An understanding of the determinants of cardiac
output is essential to both medical specialists in their dealing with heart disease and hypertension,
and to surgical specialists who deal with shock states and the maintenance of adequate
circulation during surgical procedures. In this program, I’ll introduce you to some
fundamental yet often misunderstood concepts about the determinants of cardiac output by
examining this hydraulic model of the cardiovascular system. A model gives us a unique opportunity to directly
observe phenomena that we can measure only indirectly in the human body.
Any model is as potentially useful as its ability to replicate the body’s response to
identical stimuli. As you will see during the program, this model
will mimic physiologic responses very well because of a special component: The pump.
The pump is a homologue of the heart. Each of the two pumps has a ventricle, an
inlet and an outlet valve, and an atrium. The left pump is connected to a simulated
aorta, through which fluid flows to systemic arterioles and a distensible capillary bed,
which empties into venioles, a vena cava, and back to the right heart pump.
The pulmonary circuit has a pulmonary artery, arterioles, a compliant capillary bed, emptying
into simulated venioles and pulmonary veins, back to the left pump.
At this point, the systemic and pulmonary circuits cross, making this system a single
circuit with the two pumps in series, just like in the human cardiovascular system.
As previously stated, the most significant characteristic of the model – and the one
that allows it to reproduce cardiovascular phenomena – is the pump.
These pumps, unlike most, do not suck at their inlets to fill. Let’s compare this non-sucking
pump to one that does suck to fill. This is a standard roller pump commonly used
in cardiopulmonary bypass. The rollers compress the tubing to push fluid
forward. The tubing recoils to its original shape behind
the roller, thereby generating suction that refills the tubing with fluid.
Since the tubing is always full because of the suction, the output is determined by the
speed of the pump. Pump output is therefore equal to stroke rate
times stroke volume. That is, the speed of the pump times the volume of the fluid between
the rollers. This pump therefore not only moves the fluid
but determines the flow rate by virtue of pump speed.
External or systemic factors, such as increase in hydrostatic pressure generated by lifting
the fluid container above the level of the pump, do not alter the pump output. In contrast, this non-sucking pump has a ventricle
that is normally flat instead of round on cross-section.
After this ventricle is compressed, it does not rebound and suck as in the other pump.
It fills passively after being emptied. If I turn the pump on at a rate of 80 beats
per minute, you can see that there is no flow. Even if I increase the rate above 80 beats
a minute, and increase the strength of the driving force of the impellers by hand-cranking
the pump, there is no output. The pressure in the system is below pump level.
Since the pump cannot suck to fill, no fluid runs into the ventricles, so there can be
no output. It is only when the bottle is raised above
pump level that flow occurs. Therefore, flow in a non-sucking pump is controlled
by the amount of pressure in the system. Increasing the pressure increases the flow. Decreasing
the pressure decreases the flow. So the output of a sucking pump is controlled
by pump factors, whereas the output of a non-sucking pump is controlled by systemic factors.
Now let’s go back to the model and see what this non-sucking pump does in that system. With ventricular capacity of 100 CCs, these
pumps are capable of pumping 8 liters a minute at the current rate of 80 beats a minute,
yet no circulation is occurring. Increasing the pump rate and strength of contraction
by hand-cranking also effects no flow. But remember, we just observed that non-sucking
pumps cannot pump without there being pressure in the system.
You can see that the compliant beds are flaccid, so perhaps there is insufficient pressure
in the system. A U-tube connected to the arteries allows
me to confirm that the pressure in the system is below pump level, this black line being
equal to the pump level, and the green fluid equal to the system pressure.
The pressure is low because of the low volume of fluid in the system.
The model is in hypovolemic shock. Just as in the human with inadequate pressure
in the cardiovascular system from low fluid volume, increasing the heart rate or strength
of contraction does not improve cardiac output. I can increase the fluid volume in this system
through this intravascular line. I’ll add 250 CCs of fluid and see if that’s
enough to promote flow. As you can see, this amount of fluid did not
increase the flow. And correspondingly, that amount of fluid
did not fill this flaccid system to a level above the pump level.
Therefore, if that was an inadequate amount, we’ll add 250 CCs more and see if that will
start the flow. That did cause some flow. So we now have one-and-a-half liters a minute
flow. Correspondingly, the pressure within the system
is now above pump level. If a small amount of fluid caused that amount
of flow, let’s see what an additional 250 CCs will do. This additional 250 CCs caused a marked difference
in flow. As you can see, we now have four liters a
minute. With this increased flow, we also observe
that the pressure in the system is now much higher than it was before.
We have now seen a significant increase in flow.
So what we have seen is that increase in fluid volume in the vascular system increases the
output. Although the increase was not linear, since
the 250 CCs I put in last changed the flow rate much more than the 500 CCs that was put
in during the first two transfusions.