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Chapter 13
Lecture
Outline
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Chapter 13 Outline
Functions
and Components of the Circulatory System
Composition of Blood
Structure of the Heart
Cardiac Cycle and Heart Sounds
Electrical Activity of the Heart and the ECG
Blood Vessels
Atherosclerosis and Cardiac Arrhythmias
Lymphatic System
13-2
Functions and Components of the
Circulatory System
13-3
Functions of Circulatory System
Plays
roles in transportation of respiratory gases,
delivery of nutrients and hormones, and waste removal
And in temperature regulation, clotting, and immune
function
13-4
Components of Circulatory System
Include
cardiovascular and lymphatic systems
Heart pumps blood thru cardiovascular system
Blood vessels carry blood from heart to cells and
back
Includes arteries, arterioles, capillaries, venules,
veins
Lymphatic system picks up excess fluid filtered out in
capillary beds and returns it to veins
Its lymph nodes are part of immune system
13-5
Composition of the Blood
13-6
Composition of Blood
Consists
of formed elements (cells) suspended and
carried in plasma (fluid part)
When centrifuged, blood separates into heavier
formed elements on bottom and plasma on top
13-7
Composition of Blood
Total
blood volume is about 5L
Plasma is straw-colored liquid consisting of H2O and
dissolved solutes
Includes ions, metabolites, hormones, antibodies
Red blood cells (RBCs) comprise most of formed
elements
% of RBCs in centrifuged blood sample = hematocrit
Hematocrit is 36-46% in women; 41-53% in men
13-8
Plasma Proteins
Constitute
7-9% of plasma
3 types of plasma proteins: albumins, globulins, and
fibrinogen
Albumin accounts for 60-80%
Creates colloid osmotic pressure that draws H2O
from interstitial fluid into capillaries to maintain
blood volume and pressure
Globulins carry lipids
Gamma globulins are antibodies
Fibrinogen serves as clotting factor
Converted to fibrin
Serum is fluid left when blood clots
13-9
Formed Elements
Are
erythrocytes (RBCs) and
leukocytes (WBCs)
RBCs are flattened biconcave
discs
Shape provides increased
surface area for diffusion
Lack nuclei and mitochondria
Each RBC contains 280
million hemoglobin molecules
About 300 billion RBCs are
produced each day
13-10
Leukocytes
Have
a nucleus, mitochondria, and amoeboid motion
Can squeeze through capillary walls (diapedesis)
Granular leukocytes help detoxify foreign
substances and release heparin
Include eosinophils, basophils, and neutrophils
13-11
Leukocytes continued
Agranular
leukocytes
are phagocytic and
produce antibodies
Include
lymphocytes and
monocytes
13-12
Platelets (thrombocytes)
Are
smallest of formed elements,
lack nucleus, are not true cells
Are fragments of megakaryocytes
from bone marrow
Constitute most of mass of blood
clots
Release serotonin to vasoconstrict
and reduce blood flow to clot area
Secrete growth factors to maintain
integrity of blood vessel wall
Survive 5-9 days
13-13
Hematopoiesis
Is
formation of blood cells from stem cells in bone
marrow (myeloid tissue) and lymphoid tissue
Marrow produces about 500 billion blood cells/day
In fetus occurs in liver
13-14
Hematopoiesis continued
Erythropoiesis
is formation of RBCs
Stimulated by erythropoietin from kidney
Leukopoiesis is formation of WBCs
Stimulated by variety of cytokines
= autocrine regulators secreted by immune
system
13-15
Erythropoiesis
2.5
million RBCs are
produced/sec
Lifespan of 120
days
Old RBCs removed
from blood by
phagocytic cells in
liver, spleen, and
bone marrow
Iron recycled
back into
hemoglobin
production
13-16
RBC Antigens and Blood Typing
Antigens
present on RBC surface specify blood type
Major antigen group is ABO system
Type A blood has only A antigens
Type B has only B antigens
Type AB has both A and B antigens
Type O has neither A or B antigens
13-17
Transfusion Reactions
 People
with Type A blood
make antibodies to Type B
RBCs, but not to Type A
 Type B blood has antibodies
to Type A RBCs but not to
Type B
 Type AB blood doesn’t have
antibodies to A or B
 Type O has antibodies to
both Type A and B
 If incompatible blood types
are mixed, antibodies will
cause mixture to agglutinate
13-18
Transfusion Reactions continued
 If
blood types incompatible,
recipient’s antibodies
agglutinate donor’s RBCs
 Type O is “universal donor”
because lacks A and B
antigens
 Recipient’s antibodies
won’t agglutinate donor’s
Type O RBCs
 Type AB is “universal
recipient” because doesn’t
make anti-A or anti-B
antibodies
 Won’t agglutinate
donor’s RBCs
13-19
Rh Factor
Is
another type of antigen found on RBCs
Rh+ has Rho(D) antigens; Rh- does not
Can cause problems when Rh- mother has Rh+
babies
At birth, mother may be exposed to Rh+ blood of
fetus
In later pregnancies mom produces Rh antibodies
In Erythroblastosis fetalis, Rh antibodies from
mom cross placenta and combine with
Rh+antigens on fetal blood cells causing
hemolysis of fetal RBCs
13-20
Hemostasis
Is
cessation of bleeding
Promoted by reactions initiated by vessel injury:
Vasoconstriction restricts blood flow to area
Platelet plug forms
Plug and surroundings are infiltrated by web of
fibrin, forming clot
13-21
Role of Platelets
 Platelets
don't
stick to intact
endothelium
because of
presence of
prostacyclin (PGI2-a prostaglandin)
and NO
 Keep clots from
forming and are
vasodilators
13-22
Role of Platelets
 Damage
to endothelium
allows platelets to bind to
exposed collagen
 von Willebrand factor
increases bond by
binding to both collagen
and platelets
 Platelets stick to
collagen and release
ADP, serotonin, and
thromboxane A2
 = platelet release
reaction
13-23
Role of Platelets continued
 Serotonin
and thromboxane
A2 stimulate
vasoconstriction, reducing
blood flow to wound
 ADP and thromboxane A2
cause other platelets to
become sticky and attach
and undergo platelet
release reaction
 This continues until
platelet plug is formed
13-24
Role of Fibrin
Platelet
plug becomes infiltrated by meshwork of fibrin
Clot now contains platelets, fibrin and trapped RBCs
Platelet plug undergoes plug contraction to form
more compact plug
13-25
Conversion of Fibrinogen to Fibrin
 Can
occur via 2 pathways:
 Intrinsic pathway clots damaged vessels and blood left in test
tube
 Initiated by exposure of blood to negatively charged
surface of glass or blood vessel collagen
 This activates factor XII (a protease) which initiates a
series of clotting factors
 Ca2+ and phospholipids convert prothrombin to
thrombin
 Thrombin converts fibrinogen to fibrin which
polymerizes to form a mesh
 Damage outside blood vessels releases tissue
thromboplastin that triggers a clotting shortcut (= extrinsic
pathway)
13-26
13-27
13-28
Dissolution of Clots
When
damage is repaired, activated factor XII causes
activation of kallikrein
Kallikrein converts plasminogen to plasmin
Plasmin digests fibrin, dissolving clot
13-29
Anticoagulants
can be prevented by Ca+2 chelators (e.g.
sodium citrate or EDTA)
or heparin which activates antithrombin III (blocks
thrombin)
Coumarin blocks clotting by inhibiting activation of Vit
K
Vit K works indirectly by reducing Ca+2 availability
Clotting
13-30
Structure of the Heart
13-31
Structure of Heart
 Heart
has 4 chambers
 2 atria receive blood from venous system
 2 ventricles pump blood to arteries
 2 sides of heart are 2 pumps separated by muscular septum
13-32
Structure of Heart continued
Between
atria and ventricles is layer of dense
connective tissue called fibrous skeleton
Which structurally and functionally separates the
two
Myocardial cells of atria attach to top of fibrous
skeleton and form 1 unit (or myocardium)
Cells from ventricles attach to bottom and form
another unit
Fibrous skeleton also forms rings, the annuli fibrosi,
to hold heart valves
13-33
Pulmonary and Systemic Circulations
Blood
coming from
tissues enters
superior and inferior
vena cavae which
empties into right
atrium, then goes to
right ventricle which
pumps it through
pulmonary arteries
to lungs
13-34
Pulmonary and Systemic Circulations continued
Oxygenated
blood
from lungs passes
thru pulmonary
veins to left atrium,
then to left ventricle
which pumps it
through aorta to
body
13-35
Pulmonary and Systemic Circulations continued
 Pulmonary
circulation is
path of blood from right
ventricle through lungs
and back to heart
 Systemic circulation is
path of blood from left
ventricle to body and
back to heart
 Rate of flow through
systemic circulation =
flow rate thru pulmonary
circuit
13-36
Pulmonary and Systemic Circulations continued
Resistance
in systemic circuit > pulmonary
Work done by left ventricle pumping to systemic is
5-7X greater
Makes left ventricle more muscular (and 3-4X
thicker)
13-37
Cardiac Cycle and Heart Sounds
13-38
Atrioventricular Valves
 Blood
flows from atria
into ventricles thru 1way atrioventricular
(AV) valves
 Between right
atrium and
ventricle is
tricuspid valve
 Between left
atrium and
ventricle is
bicuspid or mitral
valve
13-39
Atrioventricular Valves continued
Opening
and closing of valves results from pressure
differences
High pressure of ventricular contraction is prevented
from everting AV valves by contraction of papillary
muscles which are connected to AVs by chorda
tendinea
13-40
Semilunar Valves
During
ventricular
contraction blood
is pumped
through aortic
and pulmonary
semilunar valves
Close during
relaxation
13-41
Cardiac Cycle
13-42
Cardiac Cycle
Is
repeating pattern of contraction and relaxation of
heart
Systole refers to contraction phase
Diastole refers to relaxation phase
Both atria contract simultaneously; ventricles follow
0.1-0.2 sec later
13-43
Cardiac Cycle
End-diastolic
volume is volume of blood in ventricles at
end of diastole
Stroke volume is amount of blood ejected from
ventricles during systole
End-systolic volume is amount of blood left in
ventricles at end of systole
13-44
Cardiac Cycle continued
 As
ventricles contract, pressure rises, closing AV valves
 Called isovolumetric contraction because all valves are
closed
 When pressure in ventricles exceeds that in aorta,
semilunar valves open and ejection begins
 As pressure in ventricle falls below that in aorta, back
pressure closes semilunars
 All valves are closed and ventricles undergo isovolumetric
relaxation
 When pressure in ventricles falls below atria, AVs open
and ventricles fill
 Atrial systole sends its blood into ventricles
13-45
13-46
Heart Sounds
Closing
of AV and semilunar valves produces sounds
that can be heard thru stethoscope
Lub (1st sound) produced by closing of AV valves
Dub (2nd sound) produced by closing of semilunars
13-47
Heart Murmurs
Are
abnormal sounds produced by abnormal patterns
of blood flow in heart
Many caused by defective heart valves
Can be of congenital origin
In rheumatic fever, damage can be from antibodies
made in response to strep infection
13-48
Heart Murmurs continued
In
mitral stenosis, mitral valve becomes thickened and
calcified, impairing blood flow from left atrium to left
ventricle
Accumulation of blood in left ventricle can cause
pulmonary hypertension
Valves are incompetent when don't close properly
Can be from damage to papillary muscles
13-49
Heart Murmurs continued
 Murmurs
caused by septal defects are usually congenital
 Due to holes in septum between left and right sides of heart
 Pressure causes blood to pass from left to right
13-50
Electrical Activity of Heart and the ECG
13-51
Electrical Activity of Heart
Myocardial
cells are short, branched, and
interconnected by gap junctions
Entire muscle that forms a chamber is called a
myocardium or functional syncytium
Because action potentials originating in any cell are
transmitted to all others
Chambers separated by nonconductive tissue
13-52
SA Node Pacemaker
In
normal heart, SA
node functions as
pacemaker
Depolarizes
spontaneously to
threshold
(= pacemaker
potential)
13-53
SA Node Pacemaker continued
 Membrane
voltage begins
at -60mV and gradually
depolarizes to -40
threshold
 Spontaneous
depolarization is caused
by Na+ flowing through
channel that opens when
hyperpolarized (HCN
channel)
 At threshold V-gated Ca2+
channels open, creating
upstroke and contraction
 Repolarization is via
opening of V-gated K+
channels
13-54
Ectopic Pacemakers
Other
tissues in heart are spontaneously active
But are slower than SA node
Are stimulated to produce action potentials by SA
node before spontaneously depolarize to threshold
If action ptentials from SA node are prevented from
reaching these, they will generate pacemaker
potentials
13-55
Myocardial Action Potentials
cells have RMP of –90 mV
Depolarized to threshold by action potentials
originating in SA node
Myocardial
13-56
Myocardial APs continued
 Upstroke
occurs as
V-gated Na+ channels
open
 MP rapidly declines to
15mV and stays there
for 200-300 msec
(plateau phase)
 Plateau results from
balance between
slow Ca2+ influx and
K+ efflux
 Repolarization due to
opening of extra K+
channels
13-57
Conducting Tissues of Heart
 Action
potentials from
SA node spread
through atrial
myocardium via gap
junctions
 But need special
pathway to ventricles
because of nonconducting fibrous
tissue
 AV node at base of
right atrium and
bundle of His
conduct Act. Pot. to
ventricles
13-58
Conducting Tissues of Heart continued
 In
septum of ventricles,
bundle of His divides
into right and left bundle
branches
 Which give rise to
Purkinje fibers in
walls of ventricles
 These stimulate
contraction of
ventricles
13-59
Conduction of Action Potentials
Act.
Pot. from SA node spread at rate of 0.8 -1 m/sec
Time delay occurs as Act. Pot. pass through AV node
Has slow conduction of 0.03– 0.05 m/sec
Act. Pot. speed increases in Purkinje fibers to 5 m/sec
Ventricular contraction begins 0.1–0.2 sec after
contraction of atria
13-60
Excitation-Contraction Coupling
of myocardial cells opens V-gated Ca2+
channels in sarcolemma
This depolarization opens V-gated and Ca2+ release
channels in SR (calcium-induced-calcium-release)
Ca2+ binds to troponin and stimulates contraction
(as in skeletal muscle)
During repolarization Ca2+ pumped out of cell and
into SR
Depolarization
13-61
Refractory Periods
 Heart’s
Act. Pot. lasts
about 250 msec
 Has refractory periods
almost as long as Act.
Pot.
 Cannot be stimulated
to contract again until
has relaxed
13-62
Electrocardiogram (ECG/EKG)
Is
a recording of electrical activity of heart conducted
thru ions in body to surface
13-63
Types of ECG Recordings
 Bipolar
leads record
voltage between
electrodes placed on
wrists and legs (right leg is
ground)
 Lead I records between
right arm and left arm
 Lead II: right arm and left
leg
 Lead III: left arm and left
leg
13-64
Types of ECG Recordings continued
 Unipolar
leads record
voltage between a single
electrode placed on body
and ground built into ECG
machine
 Limb leads go on right
arm (AVR), left arm
(AVL), and left leg (AVF)
 The 6 chest leads,
placed as shown, allow
certain abnormalities to
be detected
13-65
ECG
3
distinct waves are produced during cardiac cycle
P wave caused by atrial depolarization
13-66
ECG
QRS
complex is caused by ventricular depolarization
T wave results from ventricular repolarization
13-67
Correlation of ECG with Heart Sounds
 1st
heart sound
(lub) comes
immediately after
QRS wave as AV
valves close
 2nd heart sound
(dub) comes as T
wave begins and
semilunar valves
close
13-68
Blood Vessels
13-69
Structure of Blood Vessels
Innermost
layer of all vessels is the endothelium
Capillaries are made of only endothelial cells
Arteries and veins have 3 layers called tunica externa,
media, and interna
Externa is connective tissue
Media is mostly smooth muscle
Interna is made of endothelium, basement
membrane, and elastin
Although have same basic elements, arteries and
veins are quite different
13-70
Arteries
Large
arteries are muscular and elastic
Contain lots of elastin
Expand during systole and recoil during diastole
Helps maintain smooth blood flow during diastole
13-72
Arteries
 Small
arteries and arterioles are muscular
 Provide most resistance in circulatory system
 Arterioles cause greatest pressure drop
 Mostly connect to capillary beds
 Some connect directly to veins to form arteriovenous
anastomoses
13-73
Capillaries
Provide
extensive surface area for exchange
Blood flow through a capillary bed is determined by
state of precapillary sphincters of arteriole supplying it
13-74
Types of Capillaries
 In
continuous capillaries, endothelial cells are tightly joined
together
 Have narrow intercellular channels that permit exchange
of molecules smaller than proteins
 Present in muscle, lungs, adipose tissue
 Fenestrated capillaries have wide intercellular pores
 Very permeable
 Present in kidneys, endocrine glands, intestines.
 Discontinuous capillaries have large gaps in endothelium
Are large and leaky
Present in liver, spleen, bone marrow
13-75
Veins
Contain
majority of blood in circulatory system
Very compliant (expand readily)
Contain very low pressure (about 2mm Hg)
Insufficient to return blood to heart
13-76
Veins
 Blood
is moved
toward heart by
contraction of
surrounding skeletal
muscles (skeletal
muscle pump)
 And pressure
drops in chest
during breathing
 1-way venous
valves ensure
blood moves only
toward heart
13-77
Atherosclerosis and Cardiac
Arrhythmias
13-78
Atherosclerosis
 Is
most common form
of arteriosclerosis
(hardening of arteries)
 Accounts for 50% of
deaths in US
 Localized plaques
(atheromas) reduce
flow in an artery
 And act as sites for
thrombus (blood
clots)
13-79
Atherosclerosis
Plaques
begin at
sites of damage to
endothelium
e.g. from
hypertension,
smoking, high
cholesterol, or
diabetes
13-80
Atherosclerosis
Plaques
begin at
sites of damage to
endothelium
E.g. from
hypertension,
smoking, high
cholesterol, or
diabetes
13-81
Cholesterol and Plasma Lipoproteins
 High
blood cholesterol
is associated with risk
of atherosclerosis
 Lipids, including
cholesterol, are carried
in blood attached to
LDLs (low-density
lipoproteins) and HDLs
(high-density
lipoproteins)
13-82
Cholesterol and Plasma Lipoproteins
LDLs
and HDLs are produced in liver and taken into
cells by receptor-mediated endocytosis
In cells LDL is oxidized
Oxidized LDL can injure endothelial cells
facilitating plaque formation
Arteries have receptors for LDL but not HDL
Which is why HDL isn't atherosclerotic
13-83
Ischemic Heart Disease
Is
most commonly due to atherosclerosis in coronary
arteries
Ischemia occurs when blood supply to tissue is
deficient
Causes increased lactic acid from anaerobic
metabolism
Often accompanied by angina pectoris (chest pain)
13-84
Ischemic Heart Disease continued
Detectable
by changes in S-T segment of ECG
13-85
Ischemic Heart Disease continued
Myocardial
infarction (MI) is a heart attack
Usually caused by occlusion of a coronary artery
Causing heart muscle to die
Diagnosed by high levels of creatine
phosphokinase (CPK) and lactate dehydrogenase
(LDH)
 And presence of plasma troponin T and I from
damaged muscle are now important for
diagnosis of MI
Dead cells are replaced by noncontractile scar
tissue
13-86
Arrhythmias Detected on ECG
Arrhythmias
are abnormal heart rhythms
Heart rate <60/min is bradycardia; >100/min is
tachycardia
13-87
Arrhythmias Detected on ECG continued
 In
flutter, contraction rates can be 200-300/min
 In fibrillation, contraction of myocardial cells is uncoordinated
and pumping ineffective
 Ventricular fibrillation is life-threatening
 Electrical defibrillation resynchronizes heart by
depolarizing all cells at same time
13-88
Arrhythmias Detected on ECG continued
AV
node block occurs when node is damaged
First–degree AV node block is when conduction
through AV node > 0.2 sec
Causes long P-R interval
Second-degree AV node block is when only 1 out of 24 atrial Act. Pot. can pass to ventricles
Causes P waves with no QRS
In third-degree or complete AV node block no atrial
activity passes to ventricles
Ventricles are driven slowly by bundle of His or
Purkinje fibers
13-89
Arrhythmias Detected on ECG continued
In
third-degree or complete AV node block, no atrial
activity passes to ventricles
Ventricles are driven slowly by bundle of His or
Purkinjes
13-92
Lymphatic System
13-93
Lymphatic System
Has
3 basic functions:
Transports interstitial fluid (lymph) back to blood
Transports absorbed fat from small intestine to
blood
Helps provide immunological defenses against
pathogens
13-94
Lymphatic System continued
Lymphatic
capillaries
are closed-end tubes
that form vast
networks in
intercellular spaces
Very porous,
absorb proteins,
microorganisms,
fat
13-95
Lymphatic System continued
Lymph
is
carried from
lymph
capillaries to
lymph ducts to
lymph nodes
13-96
Lymphatic System continued
 Lymph
nodes filter
lymph before returning
it to R. & L. subclavian
veins via thoracic duct
or right lymphatic duct
 Nodes make
lymphocytes and
contain phagocytic
cells that remove
pathogens
 Lymphocytes also
made in tonsils, spleen,
thymus
13-97