How do we move blood in the body?
February 3 and 5
Completion of Chapter 18- oxygen binding curves
 Today’s Goals (CH19): What are the major
features of our pump called the heart?
 How is the circulation divided into two loops with
different pressure and degrees of hemoglobin
oxygenation?
 What are the characteristics of a single cardiac
myocyte?
 What are the three layers of the heart?
 How do the cardiac valves determine the direction
of blood flow in the heart?
 How dependent is the heart upon oxygen supplies?
 How does blood reach the different regions of the
heart?
Taking Tests and Grades
A=+90% n=
B=+80% n=
C=+70% n=
D=+60% n=
F=-60% n=
Most persons find that studying for AP 212 is
different from AP 211
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Most persons find AP 212 requires less memorization and more
application
Most persons find that each hour of lecture requires 2-3 hours of
study time put in as you go (not just before the test) to be in ballpark
for a “B” or better.
If your study methods worked, use them again.
If they did not, reassess and try something else.
Essay Hint #1: remember to answer only the question being asked.
Essay Hint #2: be able to use specifics when you answer a general
question.
globin has a heme at its center. Each heme holds a single Fe++
and can hold a single O2 molecule (4 O2 /hemoglobin).
There are about 380,000,000 hemoglobins in each erythrocyte!
Each erythrocyte can carry up to about 4X380,000,000 oxygens!
Hemoglobin has 4 globins, 4 hemes, 4 Fe++,
and binds up to a maximum of 4 O2 (or No O2 at all)
The protein subunits are called “globins”
Two can be “alpha” in adult or fetus
Two can be “beta” in adult-appear just before birth
Two can be “gamma” in fetus-lost right around birth
The “HEME” is a ring like structure that has Fe++ in the
center. Oxygen is attracted to the Fe++ that binds it
temporarily and releases it later where needed.
Attachment and release is determined by concentration
gradients (What are gradients in LUNG or HEART?)
Oxygen tends to fall of the heme if there is little oxygen
around the heme….so oxygen is then supplied to tissues.
Oxygen binds to the heme when there is plenty of oxygen
available and none is attached to the heme…this condition
occurs when erythrocytes are in the capillaries that line the
alveoli of the lung.
“Cooperativity” describes how the four globins of
hemoglobin interact with each other and oxygen.
When all 4 hemes are without oxygen (empty) affinity is low, but
gradient is high.
The binding of oxygen to any one heme affects the remaining
three and makes them more likely to bind oxygen.
When another oxygen binds, it makes the remaining two even
more likely to bind oxygen.
Binding of a third oxygen tremendously increases the affinity of
the last empty heme to find and oxygen.
Assuming an oxygen can bind the heme, the hemoglobin is now
filled (100% saturated) with oxygen.
INVERSE: When any single heme in the hemoglobin looses an
oxygen, the other three are more likely to lose an oxygen, etc…
Net Result? Hemes want to be completely filled with oxygen or
completely empty! This gives the binding curve a “sigmoid” shape.
This is HUGELY important physiologically!
Myoglobin in muscle has one heme and globin (No Cooperativity).
Hemoglobin in a erythrocyte has four hemes and globins.
Why do the oxygen binding characteristics of these two proteins
look so different? Hyperbolic vs. Sigmoid Curve
Oxygen is
bound to
almost
100% of
available
Hb-hemes
in the lung.
1) Oxygen is removed from the hemoglobin
2) Percent saturation reduced (oxygen used).
Hb has “Cooperativity”--------- Mb has NO “Cooperativity”!
Why would you want fetal hemoglobin (2 gamma subunits) to bind
oxygen much more tightly than adult hemoglobin? Is there more oxygen
in the blood of the fetus or the mother? Like all molecules oxygen can
only diffuse down concentration gradients in the body.
DANGER! Carbon monoxide has an extremely high affinity for Hb
(Hb-CO), so oxygen cannot bind Hb in the lung!
The Bohr Effect is amazing!
Acids accumulate ( ↓pH) in metabolically active tissues!
This is a signal that oxygen needs have increased in the tissue!
If oxygen needs increase, oxygen delivery needs to increase! HOW IS
THIS DONE?
Protons (H+ or acids) are a signal that cause the hemoglobins to DUMP
their oxygen in acidic tissues that should also be hypoxic!
The Bohr Effect says that as conditions become more acidic (even
slightly) the hemoglobin is more likely to release its oxygen.
The reverse can also occur…..remember hyperventilating as a kid?
This causes your blood pH to become alkaline and you pass out because
you have plent of oxygen in the blood, you cannot remove the oxygen
from your hemoglobin properly in your brain!
What are some common plasma/blood electrolyte
imbalances and the terminologies used to describe them?
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Ion----[Plasma]---[ICF]----Deficiency Term-------Excess Term
↓↓
↓↓
Na+--142-----------10------Hyponatremia---------Hypernatremia
K+----5--------------141----Hypokalcemia----------Hyperkalcemia
Ca++-5-------------<1------Hyopocalcemia--------Hypercalcemia
Cl-----103-----------4--------Hypochloremia--------Hypochloremia
PO4---4-------------75-------HyperphosphatemiaHypophosphatemia
The plasma levels are often evaluated in a panel test:
Lipoproteins are large particles in the plasma that are
specialized for carrying non-water soluble lipids. These are
also VERY important items for this unit on cardiac function.
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Chylomicron: largest and synthesized by intestine
Carry_____________from the _______to the ______________
 Very Low Density Lipoprotein: VLDL: Big and synthesized by liver
Carry______________from the _______to the ______________
 Low Density Lipoprotein: LDL: VLDL-left over!
Carry______________from the _______to the ______________
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High Density Lipoprotein: HDL: smallest and synthesized by liver
Carry______________from the _______to the ______________
HDL is called “Good Cholesterol”
and
LDL is called “Bad
Cholesterol”
Plasma cholesterol and coronary heart disease/stroke risk:
Dietary influence:
Genetic Influence:
Why do we often die of a heart attack a few hours after a fatty
Christmas dinner? Look and see!
REVIEW: BLOOD CELLS HAVE AN ANTIGENIC
PROPERTY CALLED BLOOD TYPE.
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Agglutinogens: Polysaccharides on outside of RBC (antigens)
Agglutinins: Plasma antibodies that seek non-native
agglutinogens in your blood
Agglutination/hemolysis: This occurs when your antibodies
observe foreign antigens (foreign erythrocytes) in your blood
and bind to these cells. Antibodies bound to foreign cells then
bind other bound foreign cells and create clumps that clog
capillaries and lead to cellular hemolysis, possible death from a
bad transfusion.
Blood Banking/ABO designation refers to antiGENS found on
your RBCs, so your blood destroys RBCs with other antigens.
Type-O Type-A Type-B
Type-AB
Transfusions- Blood or Plasma?
Plasma transfusions:Long shelf-life but fewer risks/benefits!
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IgG proteins and Rhesus designations- Rh+ or Rh-
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Hemolytic Disease of the Newborn (HDN)/Erythroblastosis fetalis
First fetus gets off free! Following fetuses at risk of maternal Abs!
HDN: Fetal lysis, Bilirubin, Liver function, and UV-phototherapy
Universal Donor is Type-O and has anti-A and B antibodies and cannot accept A, B or AB blood.
Universal Recipient has Type AB antibodies on their erythrocytes and has NO antibodies for A or
B, if they did they would destroy their own blood. They are the universal recipient
Rh problems: second Rh+ fetus in an Rh- mother (first is usually ok because mother is not exposed
to enough fetal blood (Rh+) to created antibodies to fetal Rh+ until parturition occurs (birth).
Second birth is problematic because her body needs far less Rh+ to create a response form memory
lymphocytes.
One more review: The shift in the oxygen binding curve to the right
means less oxygen will be attached to the hemoglobins in an acidic region!
So oxygen leaves the hemoglobin and can be delivered to where it is
needed most! ↑Carbon dioxide and ↑Temperature have similar effects.
Lets Talk about your HEART!
WHAT ARE THE PRIMARY ANATOMICAL
FEATURES OF THE HEART?
Key Features:
 4 chambers
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Base (Top) vs. Apex (Bottom)
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Sides: Anterior vs. Posterior vs. L/R Lateral
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Location in pericardial sac and thoracic cavity
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Cycles of Activity: Systole vs. Diastole
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In Lab: Remember to identify the anterior surface by
looking for the more prominent anterior interventricular
sulcus (posterior sulcus is less prominent), then you also
know left vs. right, anterior/posterior.
Why is blood flow in the body divided into
two very different loops?
2 Pressure loops:
Low mmHg vs. High mmHg
2 Anatomical loops:
 Pulmonary vs. Systemic
2 Oxygenation loops:
Oxygenated vs
Deoxygenated
Blood/body colors:
Bright red vs Cyanotic
Blood Volumes in 2 circuits:
Resistance vs. Capacitance
What is the expense of
pressure? WORK!!!
WHAT ANATOMICAL CHARACTERISTICS OF
CARDIAC MYOCYTES MAKE THEM UNIQUE?
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Why do these cells function the way they do?
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Intercalated discs
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Striations
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Mitochondria
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Gap junctions
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Why is the cardiac cell very different from smooth
muscle or skeletal muscle cells?
WHAT IS THE SIGNIFICANCE OF HAVING THE WALL OF
THE HEART DIVIDED INTO THREE DISTINCT LAYERS?
1) Endocardium: prevent clotting/infection
2) Myocardium: force generation
3) Epicardium: parietal vs. visceral
Ischemia: local hypoxia/injury
Infarct: cell death
Post Infarct: tissues consist mostly of non-contractile
collagen deposited by fibroblasts (Scar Tissue)!
What keeps the heart from smashing/bruising itself to
pieces?
 Fat:
 Fluid:
 What protects the heart from the outside?
If excess fluids accumulate in the pericardial
cavity and put pressure on the heart, it
cannot be filled with venous return.
HOW DO THE HEART VALVES ENSURE ONE-WAY
FLOW OF BLOOD? WHY IS THIS CRITICAL?
Blood flow through valves requires a pressure gradient.
Two sets of Atrioventricular valves:
Right AV vs. Left AV
Tricuspid vs. Bicuspid (mitral)
Two sets of Semilunar valves:
Pulmonic vs. Aortic
DISEASE: Valvular stenosis vs. Mitral valve prolapse
Streptococcal infection in childhood? Why at the valves?
Thrombosis formation: Why at the valves?
Why does cardiac work increase dramatically when the
valves of the heart fail?
Can you name all the structures of the heart that blood
would move across in moving from the vena cava to the
aorta? Can you also describe the degree of oxygenation at
these points?
BASE
RIGHT AV Valve
LT AV Valve
APEX
WHY IS CIRCULATION THROUGH THE HEART SO
VERY COSTLY FOR THE BODY? THE STATISTICS:
1) About 5% of CARDIAC OUTPUT goes right back into heart.
The more blood you move, the more energy you USE!
2) Your heart USES about 10% of the oxygen consumed by the
body! (This is called a HIGH extraction ratio)
3) The cardiac tissues mostly desaturate (remove oxygen from) the
hemoglobin in the blood that passes thorough it! Does this leave
much oxygen in reserve? How do you supply more oxygen?
4) Cardiac metabolism is mostly aerobic (mitochondria), why?
5) Anaerobic Metabolism in the heart is mostly a back-up and
works largely via lactic acid and lactate dehydrogenase (LDH)
Blood and O2 are only pumped to cardiac cells during diastole
(cardiac period of rest or quiescence).
Your heart never “rests” longer than about 0.5-0.75 second!
VIP: What happens to the time available for blood flow into the
heart when it spends more time contracted, as happens when the
heart beats very rapidly (tachycardia)?
WHAT ARE THE PRIMARY VESSELS SUPPLYING
BLOOD TO THE HEART?
Two Major Coronary Arteries Supply the Heart!
 Left Coronary Artery (the “Widow Maker”?)splits
Left Anterior Descending or Circumflex Artery
 Right Coronary ArteryPosterior Interventricular Artery
How do you predict the risk of a heart attack in any one part
of the heart?
5) Does the region receive blood flow from a single artery?
4) Does the region receive blood from 2 or more arteries
3) Is the ventricular wall thick of thin?
2) Are coronary arteries occluded by a thrombosis/plaque?
#1) Most important question: HOW MUCH WORK IS
THE HEART DOING?
Heart Attack (Infarct) is relatively rare in the atria because of their
low work load!
(In the figure, dotted line means posterior aspect of heart).
An obstruction (thrombosis) of an artery can prevent
oxygen delivery to dependent tissues!
Some regions of cardiac tissue can be perfused with blood from
two or three coronary arteries! (“collateral flow”)
 i.e. Apex (bottom): infarct here is rare because these tissues are
perfused with blood originating from the LAD and right
posterior descending!
 i.e. Left lateral aspect of left ventricle: only gets perfussion
form one artery: circumflex! HIGH RISK for thrombosis!
Why do more anastomoses/collateral flow improve your chances
for heart attack survival?
Venous drainage during diastole occurs via the great cardiac
veins, with some blood entering coronary sinus.
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Fetal Adaptations: Ductus arteriosus and Foramen ovale
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What purpose do these fetal structures provide?
Your heart pumps blood using a five step Cardiac Cycle:
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Remember the two equal cycles: Pulmonary AND
Systemic
1) Diastolic Filling of Atria and Ventricles (V. Diastole)
 Semilunars are closed and AV valves are open!
2) Atrial Systole (VIP: occurs towards the end of V.
Diastole)
 Ventricles are primed with atrial blood (“topped off”)
 Semilunar valves closed
3) Isovolumetric Ventricular Contraction (V. Systole)
 Semilunar valves remain closed, AV valve flaps are
close by back flow of blood into atria when the
ventricular pressure begins to increase.
 Pressure is generated until
Ventricular mmHg > Arterial mmHg
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4) Ventricular Ejection (V. Systole)
 When Vent P > Arterial P, semilunars open and blood can
exit the ventricle
 Volume of blood ejected from ventricle is dependent on
magnitude of pressure gradient
 Semilunar valves must open before ejection can begin!
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5) Isovolumetric Ventricular Relaxation (V. Diastole)
 End of contraction, semilunars close when VentP<
Arterial P
 AV valves open and diastolic filling begins next cycle
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Remember the two ventricles BOTH do these activities at
about same time with the same volumes at two different
pressures!
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While “Atrial” Systole does occur, it is not as clinically
important because the atria only do about 5% of the work
done by the ventricles, so they just don’t use as much ATP
Remember that the AV and semilular valves close to
prevent flow of blood from high to low pressure back into
the atria or ventricles!