Control of MAP
1. Short-term (seconds) - baroreceptors
CV 6
•Control of MAP
•Microcirculation
•Problem solving
•Mid term tests
•
Neural control via SNS, PNS
2. Intermediate (minutes)
•
Hormonal, esp SNS→Epi from adrenal
medulla and ADH regulation of blood
volume
3. Long-term (hours, days)
•
Blood volume regulation by kidney (ADH)
Control of MAP
Sensors
1. Carotid sinus
baroreceptor
2. Aortic arch
baroreceptor
3. Atrial stretch
Baroreceptors
# Action potentials
from receptor
50
80
MAP
150
1
Baroreceptors
Baroreceptors
accommodate to chronic high MAP
↑MAP → ↑AP from receptors → ↓SNS, ↑PNS
↓MAP → ↓ AP from receptors → ↑SNS, ↓PNS
# Action potentials
from receptor
With chronically high MAP
(2 days), receptors adapt
Processing in higher brain centers
In short term, baroreceptors can respond to changes in MAP
The end effect is to try to maintain MAP near normal
50
80
MAP
150
Increase in MAP leads to
increase receptor activity
Atrial Stretch receptors
• If more blood returns to atria, walls are stretched
• Leads to increase heart rate
• Arial Stretch receptors also regulate
ADH/vasopressin release from pituitary
– Bainbridge Reflex
• Helps to clear blood from venous side
↑ Vol in atria → ↑ stretch → ↓ADH
→ vasodilation & increase water loss from kidney
(decrease blood volume)
HR
volume
2
Summary of neural reflexes
Baroreceptors and atrial stretch have
opposing effects on HR but similar effect
on vasodilation
They are sensitive to changes in different
compartments:
Baroreceptors → arterial side
Atrial Stretch → venous side
• Long-Term MAP regulation
– Kidney
– Relationship between blood volume & MAP
↑MAP
↑ blood volume
↑water and Na+ loss from kidney
↑ Venous return
↓ blood volume
↑ Cardiac output
↓ venous return
↑ MAP
↓ cardiac output
↑water and Na+ loss from kidney
↓ MAP
↓ blood volume
Microcirculation
capillaries & lymph
Capillaries
• Most cells within 100 μm of a capillary
– Short diffusion distance
• Each capillary a few mm long, 5 μm
diameter (hair 100 μm)
3
Transport between capillary
and interstitial fluid
98% of exchange by diffusion
→ concentration gradients & permeability
• Lipid-soluble pass through endothelial cell
• Non-soluble through water-filled channels
Plasma
– Intracellular cleft & vesicle channels
• Not very permeable to protein
RBC
– Some endo- and exocytosis for proteins
Capillary endothelium
Transcapillary gradient
• Between plasma and interstitial fluid
CO2
least
brain
leakiness
CO2
liver
No intracellular clefts
huge intracellular clefts
Only carrier mediated-transport
Very permeable (even proteins)
Blood-brain barrier
CO2
most
cell
RBC
O2
glucose
O2
glut
glucose
4
Transport between capillary
and interstitial fluid
• Bulk flow determined by:
1. Pressure – capillary vs interstitial
2. Osmosis – plasma vs interstitial
Bulk Fluid Flow
remaining 2% of exchange
Capillary
Pressure
(PC)
Extracellular Fluid
filtration
Plasma
absorption
Total Vol =10L
Net Filtration Pressure(NFP) = (PC-PIF) – (πP- πIF)
Interstitial fluid can supply or receive fluid from plasma
• PC at arteriole end of capillary > PC at
venule end
• All others remain constant
venule end
Arterial end
(PC = 35)
(πP =28)
Osmotic Force
Interstitial Fluid
Protein
(πIF)
Interstitial Fluid
Pressure
(PIF)
Interstitial Fluid
Total Vol = 5L
Osmotic Force
Plasma Protein
(πP)
(πP =28)
No fluid movement
Pressure
(mm Hg)
10
Filtration
Fluid out
(PC = 15)
Δπ
0
(PIF=0)
(πIF =3)
NFP = (35-0) – (28 - 3)
= 10 mm Hg
Filtration (fluid out)
(πIF =3)
(PIF=0)
NFP = (15-0) – (28 - 3)
= -10 mmHg
Absorption (fluid in)
Absorption
Fluid in
-10
Arteriole
end
ΔP
Venule
end
5
The main factor influencing Pc is
volume in capillary
↑ volume ↑ Pc
Arterial side:
vasoconstriction ↓ flow into
capillary ∴ ↓ volume, ↓ Pc
vasodilation ↑flow into capillary
∴ ↑volume, ↑ Pc
Venous side:
venoconstriction ↓ flow out of
capillary ∴ ↑ volume, ↑ Pc
venodilation ↑flow out of capillary
∴ ↓volume, ↓ Pc
• Ratio Reabsorption / Filtration = 0.85
• Remaining 15% of fluid is picked up by
lymphatic system
Pc
• When, excess interstitial fluid accumulates
– edema
Factors affecting fluid movement
from capillary
1. Vasodilation of arterioles → ↑ blood vol
in capillary → ↑ Pc → ↑ filtration
2. Vasoconstriction of arterioles → ↓ blood
vol in capillary → ↓ Pc → ↓ filtration
3. ↓ plasma volume → ↑ πp → ↑ reabsorp
1. Arteriole vasodilation
More fluid out
Pressure
(mm Hg)
10
Δπ
0
-10
Filtration
Fluid out
Arteriole
end
ΔP
Absorption
Fluid in
Venule
end
6
2. Arteriole vasoconstriction
3. ↓plasma volume
less fluid out
less fluid out
Δπ
Pressure
(mm Hg)
Filtration
Fluid out
Arteriole
end
Absorption
Fluid in
Δπ
Pressure
(mm Hg)
Absorption
Fluid in
Filtration
Fluid out
ΔP
Arteriole
end
Venule
end
ΔP
Venule
end
1. Lymphatic system
•
•
gathers excess fluid and protein
delivers it back to the CV system
2. Important determinant of PIF & πIF
3. Slow ~2 L / day (compare to CO=5 L/min)
πc
Pc
PIF Protein & fluid
πIF
lymph
7
• Pc too high, or [protein]plasma too low, drives
fluid into interstitial space
• If lymph drainage blocked, then protein
accumulates in interstitial space,
• Elephantiasis
– Caused by a small parasitic
nematode (Filaria)
– Endemic to tropical regions
of Asia, Africa, and South
America
– Infection by transfer of
larvae from mosquitoes
– Larvae enter into lymphatic
vessels and block them
– ↑ πIF, draws fluid into IF space
πc
Pc
If lymph drainage disrupted,
↑ πIF →↑ PIF
PIF Protein & fluid
πIF
lymph
Aortic pressure
Bainbridge reflex
CV Summary & Problem Solving
1.
2.
3.
4.
5.
6.
Pressure ∝ (volume, compliance)
CO=HR(EDV-ESV)
Q=(P1-P2)/Resist R∝(η,L,1/r4)
MAP=CO x TPR
CO = VR
NFP = (PC-PIF) – (πP- πIF)
viscosity
MAP = HR x (EDV-ESV) x TPR
VR
Venous
pressure
SNS
radius
PNS
Blood volume
Muscle pumps
Respiration pump
Hormones
i.e. Epi
autoregulation
Metabolic / local
Hormones
i.e. AngII, ADH, ANP
8
Problem Solving:
1. What is the initial challenge?
2. What receptors respond and what
sequence?
3. What reflexes occur?
4. What is the final outcome?
Question:
What is the physiological response to intravenous infusion of 3L iso-osmotic saline?
1. ↑ BV on venous side, ↑ VR
2. Recruit atrial stretch receptors
2. Why does a decrease in total peripheral
resistance increase cardiac output? (direct
not reflexes)
↑ HR
↓ ADH → ↑ water loss from kidney
-
-
-
vasodilation → ↑ Pc → ↑ filtration
→ ↓πc → ↑ filtration
3. ↑ VR → ↑ SV (frank-starling) →↑ CO → ↑ MAP
4. Recruit baroreceptors
↓ SNS, ↑ PNS
-
-
-
CO
VR
(l/min)
RAP
→ vasodilation & ↓ TPR
CO=VR=HR(EDV-ESV), no change in Psf
→ ↓ venous tone → ↓ VR
Decreased TPR, lead to increase VR.
Increase VR, lead to increase EDV
Increase EDV lead to increase SV (frank-starling)
Increase SV lead to increase CO
→ ↓ HR → ↓CO
→ ↓ contractility → ↓CO
5. Overall, ↓ BV and ↓CO, ↓TPR would restore
system towards normal
Since CO=VR, CO increases
9
3. Why does damage to the right ventricle lead to
fluid accumulation in the tissue?
↓ right ventricle function, ↑Central Venous
Pressure, leads to ↓VR
Leads to increase blood volume in veins
Leads to ↑Pvein, leads to↑Pcapillary
Since NFP=(Pc-PIF) – (πP- πIF)
↑Pc will lead to ↑ΔP, increase hydrostatic pressure
driving fluid out of capillary
10