Venous return in CC and shock. Pathophys. Funk et al. 2013. CC med Flashcards
What percentage of blood volume do veins contain compared to arteries
- 70% of blood volumes in veins
- 18% of blood volumes in arteries
What percentage of blood volume does the venous circulation of the splanchnic bed hold?
20-33%
Describe the Hagen-Poiseuille’s law
The Hagen-Poiseuille’s law describes how fluid flow through a system depends on the pressure gradient between points and the resistance of the system
i.e., pressure difference of vascular structures and vascular resistance
How can you modify the Hagen-Poiseuille’s law to describe cardiac output?
cardiac output is the flow and MAP is the starting pressure point (P1) and RA pressure is the end pressure point (P2)
systemic vascular resistance is the resistance to flow through the circuit
Explain the modification of Hagen-Poiseuille’s law to describe venous return and how does this put the arterial circulation into perspective?
The venous return (i.e. flow) is determined by the upstream pressure of the venous circulation/mean systemic pressure (Pms) (i.e., P1) and the RA pressure (P2), the venous vascular resistance is R
The arterial circulation is not included in this calculation and implies that the aerterial pressure is unrelated to VR, other than maintaining to volume of the venous reservoir
Describe the calculation for vascular resistance
Resistance is calculation is
- directly proportional to the viscosity of blood, the length of the vessel
- indirectly proportional to the radius of the vessel
When assessing the calculation for vascular resistance, in what clinical settings does viscosity matter?
after administration of large amounts of low-viscosity fluids, i.e., hemodilution, the contribution of viscosity of vascular resistance may become more significant
How can alterations in cardiac function affect venous return?
decreased cardiac function may increase RA pressure, and therefore decrease the driving pressure/pressure gradient between venous circulation and RA for venous return
What is the normal pressure in venules compared to the RA?
8-12 mm Hg in the venules and 1-2 in the RA/vena cava
What calculation describes mean systemic pressure Pms?
the mean systemic pressure can be calculated with the stressed blood volume over the compliance of the venous reservoir (i.e., venosu vessels)
stressed blood volume = total blood volume - unstressed blood volume
Explain stressed and unstressed blood volume
unstressed blood volume is the volume of blood required to fill the circulatory system to capacity without an increase in transmural pressure
stressed blood volume is the volume of blood added on top of the unstressed blood volume to achieve the vascular transmural pressure
According to Pms = (Vt - V0)/C how can Pms be altered
Pms may be altered through 2 mechanisms:
- change in total blood volume
- change in the proportion of stressed and unstressed blood volume
in this model C (vessel compliance) is viewed as an aggregrate static mechanical proprty of the vessel wall
What may change the proportion of unstressed blood volume to stressed blood volume
- alteration in autonomic tone
- catecholamines
- administration of exogenous vasoactive substances
in this model C (vessel compliance) is viewed as an aggregrate static mechanical proprty of the vessel wall
What percentage of the human blood volume is normally stressed volume?
20-30%
What is the normal Pms in people?
8-10 mm Hg
When assessing reservoir volume and vascular resistance how do venules and the vena cavas compare?
venules contribute little to venous vascular resistance and serve mainly as a blood reservoir
the large veins account for the majority of venous vascular resistance and make a relatively small contribution to volume
Explain how vasopressors can have increasing as well as decreasing effects on venous return.
vasopressors will increase the proportion of stressed blood volume, which will increase Pms and therefore increse the driving pressure for venous return
vasopressors may also increase venous vascular resistance by decreasing the radius of the vena cava and other large veins, having a negative impact on venous return
describe the time constant of venous blood flow through vascular beds and how this affects vascular resistance
the time constants describes the difference between longer vascular beds (e.g., skin) with slow blood flow and shorter vascular beds (e.g., renal) with fast blood flow.
the time constant is determined by the volume in the vascular bed divided by the flow through the bed
This way blood flowing through vascular beds can be divided into fast flow and slow flow beds.
distributing more blood from slow flow to fast flow vascular beds will decreased vascular resistance and increase venous return
Explain how venous return plateaus during inspiration (i.e., when PRA becomes 0 mm Hg)
normally the upstream pressure for venous return (VR) is Pms and the downstream pressure is PRA
during inspiration the PPl (pleural pressure) becomes negative → transmits to PRA which then also decreases and falls below Patm
Patm then becomes the downstream pressure for VR
large vessels collapse when entering the thorax and act as starling resistors
→ blood flow ceases
→ pressure in large intrathoracic vessels rises → large vessels in thorax open up again → flow is reestablished
⇒ VR will plateau when PRA is 0 mm Hg (equal to atmospheric pressure)
Explain the graph
The venous return on the y axis the PRA on the x axis
when PRA reaches 0 mm Hg (=atmospheric pressure) the VR plateaus. The VR is zero when PRA equals Pms
The angle of the slope describes venous resistance
Explain how changes in Pms will affect the venous return curve
An increase in Pms will increase venous return and a decrease will decrease VR, both without changing the angle of the slope (because resistance is not affected)
the change in Pms will change the PRA at which VR is zero (where PRA and Pms are the same)
Explain how changes in resistance will affect the venous return curve
changes in resistance will not change the point at which VR becomes zero (Pms equals PRV) but will change the angle of the slope
increased resistance will decrease VR and the slope becomes more shallow
decreased resistance will increase VR and the slope becomes steeper
Explain what may causes these changes in the Starling cardiac function curve
increased contractility or decreased afterload will elevate the cardiac function curve
decreased contractiltiy of increased afterload will lower the cardiac function curve
isolate diastolic dysfunction or decrease in cardiac compliance will shift the curve to the right
What is the Anrep effect?
homeometric autoregulation
increases of the RV contractility as a response to increases in RV afterload
Explain these superimposed graphs
at steady state venous return and CO must be equal
both the VR and cardiac function curve use the RA pressure as the x axis constant and can therefore be superimposed
where the curves cross each other describes the common CO/VR
Explain the different steps in CO/VR changes from whole blood or crystalloid boluses on this graph.
when administering whole blood → does not change R because same viscosity but will increase Pms through increase in total blood volume and stressed blood volume
→ will shift the VR curve to the right and up → increased VR (B)
→ the VR curve will then intersect at a higher point of CO with the cardiac function curve
when administering crystalloids → leads to hemodilution and resistance decreases → will increse VR and make the slope of VR curve steeper (C)
→ decreased viscosity will also reduce the afterload → cardiac function curve is elevated (D)
With the graph below describe effects of pure vasopressors on CO and VR
pure vasopressors (e.g., phenylephrine, vasopressine) will increase vascular resistance → will reduce VR and make VR slope more shallow (B)
→ vasoconstriction will increase the stressed to unstressed blood volume and therefore increase Pms → will then slightly increase VR and move abscissa to the right (C)
vasoconstriction of the arterial system will increase afterload and therefore lower the CO curve (D)
the net effect of pure vasopressors will be decreased VR and CO, eventhough RA pressure increases, highlighting how e.g., cental venous pressure can falsely indicate CO and volume responsiveness in patients
With the graph below describe the effects of inodilators on the CO and VR curves
administration of inodilators (e.g., dobutamine, milrinone)
→ venodilation → decreased venous resistance → steeper VR curve with increased VR (B) slope becomes steeper
→ venodilation also reduces the stressed blood volume to unstressed blood volume ration which will decrease Pms and somewhat offset the increase in VR (C) abscissa moves to the left
→ arterial vasodilation and cardiac inotropic effect (increased contractility) will elevate the cardiac function curve (D)
→ in summary increase in VR and CO with a decrease in PRA
With the graph below describe how vasopressors with inotropic activity affect the VR and CO curves
When adminsitering inotropic vasopressors (e.g., dopamine, norepinephrine) the venous vascular resistance increases → making the VR curve more shallow and reducing VR (B)
vasoconstriction will increase the stressed to unstressed blood volume and therefore increase Pms which will then elevate the VR curve and shift abscissa to the right (C)
the arterial vasoconstriction (increased afterload) will partially offset the increased CO from increased contractility → the elevation of the cardiac function curve is not as prominent as from inodilators (D)
in summary inotropic vasopressors will incrase VR and CO but not as pronounced as from inodilators and the PRA is almost unchanged due to counterbalancing effects
