1. BIOLOGY 2402
STUDY GUIDE
QUIZ I
CHS. 17 & 18 { TEXT }
LAB EXS. 21, & 23
1. List the 3 main functions of the blood.
1. Distribution functions:
Transport O2 from the lungs and nutrients from the digestive tract to the
cells.
Transport metabolic waste products from cells to elimination sites – CO2 to
the lungs and nitrogenous wastes like urea to kidneys.
Transport hormones from the endocrine glands to their target sites.
2. Regulatory functions:
Plays a role in regulating body temperature.
Plays a role in maintaining pH in body tissues.
Plays a role in maintaining adequate fluid volume in the circulatory system.
3. Protective functions:
Preventing blood loss – when blood vessel is damaged hemostasis prevents
blood loss.
Preventing infection – protecting against disease.
2. Know the following about blood volume:
a. Total volume in males.
5-6 liters.
b. Total volume in females.
4-5 liters
c. Why does the volume of blood per unit of body weight decrease as the
proportion of adipose tissue increases?
Volume of blood varies with lean both lean body weight. {79ml/kg of lean
body weight}
However adipose tissue has little vascular volume, so the volume of blood per
unit of body weight declines as the proportion of adipose tissue in the body
decrease.
The 2 components of blood is the liquid component which is the plasma and the
formed elements { blood cells}
3. Know the following about plasma: { Plasma = Whole blood – Formed Elements}
a. Percentage of blood volume.
55% of total blood volume.
b. The major component of plasma and its percentage.
Major component of plasma is water – 90%.
c. Percentage of dissolved solids in plasma.
The remaining 10% of plasma consists of various solids dissolved in the
water of the plasma.

2. These dissolved solids include:
1. Plasma proteins – 6-8% - so largest group of dissolved solids.
These include:
a. Albumins - responsible for the osmotic pressure of blood.
b. Globulins – antibodies in the blood .
c. Fibrinogen – clotting protein
d. Enzymes and protein hormones
2. Glucose { blood sugar}
3. Amino acids and fatty acids.
4. Electrolytes – Na+, Cl-, K+, Mg++, etc.
4. Know the following about the formed elements {blood cells}: { Formed elements =
Whole blood – Plasma}
a. Percentage of blood volume.
45% of total blood volume.
b. 3 major classes of formed elements:
Erythrocytes {RBC’s}, leukocytes {WBC’s}, and thrombocytes { Platelets}
c. Know the following about erythrocytes:
1. Normal counts for both males and females.
Most abundant of the formed elements.
Males – 5.1 – 5.8 million per mm3 of blood.
Females – 4.3 – 5.2 million per mm3 of blood.
2. Structure.
Circular biconcave discs.
Mature RBC’s are non nucleated.
Also lack many other cell organelles.
Lack mitochondria so anaerobic.
Filled with red pigments called hemoglobin.
They are flexible and elastic.
3. Functions:
Main function is to transport oxygen to the cells.
RBC’s have a remarkable ability to transport O2 because of their
large number of hemoglobin molecules.
A single RBC may contain up to 300 million hemoglobin molecules,
and each hemoglobin molecule can carry as many as 4 oxygen
molecules. { so 1 hemoglobin molecule carry up to 1.2 billion O2
molecules}
Lesser function is to transport carbon dioxide away from cells.
4. Composition and structure of hemoglobin.
Each hemoglobin molecule consists of:
1. The protein globin, which consists of 4 polypeptides chains – 2
beta chains and 2 alpha chains.
2. 4 non protein groups called heme groups.
1 heme group bound to each polypeptide chain.

3. Each heme group contains a central Fe atom which bounds
reversibly with O2.
So each hemoglobin molecule can transport 4 O2’s.
5. Normal hemoglobin count for both males and females.
Normal count for males is 14-18 grams per 100 ml of blood.
Normal count for females is 12-16 grams per 100 ml of blood.
6. Distinguish between oxyhemoglobin and reduced hemoglobin.
When hemoglobin is combined with O2 called oxyhemoglobin, which
is a scarlet red color.
When not carrying O2 called reduced hemoglobin, which is a dull red
color.
Hb + O  HbO2
7. Site of
erythrocyte production.
Develop from cells in the red bone marrow.
8. Describe erythrocyte formation { erythropoiesis }.
All blood cells { formed elements} develop from cells called
hemocytoblasts.
Sequence of steps in erythropoiesis:
Hemocytoblasts  Proerythroblast { at this stage committed to be a
RBC}  Basophilic erythroblast { produces large numbers of
ribosomes}  Polychromatophilic erythroblast{ hemoglobin
synthesis begins}  Normoblasts { hemoglobin synthesis continues
and when it has accumulated almost all of its hemoglobin it ejects its
nucleus and most of its organelles  Reticulocytes { enter the blood
stream – immature RBC’s- within 1 to 2 days mature into} 
Erythrocytes.
After normoblast stage { reticulocytes and erythrocytes} the cells are
non nucleated.
9. Explain how the hormone erythropoietin regulates erythropoiesis.
A hormone called erythropoietin produced by kidneys plays a major
role in regulating erythrocyte production.
This regulation involves a negative feedback mechanism that is
sensitive to the amount of O2 delivered to the tissues.
If inadequate supply of O2 to the tissues  the kidneys produce more
erythropoietin  thereby increasing erythrocyte production.
With an increased supply of O2 to the tissues  the kidneys reduce
their production of erythropoietin  thereby decreasing erythrocyte
production.
10. Average life span of erythrocyte.
About 120 days.
9. Explain how the hormone 10.Average life span of
erythrocyte.

4. 11. Explain how abnormal, defective, or aged erythrocytes are disposed of
and the fates of the breakdown products of hemoglobin.
Ages, abnormal, or damaged erythrocytes disintegrate and are
disposed of by phagocytic cells.
This occurs mainly in the spleen, liver, and bone marrow - especially
the spleen.
Once an RBC has been engulfed and broken down by a phagocytic
cell each component of the hemoglobin has different fates.
These fates are:
The globin protein is broken down to amino acids which can be used
to synthesize new proteins.
The Fe is removed from the heme groups, and is either stored in the
liver and spleen or used in the red bone marrow in the synthesis of
new hemoglobin.
The rest of the heme group { heme group minus the Fe} is converted
to bilirubin which is taken up by the liver and becomes part of the
bile.
This recycling process is very efficient - 26 mg of Fe is reused in
synthesis of hemoglobin per day.
The daily requirement of Fe is 1 – 2 mg .
12. Definition of anemia.
A condition characterized by either a decreased number of
erythrocytes or by a decreased concentration of hemoglobin; so the
tissues are receiving an inadequate supply of O2.
Since tissues are receiving in adequate O2, anemia is associated with
lack of energy, fatigue, and listlessness.
13. Causes of anemia.
1. Low RBC’s count.
2. Reduced amounts of hemoglobin per cell.
3. Reduced amounts of whole blood.
14. Describe the types of anemia.
Several types of anemia:
1. Hemorrhagic anemia:
Caused by the loss of substantial quantities of blood.
In acute hemorrhagic anemia, such as a wound, blood loss is
rapid and is treated by blood replacement.
Slight but persistent blood loss { bleeding ulcers,
hemorrhoids,etc} causes chronic hemorrhagic anemia.
Once the primary problem is solved, normal erythrocyte
production replaces the RBC’s.
2. Iron deficiency anemia:
Caused by a deficiency of Fe therefore low hemoglobin counts.
Caused by inadequate intake of iron-containing foods and
impaired Fe absorption.
3. Hemolytic anemia:
The rate of RBC destruction is increased due to fragile or
defective cells.

5. Caused by hemoglobin abnormalities, transfusion of
mismatched blood, and certain bacterial and parasitic
infections.
Example: Sickle cell anemia.
4. Pernicious anemia:
Due to a deficiency of vitamin B12.
Vitamin B12 is essential to proper maturation of RBC’s.
Rarely caused by lack of vitamin B12 in the diet, but by a
deficiency of intrinsic factor produced by mucosa of stomach.
Intrinsic factor is necessary for the absorption of vitamin B12.
15. Description of polycythemia, and a possible cause and harmful side
effects
of this condition.
Highly elevated RBC counts.
2 types:
Secondary polycythemia:
Results from an individual becoming acclimated to high elevations.
Polycythemia Vera:
Caused by tumorous abnormalities of the red bone marrow.
Both types increase the viscosity of the blood, thereby increasing
blood pressure and stressing the heart.
d. Know the following about leukocytes:
1. Normal count.
5000-10,000 per mm3 of blood.
2. The main way they differ structurally from RBC's.
The mature WBC’s are nucleated and lack hemoglobin.
The RBC’s remain in the bloodstream; whereas WBC’s can move out
of bloodstream into the tissues.
3. Site of production.
Originate from hemocytoblasts in the red bone marrow.
4. Functions.
Protection against disease.
5. Distinguish between the 2 classes of leukocytes.
Granular leukocytes:
Have noticeable granules in their cytoplasn.
These granules are stained lysosomes and other vesicles.
The 3 types are distinguished by the color these granules stain
Some are polymorphonuclear – that is have multi-lobed nuclei.
Agranular leukocytes:
Do not have noticeable granules in their cytoplasm.
Nuclei are not normally lobed.
6. Describe the structure, percentage of total WBC count, and the functions
of the 5 types of leucocytes.
Granular Leukocytes:
1. Neutrophils:
Most numerous of the WBC’s – make up 60-70% of total
WBC count.
Granules stain light pink to lilac color with Wright’s stain.

6. Multi-lobed nuclei.
Function:
Phagocytize bacteria.
2. Eosinophils:
2-4% of total WBC count.
Granules stain reddish-orange with Wright’s Stain.
Bilobed nuclei.
Function:
Most important role is to mount a defense against parasitic
worms that are too large to be phagocytized. { Release
enzymes on the worm’s surface and digest it away.}
Have roles in other diseases such allergies and asthma.
3. Basophils:
Least abundant of WBC’s – 0.5% 0f total WBC count.
Bilobed nucleus.
Have the largest granules that stain purplish-black with
Wright’s stain.
These large dark granules obscure the nucleus.
Function:
Main function – they release histamines which stimulate the
inflammatory responses.
Connective tissue cells called mast cells are similar to basophils
and also release histamines.
Also release heparin which is an anticoagulant.
Agranular Leukocytes:
4. Monocytes:
4-8% of total WBC count.
Largest leukocytes.
Pale blue cytoplasm with a kidney shaped nucleus.
Function:
When leave the bloodstream develop into highly mobile cells
called macrophages.
Very active phagocytes which play a crucial role in body’s
defense against viruses, intracellular bacteria, and chronic
infections like T.B.
5. Lymphocytes:
21-30% of total WBC count.
Has a large nucleus which occupies most of the cell’s volume.
Nucleus surrounded by thin rim of clear cytoplasm.
Function:
Mount immune responses by producing antibodies or cytotoxic
T cells.
7. List the WBC’s from most numerous to least numerous.
Neutrophils  Lymphocytes  Monocytes  Eosinophils 
Basophils.

7. { Never Let Monkeys Ear Banannas}
. Describe the causes and the harmful effects
of leukemia.
8. Describe the causes and harmful effects of leukemia.
In leukemia there is an overproduction of WBC’s.
It’s a group of cancerous conditions of WBC’s.
It can be acute {fast advancing} if it derives from blast cells like
lymphoblasts.
It’s chronic {slow advancing} if derived from cyte cells like
myelocytes.
The red bone marrow becomes overrun by cancerous leukocytes and
immature WBC’s flood the bloodstream.
Other blood cells, RBC’s and platlets, are crowed out resulting in
severe anemia and bleeding problems.
9. Describe leucopenia.
Abnormally low WBC count.
Commonly caused by drugs like glucocorticoids and anticancer
agents.
e. Know the following about thrombocytes{ Platelets}
1. Normal count:
150,000 – 400,000.
2. Structure and origin:
Platelets are not cells but are cytoplasmic fragments of large cells
called megakaryocytes.
3. Functions:
Essential for the process of hemostasis.
5. Know the following about hemostasis:
a. Definition:
The arrest {stopping} of bleeding from a damaged blood vessel.
b. List the 5 processes.
1. Vascular Constriction
2. Formation of Platelet Plug
3. Blood Clotting
4. Clot Retraction and Repair
5. Clot Dissolution
c. Describe vascular constriction and its significance.
When a blood vessel is cut or ruptured, the first response is the constriction
of that vessel.
This decreases or stops blood flow through the damaged vessel allowing
more time for the other processes of hemostasis.
Factors triggering vascular constriction are direct injury to the smooth
muscle, chemicals released by the injured tissue and platelets, and reflexes
stimulated by pain receptors.
d. Explain how the platelet plug is formed and its significance.
At the damage site platelets begin to aggregate.
They become swollen, sprout long projections, and stick together.

8. They also secrete a substance {ADP} which attracts other platelets to the
growing pile.
The layers build up forming the platelet plug.
Platelets do not adhere to the endothelial walls of undamaged vessels.
But when endothelium is damaged underlying collagenous fibers are exposed
and the platelets adhere to them starting the formation of the plug.
The platelet plug temporarily seals the break in the vessel wall.
It also helps to orchestrate events that lead to blood clot formation.
e. Describe the blood clotting mechanism.
Blood clotting is a complex process that involves a number of different
factors, most of which are found in the plasma.
Most clotting factors are plasma proteins synthesized by the liver.
They are numbered from I to XII in order of their discovery.
The clotting factors are activated into enzymes by clipping off a piece of the
protein.
Once a clotting factor is activated it activates the next clotting factor in the
sequence resulting in a cascade of reactions ultimately resulting in formation
of the clot. { see figure 17.14}
This sequence of reactions can be divided into 3 parts:
1. Intrinsic Pathway:
Called intrinsic because the factors needed are present within the
blood.
Triggered by negatively charged surfaces such as activated platelets,
collagen, and glass.
Results in the formation of a substance called prothrombin activator.
Slower than extrinsic pathway because has many intermediate steps.
2. Extrinsic Pathway:
Triggered by exposing blood to a factor released from injured tissue.
This factor called tissue factor {TF} or factor III.
Called extrinsic because the TF is formed outside the blood.
Also results in the formation of prothrombin activator.
Faster than the intrinsic pathway because fewer steps.
3. Common pathway:
Begins with prothrombin activator formed by both the intrinsic and
extrinsic pathways and ends with formation of the blood clot.
This entire sequence of reactions can be summarized into 4 basic processes.
4 basic processes of the blood clotting mechanism:
1. Formation of prothrombin activator by both the intrinsic and
extrinsic pathways.
2. Prothrombin activator converts prothrombin into the active enzyme
thrombin. {Prothrombin is always in the blood}
3. Thrombin converts fibrinogen to fibrin. {fibrinogen is always in the
blood}
4. Fibrin threads plus the trapped formed elements form the blood clot.

9. The fibrin threads adhere to the damage site and anchor the platelet plug,
thereby sealing the break in the vessel.
Clot formation is normally completed 3 – 6 minutes after blood vessel
damage.
During the process blood is transformed from a liquid to a gel.
Role of vitamin K:
Even though it is not directly involved in the blood clotting mechanism it is
necessary for the synthesis of prothrombin and 3 other clotting factors.
f.. Describe clot retraction and repair.
Within 30 -60 minutes the clot is further stabilized by clot retraction.
The fibrin network shrinks and becomes denser and stronger.
The trapped platelets play a major role in this process – they contain the
contractile proteins actin and myosin; so they can contract similar to
muscles.
This pulls the fibrin threads closer together compacting the clot and
bringing the broken edges of vessel together.
P.D.G.F. { Platelet Derived Growth Factor} released by the platelets
stimulates smooth muscle cells and fibroblasts to divide and
rebuild the vessel wall.
As the clot retracts it squeezes a fluid from the clot called serum.
Serum then is plasma lacking the clotting factors.
g. Describe clot dissolution.
It is not intended for the clot to remain indefinitely – once the damaged
vessel wall is repaired the clot is removed by dissolving.
An enzyme called plasmin is formed and decomposes the fibrin dissolving
the clot.
Formation of plasmin:
It is formed from an inactive form called plasmonogen.
Plasminogen circulates in the blood stream.
Large amounts of plasminogen are incorporated into the forming clot, where
it remains inactive until the appropriate signals reach it.
tPA produced by endothelial cells near the clot and thrombin and activated
factor XII formed during the clotting process convert the plasmonogen to
plasmin.
h. What prevents blood from clotting within normal blood vessels?
Normally anticoagulants in the blood dominate and clotting is prevented.
Only when a vessel is ruptured in coagulant activity in that area is greatly
increased does a clot form.
Factors that preventing clotting in undamaged vessels:
As long as the endothelium is smooth and intact, platelets are prevented
from clinging and piling up.
Anticoagulants in the plasma such as heparin and antithrombin III prevent
clot formation by inactivating thrombin and inhibiting the intrinsic
pathway.
i. Distinguish between a thrombus and an embolus.
Despite the many safeguards undesirable intravascular clotting sometimes
occurs.
2Types of intravascular clots:

10. 1. Thrombus:
A fixed clot – one that adheres to the vessel wall
Example – coronary thrombus
2. Embolus:
A clot that is not fixed but floats within the blood.
Example – pulmonary embolism
From prepared slide of human blood, distinguish erythrocytes from leukocytes.
From figures 21.13, 21.14, 21.15, 21.16 and 21.17 in lab manual, and from slides
identify the following WBC’s.
Neutrophils Lymphocytes
Eosinophils Monocytes
Basophils
Perform and explain how a differential white blood cell count is made.
ABO Blood groups:
a. Know the antigens and antibodies present in each of the 4 ABO blood groups.
Type A – antigen A on RBC and antibody B in plasma.
Type B – antigen B on RBC and antibody A in plasma.
Type AB – both antigen A and B on RBC and neither antibody A nor B in
the plasma.
Type O – lack both antigen A and B but both antibody A and B in plasma.
b. Why must care be taken that blood types are compatible before a transfusion with
whole blood?
Insure that the donor’s antigens are compatible with the recipient
antibodies.
c. What blood group is the universal donor? Why?
Type O because lacks both antigens A and B.
d. What blood group is the universal recipient? Why?
Type AB because lacks both antibodies A and B.
e. Perform and explain the technique used to type ABO blood groups.
If it agglutinates with the anti- A sera but not the anti-B sera the blood is
type A.
If it agglutinates with the anti- B sera but not the anti-A sera the blood is
type B.
If it agglutinates with the anti- A sera and the anti-B sera the blood is type
AB.
If it does not agglutinate with the anti- A sera and the anti-B sera the blood
is type O.
Rh blood groups:
a. Distinguish between Rh positive and Rh negative. The percentage of occurrence
of each.
If the RBC’s have the Rh antigen on their plasma membranes the blood is
Rh positive. Percentage of occurrence is 85%.

11. If the RBC’s do not have the Rh antigen on their plasma membranes the
blood is Rh negative. Percentage of occurrence is 15%.
b. Explain the cause of erythroblastosis fetalis.. {Pages 425 - 426 in lab. manual }
c. Perform and explain the technique used to type for the Rh factor.
If it agglutinates with the anti- D sera the blood is Rh positive.
If it does not agglutinate with the anti- D sera the blood is Rh negative
Red blood cell volume percentage:
a. Define hematocrit.
Per cent of total blood volume occupied by the erythrocytes.
b. Give the normal hematocrit values for both males and females.
Males – 47 plus or minus 5%.
Females – 42 plus or minus 5%.
Hemoglobin measurement:
a. Identify the instrument used to measure hemoglobin.
Hemoglobinometer.
b. Use the hemoglobinometer to measure your hemoglobin content.
From fig. 23.19 in lab manual, identify all of the labeled structures.
Trace the pathway of blood through the heart and lung circuit. At each site indicate if the
blood is oxygenated or unoxygenated.
Unoxygenated blood enters the right atrium by way of the superior and inferior
vena cavas  as the atria contract the unoxygenated blood in the right atrium
moves through the tricuspid valve into the right ventricle  as the ventricles
contract the unoxygenated blood in the right ventricle moves through the
pulmonary semilunar valve into the pulmonary trunk  the pulmonary arteries
carry the unoxygenated blood into the lungs  in the lungs the blood becomes
oxygenated  the oxygenated blood is carried by the pulmonary veins to the left atrium
 as the atria contract the oxygenated blood in the left atrium moves through the bicuspid
valve into the left ventricle  as the ventricles contract the oxygenated blood in the left
ventricle moves through the aortic semilunar valve into the aorta where it’s carried to all
parts of the body.
Know the functions of the following heart structures:
Right atrium – receives unoxygenated blood from the vena cavas.
Right ventricle – pumps unoxygenated blood into the pulmonary trunk where it is
carried to the lungs.
Left atrium – receives oxygenated blood from the pulmonary veins.
Left ventricle – pumps oxygenated blood into the systemic aorta where it is carried
to all parts of the body.
Tricuspid valve – prevents backflow of blood from the right ventricle into the right
atrium when ventricles are contracting.
Bicuspid valve – prevents backflow of blood from the left ventricle into the left
atrium when the ventricles are contracring.
Pulmonary semilunar valve – prevents backflow of blood from the pulmonary trunk
into the right atrium when ventricles are relaxing.
Aortic semilunar valve - – prevents backflow of blood from the systemic aorta
into the left atrium when ventricles are relaxing.

12. Chordae tendineae – anchors the tricuspid and bicuspid valves.
Foramen ovale – opening in the interatrial septum that allows blood to flow from the
right atrium into the left atrium. Only found in the fatal heart. It shunts blood
around the lungs. At or shortly after birth it closes and it’s remnant is called the
fossa ovalis.
Ductus arteriosus – a vessel in the fetal circulation that carries blood from the
pulmonary trunk to the systemic aorta, thereby shunting blood around the lungs.
At or shortly after birth it closes and it’s remnant is called the ligamentum
arteriosum.
From the heart model and sheep heart, identify the following structures:
Right atrium Tricuspid valve
Right ventricle Pulmonary semilunar valve
Left atrium Bicuspid valve
Left ventricle Aortic semilunar valve
Aorta Chordae tendineae
Superior vena cava Papillary muscles
Inferior vena cava Ligamentum arteriosum
Describe the coverings of the heart.
Heart is enclosed in a double-walled sack called the pericardium.
It consists of the 2 parts:
1.
Fibrous pericardium:
Tough dense irregular connective tissue that stabilizes the heart within
ediastinum.
2.
Serous pericardium:
A thinner membrane that forms a double layer around the heart.
Parts of serous membrane:
1.
Parietal pericardium:

13. Outer layer of serous pericardium.
Fuses with the inner layer of the fibrous pericardium.
2.
Visceral pericardium:
Adheres tightly to the surface of the heart.
Also called the epicardium.
3.
Pericardial cavity:
Space between the parietal and visceral pericardium.
Filled with a serous fluid called pericardial fluid.
18. Describe the 3 layers of the heart wall:
1. Epicardium:
Outer layer.
Same as the visceral pericardium.
2. Myocardium:
Middle layer.
Composed mostly of cardiac muscle.
The layer that contracts.
3. Endocardium:
Inner layer.
A thin layer of simple squamous tissue called endothelium overlying a thin
layer of connective tissue.
Lines the heart chambers and covers the heart valves.
19. From the heart model and from figures 23.14 and 23.16 in lab manual, identify the
following coronary vessels:
Right coronary artery

14. Great cardiac vein
Left coronary artery
Posterior vein
Interventricular artery
Middle cardiac vein
Anterior interventricular artery
Coronary sinus
Circumflex artery
20. Describe the circulation of blood through the coronary vessels.
The aorta gives rise to the right and left coronary arteries just past the aortic
semilunar valve.
The right coronary artery gives off branches that supply the right atrium and
ventricles, and a major branch called the posterior interventricular artery which
supplies the posterior surface of both ventricles.
The left coronary artery divides to form the anterior interventicular artery which
supplies the anterior surface of both ventricles, and the circumflex artery supplies
the posterior of both the left atrium and left ventricle.
After passing through an extensive capillary network in the myocardium, the blood
is drained by coronary veins.
The major veins are the great cardiac vein, posterior vein, and the middle cardiac
vein.
These coronary veins join to form a large vessel called the coronary sinus which
empties into the right atrium .
21. From fig. 23.31 in lab manual, identify the P wave, the QRS complex, and the T wave.
Also know what each of these waves represent.
The electrical events produced by the contracting heart can be detected by
electrodes on the surface of the body.
A recording of these events called electrocardiogram {ECG}.
Normal ECG shows 3 distant waves:
1.
P wave:
Small upward wave.
Represents the depolarization of the SA node and the atrial

15. myocardium.
Approximately 0.1 sec after the P wave atrial contraction begins.
2.
QRS complex:
Follows the P wave.
Represents the electrical activity produced by the depolarization of the
ventricular myocardium.
Precedes ventricular contraction.
3.
T wave:
Follows the QRS complex.
Represents the repolarization of the ventricular myocardium.
22. Know the following about the heartbeat:
a..Explain the automatic contraction of the cardiac muscle.
Some of the cardiac cells are self excitable{ conducting cells}. That is they generate
action potentials without external stimulation. These action potentials are then
spread the other cardiac muscles cells making them contract.
b.. Distinguish between the 2 types of cardiac muscle cells:
1. Contractile cells:
They provide the powerful contractions that propel the blood. They also form the
bulk of the atrial and ventricular walls, making up 99% of the muscle cells.
2. Conducting cells:
Specialized cardiac muscle cells that control and coordinate the activities of the
contractile cells. They spontaneously generate action potentials which spread to
the contractile cells.
c. Describe the origin and conduction of an action potential in cardiac muscle
The resting potential of cardiac muscle cells in the ventricles is - 90 mv, about the
same as skeletal muscle.{ about - 70 mv for neurons}.
However an action potential in a ventricular muscle cell lasts about 30 times as
long as it does in a typical muscle fiber.
Threshold depolarization is about - 75 mv; about the same as a skeletal muscle
fiber.
Once threshold is reached the action potential proceeds in 3 steps:

16. Step 1: Rapid depolarization:
The stage of rapid depolarization of a cardiac muscle cell resembles that of a
skeletal muscle cell.
At threshold depolarization, voltage regulated Na+ channels open and Na+’s rush in
resulting in rapid depolarization.
These channels are fast channels because they open quickly but remain open for
only a few milliseconds.
Step 2: The plateau:
As transmembrane potential approaches + 30 mv, the voltage regulated Na+
channels close.
As these channels close voltage regulated Ca++ channels are opening.
These are called slow channels because they open slowly and remain open for a
relatively long period of time.
As a result the transmembrane potential remains near 0 for an extended period of
time.
This portion of the action potential is called the plateau, and is the main difference
between the action potential in cardiac muscle cells and skeletal muscle fibers.
Step 3: Repolarization:
As the plateau continues, voltage regulated Ca++ channels begin closing, and the
voltage regulated K+ channels remain open until the resting potential is restored.
d. Explain the refractory period as it occurs in cardiac muscle.
After an action potential begins, the membrane will not respond to a 2nd
stimulus until the resting potential is restored. This time interval is called the
refractory period . Because of the plateau phase it is longer in cardiac cells
than skeletal muscle fibers{ about 250msec}. In fact in cardiac muscle cells
the refractory period continues until relaxation is underway; so they
are not capable of tetanus like skeletal muscle fibers. This is important because a
heart in tetany could not pump any blood.
e. Explain the role of calcium ions in cardiac contractions.
The role of Ca++’s in cardiac muscle contraction is the same as it is in skeletal
muscle fibers; that is to bind to the troponin. The difference is in cardiac
muscle cells 20% of the Ca++’s required for contraction enter the cell during the
plateau phase, and the rest from the sarcoplasmic reticulum. In skeletal
muscle fibers it all comes from the sarcoplasmic reticulum.
23. Describe the conducting system of the heart regarding the S-A node, A-V node, bundle of
HIS{A-V bundle}, and Purkinje fibers.
S-A node { Sinoatrial node}
Specialized conducting cells located in the wall of the right atrium near the openings
of the vena cavas.
A-V node:
Group of specialized cardiac muscles located within the interatrial septum.
Bundle of HIS { A-V bundle:
Specialized tissue that travels down the interventricular septum
Purkinze fibers:

17. Terminal branches of the bundle of HIS which transmit nerve impulses to the
contractile cells of the ventricles.
Steps:
1. Nerve impulses for contraction begin in SA node because these conducting
cells generate nerve impulses at a faster rate than the other conducting cells of
the heart - these nerve impulses are rapidly spread by gap junctions to all
the conducting cells of the atria - so both atria contract simultaneously.
2. These nerve impulses also spread to the AV node - after a 0.1 sec delay these
conducting cells generate nerve impulses at the same rate as the SA node
conducting cells - this insures that the ventricles will not contract while the
atria are contracting.
3. Nerve impulses from AV node move along the Bundle of His to Purkinje
fibers.
4. The Purkinje fibers spread the nerve impulses to the contracting cells of both
ventricles - this is very rapid so both ventricles contract simultaneously .
24. Know the following about the cardiac cycle:
a. Distinguish between systole and diastole.
To function as a pump the heart repeats 2 alternating phases:
Systole:
The contraction of the heart chambers forcing blood out.
Diastole:
The time when the heart chambers are relaxing and filling with blood.
b. Describe the sequence of atrial systole, ventricular systole, atrial diastole,
and ventricular diastole.
The heart contracts in a wavelike pattern – the atria contract first followed by
the ventricles.
Sequence:
Atrial systole – Ventricular diastole { ventricles filling with blood from the
atria}
Atrial diastole – Ventricular systole { blood moving from ventricles into the
pulmonary trunk and systemic aorta}
Atrial diastole – Ventricular diastole { so for a brief time the entire heart, both
the atria and the ventricles, are in diastole. This allows the atria to fill with
blood. Also at this time most of the blood {70%} moves through the atria into
the ventricles. The contraction of the atria just puts the final amount of blood
into the ventricles.}
Each cardiac cycle lasts 0.8 sec.
During each cycle the atria are in systole 0.1 sec and the ventricles 0.3sec.
So during each cycle the atria are in diastole 0.7sec and the ventricles 0.5 sec.
25. Know the following about heart sounds:

18. a. The characteristics sounds of a healthy heart.
The characteristic sound of a healthy is described as a Lub – Dub sound.
b. The causes of these sounds.
These sounds are caused by the closing of the heart valves.
Lub sound – caused by the closing of the tricuspid and bicuspid valves {atria-
ventricular valves}. Corresponds to ventricular systole.
Dub sound – caused by the closing of the pulmonary and aortic semilunar
valves. Corresponds to ventricular diastole.
c. Description and causes of a heart murmur.
An abnormal heart sound caused by a faulty valve.
26. Know the following about cardiac output:
a. Definition.
The volume of blood pumped per minute by either ventricle.
b. The 2 factors that determine cardiac output.
Heart rate and stroke volume.
c. Formula for cardiac output.
Cardiac Output = Heart Rate X Stroke Volume
d. The normal cardiac output for resting conditions.
C.O. = 70 beats/minute X 75 ml/beat = 5250 ml/minute
Or between 5 - 6l per minute.
e. What is cardiac reserve?
Under stressful conditions cardiac output can be greatly increased - up to 4
times in normal person and up to 7 times in a trained athlete. This is called
cardiac reserve. The formula is:
Cardiac Reserve = C.O. under stressful conditions - C.O. under restful
conditions.
27. Know the following about control of heart rate:
a. The most important factor controlling heart rate?
The most important factor are the effects produced by the autonomic nervous
system.
b. Describe how the sympathetic division effects heart rate.
Stimulation of the sympathetic nerves to the heart increase the heart rate with
maximum stimulation almost tripling the heart rate. They do this by releasing
norepinephrine which does the following:
1. Increase the rate of discharge of the S-A node.
2. Decrease conduction time through the A-V node.
3. Increase the excitability of all portions of the heart.
c. Describe how the parasympathetic division effects heart rate.
Stimulation of the parasympathetic nerves to the heart decrease the heart rate.
They do this by releasing acetyl choline which does the following:
1. Decrease the rate of discharge of the S-A node.
2. Increase conduction time through the A-V node.
3. Decrease the excitability of portions of the heart.

19. d. Explain how the heart rate at any given point is determined by the balance
between the effects of the sympathetic and parasympathetic divisions.
At any given moment the heart rate is largely determined by the stimulating
effects of the sympathetic nerves and the inhibiting effects of the
parasympathetic nerves. If the sympathetic nerves to the heart are blocked
and the parasympathetic activity is unopposed the heart rate will decrease. If
parasympathetic nerves are blocked and sympathetic activity is unopposed the
heart rate will increase. In a resting individual the parasympathetic activity is
dominant, because the inherent rate of discharge of the S-A node is about 100
beats/minute.
28. Know the following about control of stroke volume:
a. Distinguish between End Diastolic Volume and End Systolic Volume, and
explain how these relate to stroke volume.
End Diastolic Volume - the volume of blood within the ventricles at the end of
diastole just as systole begins.
End Systolic Volume - the volume of blood remaining within the ventricles
when the semilunar valves close at the end of systole.
Stroke Volume = End Diastolic Volume - End Systolic Volume
b. List and explain the 2 main factors that determine end diastolic volume.
1. Length of Diastole
The longer the time of diastole, the more time for the filling of the ventricle
therefore the larger the end diastolic volume.
The shorter the period of diastole the smaller the end diastolic volume.
2. Venous Return
The volume of blood that returns from the veins to one side of the heart in
a given time.
If the length of diastole is constant an increased venous return leads to
increased ventricular filling therefore a larger end diastolic volume.
If the length of diastole is constant a decreased venous return leads to
decreased ventricular filling therefore a smaller end diastolic volume.
c. The main factor determining end systolic volume.
Depends on the amount of blood ejected from the ventricle during contraction
{stroke volume}. The main factor is the strength of ventricular contraction.
d. Explain the Frank-Starling law of the heart and its significance.
States that within limits, as cardiac muscle is stretched its force of contraction
increases. This helps to ensure that over any period of time the normal heart
ejects the same amount of blood from each ventricle.
e. Explain how the sympathetic nervous system influences the strength of ventricular
contraction.
The norepinephrine released by the sympathetic nerves increases
the strength of ventricular contraction. It increases the contractile strength of
the cardiac muscle cells by increasing the membrane’s permeability to Ca.
29. Describe how the following factors influence cardiac functions:

20. a. Cardiac Center:
Neurons in the medulla that control both the sympathetic and
parasympathetic
nerves to the heart.
It receives neural input from higher brain centers, and from various receptors
associated with the cardiovascular system.
It reacts to this neural input by either increasing sympathetic stimulation to
the heart, increasing heart rare, or parasympathetic stimulation to the heart,
decreasing heart rate.
Sympathetic stimulation also increases strength of ventricular
contraction, increasing stroke volume.
So by effecting both heart rate and stroke volume the cardiac center plays a
role in regulating cardiac output.
b. Exercise:
Chronic heavy exercise causes the cardiac muscle tissue to hypertrophy,
thereby increasing the strength of ventricular contraction which increases
stroke volume.
Compared to a heart with a smaller stroke volume, a heart with a larger
stroke volume can achieve same cardiac output with a lower heart rate.
So both at rest and during exercise, an individual in good physical condition
can maintain the cardiac output required with a lower heart rate.
Exercise also increases one’s cardiac reserve.
c. Temperature:
When the heart is warmed the rate of discharge of the S-A node increases,
thereby increasing the heart rate.
A rise in the body temperature of 1o C increases the heart rate 12 – 20
beats/min.
This may account for the rapid heart rate that accompanies a fever and
during exercise.
d. Ions:
The levels of various ions in the blood and interstitial fluid can have an effect
on cardiac function.
Examples:
If levels of potassium ions increase substantially in the blood the heart rate
drops and the heart becomes dilated flaccid and weak.
This is called hyperkalemia.
When levels of Ca++’s are increased excessively the heart contracts spastically.
A substantial increase in Na+’s slow the heart rate and depresses cardiac
function.
e. Catecholamines:
Refers to the hormones epinephrine and nor-epinephrine produced by the
adrenal medulla.
Both hormones increase both the heart rate and stroke volume, increasing
cardiac output.
They provide a relatively small but effective supplement to the sympathetic
innervation of the heart