circulatory_class_notes

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The Anatomy & Physiology of the Circulatory System
The circulatory system consists of the blood, the heart, and the vascular
system, all of which are essential to the delivery of oxygen to the body.
THE BLOOD
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Blood is made of specialized cells suspended in a liquid substance called
plasma.
These specialized cells include red blood cells (erythrocytes), white blood
cells (leukocytes), and platelets or cell fragments (thrombocytes).
Each cell type has a specific function.
Erythrocytes
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Red blood cells, or erythrocytes, make up the majority of all blood cells
In healthy adults, there are about 4 to 5 million red blood cells per cubic
millimeter of blood.
They are produced by the red bone marrow at a rate of about 2 million
cells per second.
An equal number of worn out RBCs are destroyed by the spleen and liver
These cells live for about 120 days and are confined to the bloodstream.
A key component of erythrocytes is hemoglobin
o Primarily responsible for transporting oxygen and carbon dioxide.
 Hematocrit
 The % of RBCs in relation to the total blood volume
o Adult male: 45%
o Adult female: 42%
Leukocytes
White blood cells, or leukocytes, protect the body against "invaders" such as
bacteria, viruses, parasites, toxins, and tumors.
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A healthy adult has, on average, between 4,000 and 10,000 leukocytes
per cubic millimeter of blood.
A count higher than 11,000 cells/cubic millimeter is an indication of
infection.
Unlike erythrocytes, leukocytes can leave the capillaries to do their work.
Leukocytes are grouped into two categories, based on their physical and
chemical characteristics.
o Granulocytes: These contain membrane-bound cytoplasmic
granules that can be stained for observation.
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Neutrophils
 Make up 40% to 70% of the white blood cell (WBC)
population
 Phagocytes that destroy bacteria and some fungi
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Eosinophils
 Make up 1% to 4% of WBCs
 Phagocytize antigen-antibody complexes
 Are increased in allergic conditions (asthma)
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Basophils
 Make up 1% or less of the WBC population.
 Combat allergic reactions
o Agranulocytes: These contain a spherical nucleus but no
cytoplasmic granules.
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Lymphocytes
 Found mostly in lymph tissues
 T lymphocytes
o Attack virus infected cells and tumors
 B lymphocytes
o Produce antibodies
 Proteins that inactivate antigens
 Make up 20-25% of the WBC population.
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Monocytes
 Make up 4% to 8% of the WBC count.
 Highly mobile macrophages
 Increase in chromic infections
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Also effective against viruses and certain bacterial
parasites.
Thrombocytes
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Blood platelets, or thrombocytes, are the smallest elements in the plasma.
They prevent blood loss from small vessels by clumping together to begin
the clotting process at the site of an injury.
Normal platelet count is 250,000 to 500,000 / mm3
Plasma
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The straw-colored liquid that remains when the cells are removed from the
blood.
Plasma makes up about 55% of total blood volume
About 90% of plasma is made up of water.
Serum is the fluid portion of the blood that remains when clotting factors
such as fibrinogen are removed.
o When blood is drawn for testing, various tubes are used. Some of
these tubes contain anticoagulants, while others allow the blood to
clot, leaving the serum behind for testing.
THE HEART
Physical Structure
 The heart is a hollow, muscular organ that is enclosed in the mediastinum
and rests on the top surface of the diaphragm, flanked by the lungs.
 Its four chambers include two atria (the upper right and upper left portions
of the heart) and two ventricles (the lower right and lower left portions).
 Muscular walls called septa (singular: septum) separate the two atria and
the two ventricles.
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See the graphic below for anterior and posterior views of the heart.
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Functionally, the heart is actually like two pumps. The right atrium and
ventricle act as one to pump unoxygenated blood to the lungs. The left
atrium and ventricle pump oxygenated blood through the circulatory
system. The ventricles, which are larger and more muscular than the atria,
are the key pumping chambers.
The Pericardium
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The heart is enclosed in a sac called the pericardium.
The fibrous pericardium, the tough outer layer, functions to:
o protect the heart
o anchors it to surrounding structures, such as the diaphragm and
great vessels
o prevent the heart from overfilling
The serous pericardium, the inner wall, is composed of two layers:
o Parietal layer
 Lines the inner surface of the fibrous pericardium
o Visceral layer
 Also called the Epicardium
o A film of serous fluid between the two layers allows them to glide
smoothly against one another
 This allows the heart to work in a relatively friction-free
environment.
The Wall of the Heart
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The heart wall itself is made of three layers.
Epicardium
o the visceral layer of the pericardium
o made of a layer of squamous epithelial cells over connective tissue
Myocardium
o the thick muscular middle layer forming the bulk of the heart
o the part of the heart that actually contracts
Endocardium
o A glistening white sheet of squamous epithelium that rests on a thin
connective tissue layer
o Contains small blood vessels and smooth muscle
o Located in the inner myocardial surface, it lines the chambers of the
heart.
The graphic below shows the layers of the pericardium and the heart wall.
Blood Supply of the Heart
Arterial Supply
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The heart’s blood supply comes from the aorta by way of the:
o Left coronary artery
 Circumflex artery
 Anterior interventricular artery
 Supplies blood to the left atrium and ventricle
o Right coronary artery
 Marginal artery
 Posterior interventricular artery
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 Supplies the right atrium and ventricle
Blockage of these arteries can cause a myocardial infarction (heart
attack).
Venous Supply
The venous system parallels the coronary artery system:
 Great Cardiac Veins
o collects venous blood from the anterior portion of the heart
 Middle Cardiac Vein
o collects venous blood from the posterior portion of the heart
 Coronary Sinus
o Receives blood from the great and middle cardiac veins.
 Thebesian Vein
o Empties into the right and left atria
 Part of the normal anatomic shunt
Figure 5-6 in the text shows the arterial and venous vessels of the heart.
Blood Flow
Blood flows through the heart in the following stages.
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Venous blood, which is low in oxygen and high in carbon dioxide, moves
through the inferior vena cava and superior vena cava and enters the
right atrium.
Blood flows through the tricuspid valve into the right ventricle.
The ventricles contract.
The tricuspid valve, which is located between the right atrium and
ventricle, closes to keep blood from flowing backward into the atrium.
Blood leaves the right ventricle through the pulmonary semilunar valve
and enters the pulmonary trunk.
The pulmonary valve closes to prevent blood from flowing back into the
right ventricle.
Blood enters the lungs via the right and left pulmonary arteries. (Note
that these are the only arteries in the body that normally carry
unoxygenated blood.)
Blood passes through pulmonary arterioles, pulmonary capillaries, and
pulmonary venules
The blood, which is now high in oxygen and low in carbon dioxide, passes
through the four pulmonary veins into the left atrium. (Note that these
are the only veins in the body that normally carry oxygenated blood.)
Blood flows through the mitral valve into the left ventricle.
The mitral, or bicuspid, valve closes, keeping blood from returning to the
left atrium when the ventricles contract.
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The left ventricle pumps blood through the aortic valve and into the
ascending aorta where it enters the systemic circulation.
The aortic valve closes, keeping blood from flowing back into the left
ventricle.
THE PULMONARY AND SYSTEMIC VASCULAR SYSTEMS
The circulatory system’s vascular network has two major components:
 Systemic system: begins with the aorta and ends in the right atrium
 Pulmonary system: begins with the pulmonary trunk and ends in the left
atrium
Roles and Characteristics of Arteries and Veins
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Arteries
o Strong, elastic vessels that carry blood away from the heart.
Arterioles
o Called resistance vessels because their size and pressure change
with changes in blood flow.
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o They play a major role in the distribution and regulation of blood
pressure.
Capillaries
o Sites of gas exchange
 External respiration
 Gas exchange between the alveoli and pulmonary
capillaries
 Internal respiration
 Gas exchange between the systemic capillaries and
the tissues
Venules
o Tiny veins arising from the capillaries
Veins
o Carry blood back to the heart
o Called capacitance vessels because they can hold a large amount
of blood with very little pressure change.
Neural Control of the Vascular System
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Sympathetic nerve fibers are found in the arteries, arterioles and in the
veins.
o Nerve fibers to the arterioles are most abundant
The vasomotor center in the medulla oblongata controls the number of
sympathetic impulses sent to the vascular systems.
o Normally, the vasomotor center sends steady sympathetic impulses
that result in a moderate state of vessel constriction, called
vasomotor tone.
o Response to sympathetic impulses:
 Increased impulses causes vasoconstriction
 Decreased impulses causes vasodilation
o Exception
 Arterioles of the heart, brain, and skeletal muscle dilate in
response to increased sympathetic impulses
 Increases the blood supply to these areas for “flight or
fight” responses.
The Baroreceptor Reflex
In addition, the brain and the heart regulate arterial blood pressure in
response to signals from the arterial baroreceptors. These special pressure
receptors are located in the walls of the carotid arteries and the aorta and
function as short-term regulators of arterial blood pressure.
The graphic below shows the location of the arterial baroreceptors.
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Baroreceptors regulate arterial blood pressure by initiating reflex
adjustments to changes in blood pressure.
If arterial pressure decreases, the following occur.
o The neural impulses from the baroreceptors decrease.
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o In response, the brain increases its sympathetic activity which
causes increases in:
 heart rate
 myocardial force of contraction
 arterial constriction
 Increased total peripheral resistance
 venous constriction
 Liver, spleen, pancreas, stomach, intestine, kidneys,
skin, and skeletal muscle
o The contraction force of the heart increases.
o The arteries and veins constrict.
o The final result is increased cardiac output, increased arterial
constriction, and a rise in blood pressure.
When blood pressure increases, the following occur.
o The neural impulses from the baroreceptors increase, which cause
the brain to reduce its sympathetic activity which results in
decreases in:
 cardiac output
 total peripheral resistance
o The blood pressure falls.
Baroreceptors are short-term regulators of arterial blood pressure:
o If factors responsible for altering blood pressure persist for several
days, the arterial baroreceptors will be reset and accept the higher
pressure as normal
Baroreceptors are also found in the large arteries, large veins, pulmonary
vessels, and cardiac walls.
o Function similarly to the carotid and aortic baroreceptors
o Results in increased sensitivity to venous, atrial and ventricular
pressures
PRESSURE IN THE PULMONARY AND SYSTEMIC VASCULAR SYSTEM
Pressure Types
Three types of pressure are used to study blood flow.
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Intravascular
o the actual blood pressure in the lumen of any vessel at any point,
relative to the barometric pressure
Transmural
o The difference between the intravascular pressure of a vessel and
the pressure surrounding the vessel.
 Positive transmural pressure exists when the pressure inside
the vessel exceeds the pressure outside the vessel.
 Negative transmural pressure exists when the pressure
inside the vessel is less than the pressure surrounding the
vessel.
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Driving
o the difference between the pressure at one point in a vessel and
the pressure at any other point downstream in the vessel
Figure 5-11 in the text gives a schematic illustration of these different
pressures.
THE CARDIAC CYCLE AND ITS EFFECT ON BLOOD PRESSURE
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Arterial blood pressure increases and decreases with the phases of the
cardiac cycle:
Ventricular contraction (systole)
o Systolic pressure
 The maximum pressure generated during ventricular
contraction (systole).
 The normal value is 120 mm Hg for the systemic system.
 The normal value is 25 mm Hg for the pulmonary system.
Ventricular relaxation (diastole)
o Diastolic pressure
 The lowest pressure that remains in the arteries when the
ventricles relax (diastole) before the next ventricular
contraction.
 The normal value is 80 mm Hg for the systemic system.
 The normal value is 8 mm Hg for the pulmonary system.
Circulatory System Pressures
System
Systemic
Pulmonary
Blood
Pressure
120/80 mm Hg
25/8 mm Hg
Mean
Pressure
100 mm Hg
15 mm Hg
Driving
Pressure
98 mm Hg
10 mm Hg
Driving Pressures for the Circulatory System
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Pulmonary System
o The mean pressure in the pulmonary artery is about 15 mm Hg.
o The mean pressure in the left atrium is about 5 mm Hg.
o Therefore, the driving pressure through the pulmonary system is 15
- 5 = 10 mm Hg
Systemic System
o The mean pressure in the aorta is about 100 mm Hg.
o The mean pressure in the right atrium is about 2 mm Hg.
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o Therefore, the driving pressure through the systemic system is 100
- 2 = 98 mm Hg
Compared with the pulmonary circulation, the driving pressure in the
systemic system is about 10 times greater.
Refer to the graphic below for a summary of the diastolic and systolic
pressures in the systemic and pulmonary circulation systems.
Arterial Pulses
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In the systemic circulation the arterial walls expand (ventricular
contraction) and recoil (ventricular relaxation).
This can be felt as a pulse in several systemic arteries:
o Temporal
o Carotid
o Radial
o Popliteal
o Posterior tibial
o Facial
o Brachia
o Femoral
o Dorsal pedal
The Blood Volume and its Effect on Blood Pressure
Following are some key terms pertaining to blood volume.
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Stroke volume
o the volume of blood ejected from the ventricle during each
ventricular contraction
o Normal: 40 to 80 mL
Cardiac output
o The total volume of blood discharged from the ventricles per minute
o Formula: Stroke Volume (SV) times heart rate per minute (HR)
 Example:
 If HR is 72 bpm and SV is 70 mL then,
 CO = HR x SV
 CO = 72 x 70 = 5040 mL/min
 CO = 5 L/min.
o Normal: 4 to 8 L/min.
Effect on Blood Pressure
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Normally, when stroke volume or heart rate increases, blood pressure
correspondingly increases.
When stroke volume or heart rate decreases, blood pressure decreases.
Blood volume varies with age, gender, and body size, but on average, an
adult has about 5 L.
o 75% in systemic circulation
o 15% in the heart
o 10% in the pulmonary capillary bed (capacity of 200 mL)
THE DISTRIBUTION OF PULMONARY BLOOD FLOW
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In the upright lung, the blood flow progressively decreases from the base
to the apex (or steadily increases from the apex to the base).
Distribution of blood flow is a function of gravity, cardiac output, and
vascular resistance.
Gravity
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Blood flow in the lung is gravity dependent.
Most blood flows to the lower half of the lungs.
The intraluminal pressure of the vessels in the lower lung is greater than
the pressure in the upper lung (less gravity dependent).
Higher pressure causes the vessels to distend and allows more blood
flow.
The Effects of Gravity and Alveolar Pressure on the Distribution of
Pulmonary Blood Flow
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Zone 1 (least gravity dependent area)
o PA>Pa>Pv
o Alveolar deadspace
 Normally does not occur because pressure is usually
sufficient to raise the blood to the top of the lungs
 May occur in abnormal conditions such as:
 Hemorrhage
 Dehydration
 Positive pressure ventilation
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Zone 2
o Pa>PA>Pv
o pulmonary capillaries are perfused
 the effective driving pressure steadily increases down
through this zone
o some limitation to venous flow
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Zone 3
o Pa>Pv>PA
o Blood flow throughout this region is constant
Figure 5-11 in the text gives a schematic illustration of these relationships.
Determinants of Cardiac Output
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Cardiac output is the product of the stroke volume and the heart rate.
Stroke volume is determined by the following:
o Ventricular preload
 The degree to which the myocardial fiber is stretched prior to
contraction (end diastole).
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Normally, the more a myocardial fiber is stretched, the more
strongly it contracts, allowing the heart to convert increased
venous return into increased stroke volume.
However, in disease states, if the heart is enlarged,
sometimes the ventricular fibers are overstretched, resulting
in decreased output.
The figure below illustrates the Frank-Starling curve, which
describes the relationship between myocardial stretch and
cardiac output.
o Ventricular afterload
 The force against which the ventricles must work to pump
the blood.
 The arterial systolic blood pressure best reflects the
ventricular afterload.
 As BP increases, resistance increases
 Ventricular afterload is determined by:
 The volume and viscosity of the blood ejected
 The peripheral vascular resistance
 The total cross-sectional space into which the blood is
ejected
 Afterload reduction
 Decreasing peripheral vascular resistance will
increase the stroke volume
o Myocardial Contractility
 The force generated by the myocardium when the ventricular
muscle fibers shorten.
 When the contractility of the heart increases, cardiac
output increases.
o Positive inotropism
 When the contractility decreases, cardiac output
decreases.
o
Negative inotropism
Vascular Resistance
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In general, when vascular resistance increases, blood pressure increases
(in turn increasing the ventricular afterload).
Resistance is calculated by dividing blood pressure by cardiac output.
o R = BP / CO
Active and passive mechanisms in the pulmonary system change vascular
resistance. These mechanisms are discussed below.
Active Mechanisms Affecting Vascular Resistance
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Abnormal blood gases: The pulmonary vascular system constricts or
increases resistance in response to:
o Hypoxia
 Causes pulmonary vascular constriction which shunts blood
to ventilated areas of the lung
 Sequence leading to right heart failure (cor pulmonale)
 Increased pulmonary vascular resistance (PVR)
 Elevated right ventricular pressure
 Right ventricular strain
 Right ventricular hypertrophy
 Right heart failure
o Hypercapnia
 an acute increase PCO2 in the capillary blood
 increased H+ concentration
 increased vasoconstriction
 increased PVR
o Acidemia
 a decreased pH that develops in response to either
metabolic or respiratory causes
 pulmonary vasoconstriction due to metabolic or
respiratory acidosis
Pharmacologic Stimulation
o Pulmonary vessels constrict in response to:
 Epinephrine
 Norepinephrine
 Dobutamine
 Dopamine
 Phenylephrine
o Pulmonary vessels relax in response to:
 Oxygen
 Isoproterenol
 Aminophylline
 Calcium-channel blocking agents
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Pathologic Conditions
o The following conditions can cause increases in pulmonary
vascular resistance.
 Vessel blockage or obstruction
 Vessel wall disease
 Vessel destruction
 Vessel compression
Passive Mechanisms Affecting Vascular Resistance
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Pulmonary Arterial Pressure Changes
o As pulmonary arterial pressure increases, pulmonary vascular
resistance decreases
 This occurs through:
 Recruitment
o Opening of vessels that previously closed
 Distention
o Stretching or widening of vessels that were
open but not to full capacity
 This increases the cross-sectional area of the vascular
system, decreasing PVR
Left Atrial Pressure Changes
o The pulmonary vascular resistance decreases as the left atrial
pressure increases (assuming the lung volume and pulmonary
arterial pressure remain constant).
Lung Volume Changes
o Decreased Lung Volumes (Expiration)
 At low lung volumes
 the extra-alveolar vessels narrow and vascular
resistance increases
 the alveolar vessels dilate and vascular resistance
decreases
o Increased Lung Volumes (Inspiration)
 At high lung volumes
 the extra-alveolar vessels dilate and vascular
resistance decreases
 the alveolar vessels narrow and vascular resistance
increases
o PVR is lowest at FRC and increases in response to increased and
decreased lung volumes.
Blood Volume Changes
o As blood volume increases, the pulmonary vascular resistance
tends to decrease.
 Recruitment and distention of pulmonary vessels
Blood Viscosity Changes
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o As blood viscosity increases, the pulmonary vascular resistance
increases.
o Influences on the viscosity of the blood
 Hematocrit
 Integrity of the red blood cells
 The composition of the plasma
See Table 5-4 in the text for a summary of the effects of active and
passive mechanisms on vascular resistance.
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