BLOOD NOTES
I. Body Fluids Review:
A. Intracellular - cytoplasm
B. Extracellular - outside cells
1. Interstitial
2. Blood plasma
3. Lymph
4. Aqueous humor, etc.
II. Functions of Blood
A. Transportation – of oxygen, carbon dioxide, nutrients, wastes, and hormones
B. Protection – phagocytes, clotting
C. Regulation – pH, temperature, osmotic balance
III. Characteristics of Blood:
A. pH = 7.35 - 7.45
B. Volume = 5 - 6 L in males; 4 -5 L. in females (Overall average: 5 L.)
C. Temperature = 38 C = 100.4 F
IV. Two Main Components of Blood:
A. Formed elements - RBC, WBC, platelets
hematocrit = % of blood made up of erythrocytes (RBC) 35 - 45%
B. Plasma - liquid portion, straw colored, clear liquid
1. Water - major component - primarily a solvent
2. Electrolytes - ions
3. Plasma proteins - relatively constant concentration
a. Albumin - is major protein to remain in blood
Main contributor to osmotic pressure and tendency to hold water in blood,
rather than leak out in tissues
Kwashiorkor b. Fibrinogen - involved in clotting
c. Globulins (immunoglobulins) - antibodies
C. If collect whole blood and centrifuge:
Plasma = 55% total volume
Erythrocytes = 45% total volume
Buffy coat = 1 % WBC and platelets
V. Hemopoiesis - blood development
Hemopoietic stem cells in bone marrow differentiate into 5 precursor (-blast) cells:
A. Pro-erythroblast  RBC
B. Myeloblast  Granular leukocytes (WBC), eosinophil, basophil, neutrophils
C. Monoblast  Monocytes (WBC)  macrophages
D. Lymphoblast  T and B cell Lymphocytes (WBC), B cells  plasma cells
E. Megakaryoblast  platelets
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VI. Erythrocytes (RBC) - no nuclei, biconcave discs, specialized to carry hemoglobin
(Hemoglobin carries oxygen and some CO2 - see Hg notes)
A. 4.8 – 5.6 million/ mm3 blood
B. Erythropoiesis - 2 million cells/sec. Balanced by destruction at same rate.
C. Erythropoietin (EPO) produced mainly by kidney stimulates formation of RBCs
at higher than normal levels, usually triggered by low levels of O2 in blood.
Process occurs in red bone marrow - released as reticulocytes (no nucleus) but still has
ER, mt, ribosomes. After several days, organelles are released and cell is mature RBC.
D. RBC life expectancy around 120 days. Destruction by spleen and liver
VII. Leukocytes (WBC) - stain differentially with Wright’s stain, 5 - 10,000/ mm3 blood
A. Granulocytes - staining granules in cytoplasm
1. Neutrophils - “polys” “PMNs or PMNL” - *multi lobed (3+) nucleus, Granules stain
neutral or lavender
Most numerous of WBCs (60 - 70%)
Short term phagocytes
2. Basophil - nucleus lobed, U/S shaped, * don’t usually see due to granules concealing
Granules stain basic - blue-purple
Produce heparin, histamine
Probably same as tissue mast cells
3. Eosinophil - lobed nucleus with * band in between or figure 8
Elevated in allergies and infections with parasitic worms
B. Agranulocytes - no granules staining in cytoplasm
1. Monocytes - * large kidney shaped nucleus, *largest leukocyte
Major long term phagocytes. Leave blood and migrate to tissue
“Wandering macrophages” - involved in responding to inflammation and infection
“Fixed macrophages” - stay in one tissue. EX: Kupffer cells in liver
2. Lymphocyte - * smallest leukocyte, * nucleus occupies most of cell
Involved in immunity:
T cells - tissue immunity (viruses, cancer, transplants, fungi, etc.)
B cells - humoral immunity (bacteria and toxins)
Natural killer cells - kill many different kinds of cells
20 - 25% of WBCs
VIII. Platelets (“thrombocytes”) -* cell fragments of megakaryocytes
A. 250,000 - 400,000/ mm3 blood
B. Involved in clotting
Especially sensitive to radiation therapy
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IX. Hemoglobin - 4 polypeptide chains, 2 alpha & 2 beta chains
A. Each chain has a heme portion containing iron (Fe3+ ) to which oxygen binds
Each hemoglobin molecule can carry 4- O2 molecules
Each RBC has 250-280 million hemoglobin molecules inside = >1 billion O2 molecules
B. Hemoglobin also carries about 20-25% of the CO2 - combines with the amino acids, not
the Fe3+ part of Hg
X. Formation of RBC’s – in bone marrow. Read description of stages of RBC development
XI. Destruction of RBCs
A. Macrophages ingest cells in liver, spleen, bone marrow
B. Hg: protein chains degraded to a.a. for use in synthesis of proteins
1. Heme – Fe3+ split off, carried by transferrin in blood to liver, then bone marrow to
be recycled for production of more hemoglobin
Fe also comes from food, to liver, to bone marrow
2. Heme (non-iron portion) converted to biliverdin bilirubin bile excreted
XII. Hemostasis (Clotting)
A. Platelet plug - When cells are injured, collagen fibers from connective tissue are
exposedplatelets adhere platelet plug  if more widespread clot formation
B. Clot formation (coagulation) - “cascade of proteins”. Needs calcium, liver enzymes
released into blood, cofactors, prothrombinase enzyme
C. Two mechanisms for making prothrombinase:
1. Extrinsic pathway – Rapid: Tissue Factor (TF) leaks into blood from damaged cells
outside the blood, TF + Ca2+ → activates X; X + V + Ca2+  activates
prothrombinase
2. Intrinsic - all components are in blood, takes longer, contact with collagen inside
damaged or roughened blood vessels  activates XII → → X; X + V + Ca2+
→ activates prothrombinase
3. Both pathways need Vit K produced by bacteria in large intestine to synthesize
liver clotting factors (prothrombin, VII, IX, X)
4. Once prothrombinase is activated, both pathways use a common pathway
C. Common Pathway:
Prothrombinase
Prothrombin ------------------------> Thrombin (enzyme)
(plasma protein prod by liver.)
Fibrinogen (soluble)---------------> Fibrin (insoluble)
D. Clots stop bleeding, retraction tightens clot, platelets strengthen clot, repair follows
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E. Clotting abnomalities:
1. Hemophilia - X linked recessive genetic disease, missing clotting factor (VIII)
2. Thrombus
3. Embolus
4. Thrombocytopenia
5. Disseminated intravascular coagulation (DIC)
G. Anticoagulants – Prevent clots from forming
1. Na oxalate or Na citrate - precipitates out calcium, added to blood to prevent clotting
during collection of blood
2. Heparin - natural, produced by basophil and masts cells, prevents conversion of
prothrombin to thrombin
3. Warfarin (coumadin) - synthetic, blocks Vit K. Given to reduce clotting in patients
prone to clots
H. Clot dissolving - plasminogen stored within clot + tissue plasminogen activator (tPA)
from endothelial cells activates plasmin (clot busting enzyme) → fibrinolysis
tPA now made by bacteria - used to dissolve clots in stroke or heart attack patients
XIII. ABO Blood Groups - based on antigens on surface of RBC - inherited from both parents
Refer to FIG 19.12, and Table 19.5
Know blood type, antigen on surface, antibody produced and transfusion compatibilities.
TYPE
ANTIGEN
ANTIBODY
REC’V BLOOD DONATE BLOOD
A
B
AB
O
XIV. Rh Blood Groups
Rh +
Rh Who is at greatest risk for having a baby with erythroblastosis fetalis (Hemolytic Disease
of the Newborn -HDN)?
XV. Read disorders and associate with the type of blood cell involved or function of blood cell:
Anemia, Polycythemia, Infectious mononucleosis, Leukemia, Hemophilia
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THE CARDIOVASCULAR SYSTEM: THE HEART
Introduction
I. Heart structure
A. Size
B. Location
C. Shape
II. Pericardium - 3 layered sac:
A. Fibrous pericardium
B. Serous pericardium - 2 membranes, secrete serous fluid
1. Parietal
2. Visceral (epicardium)
3. Pericardial cavity (space) - between the parietal and visceral pericardium
a. Angina
b. Cardiac tamponade
c. Pericarditis
III. Heart wall - 3 layers
A. Epicardium - visceral layer of serous pericardium
B. Myocardium
1. Characteristics
2. Desmosomes
gap junctions
3. Autorhythmicity
C. Endocardium
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IV. Structure of the Heart - 4 chambers: 2 superior atria and 2 inferior ventricles
A. Right atrium
B. Right ventricle
C. Left atrium
D. Left Ventricle
V. Specialized Muscles in the Heart
A. Pectinate
B. Trabeculae carneae
C. Papillary
VI. Valves - ensure and enforce unidirectional flow of blood
A. Atrioventricular valves (AV) - tricuspid (R) and bicuspid (mitral) (L)
1. Structure
2. Function
B. Semilunar (SL) valves - pulmonary semilunar (R) and aortic semilunar (L)
1. Structure
2. Function
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C. Valves contribute to heart sounds :
1. “Lubb” - AV valves closing
2. “Dupp” - SL valves closing
VII. Vessels
A. Veins – carry blood back to the heart
Systemic veins carry deoxygenated blood from body back to heart
Pulmonary veins carry oxygenated blood from lungs back to heart
B. Arteries – carry blood away from the heart
Systemic arteries carry oxygenated blood from heart to body
Pulmonary arteries carry deoxygenated blood from heart to lungs
VIII. Pulmonary and Systemic Systems - Tracing blood flow through the pulmonary and
systemic systems: Fig 20.7 p669, 670
**Be able to trace a drop of blood from the entry into the right atrium through its entire
journey until it returns to the R atrium.
IX. Fetal Circulation Variations ( p754). Covered in greater detail with vessels
A. Ductus arteriosus ----> ligamentum arteriosum
B. Foramen ovale  fossa ovalis
X. Heart Blood Supply
A. Coronary arteries:
1. Left coronary artery - divides
a. Anterior interventricular branch (L anterior descending - LAD)
b. Circumflex branch
2. Right coronary artery - supplies the R atrium then divides
a. Posterior interventricular branch
b. Marginal branch
3. Anastomoses
4. By-pass operations
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B. Coronary veins
1. Great cardiac vein
2. Middle cardiac vein
3. Coronary sinus - on posterior side, empties into the R atrium
C. Abnormalities
1. Ischemia
2. Angina pectoralis
3. Myocardial infarction
4. Read section on symptoms and treatment
D. Read disorders p663-665. Relate them to what you have learned about the structure and
function of the heart
XI. Intrinsic Conduction System
A. Sinoatrial (SA) node
1. Location
2. Natural “pacemaker”
AP  interatrial walls of both atria, via gap junctions
B. SA node also sends AP  atrioventricular (AV) node
1. Location
C. AV node sends AP  atrioventricular bundle (bundle of His)
1. Location
D. Bundle of His sends AP  R and L bundle branches in interventricular septum
E. Bundle branches send AP  Purkinje fibers (conduction myofibers)  apex
F. Contraction begins at apex of ventricles and moves upward
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G. Determining the heart rate:
1. SA node depolarizes 90-100 times/min : Faster and stronger than others, therefore sets
the pace = “natural pacemaker”.
2. Parasympathetic acetylcholine slows rate to 75 beats/min.
3. Hormones (epi, etc.) and neurotransmitters can increase or decrease heart rate (HR).
H. Cardiac cycle = .8 sec 1 beat
.8 sec
=
X beats
60 sec
X = 75 beats
Min
1. If SA node fails:
2. If AV node fails:
3. Physically fit heart: relaxed (filling) state .4sec. of cardiac cycle
XII. Contraction Physiology
A. Skeletal muscle AP
Cardiac muscle AP
B. Cardiac membrane potential -90mV
1. Rapid depolarization of voltage-gated Na+ channels
2. Plateau - voltage-gated slow Ca++ channels open
3. Repolarization - voltage-gated K+ channels open
4. Plateau increases absolute refractory period, which prevents summation and tetany
under normal conditions.
XIII. Electrocardiogram (ECG, old EKG)
A. Measures electrical currents associated with action potentials
1. Instrument = electrogardiograph
2. Results can detect abnormal currents, certain damage to heart, enlargement of
chambers
B. Three waves noticeble with each heartbeat:
1. P wave - atrial depolarization
2. QRS complex - ventricular depolarization
3. T wave - ventricular repolarization
4. Atrial repolarization is “hidden” in the QRS complex)
5. Variants: must note size and spacing or timing of waves
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XIV. Cardiac Cycle revisited: KNOW HOW TO INTERPRET FIG 20.13. Refers to left side,
but applies generally to both sides.
A. ECG
B. Pressure - aortic, L ventricular, L atrial
C. Volume of L ventricle
D. Remember: blood flows from regions of higher pressure to regions of lower pressure.
1. Contractions cause pressure to increase in chambers
2. Although the pressure of blood leaving R ventricle is lower than that in L
ventricle, the volume of blood is the same.
3. Both atria contract simultaneously while both ventricles relax; both ventricles
contract simultaneously while both atria relax.
E. Systole - contraction phase
F. Diastole - relaxation phase
G. Atrial systole
1. Atrial depolarization = P wave
Ventricular Filling – rapid (105 ml)
2. Atrial systole (25 ml)
3. End diastolic volume (EDV) of ventricle = 105 + 25 =130 ml
H. Ventricular systole
1. Bicuspid valve closes - atria begin filling (atrial diastole)
2. Isovolumetric contraction - all four valves are closed, blood being squeezed
upward – pressure rises
3. When ventricular pressure exceeds pressure in the arteries, the semilunar valves open
and ventricular ejection occurs
4. End systolic volume (ESV) in ventricle = 60 ml
Stroke volume = EDV – ESV (130 - 60 = 70 ml/beat)
5. T wave = ventricular repolarization
I. Relaxation – both atria and ventricles are relaxed (.4 sec)
1. ECG - begins with T wave, ventricular repolarization
2. Pressure - drops in ventricle and aorta
Dicrotic wave (notch)
3. Atrial pressure rising (filling)
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4. Isovolumetric relaxation - both bicuspid and aortic valves closed, blood volume
does not change.
5. AV valves open when ventricular pressure drops below atrial pressure.
J. Cardiac cycle = .8 sec/beat
.4 sec. = diastole
.1 sec. = atrial contraction (systole)
.3 sec. = ventricular contraction (systole)
Read section on valve abnormalities
XV. Cardiac Output: CO = Stroke volume (SV) X Heart Rate (HR)
A. CO = 70 ml X 75 beats = 5250 ml = 5.25 L
Beat
Min
Min
Min
B. Cardiac reserve:
C. Remember: force of contraction (SV) as well as # of beats (HR) will affect CO
XVI. Regulation of Stroke Volume : SV = EDV - ESV
A. Affected by preload stretch, contractility, afterload
1. Preload stretch
2. Contractility
3. Afterload
Anything that increases the preload stretching of cardiac muscle fibers increases
the contraction force of the heart = Frank-Starling law of the heart.
B. How does preload stretching affect the heart? Greater EDV stronger contractions:
1. Length of diastole – need adequate time for filling.
An increase in HR >160 beats/min will decrease EDV, decreasing SV
2. Venous return - Increase of venous return into R ventricle will  EDV. Converse true.
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3. Sides of the heart equate or compensate (F-S law)
D. Factors that affect contractility (strength of contraction):
1. Increase contractility:
a. Epinephrine and NE
b. Thyroid hormones
c. Stimulation of sympathetic ANS
d. Increase in Ca++ levels
2. Decrease contractility:
a. Inhibition of sympathetic ANS
b. Increased K+ or Na+ levels
c. Decreased body temp
E. Afterload – Pressure in ventricles must exceed pressure in pulmonary trunk
(~20mmHg) and in aorta (~80 mmHg) to eject blood through the semilunar valves.
Anything that  afterload pressure (hypertension, narrowing of the arteries, etc.) will 
SV because more blood will remain in the ventricles.
XVII. Regulation of Heart rate (HR)
A. ANS - CV center in medulla
1. Proprioreceptors
2. Chemoreceptors
3. Baroreceptors
B. Low O2 (hypoxia)
C. Low pH (acidois)
D. High pH (alkalosis)
E. Temperature
F. Hormones
G. Ions
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H. Age, sex, physical fitness
I. Congestive heart failure 1. Pulmonary congestion
2. Peripheral congestion
XVIII. Risk Factors for Heart Disease:
A. High blood cholesterol levels
TC 150mg/dl
 200mg/dl
Desirable levels:
TC < 200mg/dl
LDL < 130 mg/dl
HDL > 40 mg/dl
Triglycerides 130-159 mg/dl
TC:HDL < 4
B. High blood pressure
C. Smoking
D. Obesity
E. Lack of exercise
F. Diabetes mellitus
G. Family history (genetic predisposition)
H. Sex (male ; after age 70 - same)
Read sections on plasma lipids and exercise
XIX. Development of Circulatory System
A. Heart begins to beat 22 days after conception - first functional organ
Read disorder section - will be covered fully in pathophysiology and nursing courses
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BLOOD VESSELS AND HEMODYNAMICS
I. Types of Blood Vessels
A. Arteries B. Veins
C. Capillaries
II. Arteries
A. More rounded
B. Thicker tunica media
C. Elastic tissue
D. Adventitia
III. Veins
A. Valves to prevent backflow
B. Muscular pump
C. Pulmonary pump
IV. Capillaries
A. One cell thick
B. Low pressure
C. Low velocity
D. Large numbers
E. Large cross sectional area
F. Capillary Bed
1. Arteries  arterioles  metarterioles  capillaries  venules  veins
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2. Thoroughfare channels
3. Precapillary sphincters
G. Note structure of capillaries in FIG 21.4
1. Continuous
2. Fenestrated
3. Sinusoid
Note FIG 21.6 - most of blood (60%) is in veins and venules = “blood reservoir”
V.
Diffusion - important for solute exchange (ex: O2/CO2; ions, etc.)
VI.
Bulk Flow - movement in same direction of large amounts of ions, molecules, etc. carried
by water or air. Bulk flow in capillaries determined by two opposing forces:
A. Forces favoring filtration out of capillary:
1. Blood Hydrostatic pressure - (BHP) pressure squeezing fluid across capillary
membrane
2. Interstitial fluid osmotic pressure (IFOP) – interstitial solutes pulling fluid out
B. Forces favoring reabsorption of fluid into capillary
1. Blood colloid osmotic pressure (BCOP) – proteins and solutes in blood pulling fluid
back into capillary
2. Interstitial fluid HP (IFHP) - negligible
Refer to FIG 21.7:
Arterial end
BHP = 35mmHg
BCOP = 26mmHg
IFOP = 1mmHg
IFHP = 0mmHg
Venule end
BHP = 16mmHg
BCOP = 26mmHg
Net filtration pressure (NFP) = net filtration (out) - net reabsorption (in)
(BHP + IFOP) – (BCOP + IFHP)
NFP = (35 + 1) - (26 +0)
= +10 mmHg
Net flow out of capillary
NFP = (16 + 1) - (26 + 0)
= -9 mmHg
Net flow into capillary
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Edema = Filtration>> reabsorption
VII. Blood Pressure
A. Blood Pressure Average = 120 systole
80 diastole
B. Pulse pressure = 40 (difference between systole - diastole)
C. Mean arterial blood pressure (MABP or MAP) = diastolic BP + 1/ 3 (systolic -diastolic)
EX:
= 80 + 1/ 3 (120 - 80)
= 93
D. MABP = CO X Resistance (SVR)
E. Read measurement of blood pressure (p. 714, Fig 21.15 p 715)
1. sphygmomanometer
2. Korotkoff sounds
VIII. Factors Affecting Blood Flow
A. Blood Pressure: MABP = CO X SVR
(remember: CO = SV X HR)
1. Resistance affected by:
a. Diameter of vessels
Arteries - expand, recoil
Arterioles - dilate, constrict
Sympathetic ANS - short term control (see below)
(Remember cardiovascular center is in medulla oblongata)
b. Blood viscosity
c. Total length of vessels
B. Venous return (an  in blood volume, skeletal muscle pump, respiratory pump, or
venoconstriction will  return)
C. Velocity of Blood Flow (Fig 21.11 p709)
D. Factors affecting CO:
1. Venous return
2. Change in HR (ANS input)
3. Change in SV (sympathetic ANS input, venous return)
Good review Fig 21.10
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IX. Control of Blood Pressure
A. Long term control of BP is renal function - to be discussed in renal physiology section
B. Short Term Control of BP:
1. Baroreceptors in aortic arch, carotid sinuses, some veins – an increase or decrease in
stretching sends impulses to CV center in medulla
a. If BP is elevated: stretch is . The CV center  parasympathetic impulses and
 sympathetic impulses to heart.
Remember, an  in parasympathetic impulses to the heart will  HR, and
 contractility (SV) =  CO
The CV center also  sympathetic impulses to the vessels which vasoconstriction.
This effect causes vasodilation, reducing resistance in the vessels. ( SVR).
If CO and SVR both decline, so will the MAP, bringing blood pressure down to
normal.
b. If BP is too low: stretch is . The CV center  sympathetic impulses to the heart
and  secretion of epi and NE
These will  HR,  contractility =  CO
An  in sympathetic impulses to the vessels will  vasoconstriction =  resistance.
If both CO and SVR increase, the MAP will also increase, bringing blood
pressure back to normal.
2. Chemoreceptors - detect O2/CO2 and certain hormone levels
Low O2, acidosis, or high CO2 stimulates CV center   symapthetic impulses
which cause vasoconstriction which  BP.
X. Hormonal Regulation of BP:
A. Renin - angiotensin - aldosterone system
B. Epinephrine and NE
C. ADH
D. Atrial natriuretic peptide (ANP)
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XI. Shock - failure of CV system to deliver O2 to cells. Read p 715-717.
A. Causes:
1. Hypovolemic -decrease in blood volume due to loss of fluid (hemorrhage,
dehydration, burns, etc.)
2. Cardiogenic – poor heart function (ex: heart attack)
3. Vascular – inappropriate vasodilation (ex: anaphylactic shock)
4. Obstructive – block of blood flow (ex: pulmonary embolism)
B. Stages of shock
1. Stage I - compensated (nonprogressive) Renin-Angiotensin-Aldosterone system,
ADH, sympathetic ANS activation. Review Fig 21.16
2. Stage II - decompensated (progressive)
3. Stage III - irreversible
C. Signs of shock: Read p 717
XII. Pulmonary Circulation – review P753, Fig 21.30
XIII. Hepatic Portal Circulation – review p752, Fig 21.29
XIV. Fetal Circulation – review p 752-755, Fig 21.31 p 754 - 755
A. Umbilical vein
B. Ductus venosus
C. Foramen ovale
D. Ductus arteriosus
E. Umbilical arteries
F. Changes after birth:
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