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Cardio # 96
Mon 02/04/03 10am
Dr. M. Smith
Bryan Massey
Proscribe Samera Kasim
Page 1 of 3
Venous Return and Cardiac Output
I. Coupling of the heart and Circulation
a. Cardiac function curve
i. This was introduced by Dr. Downey
ii. CO v. Preload curve (starling curve)
b. Venous Return curve
i. Aka vascular function curve
ii. 3 things effect it:
1. RAP (right atrial pressure)
a. Related to preload
b. Defines the curve
2. Mean circulatory filling pressure (MCFP)
3. systemic vascular resistance
a. together, #2 and 3 alter the form of the curve
II. Vascular function curve
a. Venous return v. Venous pressure
i. Venous pressure is the same as RAP
b. Increasing RAP results in a decr venous return
c. Pressure gradient is the key
d. As RAP continues to increase, there is less blood flow through the heart
and thus less flow through the system. As a result, there is less flow
returning to the heart.
e. Negative values for RAP creates a suction-like environment that
counterbalances the tendency for veins with low pressure to collapse.
a. “the equilibrium pressure which prevails in the circulatory system in the
absence of blood flow (Q).” -levy
i. note, there’s a really good explanation of this in the book that
corresponds with fig 29-2, p460. it was recommended that you
look at the figure.
b. Explanation of the chart:
i. The pressure gradient between Pv (venous pressure) and Pa
(arterial Pressure) determines Q.
ii. At t=0, the heart is functioning properly and Q is normal at
5L/min. pressures are also normal
iii. At t = 5, Q has decreased because of fibrillations or cardiac arrest;
there is a resultant change in the Pa and Pv.
1. Pv increases because blood is getting “backed up” since it’s
not being pumped out
2. Pa is decreasing because it’s not getting much blood
pumped out of the heart.
Cardio # 96
Mon 02/04/03 10am
Dr. M. Smith
Bryan Massey
Proscribe Samera Kasim
Page 2 of 3
iv. At t = 10, Pa and Pv have equilibrated; there is no longer a
driving force (pressure gradient) for venous return so Q = 0
1. this is the mean circulatory filling pressure
c. What effects MCFP? – 2 things…
i. Blood volume (graph)
1. Transfusion (added vascular volume) OR venoconstriction
results in increase venous return and increases the MCFP
2. Hemmorrhage or venodilation results in decr venous return
and decreases the MCFP value
3. REMEMBER that venous return (or the right atrial
pressure) must = cardiac output.
ii. Sympathetic activation in the form of venoconstriction OR
1. this is where veins and arteries are different. Most
sympathetic nerves go to the arterioles on the arterial side
of the system because they’re the big resistors (as explained
later this afternoon by Dr. Downey)
2. there is little sympathetic effect on lg arteries, such as the
3. venous innervation is diffuse and occurs across the entire
vessel, thus venoconstriction causes a generalized
constriction, resulting in “stiffness” and decrease
compliance of the vessel.
4. veins are able to equilibrate with arteries because they are
very compliant
IV. Vascular compliance curves
a. What happens to compliance at MCFP?
b. Well, as it was mentioned above, the venous volume increases until it
reaches a pressure of 7 and the arterial vol decreases until it reaches a
pressure of 7.
c. Veins become more distended with incr volume
d. It is very important to note that the change arterial volume is VERY
SLIGHT. Look at the graph and see how shallow the slope is.
V. Arterial compliance curve
a. Reiterating what was mentioned above, if you stop Q, the Vascular
volume of the arteries will decrease until they reach a pressure of 7
mmHg, wherein they will have equilibrated with the Pv.
b. Clinically, we increase the blood volume (or vascular volume) in
hypotensive pts.
i. Note, the fluid does not have to be blood; it could be plasma, etc.
VI. Vascular function curve
Cardio # 96
Mon 02/04/03 10am
Dr. M. Smith
Bryan Massey
Proscribe Samera Kasim
Page 3 of 3
a. Demonstrates the effect of systemic vascular resistance
i. Ex: An increase in R decr Q, resulting in decr Venous Return and
decr CO (this is all a chain of events…)
ii. Homeostasis occurs upon vasoconstriction
b. Graph (slide #11) – decrease vascular R (vasodilation) or incr vascular R
(vasoconstriction) does not change MCFP
c. At the arterial level, vasoconstriction slows Q, thus slows venous return
d. Stated another way, in the presence of vascular resistance, Q is altered
(decr) in able to maintain Cardiac Output.
VII. Coupling of Cardiac and Vascular Function
a. This is putting together 2 graphs that we should definitely be able to
recognize and understand.
b. Don’t make superimposing these graphs too complex. They no longer
make this too elaborate on the boards.
c. The point where the 2 curves intersect is the value for normal CO and
venous return. (because of course you know they’re equal at ~5L/min)
d. In the event of increase contractility,
i. cardiac function improves and the curve shift upward
ii. CO, SV, and Venous return increase while the ESV, EDV and
Preload decrease
1. remember this is because with constant heart rate and flow,
there will be less blood left in the ventricles after systole.
2. if the same amount of blood is coming into the ventricles,
but they’re emptier than before, then EDV also decr
iii. venous return increases to match CO.
e. In the event of a change in blood volume,
i. This assumes no change in contractility
ii. A hemorrhage (dotted line) would result in decr volume.
iii. This pretty much causes everything else to fall too:
1. MCFP, pressure gradient, venous return, preload, and
cardiac output would decrease
2. again, CO decreases because it matches Venous return.