bronchi, and lungs

1. Can be divided into two: upper and lower

respiratory systems

o Some consider the larynx part of

the lower respiratory tract. Here

we will consider the larynx part of the upper respiratory tract

B. Respiration

1. External

2. Exchanging gases between environment and cells

3. Involves 4 major steps

o Atmosphere to lungs = ventilation

o Gas exchange from lungs to blood

o Transport of gases through blood

o Exchange of gases between blood and tissues

C. Respiratory epithelium

1. Designed to help remove dust and debris

o Epithelium

à many parts of airways contains ciliated cells

(cells with cilia attached to them) and

scattered goblet cells that secrete mucus.

o Cilia

à short, hairlike projections that extend from surface of a cell.

à in the nose moves mucus and trapped particles down toward the pharynx

à in the larynx, trachea, bronchi, and bronchioles moves these substances

up toward the pharynx.

o Mucosa

à or mucous membrane, consists of a layer of epithelial cells and an

underlying layer of connective tissue

à Mucus is a sticky secretion that traps inhaled particles and serves as a

lubricant for the lining of the respiratory tract.

o Mucociliary escalator

à refers to movement of mucus along respiratory tract toward the pharynx.

à once mucus and trapped particles reach the pharynx, they can be

swallowed or expectorated (spit out).

à movement of cilia is paralyzed by nicotine. For this reason, smokers cough

often to remove foreign particles from their airways.

D. Movement of air

1. Brought in by nose

2. Enters pharynx

o Common passageway for food, liquid, and air

3. Larynx routes air into proper channels

o Also where vocalization takes place

4. Trachea carries air to bronchi

5. Primary bronchi transport air to lungs

6. Branching of the respiratory tract

E. Lungs

1. Paired, cone shaped

2. Located in thoracic cavity

3. Covered by pleura membrane

4. Contain most of the components of the respiratory tract

o Terminate at the alveoli

F. Alveoli

1. Single layer of epithelium

o Two types of cells

à Type I alveolar cells

§ 95% of alveolar

surface

à Type II alveolar cells

§ Secrete surfactant

G. Capillaries

1. Fill about 80-90% of space between alveoli

2. Interstitial fluid

o Very little

o Maximizes gas exchange

H. Zones of the respiratory system

1. Conducting zone

o Prepares air

2. Respiratory zone

o Where gas exchange takes place

I. Blood flows to the lungs

1. Network of capillaries

2. Blood flow is high

3. Entire Cardiac Output from Right Ventricle

4. Blood pressure is low

o 25/8 mmHg

IV. Ventilation

A. Defined as breathing

B. Mechanical flow of air into and out of the lungs

1. Dependent on

o Atmospheric pressure - pressure of the air in the atmosphere, which at sea

level is about 760 millimeters of mercury (mmHg), or 1 atmosphere (atm).

o Alveolar pressure - pressure of air within the alveoli of the lungs. Depending

on the stage of the breathing cycle, it may be equal to, lower than, or higher

than atmospheric pressure. Air flows into or out of the lungs because a

pressure gradient exists between the atmosphere and the alveoli. Air moves

into the lungs when alveolar pressure is lower than atmospheric pressure. Air

moves out of the lungs when alveolar pressure is higher than atmospheric

pressure.

o Intrapleural pressure - pressure within the pleural cavity. Recall that the

pleural cavity is the space between the parietal and visceral layers of the

pleura. A small amount of intrapleural fluid is present in this space.

Intrapleural pressure is always a negative pressure (lower than atmospheric

pressure), ranging from 754–756 mmHg during normal quiet breathing.

Because the pleural cavity has a negative pressure, it essentially functions as

a vacuum. The suction of this vacuum couples the lungs to the chest wall via

the pleura to form the lung–chest wall system. Thus, if the thoracic cavity

increases in size, the lungs also expand; if the thoracic cavity decreases in

size, the lungs recoil (become smaller). The changes in lung volume caused by

alterations in thoracic cavity size in turn cause a change in alveolar pressure.

C. Air flow is dependent on pressure gradients

1. Boyle’s Law and the lungs

D. Breathing cycle

1. Has three phases:

o Rest

à No air movement into or out of lungs

o Inspiration

à Bringing air into lungs from

atmosphere

o Expiration

à Expelling air into the environment from the lungs

2. Inspiration

o Respiratory muscles contract to cause a change in thoracic volume

à During a normal quiet inspiration, the diaphragm and external

intercostals contract, the lungs expand, and air moves into the lungs

o Results in a drop in alveolar pressure

o Air moves into lung

3. Expiration

o Respiratory muscles relax

à during a normal quiet expiration,

the diaphragm and external

intercostals relax, and lungs recoil

inward, forcing air out of the lungs

o Rib cage decreases volume

o Alveolar pressure increases

o Air flows out

E. Factors affecting ventilation

1. Surface tension of alveolar fluid

o A thin layer of alveolar fluid coats the luminal surface of alveoli and exerts a

force known as surface tension. Surface tension arises at all air–water

interfaces because the polar water molecules are more strongly attracted to

each other than they are to the nonpolar gas molecules in the air. When liquid

surrounds a sphere of air, as in an alveolus or a soap bubble, surface tension

produces an inwardly directed force. Soap bubbles burst because they

collapse inward due to surface tension. In the lungs, surface tension causes

the alveoli to assume the smallest possible diameter. During breathing,

surface tension must be overcome to expand the lungs during each

inspiration. Surface tension also accounts for two-thirds of lung elastic recoil,

which decreases the size of alveoli during expiration.

o The surfactant in alveolar fluid reduces surface tension. Surfactant, a surface

active agent, is a complex mixture of lipids and proteins secreted by type II

alveolar cells of the lungs. It intersperses between the water molecules at the

air–water interface. This disrupts the cohesive forces between water

molecules, causing a marked decrease in surface tension. The presence of

surfactant in alveolar fluid reduces the work of breathing and increases lung

compliance (described shortly).

o A deficiency of surfactant in premature infants causes respiratory distress

syndrome (RDS), in which the surface tension of alveolar fluid is greatly

increased so that many alveoli collapse at the end of each expiration.

Treatment involves the administration of surfactant directly into the lungs.

2. Compliance of lungs

o refers to how much effort is required to stretch lungs and chest wall. High

compliance means that lungs and chest wall expand easily; low compliance

means that they resist expansion. By analogy, a thin balloon that is easy to

inflate has high compliance, and a heavy and stiff balloon that takes a lot of

effort to inflate has low compliance. In lungs, compliance is related to two

principal factors: elasticity and surface tension. Lungs normally have high

compliance and expand easily because elastic fibers that are present in lung

tissue are easily stretched and surfactant in alveolar fluid reduces surface

tension. Decreased compliance is a common feature in pulmonary conditions

that (1) scar lung tissue, (2) cause lung tissue to become filled with fluid

(pulmonary edema), (3) produce a deficiency in surfactant, or (4) impede

lung expansion in any way (for example, paralysis of the intercostal muscles).

By contrast, increased lung compliance occurs in emphysema because there

is less elastic recoil of lungs due to destruction of elastic fibers in alveolar

walls.

3. Airway resistance

o Like the flow of blood through blood vessels, the rate of airflow through the

airways depends on both the pressure gradient and the resistance: Airflow

equals the pressure gradient between the alveoli and the atmosphere divided

by the resistance. The relationship among airflow, the pressure gradient, and

resistance is given by the following equation:

o The walls of the airways, especially the bronchioles,

offer some resistance to the normal flow of air into and out of the lungs.

(Larger-diameter airways have decreased resistance.) As the lungs expand

during inspiration, the bronchioles enlarge because their walls are pulled

outward in all directions. Airway resistance then increases during expiration

as the diameter of bronchioles decreases. Airway diameter is also regulated

by the degree of contraction or relaxation of smooth muscle in the walls of

the airways. Signals from the sympathetic division of the autonomic nervous

system (ANS) cause relaxation of bronchiolar smooth muscle, which results in

bronchodilation and decreased resistance. Signals from the parasympathetic

division of the ANS cause contraction of bronchiolar smooth muscle,

resulting in bronchoconstriction and increased resistance.

o Any condition that narrows or obstructs the airways increases resistance so

that more pressure is required to maintain the same airflow. The hallmark of

asthma or chronic obstructive pulmonary disease (COPD)—emphysema or

chronic bronchitis—is increased airway resistance due to obstruction or

collapse of airways.

V. Lung Volumes and Capacities

A. Lung volumes - Measured to assess lung function

B. Lung capacities - Combinations of lung volumes

C. These can all be measured using a spirogram - Can also use these to measure minute

ventilation

D. Lung volumes and lung capacities

1. Tidal volume (VT) - volume of air inspired or expired during a single breathing cycle

under resting conditions. It equals 500 mL in an average adult male or female.

2. Inspiratory reserve volume (IRV) - maximum volume of air that can be inspired after

a normal inspiration. It is about 3100 mL in an average adult male and 1900 mL in an

average adult female.

3. Expiratory reserve volume (ERV) - maximum volume of air that can be expired after a

normal expiration. It averages 1200 mL in males and 700 mL in females.

4. Residual volume (RV) - volume of air that remains in the lungs after a maximum

expiration. It amounts to

about 1200 mL in males

and 1100 mL in females.

This air remains in the

lungs because the

subatmospheric

intrapleural pressure

keeps the alveoli slightly

inflated, and some air also remains in the noncollapsible airways. Because it does

not leave the lungs, RV and any lung capacity that includes the RV cannot be

measured with a spirometer.

5. Functional residual capacity (FRC) - volume of air in the lungs at the end of a normal

expiration. It is the sum of residual volume and expiratory reserve volume (1200 mL

+ 1200 mL = 2400 mL in males and 1100 mL + 700 mL = 1800 mL in females).

6. Inspiratory capacity (IC) - maximum volume of air that can be inspired after a

normal expiration. It is the sum of tidal volume and inspiratory reserve volume (500

mL + 3100 mL = 3600 mL in males and 500 mL + 1900 mL = 2400 mL in females).

7. Vital capacity (VC) - maximum volume of air that can be expired after a maximum

inspiration. It is equal to the sum of inspiratory reserve volume, tidal volume, and

expiratory reserve volume (4800 mL in males and 3100 mL in females). A term

related to the VC is the forced expiratory volume in 1 second (FEV1), the volume of air

that can be exhaled from the lungs in 1 second with maximal effort following a

maximal inspiration. Under normal conditions, the FEV1 is about 80% of the VC.

Typically, chronic obstructive pulmonary disease (COPD) greatly reduces FEV1

because COPD increases airway resistance.

8. Total lung capacity (TLC) - total volume of air in the lungs after a maximum

inspiration. It is the sum of vital capacity and residual volume (4800 mL + 1200 mL =

6000 mL in males and 3100 mL + 1100 mL = 4200 mL in females).

VI. Exchange of Oxygen and Carbon Dioxide

A. Occurs via passive diffusion

B. Governed by the behavior of gasses

1. Explained by two laws

o Dalton’s law

à Each gas in a mixture of gases exerts its own pressure as if there were

no other gases present

à The pressure that a specific gas exerts is called the partial pressure (Px)

o Henry’s Law

à Quantity of a gas that will dissolve in a liquid is proportional to the

partial pressure of the gas and its solubility

à Oxygen has a lower solubility than carbon dioxide

C. Two types

1. Pulmonary gas exchange

o Converts deoxygenated blood into

oxygenated blood

2. Systemic gas exchange

o Allows peripheral tissues to use the

oxygen that is in the blood

VII. Transport of Oxygen and Carbon Dioxide

A. Oxygen transport

1. Oxygen has poor solubility

2. 98.5% is bound to hemoglobin and transported in red blood cells

3. Referred to differently when there is O2 attached

o Deoxyhemoglobin

à Without O2

o Oxyhemoglobin

à With O2

4. Partial pressure of oxygen determines how much binds to hemoglobin

5. Factors affecting oxygen affinity to hemoglobin

o Acidity (pH) - As acidity increases (pH decreases), the

affinity of hemoglobin for O2 decreases, and O2 dissociates

more readily from hemoglobin. In other words, increasing

acidity enhances the unloading of oxygen from

hemoglobin. The main acids produced by metabolically active tissues are lactic

acid and carbonic acid. When pH decreases, the entire oxygen–hemoglobin

dissociation curve shifts to the right; at any given PO2, hemoglobin is less

saturated with O2, a change termed the Bohr effect.

o Partial pressure of carbon dioxide - CO2 can also bind to hemoglobin, and

the effect is similar to that of H+ (shifting the curve to the right). As PCO2 rises,

hemoglobin releases O2 more readily. PCO2 and pH are related factors because

low blood pH (acidity) results from high PCO2. As CO2 enters the blood, much of

it is temporarily converted to carbonic acid (H2CO3), a reaction catalyzed by

an enzyme in erythrocytes called carbonic anhydrase (CA):

The carbonic acid thus formed in erythrocytes dissociates into hydrogen ions

and bicarbonate ions. As the H+ concentration increases, pH decreases. Thus,

an increased PCO2 produces a more acidic environment, which helps release O2

from hemoglobin. During exercise, lactic acid—a by-

product of anaerobic metabolism within muscles—also

decreases blood pH. Decreased PCO2 (and elevated pH)

shifts the saturation curve to the left.

o Temperature - Within limits, as temperature increases,

so does the amount of O2 released from hemoglobin. Heat is a by-product of

the metabolic reactions of all cells, and the heat released by contracting

muscle fibers tends to raise body temperature. Metabolically active cells

require more O2 and liberate more acids and heat. The acids and heat in turn

promote release of O2 from oxyhemoglobin. Fever

produces a similar result. By contrast, during

hypothermia (lowered body temperature) cellular

metabolism slows, the need for O2 is reduced, and

more O2 remains bound to hemoglobin (a shift to the

left in the saturation curve).

o Biphosphoglycerate (BPG) - A substance

found in erythrocytes called 2,3-

bisphosphoglycerate (BPG), previously

called diphosphoglycerate (DPG), decreases

the affinity of hemoglobin for O2 and thus

helps unload O2 from hemoglobin. BPG is

formed in erythrocytes when they break

down glucose to produce ATP during

glycolysis. When BPG combines with hemoglobin by binding to the terminal

amino groups of the two beta globin chains, the hemoglobin binds O2 less

tightly at the heme group sites. The greater the level of BPG, the more O2 is

unloaded from hemoglobin. Certain hormones, such as thyroxine, growth

hormone, epinephrine, norepinephrine, and testosterone, increase the

formation of BPG. The level of BPG is also higher in people living at higher

altitudes.

o Fetal hemoglobin - differs from adult hemoglobin (Hb-A) in structure and in

its affinity for O2. Hb-F has a higher affinity for O2 because it binds BPG less

strongly. Thus, when PO2 is low, Hb-F can carry up

to 30% more O2 than maternal Hb-A. As the

maternal blood enters the placenta, O2 is readily

transferred to fetal blood. This is very important

because the O2saturation in maternal blood in the

placenta is quite low, and the fetus might suffer

hypoxia were it not for the greater affinity of fetal hemoglobin for O2.

B. Carbon dioxide transport

1. Is transported through the blood in three ways:

1. Dissolved in the plasma

o 7% - Upon reaching the lungs, it diffuses into alveolar air and is exhaled.

2. Carbamino compounds

o 23% - combines with the amino groups of amino acids and proteins in

blood to form carbamino compounds. Because the most prevalent protein

in blood is hemoglobin (inside erythrocytes), most of the CO2 transported

in this manner is bound to hemoglobin. The main CO2 binding sites are the

terminal amino acids in the two alpha and two beta globin chains.

3. Bicarbonate ions

o 70% - As CO2 diffuses into systemic capillaries and enters erythrocytes, it

reacts with water in the presence of the enzyme carbonic anhydrase (CA)

to form carbonic acid, which dissociates into H+ and HCO3 −

Gas Exchange and Transport Can Be Summarized: Deoxygenated blood returning to the pulmonary

capillaries in the lungs contains CO2 dissolved in blood plasma, CO2 combined

with globin as carbaminohemoglobin (Hb–CO2), and CO2 incorporated into

HCO3 − within erythrocytes. The erythrocytes have also picked up H+, some of

which binds to and therefore is buffered by hemoglobin (Hb–H). As blood

passes through the pulmonary capillaries, molecules of CO2 dissolved in blood

plasma and CO2 that dissociates from the globin portion of hemoglobin diffuse

into alveolar air and are exhaled. At the same time, inhaled O2 diffuses from

alveolar air into erythrocytes and is binding to hemoglobin to form

oxyhemoglobin (Hb–O2). Carbon dioxide is also released from HCO3 − when H+

combines with HCO3 − inside erythrocytes. The H2CO3 formed from this reaction

then splits into CO2, which is exhaled, and H2O. As the concentration of HCO3 − declines inside

erythrocytes in pulmonary capillaries, HCO3 − diffuses in from the blood plasma, in exchange for Cl−. In

sum, oxygenated blood leaving the lungs has increased O2 content and decreased amounts of CO2 and

H+. In systemic capillaries, as cells use O2 and produce CO2, the chemical reactions reverse.

VIII. Control of Ventilation

A. Respiratory centers control breathing

1. Cluster of neurons in the brainstem collectively known as the respiratory center

o Divided

à Medullary respiratory center – dorsal respiratory group (DRG) and

ventral respiratory group (VRG)

§ Located in the VRG is a cluster of neurons called the pre-

Bötzinger complex that is believed to be important in the

generation of the rhythm of respiration

à Pontine respiratory center – pneumotaxic area (also known as pontine

respiratory group) and apneustic area

B. Respiratory centers are subject to regulation

1. Cortical influences -Because the cerebral cortex has connections with the respiratory

center, we can voluntarily alter our pattern of breathing. We can even refuse to

breathe at all for a short time. Voluntary control is protective because it enables us to

prevent water or irritating gases from entering the lungs. The ability not to breathe,

however, is limited by the buildup of CO2 and H+ in the body. When PCO2 and H+

concentrations increase to a certain level, the DRG neurons of the medullary

respiratory center are strongly stimulated, action potentials are sent along the

phrenic and intercostal nerves to inspiratory muscles, and breathing resumes,

whether the person wants it to or not. It is impossible for small children to kill

themselves by voluntarily holding their breath, even though many have tried in

order to get their way. If breath is held long enough to cause fainting, breathing

resumes when consciousness is lost. Action potentials from the hypothalamus and

limbic system also stimulate the respiratory center, allowing emotional stimuli to

alter respirations as in, for example, laughing and crying.

2. Chemoreceptor regulation - Certain chemical stimuli modulate

how quickly and how deeply we breathe. The respiratory system

functions to maintain proper levels of CO2 and O2 and is very

responsive to changes in the levels of these gases in body fluids.

Chemoreceptors are sensory receptors that are responsive to

chemicals. Chemoreceptors in two locations monitor levels of

CO2, H+, and O2 and provide input to the respiratory center.

The central and peripheral chemoreceptors participate in a negative feedback system that regulates

the levels of CO2, O2, and H+ in the blood. As a result of increased PCO2,

decreased pH (increased H+), or decreased PO2, input from the central and

peripheral chemoreceptors causes the DRG to become highly active, and

the rate and depth of breathing increase. Rapid and deep breathing,

called hyperventilation, allows the inhalation of more O2 and expiration

of more CO2 until PCO2 and H+ are lowered to normal.

3. Proprioceptor stimulation of breathing - As soon as you

start exercising, your rate and depth of breathing

increase, even before changes in PO2, PCO2, or H+ level

occur. The main stimulus for these quick changes in

respiratory effort is input from proprioceptors, which

monitor movement of joints and muscles. Action

potentials from the proprioceptors stimulate the DRG

of the medulla oblongata. At the same time, axon collaterals (branches) of upper

motor neurons that originate in the primary motor cortex also feed excitatory

signals into the DRG.

4. The inflation reflex - Similar to those in the blood vessels, stretch-sensitive

receptors are located in the walls of bronchi and bronchioles. When these receptors

become stretched during overinflation of the lungs, action potentials are sent along

the vagus (X) nerves to the dorsal respiratory group (DRG) in the medullary

respiratory center. In response, the DRG is inhibited and the diaphragm and external

intercostals relax. As a result, further inspiration is stopped and expiration begins.

As air leaves the lungs during expiration, the lungs deflate and the stretch receptors

are no longer stimulated. Thus, the DRG is no longer inhibited, and a new inspiration

begins. This reflex is referred to as the inflation (Hering–Breuer) reflex. In infants,

the reflex appears to function in normal breathing. In adults, however, the reflex is

not activated until tidal volume (normally 500 mL) reaches more than 1500 mL.

Therefore, the reflex in adults is a protective mechanism that prevents excessive

inflation of the lungs, for example, during severe exercise, rather than a key

component in the normal control of respiration.

5. Limbic system - Anticipation of activity or emotional anxiety may stimulate the

limbic system, which then sends excitatory input to the DRG, increasing the rate and

depth of ventilation.

6. Temperature - An increase in body temperature, as occurs during a fever or vigorous

muscular exercise, increases the rate of ventilation. A decrease in body temperature

decreases respiratory rate. A sudden cold stimulus (such as plunging into cold water)

causes temporary apnea, an absence of breathing.

7. Pain - A sudden, severe pain brings about brief apnea, but a prolonged somatic pain

increases respiratory rate. Visceral pain may slow the rate of ventilation.

8. Stretching the anal sphincter muscle - This action increases the respiratory rate

and is sometimes used to stimulate ventilation in a newborn baby or a person who

has stopped breathing.

9. Irritation of airways - Physical or chemical irritation of the pharynx or larynx brings

about an immediate cessation of breathing followed by coughing or sneezing.

10. Blood pressure - The carotid and aortic baroreceptors that detect changes in blood

pressure have a small effect on breathing. A sudden rise in blood pressure decreases

the rate of respiration, and a drop in blood pressure increases the respiratory rate.

VI.Blood Groups and Blood Types

A. The surfaces of erythrocytes contain a genetically determined assortment of antigens

that includes carbohydrates and proteins. These antigens, called agglutinogens occur in

characteristic combinations. Based on the presence or absence of various antigens,

blood is categorized into different blood groups. Within a given blood group, there may

be two or more different blood types. There are at least 24 blood groups and more than

100 antigens that can be detected on the surface of erythrocytes. Here, two major blood

groups—ABO and Rh—are discussed.

B. The incidence of ABO and Rh blood types varies among different

population groups, as indicated in the table below.

C. ABO Blood Group Is Determined by the Presence or Absence of A and B Antigens

à The ABO blood group is based on two glycolipid antigens called A and B. People

whose erythrocytes display only antigen A have type A blood. Those who have only

antigen B are type B. Individuals who have both A and B antigens are type AB; those

who have neither antigen A nor B are type O.

Plasma usually contains antibodies called agglutinins that react with the A or B antigens if the two are

mixed. These are the anti-A antibody, which reacts with antigen A, and the anti-B antibody, which

reacts with antigen B. The antibodies present in each of the four blood types are shown above. You do

not have antibodies that react with the antigens of your own erythrocytes, but you do have antibodies

for any antigens that your erythrocytes lack. For example, if your blood type is B, you have B antigens

on your erythrocytes, and you have anti-A antibodies in your plasma. Although agglutinins start to

appear in the blood within a few months after birth, the reason for their presence is not clear. Perhaps

they are formed in response to bacteria that normally inhabit the gastrointestinal tract. Because the

antibodies are large IgM-type antibodies that do not cross the placenta, ABO incompatibility between

a mother and her fetus rarely causes problems.

D. An Incompatible Transfusion Causes Agglutination

à Despite the differences in erythrocyte antigens reflected in the blood group

systems, blood is the most easily shared of human tissues, saving many thousands

of lives every year through transfusions. A transfusion is the transfer of whole blood

or blood components (erythrocytes only or plasma only) into the bloodstream or

directly into the red bone marrow. A transfusion is most often given to alleviate

anemia, to increase blood volume (for example, after a severe hemorrhage), or to

improve immunity. However, the normal components of one person's erythrocyte

plasma membrane can trigger damaging antigen–antibody responses in a

transfusion recipient. In an incompatible blood

transfusion, antibodies in the recipient's plasma

bind to the antigens on the donated erythrocytes,

which causes agglutination, or clumping, of the

erythrocytes. Agglutination is an antigen–antibody

response in which erythrocytes become cross-

linked to one another. (Note that agglutination is

not the same as blood clotting.) When these

antigen–antibody complexes form, they activate

plasma proteins of the complement family. In

essence, complement molecules make the plasma

membrane of the donated erythrocytes leaky, causing hemolysis (rupture) of the

erythrocytes and the release of hemoglobin into the plasma. The liberated

hemoglobin may cause kidney damage by clogging the filtration membranes.

à Consider what happens if a person with type A blood receives a transfusion of type B

blood. The recipient's blood (type A) contains A antigens on the erythrocytes and

anti-B antibodies in the plasma. The donor's blood (type B) contains B antigens and

anti-A antibodies. In this situation, two things can happen. First, the anti-B

antibodies in the recipient's plasma can bind to the B antigens on the donor's

erythrocytes, causing agglutination and hemolysis of the erythrocytes. Second, the

anti-A antibodies in the donor's plasma can bind to the A antigens on the

recipient's erythrocytes, a less serious reaction because the donor's anti-A

antibodies become so diluted in the recipient's plasma that they do not cause

significant agglutination and hemolysis of the recipient's erythrocytes.

People with type AB blood do not have anti-A or anti-B antibodies in their blood plasma. They

are sometimes called universal recipients because theoretically they can receive blood from

donors of all four blood types. They have no antibodies to attack antigens on donated

erythrocytes. People with type O blood have neither A nor B antigens on their erythrocytes

and are sometimes called universal donors because theoretically they can donate blood to all

four ABO blood types. Type O persons requiring blood may receive only type O blood. In

practice, use of the terms universal recipient and universal donor is misleading and dangerous.

Blood contains antigens and antibodies other than those associated with the ABO system that

can cause transfusion problems. Thus, blood should be carefully cross-matched or screened

before transfusion. In about 80% of the population, soluble antigens of the ABO type appear

in saliva and other body fluids, in which case blood type can be identified from a saliva sample.

E. Rh Blood Group Is Based on the Presence or Absence of Rh Antigens

à The Rh blood group is so named because the antigen was discovered in the blood of

the Rhesus monkey. The alleles of three genes may code for the Rh antigen, which is

a protein. People whose erythrocytes have Rh antigens are designated Rh+ (Rh

positive); those who lack Rh antigens are designated

Rh− (Rh negative). Normally, plasma does not contain

anti-Rh antibodies. If an Rh− person receives an Rh+

blood transfusion, however, the immune system

starts to make anti-Rh antibodies that remain in the

blood. If a second transfusion of Rh+ blood is given

later, the previously formed anti-Rh antibodies would

cause agglutination and hemolysis of the erythrocytes

in the donated blood, and a severe reaction may occur.

F. Hemolytic disease of the newborn (HDN)

à Most common problem with Rh incompatibility

à May arise during pregnancy

à Normally, no direct contact occurs between maternal and fetal blood while a

woman is pregnant. However, if a small amount of Rh+ blood leaks from the fetus

through the placenta into the bloodstream of an Rh− mother, the mother starts to

make anti-Rh antibodies.

à Because the greatest possibility of fetal blood leakage into the maternal circulation

occurs at delivery, the firstborn baby usually is not affected. If the mother becomes

pregnant again, however, her anti-Rh antibodies can cross the placenta and enter

the bloodstream of the fetus. If the fetus is Rh−, there

is no problem because Rh− blood does not have the Rh

antigen. If the fetus is Rh+, however, agglutination

and hemolysis brought on by fetal–maternal

incompatibility may occur in the fetal blood.