Download Cardiovascular Physiology

Cardiovascular
Physiology
Lectures by
Jan Machart
University of Texas, Austin
Copyright © 2009 Pearson Education, Inc.
Overview: Cardiovascular System
Veins
Capillaries
Arteries
Head and
Brain
Arms
Lungs
Superior vena cava
Pulmonary
arteries
Right atrium
Pulmonary
veins
Ascending arteries
Aorta
Left atrium
Coronary arteries
Left ventricle
Abdominal aorta
Right ventricle
Heart
Inferior vena cava
Trunk
Hepatic artery
Hepatic portal vein
Hepatic
vein
Digestive
tract
Liver
Ascending veins
Renal
veins
Renal
arteries
Descending arteries
Venous valve
Kidneys
Pelvis and
Legs
Copyright © 2009 Pearson Education, Inc.
Figure 14-1
Pressure Gradient in Systemic Circulation
• Blood flows down pressure gradients
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Figure 14-2
Pressure Change
• Pressure created by contracting muscles is
transferred to blood
• Driving pressure for systemic flow is created
by the left ventricle
• If blood vessels constrict, blood pressure
increases
• If blood vessels dilate, blood pressure
decreases
• Volume changes greatly affect blood
pressure in CVS
Copyright © 2009 Pearson Education, Inc.
Structure of the Heart
• The heart is composed mostly of myocardium
STRUCTURE OF THE HEART
Aorta
Superior
vena cava
Pericardium
Right
atrium
Right
ventricle
Pulmonary
artery
Auricle of
left atrium
Coronary
artery
and vein
Left
ventricle
Diaphragm
(e) The heart is encased within
a membranous fluid-filled
sac, the pericardium.
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(f) The ventricles occupy the bulk of
the heart. The arteries and veins all
attach to the base of the heart.
Figure 14-7e–f
Structure of the Heart
• The heart valves ensure one-way flow
Aorta
Pulmonary
semilunar valve
Right
pulmonary
arteries
Superior
vena cava
Left pulmonary
arteries
Left pulmonary
veins
Left atrium
Right atrium
Cusp of the AV
(bicuspid) valve
Cusp of a right AV
(tricuspid) valve
Chordae tendineae
Papillary muscles
Left ventricle
Right ventricle
Inferior
vena cava
Descending
aorta
(g) One-way flow through the heart
is ensured by two sets of valves.
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Figure 14-7g
Cardiac Muscle
(a)
Intercalated disk
(sectioned)
Nucleus
Intercalated disk
Mitochondria
Cardiac muscle cell
Contractile fibers
(b)
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Figure 14-10
Cardiac Muscle
• Excitation-contraction coupling and relaxation
in cardiac muscle
10
Ca2+
1
ECF
2 K+
ATP
ICF
1 Action potential enters
from adjacent cell.
9
3 Na+ Ca2+
NCX
3 Na+
RyR
2
Ca2+
2+
2+
3 Ca induces Ca release
through ryanodine
receptor-channels (RyR).
2
3
L-type
Ca2+
channel
SR
Ca2+
Sarcoplasmic reticulum
(SR)
release causes
4 Local
Ca2+ spark.
Ca2+ stores
4
ATP
Ca2+ sparks
T-tubule
Voltage-gated Ca2+
channels open. Ca2+
enters cell.
2+
5 Summed Ca sparks
create a Ca2+ signal.
8
2+
6 Ca ions bind to troponin
to initiate contraction.
5
Ca2+ signal
6
Contraction
Ca2+
7 Relaxation occurs when
Ca2+ unbinds from troponin.
Ca2+
7
7
Relaxation
Actin
Myosin
2+
8 Ca is pumped back
into the sarcoplasmic
reticulum for storage.
2+
9 Ca is exchanged with
Na+ by the NCX antiporter.
10 Na+ gradient is maintained
by the Na+-K+-ATPase.
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Figure 14-11
Myocardial Contractile Cells
• Action potential of a cardiac contractile cell
Membrane potential (mV)
1
+20
PX = Permeability to ion X
PNa
2
PK and PCa
0
–20
3
–40
0
–60
PNa
–80
4
PK and PCa
4
–100
0
Phase
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100
200
Time (msec)
300
Membrane channels
0
Na+ channels open
1
Na+ channels close
2
Ca2+ channels open; fast K+ channels close
3
Ca2+ channels close; slow K+ channels open
4
Resting potential
Figure 14-13
Electrical Conduction in Myocardial Cells
Membrane potential
of autorhythmic cel
Membrane potential
of contractile cell
Cells of
SA node
Contractile cell
Intercalated disk
with gap junctions
Depolarizations of autorhythmic cells
rapidly spread to adjacent contractile
cells through gap junctions.
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Figure 14-17
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5
Depolarization wave
spreads upward from
the apex.
AV node
AV bundle
4
Bundle
branches
Purkinje
fibers
5
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Figure 14-18
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
THE CONDUCTING SYSTEM
OF THE HEART
SA node
Internodal
pathways
AV node
AV bundle
Bundle
branches
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Purkinje
fibers
Figure 14-18, step 1
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
Internodal
pathways
AV node
AV bundle
Bundle
branches
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Purkinje
fibers
Figure 14-18, steps 1–2
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
AV node
AV bundle
Bundle
branches
Copyright © 2009 Pearson Education, Inc.
Purkinje
fibers
Figure 14-18, steps 1–3
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
AV node
AV bundle
4
Bundle
branches
Copyright © 2009 Pearson Education, Inc.
Purkinje
fibers
Figure 14-18, steps 1–4
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5
Depolarization wave
spreads upward from
the apex.
AV node
AV bundle
4
Bundle
branches
Purkinje
fibers
5
Copyright © 2009 Pearson Education, Inc.
Figure 14-18, steps 1–5
Electrical Conduction
• AV node
• Routes the direction of electrical signals
• Delays the transmission of action potentials
• SA node
• Sets the pace of the heartbeat at 70 bpm
• AV node (50 bpm) and Purkinje fibers (25-40
bpm) can act as pacemakers under some
conditions
Copyright © 2009 Pearson Education, Inc.
Einthoven’s Triangle
Right arm
Left arm
I
Electrodes are
attached to the
skin surface.
II
III
A lead consists of two
electrodes, one positive
and one negative.
Left leg
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Figure 14-19
The Electrocardiogram
• Three major waves: P wave, QRS complex,
and T wave
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Figure 14-20
Electrical Activity
• Correlation between an ECG and electrical
events in the heart
P wave: atrial
depolarization
START
P
The end
R
P
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
Q S
Atria contract
T wave:
ventricular
repolarization
Repolarization
R
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
T
P
Q S
P
ST segment
Q wave
Q
R
P
R wave
R
Q S
R
Ventricles contract
P
Q
P
S wave
Q S
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Figure 14-21
Electrical Activity
P wave: atrial
depolarization
START
P
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
Copyright © 2009 Pearson Education, Inc.
Figure 14-21 (1 of 9)
Electrical Activity
P wave: atrial
depolarization
START
P
PQ or PR segment:
conduction through
AV node and AV
bundle
P
Atria contract
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
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Figure 14-21 (2 of 9)
Electrical Activity
P wave: atrial
depolarization
START
P
PQ or PR segment:
conduction through
AV node and AV
bundle
P
Atria contract
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
P
Q wave
Q
Copyright © 2009 Pearson Education, Inc.
Figure 14-21 (3 of 9)
Electrical Activity
P wave: atrial
depolarization
START
P
PQ or PR segment:
conduction through
AV node and AV
bundle
P
Atria contract
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
P
Q wave
Q
R wave
R
P
Q
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Figure 14-21 (4 of 9)
Electrical Activity
P wave: atrial
depolarization
START
P
PQ or PR segment:
conduction through
AV node and AV
bundle
P
Atria contract
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
P
Q wave
Q
R wave
R
R
P
Q
P
S wave
QS
Copyright © 2009 Pearson Education, Inc.
Figure 14-21 (5 of 9)
Electrical Activity
P wave: atrial
depolarization
START
P
PQ or PR segment:
conduction through
AV node and AV
bundle
P
Atria contract
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
P
ST segment
R
Q wave
Q
P
R wave
R
QS
R
Ventricles contract
P
Q
P
S wave
QS
Copyright © 2009 Pearson Education, Inc.
Figure 14-21 (6 of 9)
Electrical Activity
START
P wave: atrial
depolarization
P
PQ or PR segment:
conduction through
AV node and AV
bundle
P
Atria contract
T wave:
ventricular
repolarization
R
T
P
Repolarization ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
QS
P
ST segment
R
Q wave
Q
P
R wave
R
QS
R
Ventricles contract
P
Q
P
S wave
QS
Copyright © 2009 Pearson Education, Inc.
Figure 14-21 (7 of 9)
Electrical Activity
START
P wave: atrial
depolarization
P
The end
R
P
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
QS
Atria contract
T wave:
ventricular
repolarization
R
T
P
Repolarization ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
QS
P
ST segment
R
Q wave
Q
P
R wave
R
QS
R
Ventricles contract
P
Q
P
S wave
QS
Copyright © 2009 Pearson Education, Inc.
Figure 14-21 (8 of 9)
Electrical Activity
START
P wave: atrial
depolarization
P
The end
R
P
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
QS
Atria contract
T wave:
ventricular
repolarization
R
T
P
Repolarization ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
QS
P
ST segment
R
Q wave
Q
P
R wave
R
QS
R
Ventricles contract
P
Q
P
S wave
QS
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Figure 14-21 (9 of 9)
Electrical Activity
• Comparison of an
ECG and a
myocardial action
potential
1 mV
1 sec
(a) The electrocardiogram represents the summed
electrical activity of all cells recorded from the
surface of the body.
110
mV
1 sec
(b) The ventricular action potential is recorded from
a single cell using an intracellular electrode.
Notice that the voltage change is much greater
when recorded intracellularly.
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Figure 14-22
Electrical Activity
• Normal and abnormal electrocardiograms
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Figure 14-23
Mechanical Events
• Mechanical events of the cardiac cycle
1
Late diastole—
diastole—both sets of
chambers are relaxed and
ventricles fill passively.
START
5
Isovolumic ventricular
relaxation—
relaxation—as ventricles
relax, pressure in ventricles
falls, blood flows back into
cusps of semilunar valves
and snaps them closed.
2
Atrial systole—
systole—atrial contraction
forces a small amount of
additional blood into ventricles.
3
Isovolumic ventricular
contraction—
contraction—first phase of
ventricular contraction pushes AV
valves closed but does not create
enough pressure to open semilunar
valves.
S1
S2
4
Ventricular ejection—
ejection—
as ventricular pressure
rises and exceeds pressure
in the arteries, the semilunar
valves open and blood is
ejected.
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Figure 14-24
Mechanical Events
1
Late diastole—
diastole—both sets of
chambers are relaxed and
ventricles fill passively.
START
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Figure 14-24, step 1
Mechanical Events
1
Late diastole—
diastole—both sets of
chambers are relaxed and
ventricles fill passively.
START
2
Atrial systole—
systole—atrial contraction
forces a small amount of
additional blood into ventricles.
S1
Copyright © 2009 Pearson Education, Inc.
Figure 14-24, steps 1–2
Mechanical Events
1
Late diastole—
diastole—both sets of
chambers are relaxed and
ventricles fill passively.
START
2
Atrial systole—
systole—atrial contraction
forces a small amount of
additional blood into ventricles.
S1
S2
3 Isovolumic ventricular
contraction—
contraction—first phase of
ventricular contraction pushes AV
valves closed but does not create
enough pressure to open semilunar
valves.
Copyright © 2009 Pearson Education, Inc.
Figure 14-24, steps 1–3
Mechanical Events
1
Late diastole—
diastole—both sets of
chambers are relaxed and
ventricles fill passively.
START
2
Atrial systole—
systole—atrial contraction
forces a small amount of
additional blood into ventricles.
S1
S2
4
Ventricular ejection—
ejection—
as ventricular pressure
rises and exceeds pressure
in the arteries, the semilunar
valves open and blood is
ejected.
Copyright © 2009 Pearson Education, Inc.
3 Isovolumic ventricular
contraction—
contraction—first phase of
ventricular contraction pushes AV
valves closed but does not create
enough pressure to open semilunar
valves.
Figure 14-24, steps 1–4
Mechanical Events
1
Late diastole—
diastole—both sets of
chambers are relaxed and
ventricles fill passively.
START
5
Isovolumic ventricular
relaxation—
relaxation—as ventricles
relax, pressure in ventricles
falls, blood flows back into
cusps of semilunar valves
and snaps them closed.
2
Atrial systole—
systole—atrial contraction
forces a small amount of
additional blood into ventricles.
S1
S2
4
Ventricular ejection—
ejection—
as ventricular pressure
rises and exceeds pressure
in the arteries, the semilunar
valves open and blood is
ejected.
Copyright © 2009 Pearson Education, Inc.
3 Isovolumic ventricular
contraction—
contraction—first phase of
ventricular contraction pushes AV
valves closed but does not create
enough pressure to open semilunar
valves.
Figure 14-24, steps 1–5
Cardiac Cycle
• Left ventricular pressure-volume changes
during one cardiac cycle
Stroke volume
120
Left ventricular pressure (mmHg)
KEY
EDV = End-diastolic
volume
ESV = End-systolic
volume
ESV
D
80
C
One
cardiac
cycle
40
B
EDV
A
0
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65
100
Left ventricular volume (mL)
135
Figure 14-25
Wiggers Diagram
Time (msec)
0
Electrocardiogram
(ECG)
100
200
300
400
500
600
700
800
QRS
complex
QRS
complex
P
T
P
120
B
90
Dicrotic notch
Pressure
(mm Hg)
A
60
Left
venticular
pressure
30
Left atrial
pressure
0
D
C
S1
Heart sounds
135
S2
E
Left
ventricular
volume (mL)
F
65
Atrial
systole
Atrial
systole
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Ventricular
systole
Ventricular
diastole
Isovolumic Ventricular
Early
Late
ventricular
systole
ventricular ventricular
contraction
diastole
diastole
Atrial
systole
Atrial
systole
Figure 14-26
Stroke Volume and Cardiac Output
• Stroke volume
• Amount of blood pumped by one ventricle
during a contraction
• EDV – ESV = stroke volume
• Cardiac output
• Volume of blood pumped by one ventricle in a
given period of time
• CO = HR × SV
• Average = 5 L/min
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Autonomic Neurotransmitters Alter Heart Rate
KEY
Integrating center
Cardiovascular
control
center in medulla
oblongata
Efferent path
Effector
Tissue response
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Sympathetic neurons
(NE)
Parasympathetic
neurons (Ach)
β 1-receptors of
autorhythmic cells
Muscarinic receptors
of autorhythmic cells
Na+ and Ca2+ influx
K+ efflux; Ca2+ influx
Rate of depolarization
Hyperpolarizes cell and
rate of depolarization
Heart rate
Heart rate
Figure 14-27
Stroke Volume
• Frank-Starling law states
• Stroke volume increase as EDV increases
• EDV is affected by venous return
• Venous return is affected by
• Skeletal muscle pump
• Respiratory pump
• Sympathetic innervation
• Force of contraction is affected by
• Stroke volume
• Length of muscle fiber and contractility of heart
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Inotropic Effect
• The effect of norepinepherine on contractility
of the heart
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Figure 14-29
Stroke Volume and Heart Rate Determine Cardiac
Output
CARDIAC OUTPUT
is a function of
Heart rate
Stroke volume
determined by
determined by
Rate of depolarization
in autorhythmic cells
Force of contraction in
ventricular myocardium
is influenced by
Decreases
Due to
parasympathetic
innervation
Increases
increases
Contractility
Sympathetic
innervation and
epinephrine
increases
End-diastolic
volume
which varies with
Venous constriction
Venous return
aided by
Skeletal muscle
pump
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Respiratory
pump
Figure 14-31
Summary
• Cardiovascular system—anatomy review
• Pressure, volume, flow, and resistance
• Pressure gradient, driving pressure, resistance,
viscosity, flow rate, and velocity of flow
• Cardiac muscle and the heart
• Myocardium, autorhythmic cells, intercalated
disks, pacemaker potential, and If channels
• The heart as a pump
• SA node, AV node, AV bundle, bundle
branches, and Purkinje fibers
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Summary
• The heart as a pump (continued)
• ECG, P wave, QRS complex, and T wave
• The cardiac cycle
• Systole, diastole, AV valves, first heart sound,
isovolumic ventricular contraction, semilunar
valves, second heart sound, and stroke volume
• Cardiac output
• Frank-Starling law, EDV, preload, contractility,
inotropic effect, afterload, and ejection fraction
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Blood Flow and the
Control of Blood
Pressure
Lectures by
Jan Machart
University of Texas, Austin
Copyright © 2009 Pearson Education, Inc.
Functional Model of the Cardiovascular System
Elastic arteries
Aorta
Aortic valve
Left ventricle
Left heart
Mitral valve
Left atrium
Arteriole with
variable radius
Pulmonary veins
Lungs
Exchange of
material with
cells
Capillaries
Pulmonary artery
Pulmonary valve
Right ventricle
Right heart
Venules
Tricuspid valve
Right atrium
Venae cavae
Expandable veins
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Figure 15-1
Elastic Recoil in Arteries
Arterioles
1
Ventricle contracts.
2
Semilunar valve opens.
1
2
3
3 Aorta and arteries expand and
store pressure in elastic walls.
(a) Ventricular contraction
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Figure 15-4a
Pressure Throughout the Systemic Circulation
• Blood pressure is highest in the arteries and
decreases continuously as it flows through
the circulatory system
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Figure 15-5
Measurement of Arterial Blood Pressure
(a)
Cuff pressure
> 120 mm Hg
Inflatable
cuff
Pressure
gauge
(b)
Cuff pressure
between 80 and
120 mm Hg
Stethoscope
(c)
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Cuff pressure
< 80 mm Hg
Figure 15-7
Blood Pressure
Blood
volume
leads to
KEY
Stimulus
Integrating center
Blood
pressure
Tissue response
Systemic response
triggers
Fast response
Slow response
Compensation
by
cardiovascular
system
Vasodilation
Compensation
by kidneys
Excretion of fluid in urine
blood volume
Cardiac output
Blood
pressure
to normal
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Figure 15-9
Factors that Influence Mean Arterial Pressure
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Figure 15-10
Arteriolar Resistance
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Table 15-2
Distribution of Blood
• Distribution of blood
in the body at rest
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Figure 15-14
Blood Flow
• Blood flow through individual blood vessels is
determined by vessel’s resistance to flow
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Figure 15-15a
Blood Flow
• Flow ∝ 1/resistance
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Figure 15-15b
Velocity of Blood Flow
• Velocity of flow
depends on total
cross-sectional
area of the vessels
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Figure 15-18
Fluid Exchange at a Capillary
• Hydrostatic pressure and osmotic pressure
regulate bulk flow
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Figure 15-19a
Fluid Exchange at a Capillary
Venule
Arteriole
Net
filtration
Net
absorption
Lymph
vessels
(b) Relationship between capillaries and lymph vessels
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Figure 15-19b
Lymphatic System
Thoracic (left lymph) duct
Cervical
lymph nodes
Right lymph duct
Thymus
Thoracic duct
Lumbar
lymph nodes
Lymphatics of
upper limb
Axillary lymph nodes
Lymphatics of
mammary gland
Spleen
Pelvic
lymph nodes
Inguinal
lymph nodes
Lymphatics
of lower limb
Blind-end lymph
capillaries in the tissues
remove fluid and filtered
proteins.
Lymph fluid empties into the venous circulation.
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Figure 15-20
Edema
• Two causes
• Inadequate drainage of lymph
• Filtration far greater than absorption
• Disruption of balance between filtration and
absorption
• Increase in hydrostatic pressure
• Decrease in plasma protein concentration
• Increase in interstitial proteins
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Blood Pressure
• Components of the baroreceptor reflex
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Sympathetic
neurons
Carotid and aortic
baroreceptors
SA node
Ventricles
Veins
Arterioles
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Figure 15-22
Blood Pressure
KEY
Stimulus
Sensory receptor
Integrating center
Efferent path
Effector
Change in
blood
pressure
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Figure 15-22 (1 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Integrating center
Efferent path
Effector
Change in
blood
pressure
Carotid and aortic
baroreceptors
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Figure 15-22 (2 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Integrating center
Medullary
cardiovascular
control center
Efferent path
Effector
Change in
blood
pressure
Carotid and aortic
baroreceptors
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Figure 15-22 (3 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Integrating center
Medullary
cardiovascular
control center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
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Carotid and aortic
baroreceptors
Figure 15-22 (4 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Carotid and aortic
baroreceptors
Sympathetic
neurons
Copyright © 2009 Pearson Education, Inc.
Figure 15-22 (5 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Sympathetic
neurons
Copyright © 2009 Pearson Education, Inc.
Carotid and aortic
baroreceptors
SA node
Figure 15-22 (6 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Sympathetic
neurons
Copyright © 2009 Pearson Education, Inc.
Carotid and aortic
baroreceptors
SA node
Figure 15-22 (7 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Sympathetic
neurons
Carotid and aortic
baroreceptors
SA node
Ventricles
Copyright © 2009 Pearson Education, Inc.
Figure 15-22 (8 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Sympathetic
neurons
Carotid and aortic
baroreceptors
SA node
Ventricles
Arterioles
Copyright © 2009 Pearson Education, Inc.
Figure 15-22 (9 of 10)
Blood Pressure
KEY
Stimulus
Sensory receptor
Medullary
cardiovascular
control center
Integrating center
Efferent path
Effector
Change in
blood
pressure
Parasympathetic
neurons
Sympathetic
neurons
Carotid and aortic
baroreceptors
SA node
Ventricles
Veins
Arterioles
Copyright © 2009 Pearson Education, Inc.
Figure 15-22 (10 of 10)
Blood Pressure
• The baroreceptor
reflex: the
response to
increased blood
pressure
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Figure 15-23
Blood Pressure
• The baroreceptor
reflex: the
response to
orthostatic
hypotension
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Figure 15-24
CVD: Risk Factors
• Not controllable
• Sex
• Age
• Family history
• Controllable
•
•
•
•
Smoking
Obesity
Sedentary lifestyle
Untreated hypertension
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CVD: Risk Factors
• Uncontrollable genetic but modifiable lifestyle
• Blood lipids
• Leads to atherosclerosis
• HDL-C versus LDL-C
• Diabetes mellitus
• Metabolic disorder contributes to development of
atherosclerosis
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LDL and Plaque
• The development of
atherosclerotic
plaques
Endothelial cells
Elastic connective tissue
Smooth muscle cells
(a) Normal arterial wall
LDL cholesterol accumulates
Macrophages
Smooth muscle cells
(b) Fatty streak
A lipid core accumulates
Fibrous scar tissue
Smooth muscle cells
Calcifications are deposited
within the plaque.
(c) Stable fibrous plaque
Platelets
Macrophages
(d) Vulnerable plaque
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Figure 15-25
Hypertension
• The risk of developing cardiovascular disease
doubles with each 20/10 mm Hg increase in
blood pressure
• Essential hypertension has no clear cause
other than hereditary
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Figure 15-26
Hypertension
• Carotid and aortic baroreceptors adapt
• Risk factor for atherosclerosis
• Heart muscle hypertrophies
• Pulmonary edema
• Congestive heart failure
• Treatment
• Calcium channel blockers, diuretics, betablocking drugs, and ACE inhibitors
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Myocardial infarction
Decreased oxygen supply to the heart due to
blockage of one or more coronary arteries.
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Myocardial infarction
Drawing of the heart showing anterior left ventricle wall infarction
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Myocardial infarction
Symptoms:
A person having an acute myocard infarct usually has sudden chest
pain (called angina pectoris) that is felt behind the breast bone and
sometimes travels to the left arm or the left side of the neck.
Additionally, the person may have shortness of breath, sweating,
nausea, vomiting, abnormal heartbeats and anxiety.
Areas of pain
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Myocardial infarction
A cardiac troponin rise (as a marker of all heart muscle damage) accompanied
by either typical symptoms, pathological Q waves, ST elevation or depression,
or coronary intervention is diagnostic of MI (WHO).
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Myocardial infarction
• Etiology/Prevention:
• Lifestyle: smoking, obesity, stress, exercise, …
• Diseases: diabetes mellitus, hypertension, lipid disorders, …
• Medication: antiplatelet drugs, beta blockers, ACE inhibitors,
statins, other antihypertensive drugs, …
• Treatment angina pectoris:
• The most specific medicine to treat angina is nitroglycerin. It is a
potent vasodilator that makes more oxygen available to the heart
muscle.
• Beta blockers and calcium channel blockers act to decrease the
heart's workload, and thus its requirement for oxygen.
Copyright © 2009 Pearson Education, Inc.
Myocardial infarction
Percutaneous coronary intervention
•
•
•
During PCI, a cardiologist feeds a deflated balloon or other device on a catheter from
the inguinal femoral artery or radial artery up through blood vessels until they reach the
site of blockage in the heart and X-ray imaging is used to guide the catheter threading.
At the blockage, the balloon is inflated to open the artery, allowing blood to flow.
A stent is often placed at the site of blockage to permanently open the artery.
Coronary angiography and angioplasty
in acute myocardial infarction
left: RCA closed
right: RCA successfully dilated
Coronary artery bypass grafting (CABG), which bypasses stenotic arteries by grafting
vessels from elsewhere in the body, is an alternative treatment.
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Myocardial infarction
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Myocardial infarction
Ischemic heart disease in context of
other cardiovascular (related) diseases
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EHEALTH
Questions?
and/or
Blood Pressure Measurement
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