Download Lecture 4

Elaine N. Marieb
Katja Hoehn
Bio 401
Lecture 4
Blood vessels and
control blood flow
Human
Anatomy
& Physiology
SEVENTH EDITION
Copyright © 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Dr. Shlomoh Simchon
Exam 03/22
1. Use only short answers - key words
2. All books, notes etc, must be away, in your bag.
3. All cell phone turned off and hidden in your bag
4. Use calculators Provided.
1
1.
2.
3.
4.
5.
6.
Will have some multiple choice questions
Multiple answer
Short essay questions
Calculations (show your work)
Graphic
Matching
What to study?
Heart
• Electrical activity – action potential. Know the
ions involved in SA node action potential
(automaticity), Ventricle etc
• EKG
• Control of heart rate: SA pacemaker potential
• Sympathetic / parasympathetic
• Contractility
• Role of calcium in action potential, contraction
• Cardiac cycle
• Starling law
2
Cardiac Output (CO) and Reserve
• CO is the amount of blood pumped by each ventricle in one minute
• CO is the product of heart rate (HR) and stroke volume (SV)
CO = SV x HR
• HR is the number of heart beats per minute
• SV is the amount of blood pumped out by a ventricle with each beat
• Cardiac reserve is the difference between resting and maximal CO
• Remember
SV = EDV – ESV
Ejection Fraction = SV/EDV
Regulation of Stroke Volume
• SV = end diastolic volume (EDV) minus end
systolic volume (ESV)
• EDV = amount of blood collected in a
ventricle during diastole
• ESV = amount of blood remaining in a
ventricle after contraction
Exercise  increase HR  decrease filling time  decrease SV
increase EDV + sympathetic  increase SV
3
Factors Affecting Stroke Volume
• Preload – amount ventricles are stretched by contained
blood
• Contractility – cardiac cell contractile force due to
factors other than EDV
• Afterload – back pressure exerted by blood in the large
arteries leaving the heart
SV = EDV - ESV = Filling and Contractility
Frank-Starling Law of the Heart
• Preload, or degree of stretch, of cardiac muscle
cells before they contract is the critical factor
controlling stroke volume
• Slow heartbeat and exercise increase venous
return to the heart, increasing SV
• Blood loss and extremely rapid heartbeat
decrease SV
4
Extrinsic Factors Influencing
Stroke Volume
• Contractility is the increase in contractile
strength, independent of stretch and EDV
• Increase in contractility comes from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
Regulation of Heart Rate
• Positive chronotropic factors increase heart
rate
• Negative chronotropic factors decrease heart
rate
5
Regulation of Heart Rate:
Autonomic Nervous System
• Sympathetic nervous system (SNS) stimulation is activated by
stress, anxiety, excitement, or exercise
• Parasympathetic nervous system (PNS) stimulation is
mediated by acetylcholine and opposes the SNS
• PNS dominates the autonomic stimulation, slowing heart rate
and causing vagal tone
• Cutting Symp + Para will remove more inhibition of para
causing an increase in heart rate
6
a. Effects of Preload
The tension developed during systole depends on the cardiac fiber
length. This is known as the length-tension relationship of cardiac
muscle. The ultrastructural basis for this relationship is the amount
of overlap between the thick and thin filaments of the cardiac
muscle fibers. In the cardiac chambers, variations of the initial
fiber length are achieved by the changes in the volume of blood in
the chamber before systole commences, i.e., the end-diastolic
volume (EDV). When applying this to measurable parameters,
typically the length-tension parameters are expressed as EDV and
ventricular pressure respectively. The relationship can be seen in
the graph below. At a normal EDV, the systolic pressure is on the
ascending limb of the graph. Increase VR, increase vent. filling,
increase EDV, increase initial fiber length, increase systolic
pressure (force on contraction). This is Starling's Law of the Heart.
Summary of Preload
Intrinisic
regulation
7
THE PRESSURE-VOLUME LOOP
Ventricular
pressure, mm Hg
Aortic
valve closes
150
ejection
100
isovolumic
relaxation
50
0
mitral valve
opens
0
Resting
contraction
filling
50
100
Ventricular volume, ml
aorticvalve
opens
isovolumic
contraction
mitral valve
closes
150
b. Effects of Afterload
The velocity of fiber shortening depends on the load
against which the heart contracts. This is known as the
force-velocity relationship. In an isotonic contraction, the
velocity of fiber shortening decreases as one raises the
load. The load here is the aortic pressure.
8
Afterload
Starlings Law = Preload
Afterload = Load (arterial blood pressure) and speed of contraction
Afterload can be viewed as the "load" that the heart must eject
blood against. In simple terms, the afterload is closely related to the
aortic pressure. Hypertension is related to increased afterload
V max
Speed of contraction (V)
Arterial blood pressure (= afterload)
Afterload
V max
Speed of contraction (V)
Sympathetic
Arterial blood pressure (= afterload)
9
Afterload
V max
Speed of contraction (V)
Sympathetic
Heart Failure
Normal
Arterial blood pressure (= afterload)
Heart failure
10
Review Questions
1. Which of the following determines myocardial stiffness?
a. Contraction rate of myofibrils
b. Calcium channel antagonist binding
c. Extracellular collagen
d. Membrane-bound adenosine triphosphate
2. In the resting state, the sarcolemma membrane has the highest
conductance for which ion?
a. Calcium
b. Sodium
c. Potassium
d. Chloride
11
3 . How do calcium channel blockers decrease cardiac contractile
force?
a. By enhancing mode 1 calcium channel opening
b. By increasing calcium conductance during phase 2 of the action
potential
c. By eliciting vasodilatation and decreasing afterload
d. By blocking mode 2 calcium channel opening
12. The term “lusitropy” refers to which of the following?
?
a. Afterload
b. Inotropic state
c. Venous return
d. Intrinsic state of myofibril relaxation
12
Chemical Regulation of the Heart
• The hormones epinephrine (from adrenal
medulla) and thyroxine (thyroid hormone)
increase heart rate
13
Heart rate, stroke volume and cardiac
output
• Cardiac output = the amount of blood pumped out
from a ventricle in 1 minute ( liters/min)
• Stroke volume = the amount of blood pumped out in
a single heart beat
• Heart rate = the number of times in a minute the
heart contracts
• Cardiac output = stroke volume x heart rate
Determine the stroke volume if a young
healthy person has cardiac output of 6
liters and a pulse of 60 beats per minute.
14
On a second occasion, heart rate is 90
beats/min and stroke volume is
120ml/beat
• Determine cardiac output. Explain the
difference in CO from the 1st data set
Stroke volume
• Stroke volume is the difference between the
volume of blood in the ventricle just before
contraction ( end diastolic volume) and the
volume in the ventricle at the end of a
contraction (end systolic volume).
• SV = EDV – ESV
15
End diastolic volume
The volume of blood at the end of filling is
determined by
• Venous filling pressure = venous return
• Pressures generated during atrial contraction.
• The distensibility of the ventricular wall.
• The time available for filling.
End Systolic Volume
The volume of blood left in the heart at the end
of emptying is determined by
• Pressures generated during ventricular
contraction.
• The pressure in the outflow channels from the
heart (aortic and pulmonary arteries).
16
Ejection Fraction
The proportion of blood that leaves the ventricle
per beat. Depends upon the force of
contraction.
EF = (SV/ EDV)%
EF = {(EDV-ESV)/EDV} x 100
Calculation: find the SV and EF
• EDV is 175 ml
• ESV is 25 ml
17
Study
18
Filling Pressure
Changing filling
pressure changes stroke
volume by changing
EDV
ESV
This could be an example
of blood transfusion
SV1
EDV2
SV2
Will cause an
increase in stroke
volume
EDV1
Lowering EDV has the opposite effect
19
Blood Vessels
We will learn New Stuff:
•
•
•
•
Turbulence - Sets up murmurs
Local decrease in vessel diameter (stenosis)
Example:
Atherosclerosis narrows lumen; increases
velocity, produces murmurs
Blood
Vessels
20
Circulatory systems
All circulatory systems are comprised of:
• A pump that forces blood through the network of large
distributing vessels
• A distributing system of arteries that carries the blood to
all of the organs
• A specialized system where there is transfer by diffusion
between vessels and tissues (interstitium) (ie.:capillaries)
• A venous system that returns blood from the transfer
structures to the heart
21
Introduction to hemodynamics
• The primary function of the cardiovascular system
is to deliver oxygen and nutrients; and to remove
wastes from tissue.
• The pressure generated by cardiac contraction
provides the driving force needed for blood flow
through the vascular system.
• Hemodynamic (hemo is blood), is the area of
physiology that study the dynamic behavior of
blood.
• Hemodynamics concerns the physical factors
governing blood flow within the circulatory system.
What is the difference between
blood flow and blood velocity?
Definitions
Blood flow is the volume of blood delivered per unit time.
Volume / Unit time
example flow of 5 l/min or 5,000 ml/min is volume (5 l) of
blood delivered per min
Velocity is the displacement of blood in time.
Distance/time
example velocity of 20 cm/min is the displacement of blood / min
22
Not all tissues need or receive the same
amount of blood at rest
Series
How can organs
and tissues
receive different
flows?
What determines how much blood
will flow through a vessel?
Lung
Right
Heart
Left
Heart
Parallel
Brain
Heart
Kidney
Gut
Skin
Muscle
Hemodynamics: What determines flow
rate through vessel?
23
Poiseuille Equation
(π) (P1 – P0) (r 4)
Flow (Q) = ----- x ----------------(8)
(η) (L)
(π)
----- = correlation constant
(8)
(P1 – P0) = pressure gradient
r = radius of the pipe (blood vessel)
η = viscosity of fluid (blood) flowing through the pipe
L = length of pipe (blood vessel)
In the circulation:
 (P1 – P0) is the driving force
 r and L are geometrical factors = vascular hindrance
 Viscosity depends on the physical property of the blood = blood rheology
Simplified Poiseuille equation to study
cardiovascular hemodynamic basics
Flow (Q) =
P 1 – P0
--------------- =
(8) (η) (L)
--------------() (r 4)
ΔP (driving force)
--------------------Resistance
ΔP
Flow = --------------Resistance
24
Resistance in Series and Parallel
R1
Series
R2
RT = R1 + R2
R1
Parallel
1/RT = 1/R1 + 1/R2
R2
Distribution of
Blood flow to Various Organs




The total blood flow pumped out of
the heart (cardiac output) is about 5
L/min. This blood is then delivered to
different organs.
Liver, kidneys, and skeletal muscle
receive the largest percentage of CO.
The heart receives the lowest
percentage of flow.
Most vessels are arranged in parallel.
The capillaries throughout the
systemic circulation are in parallel
with one another.
25
Calculate Systemic Peripheral Resistance
ΔP
R = -------Q
Q = cardiac output (CO) = 5.1 L/min = 5,100 ml/min = 85 ml/sec
Systemic Vascular Resistance (SVR) = (Pa - Pv) / CO
= (102 mm Hg - 2 mm Hg) / 5.1 L/min = 19.6 mm Hg/L/min
Calculate Pulmonary Resistance
Pulmonary Vascular Resistance (PVR) = (P pulm artery - P pulm vein ) / CO
= (16 mm Hg - 4 mm Hg) / 5.1 L/min = 2.35 mm Hg/L/min
Peripheral Resistance
1. The lung is a low resistance vascular bed compared to the
systemic resistance (2.9 < 19.6 mm Hg/L/min).
2. The lung must not offer high resistance, this can lead to
pulmonary edema (pressure mediated filtration)
Pulmonary blood flow = cardiac output = Systemic blood flow
(flow the same = 5.1 L/min)
Yet pulmonary resistance is lower.
How can it be, same flow but lower resistance?
26
Graphical Presentation in Rigid Tube
Same pressure  Higher flow = low resistance
ΔP
-------↑Q
Tube A
Flow (ml/min)
↓R =
Tube B
Pressure (mmHg)
Rigid Tube
Same flow  lower pressure = lower resistance
↓ΔP
-------Q
Tube A
Flow (ml/min)
↓R =
Tube B
Pressure (mmHg)
27
Determinants of blood flow
Pumping of heart
Flow =
ΔP
-------R
Blood vessels, Blood viscosity
Calculation
Flow = 9 ml/min
P1 = 100 mmHg
P0 = 10 mmHg
Calculate R
28
Calculation
Two tubes having P1 = 100 mmHg P0 = 10 mmHg
The resistances in the 2 tubes are: R 1 =9 ; R 2 = 4.5
Calculate:
Flow 1, Flow 2
Determinants of Vascular Resistance:
1. Length: not so important because it is
constant
2. Blood Viscosity (maple syrup vs. water)
Greater viscosity = greater resistance
3. radius – the most important variable
Small changes in diameter result in large
changes in flow. Flow proportionate to
radius4
29
Viscosity
Determinants of Vascular Resistance:
1. Length: not so important because it is
constant
2. Number of vessels
3. Blood Viscosity
4. Changing radius
30
Effects of changing the radius in the control of
vascular tone
radius – the most important variable (radius4)
For each organ changes in vascular tone will determine its resistance and
therefore its blood flow.
Factors affecting vascular tone:
1. Mechanical factors
Compression of artery by surrounding tissue pressure
2. Intrinsic control (local)
Auto-regulation and myogenic regulation (will be discussed later)
Endothelium-mediated regulation
Metabolic regulation
3. Extrinsic control
Sympathetic neural vasoconstriction
Parasympathetic neural influences
Humoral (blood-borne) factors
31
BLOOD FLOW RATE vs.
VELOCITY
• Blood flow = volume of blood delivered per
unit time
Flow = Volume / Unit time
• Velocity = the displacement in time of a
particle of blood Velocity = Distance / time
BLOOD FLOW RATE vs.
VELOCITY
Relationship between blood flow and velocity:
Velocity =
Blood flow
-------------Area
cm3/min
= -------------- = cm / min = Distance / time
cm2
At constant cross section area: ↑ flow  ↑ velocity
At constant flow:
↑ cross section area  ↓ Velocity
32
How can amount of blood flowing be
adjusted to meet changing demands?
• Amount of blood flowing can be altered by
modifying pump frequency and force of
contraction.
• Pressure and blood flowing through the tube
can be altered by modifying the tube.
How can amount of blood flowing be
adjusted to meet changing demands?
P
Flow = -----------------Resistance
P = perfusion pressure = determined by the heart
Resistance = determined by blood vessels
33
How can amount of blood flowing be adjusted
to meet changing demands?
• Amount of blood flowing can be altered by
modifying pump (heart) frequency and force of
contraction.
• Pressure and blood flowing through the tube can be
altered by modifying the tube.
Blood pressure
• Always fluid in heart and blood vessels and
this exerts a pressure on the walls of the
vessels.
• During systole blood is pumped out ventricle
into aorta, increasing its blood pressure
• During diastole, the relaxed heart is filling
with blood returned via vena cava. Blood
pressure in the aorta is lowest during diastole.
34
Blood pressure
• Humans 120/80mm Hg what does this mean?
• 120 is systolic pressure i.e. pressure in the
aorta after heart has finished contracting
• 80 is the diastolic pressure; the pressure in the
aorta during the relaxation phase of the heart
while the ventricles are filling.
Control of Blood Pressure
1. Pressure-Flow Relationship and the
Resistance of the Circulation
Pressure = Cardiac output x Resistance
2. Pressure-Volume Relationship and the
Capacity of the Circulation
Pressure = Volume/capacity
35
Control of Blood Pressure
Pressure: 1. Cardiac output
2. Resistance
3. Volume
4, Capacity
Important terms we studied
•
•
Resistance vs capacitance
Elasticity of arteries
36
Blood vessels
Blood vessels are not rigid tubes…
Compliance = DV/DP
Resistance vs capacitance
Resistance (pressure-flow relation)
R = pressure / flow
Same flow  lower pressure = low resistance
↓ΔP
R
=
↓ -------Q
37
Capacitance (pressure volume relation)
• In analyzing the pressure-flow relation (resistance),
we have seen that the pressure at one section of the
vessel is compared to that at another section along the
longitudinal axis of the vessel.
• When the pressure at one section inside the vessel is
compared with the pressure outside the vessel, the
transmural pressure difference serves to distend the
vessel and increase the volume of blood contained
inside.
P0
Resistance
Pressure-Flow relation
P1
Dynamic = with flow (hemodynamic) = volume / time
Transmural pressure
P1
Pressure-volume relation
Capacitance
P0
P0
Static = no flow
The pressure in a container is exerted in all directions
38
High Compliance
Low Compliance
Arterial blood pressure and pulsatility:
review cardiac cycle
The high
capacitance and
elastic recoil help
to store blood
(during systole)
that can be used
during diastole.
39
Elastic Arteries
• Largest-diameter arteries have lot of elastic fibers
• One important function is to help propel blood onward
despite ventricular relaxation
(pressure reservoir  stretch and recoil)
Arterial Blood Pressure
120 mmHg
1/3
2/3
95 mmHg
80 mmHg
No ejection
Why pressure is not 0 mmHg
MAP = 1/3 Psystolic + 2/3 Pdiastolic
40
Static
ΔV
Compliance = -------------ΔP
Dynamics
Mean Arterial Pressure
Cardiac output = ---------------------------Peripheral Resistance
ΔV
ΔP = -------------Compliance
Stroke Volume
Pulse P = -------------------Compliance
MAP = CO x Peripheral Resistance
41
Cardiac output
5 L/min
7
10
25
50
70
Stroke volume
Cardiovascular Control Mechanisms
Regulatory Systems:
1. Volume regulation
2. Flow regulation
3. Pressure regulation
Control Systems:
1. Neural
2. Hormonal
3. Metabolic
4. Autoregulation
42
Vasoactive substances
a) a local vasodilator action
b) a local vasoconstrictor action
Neural System:
1.
2.
Hormonal System: 1.
2.
. Metabolic Effect:
3.
4.
5.
1.
2.
3.
Parasympathetic (acetylcholine).
Sympathetic (epinephrine)
Renin_Angiotensin
Antidiuretic hormone (ADH) =
vasopressin
Catecholamines
Histamine
Bradykinin
CO2
O2
Temperature
Cardiovascular System
Components
Purposes:
– Transport O2 to tissues and remove waste
– Transport nutrients to tissues
– Regulation of body temperature
It is very important to control blood flow in order to
meet the metabolic requirements of tissue
43
Overall Cardiovascular regulation
Rapid response –Short-term (seconds to minutes)
Slow response – Long-term (hours to days)
LOCAL CONTROL
Rigid tube (R constant)
Flow (ml/min)
Increase pressure  increase flow (linear)
R is constant
ΔP
Flow =-------R
In several tissues flow remains
constant, despite changes to BP
Autoregulation
Pressure (mmHg)
44
Pressure-flow curves
Elastic Tube (rubber)
↑Q=
R is constant
↑ ΔP
-------R
Pressure (mmHg)
Flow (ml/min)
↑ ΔP  expend tube ↓R (expand)
Flow (ml/min)
Slope = 1/R
↑ ΔP
↑↑ Q = -------↓R
Pressure (mmHg)
Autoregulation
Q=
↑ ΔP
-------↑ ΔP ↑ R (vasoconstriction)
↑R
Pressure (mmHg)
Pressure-flow curves
Flow (ml/min)
Flow (ml/min)
Rigid Tube
Autoregulation
Pressure (mmHg)
45
Myogenic Control
Circumferentially arranged smooth muscle fibers respond
to moderate increases in transmural pressure. These
responses vary in different vascular beds. Some vessels
respond passively to stretch, vasodilating in response to
increased intravascular pressure. Other vessels (resistance
vessels in the renal and cerebral circulations) respond by
constricting. Since blood flow is determined by the
pressure/resistance ratio, the active response serves to
maintain a relative constancy of flow with changes in
arterial pressure. This is known as autoregulation because
it is a smooth muscle cell response that does not utilize
neural or hormonal mediators. .
Myogenic response
When arterial pressure increases the arteriole is stretched
Increase of
Flow
pressure
increases
Vascular smooth muscle responds by contracting
thus increasing resistance
Increase of
vascular tone
Flow
returns to
normal
46
Local factors and blood flow
Adenosine
CO2
+
H, K
O2
+
EDRF
Endothelial
Derived
Relaxing
Factor
NO
NO
NO
NO
Endothelial
cells
NO
Flow Velocity
at vessel inner
wall (shear
stress)
NO
NO
EDRF = NO NO
NO
NO
47
Sympathetic innervation of VSM
Smooth
muscle cell
Sympathetic nerve
Lumen
Blood vessel
Sympathetic adrenergic receptors
Epi
NE
a
a
a
a
b
2
Smooth Muscle Cell
Contraction
Vasoconstriction
Relaxation
Vasodilation
48
Non-local factors
Epinephrine
(B 2-recept.)
Bradykinin
Norepinephrine
Epi (a- recept.)
ADH
Local Factors influencing arteriolar tone
Vasodilated
low PO2
low pH
adenosine, ADP
histamine
low pressure
high flow velocity
EDRF (NO)
high pressure
low flow velocity
Vasoconstricted
49
Why is blood pressure important?
From tubes to the circulation
P1
DP
Flow =
CO =
Resistance
P2
Flow
DP
Total
Peripheral
Resistance
(TPR)
DP = P1 - P2
If P1 = P and
P2 = P (0),
then D@
P P= MAP
a o r ta
v e n a c a v a
a o rta
Lung
Left
Heart
Right
Heart
P2
P1
Brain
Heart
Kidney
Gut
Skin
Muscle
50
Myogenic response
↑ Arterial Pressure
Hemodynamics
↑ Blood Flow
↓ Blood Flow
↑ Transmural Pressure
↑R
ΔP/R
Arteriolar Constriction
Stretch of Arteriolar
Smooth Muscle
Contraction Arteriolar
Smooth Muscle
Myogenic Mechanisms
Myogenic mechanisms originate in the smooth muscle of blood
vessels, particularly in small arteries and arterioles. When the
lumen of a blood vessel is suddenly expanded, as occurs when
intravascular pressure is suddenly increased, the smooth muscles
respond by contracting. Conversely, a reduction in intravascular
pressure results in smooth muscle relaxation and vasodilation.
Electrophysiological studies have shown that vascular smooth
muscle cells depolarize when stretched, leading to contraction.
Stretching also increases the rate of smooth muscle pacemaker
cells that spontaneously undergo depolarization and
repolarization.
Myogenic mechanisms may play a role in autoregulation of blood
flow and in reactive hyperemia.
51
Autoregulation of blood flow
The ability of an organ to regulate its own blood flow is termed
local regulation of blood flow and is mediated by vasoconstrictor
and vasodilator substances released by the tissue surrounding
blood vessels (vasoactive metabolites) and by the vascular
endothelium. There is also a mechanism intrinsic to the vascular
smooth muscle (myogenic mechanism) that is involved in local
blood flow regulation.
In organs such as the heart and skeletal muscle, mechanical
activity (contraction and relaxation) produces compressive forces
that can effectively decrease vessel diameters and increase
resistance to flow during muscle contraction (see extravascular
compression).
The question is: What factors cause this myogenic
response and autoregulation?
Intrinsic Control of Vascular Tone:
Metabolic Regulation
↓ Blood Flow  ↑ metabolites
Metabolic activity of a tissue generates substances with
vasodilating capacity – products of metabolism or
consequences of metabolism
Carbon dioxide
Lactic acid
Potassium
Breakdown products of ATP: ADP, phosphate and adenosine
Reduction in oxygen
These substances are involved in hyperemic responses
Active:
driven by increased metabolism
Reactive:
driven by reduction in blood flow
52
Flow (ml/min)
Control Flow
Time
53
Reactive hyperemia is the transient increase in organ
blood flow that occurs following a brief period of
ischemia (e.g., arterial occlusion).
Arterial occlusion on blood flow. During the
occlusion period, blood flow goes to zero. When the
occlusion is released, there is a rapid increase in
blood flow (hyperemia) that lasts for several minutes.
The hyperemia occurs because during the period of
occlusion, tissue hypoxia and a build up of
vasodilator metabolites dilate arterioles and decrease
vascular resistance. Then when perfusion pressure is
restored (i.e., occlusion released), flow becomes
elevated because of the reduced vascular resistance.
During the hyperemia, oxygen becomes replenished and
vasodilator metabolites are washed out of the tissue
causing the resistance vessels to regain their normal
vascular tone and thereby return flow to normal levels.
The longer the period of occlusion, the greater the
metabolic stimulus for vasodilation leading to increases
in peak reactive hyperemia and duration of
hyperemia. Depending upon the organ, maximal
vasodilation as indicated by peak flow, may occur
following less than one minute of complete arterial
occlusion, or may require several minutes of occlusion.
During surgery, arterial vessels are often clamped for a
period of time. Release of the arterial clamp results in
reactive hyperemia.
54
Orthostatic Hypotension
Stand up suddenly
Decreased venous return
Decreased cardiac output
Decreased central blood flow
Collapse
Removes hydrostatic effects
Increases venous return
Increases cardiac output
Increases cerebral perfusion
Conscious
Lab 4
Circulation: Flow in tubes and vessels;
Arteries and veins, rat and human
circulatory anatomy
Microcirculation and Lymph
09/22
Dr. Shlomoh Simchon
55
Vasculature (cardiovascular)
Tis week you will study the vasculature
In three parts :
1. An experimental model to study blood flow in vascular
system (physiology)
2. Cross anatomy of vasculature (dissect a rat)
3. Microscopic observation of blood vessels\
An
experimental model to study hemodynamics
If a tube is attached to a fluid reservoir having a pressure P and
1
the pressure at the other open end of the tube is P0 then the
pressure difference (P1- P0) will cause fluid to flow out of the
tube opening.
There are 2 more parameters
affecting blood flow related to the
geometry of tube:
radius and length of tube.
Another parameter
affecting blood flow is
(P1 - P0) = ΔP Driving force
related to the
(energy)
properties of liquid:
viscosity
P
radius
P
0
1
Length
Flow
56
Hemodynamics: What determines flow
rate through vessel?
B
A
h=2
h=1
r=1
r=2
ΔP
Flow = ----------------- ; Resistance ~ 1/ radius 4
Resistance
How can we study hemodynamics?
We can double one parameter at a time from its original value and determine
the relative change in flow rate. We can assume that each parameter had an
initial value of 1 we will then determine the relative change in flow if the
initial parameter is doubled.
Four hemodynamic parameters: a) the pressure gradient – driving force
b) the length of the tube
c) the radius of the tube - Geometrical factors
d) the viscosity of fluid – property of fluid
Example: change vessel radius  measure blood flow
Initial radius r = 1
P = 100
mmHg
Flow
r=2
1 ml/min
r=4
24 =16
44 = 256
Flow = f(r 4)
Analyze all parameters using the same strategy
57
How much will flow into the container?
Resistance a 1
Radius
D Pressure
Flow =
Resistance
4
D Pressure = 10
Radius = 2
Resistance = 1/16
Flow = “?”
Radius = 1
Resistance = 1
Flow = 10
Figure 19-6
Summary of results
A French physiologist by the name of Poiseuille studied the
relative change in flow after he doubled one parameter at a time.
initial
A. Initial condition
B. length of the tube is doubled flow is halved (inversely proportional)
C. radius (r) of tube is doubled  flow increased 16 times (r 4) (directly)
D. viscosity (η) of fluid is doubled  flow is halved (inversely)
pressure gradient is doubled  flow is also doubled (directly proportional)
Developed an equation known as the ”Poiseuille equation”
58
Fig 11.5
Double length in b  1/2 flow in b
Double ΔP + Double length in d  flow in d unchanged
(as in a)
Double radius in A  flow 16x
Hemodynamics: What determines flow
rate through vessel?
59
Simplified Poiseuille equation to study
cardiovascular hemodynamic basics
Flow (Q) =
P 1 – P0
--------------- =
(8) (η) (L)
--------------() (r 4)
ΔP (driving force)
--------------------Resistance
ΔP
Flow = --------------Resistance
Pressure, Resistance and Flow
↑2x Pressure  ↑2x Flow
↑ 2x Radius  ↑16x Flow
↓16x Resistance
60
Simplified Poiseuille equation to study cardiovascular
hemodynamic basics
P1
P0
Flow
Resistance
ΔP
Flow = --------------Resistance
Geometrical factors = vascular hindrance = Z
Property of
fluid
ηx 8xL
Resistance = ----------------π x r4
Relationships Pressure, Flow, and Resistance:
3 variables
ΔP
R
ΔP
Q = ----R
Q
ΔP
R = ----Q
ΔV (voltage)
Remind us Ohm's law:
R = ----I (current)
ΔP = Q x R
61
Lab – determinant blood flow
Calculate Resistances at 2 ΔP: Resistance R1, R2
Shut-off
valve
Fillline
Disconnect
Point
Fill
2 different tubes: R1, R2
Replaceable
Tubing
Beaker
Pa (cmH2O)
2 different heights
2 different pressures
ΔP1 and ΔP2
100mlline
Pb
ΔP = Pa – Pb
Measure Flows: Flow1, Flow2
Graduated
cylinder
Pressure, Radius and Flow
↑2 x Pressure (high of bottle)  ↑2x Flow
↑ 2 radius  ↑16x Flow (to 4th power)
62
Calculate Resistance
• Measure ΔP (high of bottle) in cm H2O
• Measure flow (stop watch) ml/min
• Calculate Resistance = ΔP / Flow
Measure flow for 2 heights and 2 tube size
Table Ia. Parameters for Setup 1 ΔP , Tube 1
ΔP = cmH2O
Flow rate = 100 ml /Time (Sec)
ΔP1
ΔP2
63
Table Ib. Parameters for Setup 2 ΔP , Tube 2
ΔP = cmH2O
Flow rate = 100 ml / Time (Sec)
ΔP1
ΔP2
Table 2a
ΔP
cmH2O
Flow rate =
ml / sec
Resistance
Set up 1
Set up 1
64
Table 2b
ΔP
cmH2O
Flow rate =
ml / sec
Resistance
Set up 2
Set up 2
The circulatory system







Heart (the pump)
Arteries (distributing vessels)
Small Arteries
Arterioles (resistive vessels)
Capillaries (exchange vessels)
Venules (collecting vessels)
Veins (capacitant vessels)
microcirculation
• Pulmonary and systemic are connected in series
• Multiple systemic organs are connected in parallel
 The lymphatic system
65
Microscopic examination
Figure 19-1. Idealized microcirculatory circuit.
66
Microcirculation
Arterioles (resistive vessels)
Capillaries (exchange vessels)
Venules (collecting vessels)
What are capillaries?
• Microscopic vessels that connect arterioles to
venules
• Found near every cell in the body but more
extensive in highly active tissue (muscles, liver,
kidneys and brain)
• Entire capillary bed fills with blood when
tissue is active
• Function is to exchange of nutrients & wastes
between blood and tissue fluid
• Structure is single layer of simple squamous
epithelium and its basement membrane
67
RBC’s in a capillary
Control of flow through capillary beds by sphincters
Precapillary
Postcapillary
a) Active muscle = Sphincters open
b) Resting muscle = Sphincters close
68
Study of capillary circulation: pressure measurements
Pressure
decrease
progressively
from arteriolar
end to venule
end
Lymphatic
An ‘open’ system of nodes
and vessels that drain into
the venous portion of the
closed cardiovascular
system
The lymphatic system is like
the blood circulation - tubes
branch through all parts of
the body like the arteries and
veins that carry blood.
Except that the lymphatic
system carries a colorless
liquid called 'lymph'.
69
1.
2.
3.
4.
5.
Precap sphincters are relax, blood flow
Fluid filtered arterial side
Fluid eabsorbed on the venous side
What is not reabsorbed will pass through lymphatics
Blood return from postcapil sphincters to the venous system
Summary Vascular network
3
2
4
1
9
5
8
7
6
70
Dissection of Rat:
Vascular Systems of Rats
Dr. Shlomoh Simchon
Lab exercise
• The rats are triple color injected:
- red is artery
- blue is vein
- yellow is hepatic portal
• Ventral (abdominal) cavity
• thoracic cavity: diaphragm, digestive system, spleen
• Cardiovascular system: Heart and associated vessels
• Urinary system: kidney etc
71
Cardiovascular
Adult:
vena cava –> right atrium (deoxygenated)–>
A-V valve –> right ventricle --> pulm valve –>
pulm art –> lung —> pulm vein (oxygenated)
—> left atrium –> A-V valve –> left ventricle –>
Aortic valve –> aorta –> body –> vena cava - >
Arterial
(red color)
72
Venous
(Blue color)
Hepatic portal
System (yellow)
73
Dr. Simchon
Dr. Simchon
74
Dr. Simchon
Dr. Simchon
75
Dr. Simchon
76