Venous Function
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Function of the venous system
Definitions
Mean circulatory filling pressure
Two compartment model
Dynamic methods of assessing volume status
Main Points
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The venous system functions to maintain filling
of the heart.
The main driving force for venous return is
MCFP.
The splanchnic vascular bed is the reservoir for
venous return.
CVP is useless for volume status unless it is at
the extremes. Dynamic measures for fluid
responsiveness is informative.
Definitions
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Venous capacity
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Venous capacitance
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Blood volume contained in a vein at a specific
distending pressure.
The relationship between contained volume and
distending pressure in a vein.
Venous compliance
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Change in volume of blood associated with a change
in distending pressure.
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Unstressed volume
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Stressed volume
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A volume of blood in a vein at a transmural pressure
= 0.
The volume of blood in a vein above a zero
transmural pressure.
The sum of stressed and unstressed volume is
the total volume of the system.
Volume
Capacity
V1
Stressed
Vu
Unstressed
0
P1
Pressure
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Stressed volume determines the MCFP and
affects venous return and cardiac output.
Unstressed volume is a reserve that can be
mobilized when needed.
It is helpful to think of the volumes as a tub.
Arterial flow
Stressed volume
Venous
resistance
CVP
Unstressed volume
Function of the Venous System
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To return blood to the heart and serve as capacitance to
maintain filling.
Veins contain 70% of the blood volume and are 30
times more compliant than arteries.
Thus they are a reservoir that can easily and
immediately change volume to maintain filling pressure
in the right heart.
The splanchnic veins contain 20% of the total blood
volume.
These are heavily populated with alpha1 and 2
receptors.
Mean Circulatory Filling Pressure
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If you stop the heart, flow through the
capillaries continues for a brief time as the low
compliant/high pressure arteries decompress
into the high compliant/low pressure veins.
Once the pressure equalizes throughout the
entire system, the MCFP can be measured.
Mean Circulatory Filling Pressure
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Flow to the heart is determined by the gradient
between the central and peripheral venous
pressure.
The driving force for venous return (VR) is:
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(MCFP-CVP)/Venous resistance
CO is determined entirely by VR as the heart
can’t pump more blood than it receives.
VR can go up by increasing MCFP or decreasing
CVP (resistance is relatively small).
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MCFP is determined by stressed volume and is
normally around 7 – 12 mmHg while CVP is 2-3
mmHg.
So why does an increase in CVP (by bolus) increase CO
in a normal heart?
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The sudden increase in preload would increase SV
temporarily but fall once the volume redistributes to the
venous system.
The stressed volume increases and increases the MCFP
greater than CVP.
The pressure gradient is thus increased and so VR goes up.
Increased VR = increased CO.
Volume
Effect of Fluid Bolus
V1
Stressed
Vu
Unstressed
0
P1
Pressure
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While venous return can be increased by a fluid
bolus which increases stressed volume which
increases MCFP (think increasing the amount of
fluid in the tub), it can also be increased by
venoconstriction.
This decreases venous capacity (not compliance)
which in turn decreases unstressed volume to
the benefit of the stressed volume.
Think moving the outlet hole down.
Arterial flow
Stressed volume
Venous
resistance
CVP
Unstressed volume
Volume
Effect of Venoconstriction
V1
Stressed
Vu
Unstressed
0
P1
Pressure
Two Compartment Model of the
Venous System
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It is helpful to think of the venous system as two
connected compartments.
The splanchnic system is very compliant and slow flow
while the non-splanchnic system is noncompliant and
fast flow.
An increase in resistance in the arteries feeding the
splanchnic veins decreases flow and shifts blood into
the system circulation.
A decrease in resistance causes blood pooling in the
veins.
Dynamic methods of assessing
volume status
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I think it goes without saying that the CVP is a
less useful measure of volume status (fluid
responsiveness) because of the many factors that
influence it.
Abdominal pressure
 Pump function
 Pericardial pressure
 Thoracic pressure
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Dynamic methods are much more useful
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On PPV, inspiration causes increased LVSV because of
compression of pulmonary veins, decreased afterload
and decreased RV volume from pulmonary
compression.
The increased thoracic pressure at end inflation
decreases the gradient for venous return at in a few
beats causes a decreased LVSV.
This variation is exacerbated by hypovolemia.
Variation greater than 12 mmHg better reflects preload
inadequacy than CVP.
How does that work?
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Hypovolemia causes a fall in the total volume in
the system.
The fall in capacity is partly compensated by an
immediate reflex venoconstriction.
MCFP initially is preserved to maintain venous
return.
Volume
Venoconstriction in Response to a Fall in Total Volume
V1
Stressed
Vu
Unstressed
0
P1
Pressure
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Once the unstressed volume is completely
mobilized into the stressed volume, further fall
in the total body volume results in a fall in
MCFP and therefore, venous return.
Volume
Unstressed Volume Exhausted, Further Fall in Volume
V1
V2
Stressed
0
P2
P1
Pressure
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Recall that venous return is:
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(MCFP-CVP)/Venous resistance
When the MCFP falls and the venous resistance rises,
the normal variation in CVP causes a greater variation
in venous return which translate into a greater variation
in cardiac output/blood pressure.
Hence why dynamic changes are more reflective of
volume status.
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CVP normally varies and subject to external influences.
Dynamic changes allows us a look into the status of the
stressed and unstressed volumes.
Main Points



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The venous system functions to maintain filling
of the heart.
The main driving force for venous return is
MCFP.
The splanchnic vascular bed is the reservoir for
venous return.
CVP is useless for volume status unless it is at
the extremes. Dynamic measures for fluid
responsiveness is informative.





Function of the venous system
Definitions
Mean circulatory filling pressure
Two compartment model
Dynamic methods of assessing volume status