Lecture 5 Blood Flow, Heart and Vascular System

5.
Regulation oI blood Ilow -

Heart and Vasculature
1
Negative Ieedback regulation
negative Ieedback
OVERRIDE
SENSOR
EFFECTOR
COORDINATING
CENTRE
Mean Arterial Pressure (MAP)
needs to be at ~ 100 mm mercury
PNS
SNS
muscle
-cardiac
-smooth
glands.
MAP
(mmHg)
100
time
pressure
receptors
(sensors)
5. Regulation oI blood Ilow -
2
Pump
Pump
transport
resistance
exchange
storage
storage transport
exchange
resistance
64
7
7
13
9
Cardiovascular system - closed circuit system
- (really just some) pumps and pipes
- functionally compartmentalized system
left Heart
arteries
body
systemic
small arteries
arterioles
capillaries
gut
over 600
skeletal muscle
etc.
veins
right Heart
lung
pulmonary
arteries
caps.
Lung
pulm. veins
pulm.
arteries
Artery - a vessel that takes blood away from the heart.
Vein - a vessel that takes blood to the heart.
2 hearts - 2 pumps
3
Silverthorn pg 413
Pumps - the heart
- 2 independent pumps that beat simultaneously
1.
tack down leaflets on inside, so that when the muscle contracts,
the leaflets will not be pushed into the right atrium
2
going out to lungs
coming back from
lung
3. mitral valve
wall of left ventricle is
very thick because the
afterload it has to work
against is immensely high
(80 mmHg)
4. aortic valve
All valves passive.
preload - volume ventricle has just prior to contraction
afterload - Load (volume) that the ventricle is working against
Q (blood flow) = P1-P2/R
heart creates P1 because if it is not the greatest pressure in the system we would have no flow
4
Conduction
Tissue Velocity (m/s)
SA node 0.05
Artial pathways 1.0
AV node 0.05
Bundle oI HIS 1.0
Purkinje system 4.0
Ventricular muscle 1.0
Trigger for contraction - AP -> start in specialized muscle cells -> nodal cells of sinoatrial node (sa node).
spontaneous depolarizers
-pacemaker cells
70-80 beats/min
atrial myocytes
ventricular myocytes
spontaneously depol.
40-60 times/min
-if sa fails can work
alone to operate heart
spontaneously depol. 15-40
times/min
need a pacemaker if both the SA and AV nodes fail
slow down AP
so that atria
contract before
ventricles
Vm
(mV)
5
Vm
(mV)
2 types of cells in the heart:
1. Nodal cells - generates APs
2. Muscle cells - generates pressure
1. Nodal cells - generate AP
- triggers for contraction
i) SA node
ii) AV node
time
(ms)
slow Na+ leak
Na+ in flux
i(current)f(funny)
if
because the SA node is connected to the rest of the system, once
the AP is started, it will spread rapidly
threshold for
volt. gated Ca++ Channels
Ca++ channels inactivate
volt. gated K+ channels
open
K+ channels close
0 200 300 100
"Effective"
refractory
period
-can't generate
another AP
relative
refractory period
-can generate
another AP
if stim. is
greater than
original
-wont be
generating an AP
in this area
200 ms
post. repolarization
refractoriness
- still cannot generate another AP
for another 200 ms
Ho: waiting for volt. dep. Ca+ channels to close
if stimulate Vm at these points, you wont get full response until all the Ca+ channels close
6
Silverthorn page 486
Changing HR:
1 SNS --> NE --> increase permeability of nodal cells to sodium
- increases our Na+ leak rate, therefore reach threshold faster
2 PNS --> Ach --> Ach dep. K+ channels --> hyperpolarize
- take more time to reach threshold therefore fewer AP/min
7
Vm
(mV)
2 muscle cell - ventricular myocyte - receives AP
threshold
volt. gated Na+
channels
-open
Na+ channels inactivate
time (ms)
0 100 200
300
K+ movement out due to its
[ ] and electrical gradient
open volt. gated Ca++ channels - L-type Ca++ channels
- trigger calcium for contraction
plateau region because Ca+ flux in = K+ flux out
volt. gated Ca++ channels inactive
K+ flux out > Ca++ flux in
volt. gated Na+ channels close
Ca++ channels close.
effective refractory period
relative
refractory
period
Ca++ channels close
(200 ms)
ion conductance
(permeability)
Na+
Ca++
K+ - must decrease K+ permeability
to prevent excess K+ loss from cell.
time (ms)
8
Berne and Levy p. 302
Effective Refractory Periods - not "absolute"
AP
duration
APD
Cycle
length
CL
CL (increase AP freq.)
APD
refractory period
9
Silverthorn p.494
ECG - tells us about electrical conductance of heart, timing of electrical activity, HR.
* wave form amplitude
and direction are a result
of electrode placement
amplitude and direction
of wave form has
nothing to do with heart
SA node
depol.
atrial depol.
AV
HIS
purkinje
vent. depol.
vent. repol.
if there is a p wave and then a long period before the QRS then you know there is a problem with either the AV, HIS or purkinje fibres
upper graph is drawn in comparison with action potential (bottom graph)
most vulnerable to fibrillation
(most cells past refractory
period). * See notes Oct. 24th *
10
P
QRS
T
delay
delay categorized as prolonged
P-R interval (check previous
slide) should be < 0.25 sec
its not really a
block, its just
been a slight
delay
P
QRS T P
heart skips a beat
All QRS preceded by P but not
all P's followed by QRS.
something wrong with AV node
QRS
P
P P P P P P
QRS
QRS
P's happening -> 70-80 times/min
QRS's -> 15-40 times/min
purkinje fibres are the spontaneous depolarizers that has a rate of 15-40 times/min thus there is a complete block
at the AV node since nothing is going through
Complete block at
AV node P waves
independent of QRS
waves.
P interferes
with T
Needs a pacemaker!
11
Aortic
EDV
ESV
Mechanics
- pressure/volume relationships in ventricles
- pressure relative to atmospheric pressure, set atmospheric pressure to zero.
left vent.
left vent.
1.
1. Diastole - ventricle is relaxed
ventricle filling (catching at the
end of filling)
*
* atrial contraction
increase in volume, increase
in pressure
2.
2. Ventricle contraction - systole
mitral valve closes due to increased pressure
aortic valve not open.
b)
b) isovulumetric contraction
increases Pressure, no change in volume
aortic pr. > vent. pr.
3
3. vent. pr. > aortic pr.
aortic valve opens

4.
4. volume ejected
5.
5. vent. relaxation
6.
6. aortic valve closes (passively - aortic pr. >
vent. pr.)
7.
7. isovolumetric relaxation - decreasing pr., no
change in volume
8. mitral valve opens - vent. pr. < atrial pr.
8
9.
9. period of rapid filling
taking volume from left ventricle and ejecting it into the next compartment
End diastolic volume (EDV)
End systolic volume (ESV)
Stroke volume = EDV - ESV = 130mL - 50mL = 80mL
(every contraction, 80 mL is ejected)
Tend to leave a little volume in the chambers so that the chambers do not collapse on themselves.
blood pr. = systolic pressure/diastolic pressure
=120 mmHg(highest pressure in Aorta)/
80 mmHg (resting pressure of Aorta)
MAP = 100 mmHg
12
Mitral
valve
opens
Mitral
valve
closes
Atrial contraction
Berne and Levy p. 326.
period of rapid filling - ventricle in diastole
atrial contraction
systole - vent.
contraction
mitral valve closes &
aortic valve isn't open
isovolumetric
contraction
increase in pressure
with no change in volume
aortic valve
opens
volume ejected from heart
>container is getting smaller,
(contracting) hence more
pressure
ventricle relaxes
>diastole
aortic valve
closes
isovolumetric
relaxation
decrease in
pressure, no change
in vol.
mitral valve opens
0
25 mmHg
if we are looking at
the right ventricle
the graphs would be
exactly the same
except the scale
would only go up to
25 mmHg for the
right because it does
not have as much
pressure
to overcome
right ventricle
uses same volume
13
2. ESV
i) intrinsic regulation
80
130
Silverthorn p. 501
Berne and Levy p. 264
- increase strength of contraction -> decrease ESV -> increase SV -> increase in CO
-> regulation by a factor originating from within the tissue
A Frank -Starling law of the heart
normal
eject
80 ml
skeletal muscle
tension
length
in the heart we
live here
thus as we
increase volume,
we increase
stretch up to
something
optimal ->
increasing
output
we live here
"optimal"
optimal stretch for
maximum force
limited due to pericardium
only have to much space to fill
14
ii) nervous innervation (extrinsic)
- direct innervation to cardiac myocytes.
SNS NE
cardiac
myocytes
-adrenergic Rm
protein kinases phosphorylation oI:
Gs
AC cAMP
1. volt. dep. Ca
channels (L-type)
# channels that open per AP
trigger Ca
.. contractility
2. Ca
pumps on SR
activity relaxation time
speed oI contraction
regulation by factors originating outside the tissue
direct SNS innervation into the myocytes
Change two things:
force
time
Beta stim-> SNS
-Epi/NE
musc. chol. stim -> PNS
(next slide)
15
iii) hormonal control
SNS EPI/NE adrenal
glands
cardiac
myocytes
PNS ACh
cardiac
myocytes
muscarinic
cholinergic Rm
protein kinases phosphorylation oI:
Gi
AC cAMP
1. volt. dep. Ca
channels (L-type)
2. Ca
pumps on SR
-adrenergic
Rm
iv) paracrine endothelial cells line the heart
v) afterload
Endothelin -> ET, or ET2 Rm - IP3 - increase in Ca++ available for contraction
Nitric oxide -> increase or decrease in force (?)
- high after load -> decrease volume out per beat
- increase ESV, decrease SV, decrease CO
16
3. HR
i) neural control
PNS ACh SA node
(AV node)
K
permeability hyperpol.
spontaneous depol. rate HR
SNS NE SA node
(AV node)
Na
'leak rate
time to threshhold HR spontaneous depol. rate
ii) hormonal control
SNS EPI/NE adrenal glands SA node
(AV node)
(as a hormone)
CO = HR x SV
(-) increase HR (220-230 bpm) -> decrease duration of diastole -> decrease filling time -> decrease
pre-load or EDV-> decrease in Sv -> decrease CO {you can't pump what you don't have}
(-) increase HR -> increase CO -> increase afterload -> decrease SV of next heartbeat -> decrease CO
(+) increase HR -> increase contractility (staircase phenomenon) -> decrease ESV -> increase SV ->
increase CO
100
CO (%)
50 100 150 200 250
HR (bpm)
~ 180 - 200 bpm
(negative CO after this point)
Olympians have low resting heart rate ~ 40 - 50 bpm
- heart is stronger, ejecting more per beat
- higher PNS control from brain stem to
spontaneous depolarizer
17
Where is CO going? (leIt ventrical CO)
Heart
Brain
Liver
Kidney
Skeletal
muscle
skin
4
14
28
20
21
8
70
84
96
308
4
8
Q (Ilow)
CO ml/min/100g tissue)
AP = Aortic pressure
VP = venous pressure (~ 7 mmHg)
> MCFP
- the heart created P1
- the rest of the system must have a lower
pressure than P1 (otherwise, no movement!)
Q = P1 - P2 / R
P1
P2
cap
bed
aterioles
resistance
Q=P1-P2/R
veins
Cap
Cap
aterioles arterioles
veins
18
Media
Intima
Adventitia
Endothelial cells
Basement membrane
Elastin
Connective Tissue
Smooth Muscle Cells
Neurons
Neurons
Macrophages
From 'Basic Histology 8th ED
Junqueria, Carneiro, Kelley, pg 213
Blood Vessels
- have very different wall characteristics
- all have variations of these layers
Only capillaries have these two
layers
lumen (blood flow)
-primary SNS
primary SNS
Fibroblasts
-outer most layer
-fairly active area
- Nerve
> releases neurotransmitters at very specific areas on nerve
> no specific neuromuscular junction
> flood region with neurotransmitter
> system a little slower to activate (10's of ms)
-> compared to skeletal muscle that only
takes ms
19
Summary of the dimensions and composition of different levels of the vasculature
endothelial
cells yes yes yes yes yes yes yes
elastic 4 4 3 - - 3 3
tissue
smooth 2 4 4 - - 2 2
muscle
Iibrous 3 2 2 - 1 2 4
tissue
Endothelial cells line all vessels oI vascular system and chambers oI the heart.
1 a little, 4 alot
# 1 40 to 2.8x10
6
2.7x10
9
1x10
7
660,000 2
110,000 to 110
radius 12.5mm 2mm 15m 4m 10m 2.5mm 15mm
wall 2mm 1mm 6m 0.5m 1m 0.5mm 1.5mm
thickness
w/r 0.16 0.5 0.4 0.13 0.1 0.2 0.1
Aorta artery arteriole capillary venule veins vena cava
Dimensions
Composition
Aorta artery arteriole capillary venule veins vena cava
adds
rigidity
just endothelial cells
we don't know how the vessel wall has so many different compartments with different compositions
smaller diameter than a red blood cell
divergence
convergence
20
0
20
40
60
80
100
120
0 1000 2000 3000 4000 5000
Volume (ml)
P
r
e
s
s
u
r
e

(
m
m
H
g
)
Nature of wall determines the nature of the vessel
large artery (like aorta)
- tiny change in volume = huge change in pressure
- wall is rigid (does not expand like a water balloon)
stiff, rigid, no-compliant compartment
small changes in volume = large changes in pressure
large veins (storage)
-very compliant (elastic -
expands)
-large changes in volume =
small changes in pressure
21
1. Aortic/arterial compartment
Time (sec)
0.8
0
- transport vessels
- low volume, high pressure vessels
120
blood from heart - aorta
aortic valve
opens
aortic valve closes
systolic pressure
~120 mmHg
to prevent back
flow into left
ventricle.
Volume (blood)
is being pushed
forward to
other parts of
the body
volume leaves
compartment
diastolic pressure
~80 mmHg
ventricular
systole
ventricular
diastole
80
compartment is strictly transporting blood from heart to other parts of body
* dicrotic notch - true measure of the pressure-volume relationship when aortic valve closes
MAP ~ 100 mmHg
- Anything that alters CO (cardiac output) will alter
MAP
- If CO increases (increased volume into aorta) and
volume out of aorta is constant -> increase volume
in aorta, increase pressure in aorta -> increase
MAP
How do we change CO? - EDV, ESV, HR
i.e. increase SNS output to ventricular myocyte ->
increase contractility -> decrease ESV -> increase
SV -> increase CO -> increase MAP
aorta
heart CO volume
into aorta
arterioles
-represent volume
out of aorta
Q=flow
22
B&L page 442
Electron micrograph oI an arteriole in cross-section (inner diameter
40m) Irom cat ventricle.
iii) radius {R (inversely related to) 1/ r4
- control of vascular smooth muscle contractile state
lumen of
blood vessel
endothelial cell
nerves
ventricular
myocytes
-tissue cells
vascular smooth muscle
blood (hormones)
nerves
endothelial cells
tissue cells
adventitial layer cells
23
Regulation oI arteriolar radius
Blood Ilow
SNS VC SNS VDil
NE
ACh
Histamine, 5HT
Tissue Metabolism
CO
2
ADO NO K
NO
EDRF
EDHF
EDCF Endothelin
PGI
2
BK
Flow
Shear
EPI
NO
NO
NO
cGMP
cGMP
Mast cells
Vascular smooth muscle
Endothelial cell
Other
Rm Rm
Rm
Rm Rm Rm Rm
Rm Rm Rm Rm
INTIMA
MEDIA
ADVENTITIA
3. paracrine -> endothelial cells are a rich source of vasoactive compounds
- blood environment will stimulate endothelial cells
- blood flow (shear) will stimulate endothelial cells
4. endocrine
- SNS -> adrenal glands -> Epi/NE
- affects differ depending on Rm
populations
> alpha - constriction, beta - vasodilation
> A2 and ADH - very potent -
vasoconstriction
> ANP - vasodilation
lumen
2. autocrine
3. paracrine - vasoactive
compounds released from
surrounding tissue cells
> Working tissue will release products to
influence blood vessel diameter
- increase tissue metabolism, increase adenosine
production, vasodilation
- "metabolic vasodilators" -> increase CO2,
decrease O2, increase adenosine, increase K+,
increase Pi, increase H+, etc
1. neural
- all blood vessels innervated by
SNS except capillaries
- arteries > veins in terms of
impact of SNS
- not equally distributed in body
- vasoconstriction powerful ->
skin, gut, kidney
- less powerful in brain, skeletal
muscle
24
Capillaries
1. Site Ior exchange oI substrates and metabolites.
2. Important Ior cell survival each cell oI the body is approx.
20um Irom a capillary.
3. Important Ior adjusting blood volume in the short term.
A. LS can diIIuse directly through endothelial cell membranes.
B. NLS (ions, glucose, water, etc.) can pass through spaces
between the cells cleIt pores.
3. Adjusting blood volume.
1. Exchange oI substrates and metabolites mostly by diIIusion
What determines Iluid movement?
i) CFC capillary Iiltration coeIIicient
- describes Iluid permeability characteristics oI capillary bed.
- dependent on:
a) endothelial cell spacing (cleIt pore size)
b) surIace area oI capillaries
c) number oI open capillaries at any given time
- usually constant
(space between two cells)
different sizes of cleft pores depending on tissue
skeletal muscle ~ 6-7 nm
essential size of cleft pore develops size filter
H2O, glucose, urea can all pass through, but not plasma proteins (hemoglobin,
albumin, etc.)
-relatively constant but can
be changed (local histamine
flux)
flowing
25
ii) Pc capillary pressure
- hydrostatic pressure in the capillary exerted by blood
- principle Iorce in capillary Iiltration
pressure to move H2O from capillaries to ISS
mAP
resistance
arterioles
P1
Q=P1-P2/R
P2
CAP
P1
P2
venous pressure
MCFP = 7 mmHg
flow through it doesn't matter, what matters is whether or not flow out is equal to flow in
Pc (pressure in capillary) is therefore related to volume in cap. bed.
a) increase mAP -> increase vol. into cap bed -> increase vol. in cap bed = increase in Pc
b) increase Venous pr. -> decreasing vol. out of cap. bed (increase P2) -> increase vol. in
capillaries -> increase Pc
c) Vasocontstrict arterioles ( Resistance) -> decr. vol. into capillary bed -> decrease vol. in
capillary bed -> decrease Pc

Example Scenarios:
Pc = whole body average = 25 mmHg
skeletal muscle ~ 30 mmHg
kidney ~ 45 mmHg
26
iii) Pt interstitial space (ISS) hydrostatic pressure (tissue pressure)
- pressure exerted by Iluid in the ISS
- ranges Irom 5 to 0 to -6 mmHg (very loose tissues have negative hydrostatic
pressures - sucking pressure)
Avg ~ -3mmHg
Net Fluid mement due to hydrostatic pressures
bl. Q
Cap lumen Pc= 25mmHg
Pt= - 3mmHg
DeltaP = Pc - Pt
= 25 - (-3)
= 28 mmHg
(+1)
TWO DIFFERENT DRIVES FOR WATER HYDROSTATIC PRESSURE AND OSMOTIC PRESSURE
27
v) t colloid osmotic pressure in the tissue
- generated by proteins Iound in ISS
- varies among tissue average approx. 8 mmHg
iv) c colloid osmotic pressure in capillaries (oncotic pressure)
- generated by plasma proteins and electrolytes conIined to the
blood compartment
pressure to move fluid by osmosis
Therefore will be a drive for H2O movement, H2O moves to dilute (due to concentrated amount of
proteins which are unable to move)-> pressure (drive) will be to move H2O from ISS to caps.
pl. proteins = 20 mmHg
electrolytes (ions bound to pl. prot.) = 5-8mmHg
25-28 mmHg
pressure to move H2O from caps to ISS.
Net fluid movement due to osmotic drives
delta Pie = Pic - Pit
=25-8
= 17 mmHg from ISS to caps.
cap lumen
iss
pic = 25 mmHg
Pit = 8 mmHg
concentrated compartment of proteins in the blood, therefore huge drive of water into cap lumen
proteins also in ISS but not as strong as blood therefore more water will move into the blood
28
Lymphatics:
- picks up Iiltrate (and protein leak) and delivers it back to blood
compartment.
- closed ended network oI tubes that originate in the tissue
- highly permeable
- drains into vascular system near the right atria
What helps lymph Ilow?
bigger pore - proteins get through
- low pressure side
1. lymph vessels have one-way valves to get directional flow (Q)
> Q into lymph: Pt > Plymph
> if Pt < Plymph: back flow in lymphatics will close valves
Pt
Plymph
Pt>Plymph
smooth muscle
pacemaker cells
> start AP (spontaneous
depolarizers)
29
100
L
y
m
p
h

Q

(
)
2. Spontaneous vasomotion - larger collector vessels are wrapped in smooth muscle -> can contract
> pacemaker cells ?
> myogenic response (stretch) ?
3. Transmural Pressure (PT)
PL
Penvironement (tissue)
4. Pt -> Q = Pt - PL/R
Pt
no change in flow
increase Pt too high
-will decrease radius of vessels
(PT)
- decrease radius, increase
resistance, decrease flow
30
Cardiovascular mechanics
These data describe the mechanical interactions between the heart and blood vessels.
The model contains two pumps and a systemic and a pulmonary vascular bed. Each
vascular bed has an arterial and a venous compartment. The pressure in a given
compartment depends on the volume oI Iluid divided by the cross-sectional area oI the bed.
The volume is distributed so that pressure gradients result in steady-state Ilows which match
pumping rates. The pumping rates depend upon ventricular Iunction 1.0 being normal.
Cardiac output is a linear Iunction oI venous Iilling pressure to approximate the Starling
eIIect. Arterial pressure has a slight loading eIIect on the stroke volume. Vascular
resistance and conductances are not inIluenced by the pressure. The model used does not
consider neural or hormonal compensations.
All values are returned to control beIore starting the next challenge. All pressures (P) are
in mmHg. Cardiac output is in L/min. All volumes (V) are in L. The systemic capillary
pressure (Pc) was estimated by solving Pc(0.25PaPv)/1.25
Where Pa is the mean arterial pressure and Pv is the systemic venous pressure. 0.25 is an
estimate oI the ratio oI systemic venous resistance to systemic arteriolar resistance.
LV: 0
Syst
Pulm
RV: 0
P:74
V:.01.007
P:64
V:1.81.2
P:13 9
V:.05.04
P:75
V:4.73.3
CO: 0
P
c
: 8.25.8
Situations:
1. Ventricular Iunction oI both ventricles was set as low as possible (0.05 oI normal, trying to
take the pump out oI the system) in an attempt to estimate mean circulatory Iilling pressure.
A) The blood volume was decreased Irom 6.5 to 4.5 L
no regulation
Pressure = mmHG
Volume = L
pulmonary veins
systemic artery
pulmonary cap. bed.
systemic veins
pulmonary atery
systemic cap. bed
Arteries = low volumes, high pressure
systems
Veins = high volume, low pressure
systems
31
LV: 0
Syst
Pulm
RV: 0
P:5 6
V:0.008 0.008
P: 5 5
V:1.5
1.5
P: 11 11
V: 0.06 0.02
P: 6 6
V: 4.4 4.4
CO:0
P
c
: 7 7
LV: 0
Syst
Pulm
RV: 0
P:4 9
V:0.006 0.013
P: 3 8
V:1 2
P: 8 17
V: 0.03
0.07
P: 4 9
V: 4.4 3.0
CO:0
P
c
: 4.8
10.6
B) The systemic arterial compliance was decreased Irom 1.5 to 0.5.
C) The systemic venous compliance was decreased Irom 1.5 to 0.5.
-decrease elasicity
1.5
1. decreased volume, same
pressure
took elastic compartment and made it rigid
2
4.44
-change delta P/volume relationship of systemic veins
0.07
10.6
displaced 1.4L
1. Challenge:
- make systemic veins less compliant (decrease
volume, increase pressure)
32
LV: 0.3
Syst
Pulm
RV: 1.0
P:15 16
V:0.25 0.25
P: 5 10
V:1.5
3.0
P: 97 60
V: 0.38 0.24
P: 5 3
V: 3.6
2.2
CO:5.1
3.1
P
c
: 23
14.4
LV: 1.0
Syst
Pulm
RV: 0.3
P:15 6
V:0.23 0.09
P: 5 2
V:1.5
0.5
P: 97 45
V: 0.38
0.18
P: 5 7
V: 3.6 4.8
CO:5.1
2.1
P
c
: 23
14.6
2. With a blood volume oI 5.5 L:
A) Normal right ventricular Iunction and the leIt ventrical Iunction was decreased to 30.
B) Normal leIt ventricular Iunction and the right ventrical Iunction was decreased to 30.
Cap
mAP
decrease in mcFP
inc. vol. out of caps
decrease vol. in
therefore decrease Pc
decrease in MAP
decrease vol into caps
decrease vol. in
decrease Pc
2.1
0.18
19.6
1. Challenge
decrease CO
RH
(cardiac
output)
2
increase in vol & press.
decrease in vol & press.
4
0.5
less volume throughout
entire pulmonary system
decrease P1 - decrease Q into left vent.
decrease EDV, decrease SV and decrease
CO
5
3
less vol. less press. due to decreased CO
6
cap bed MAP
decrease MAP
decrease vol. into cap
decrease vol. in
decrease Pc
mcFP
increase MCFP
decrease vol. out of caps
increase vol in caps
increase Pc
- left heart failure
1. challenge: decreased CO on left
side
2. decreased volume, decreased
pressure (not receiving as much in
this compartment)
- less volume in system
circulation
-less flow through
systemic circulation
3. increase in volume, increase in pressure (not
taking as much from this compartment)
(increase P2)
increase in volume
decreased flow through
pulmonary system
5. drop in volume, drop
in pressure
VR= McFP - RAP/ R(V)
- decrease McFP
-decreased VR
-decrease CO of right
heart
-therefore decrease in
volume, decrease in pressure
4. right heart
-okay
33
3.A) Systemic resistance was i) decreased Irom 1.0 to 0.5
ii) increased Irom 1.0 to 1.5
LV: 1
Syst
Pulm
RV: 1
P:15.315.7
V:.023.024
P:5.14.9
V:1.521.48
P:9754
V:.39.22
P:5.15.4
V:3.63.8
CO:5.15.4
P
c
: 2315.1
i)
LV: 1
Syst
Pulm
RV: 1
P:15.314.8
V:.023.022
P:5.15.2
V:1.521.55
P:97135
V:.39.54
P:5.14.8
V:3.63.4
CO:5.14.8
P
c
: 2330.8
ii)
vasodilation
vasocontriction
1. Challenge -> vasoconstriction
2
Q=P1-P2/ R
increase in vol. press.
decrease in vol/press
3
decrease in mCFP
increase vol out of caps
increase vol out
decrease Pc
decreased VR (venous return)
= MCFP - RAP/Rvenous
decrease CO R.H.
4
5
increased afterload increase
CO
increase vol. due to decrease in CO
L.H. in this scenario this has greater
influence, but in a test we can decide
which has greater influence
decrease vol. due to decrease CO R.H.
therefore decrease vol. pulm system
cap
bed
MAP
increase MAP
increase vol. into caps
increase vol in caps
increase Pc
dcrease MCFP
increase vol. out of caps
increase vol. in caps
decrease Pc
increase resistance
decrease vol. into caps
decrease vol. in
decrease in Pc
19.2
24.8
34
LV: 1.0
Syst
Pulm
RV: 1.0
P:15 25
V:0.23 0.38
P: 5 5
V:1.5
1.5
P: 97 96
V: 0.39
0.38
P: 5 5
V: 3.6 3.6
CO:5.1
5.0
P
c
: 23 23
3. B) Pulmonary vascular resistance was doubled
1.5
5.0
0.38
1. Challenge
2.
3
displace ~ 150 mL of volume
due to the fact that R.H pumps
5.5L the pulm arteries are very elastic
not much changed due to such low
resistance in pulm. arterioles to begin
with. Low resistance because we have
to pump 5.5L across one capillary bed
Q = P1-P2/R
35
negative Ieedback
Negative Ieedback regulation
OVERRIDE
SENSOR
EFFECTOR
COORDINATING
CENTRE
MAP
36
Sensors:
1. High pressure baroreceptors:
i) carotid artery carotid sinus
ii) wall oI the aorta aortic arch
Projections Irom baroRc medulla (brain stem)
iI AP Irequency:
a) inhibit vasoconstricter centre and cardioaccellerator centre
b) stimulate cardiodecellerator centre
c) hypothalamic nuclei that control ADH-VP secretion
2 sensors
change in pressure (change in stretch)
(Ka-rah-tid)
MAP
its importance that we live on the steep part of the curve so that
small changes in pressure will make changes to the body
we live here
slowly adapting - over days
if high blood pressure, the body will aim to keep blood
pressure at this level, very difficult to bring down
not good for long term regulation
(increase MAP)
this must be connected to nodal cells of heart
this must be connected to smooth
muscle in arteries
cells of hypothalamus stimulate release of vasodepression
37
MAP HR (EDV ESV) x TPR
endocrine
SNS
PNS
aIterload
Treppe
Iilling
time
paracrine
endocrine
SNS
Ptrans
viscosity
length, # vessels
radius (arteriolar)
auto, para, endocrine
neural
autoregulation
preload
vol. in
VR
MCFP
blood volume
SNS
(venoconstriction)
Iluid Ilux
at tissues
(Pc, Pt, c, t)
MAP = CP x TPR
staircase
changing contractility of ventricle
care about this the most
vol. back to heart
Venous Return
kidney
most potent regulators:
1 hormonal/neuronal regulation
2 volume regulation
3 pressure (afterload)
most power
least power

Lecture 5 Blood Flow, Heart and Vascular System

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Lecture 5 Blood Flow, Heart and Vascular System

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5.

Regulation oI blood Ilow -

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