So we know that one factor that determines
pressure in the system, and thus determines flow, is fluid volume. The pressure in any
hydraulic system is a product of volume and system compliance. So let’s look at the compliance
of this system. Compliance of the beds can be decreased by
contracting the muscles around the beds, thereby decreasing distensibility.
If you will notice, look at the manometer and see as I press on the beds how the pressure
increases. I’ll turn on the pump now and see if this
increase in pressure does increase the flow. As I press on the beds, you can see the increase
in flow on the flow meter. A corollary in human physiology is seen when
vasopressors increase cardiac output by decreasing vascular compliance, and when spinal anesthesia
and vasorelaxers decrease cardiac output by increasing vascular compliance.
So one determinant of output that we have observed thus far is the pressure in the vascular
system that forces fluid into the non-sucking heart and which has two components: the fluid
in the system and compliance. This pressure, which is the result of blood
volume and vascular compliance, is called mean vascular pressure, and was first described
by Weber in 1863. “Mean vascular pressure” is perhaps an unfamiliar
term to you. The mean vascular pressure is the pressure
in the vascular system with the heart stopped, after pressures have equilibrated between
the arteries, capillaries, and veins. Mean vascular pressure is normally between
16 and 18 millimeters of mercury above mid-heart level, but has been measured up to 20 to 30
millimeters in high output states, and as low as 6 to 8 millimeters of mercury in shock
states. Yet we can again confirm that with a pressure
sufficient to cause flow, an increase in rate and strength of contraction does not increase
the output. A corollary in human physiology is seen when
digitalis or an increase in pacemaker rate may not change cardiac output when there is
no myocardial energy failure. I’ll come back to this concept of energy failure in a few
minutes. So we have determined a factor that can cause
flow to increase. However, there may be other factors that can
reduce flow, even in the presence of a positive mean vascular pressure.
The most obvious candidate is resistance. Certainly a tube clamp placed partially across
a vessel will add considerable resistance to flow. Let’s see what effect such resistance
does have on pump output. Without the resistance, the pressure on the
arterial side is very low, being 80 over 20. The flow rate is now four-and-one-half liters
per minute. Now let’s see what adding a significant resistance
will do. The pressure is now 220 over 100, certainly
a significant resistance. Yet the flow remains four-and-a-half liters
per minute. The pump is strong enough to just force the
fluid right on by the resistance point. So the flow stays at four liters a minute, unchanged.
Clinically, we see a similar phenomenon with aortic stenosis, arteriolar hypertension,
and coarctation of the aorta. People with such problems still have normal cardiac output
as long as their heart is strong enough to eject its contents.
But let’s see what happens if we add a similar resistance to the inlet of the pump. Obviously a dramatic decrease in output.
But why does the resistance at the inlet of the pump slow pump output, while it has no
effect at the outlet of the pump? The difference between the two is the relative
amount of compliant bed upstream from the two resistance points.
In the case of outlet resistance, there is very little distensible bed between the resistance
point and the pump. But with inlet resistance, there is a large
compliant bed upstream. The compliant bed stores potential energy
from the pump ejection that would otherwise be in the form of kinetic energy.
But with outlet resistance, there is only minimal stored potential energy because there
is very little distensible bed upstream. Therefore there is much more kinetic energy
available to force the fluid past the resistance. Total vascular resistance therefore is not
a parameter that is a factor in determining cardiac output.
It is instead the combination of a resistance point and the vascular distensibility upstream
from that resistance point that together impede the flow to the pump inlet and decrease pump
output. “Inlet impedance” is the term we will use
to describe this combination of resistance and compliance that can decrease cardiac output.
Take note that again I am using a term that you may not be accustomed to using in this
context. The most significant factor in minimizing
inlet impedance to a non-sucking pump is the atrium.
As I turn on the pump, you will notice that the pump’s output it pulsatile, while inflow
to the pump is non-pulsatile. If I momentarily stop the atrium from working,
you can see that the venous flow becomes pulsatile, and the flow decreases significantly.
By being empty and distensible, when the inlet valve closes, the atrium allows uninterrupted
venous flow to the pump during ventricular systole.
While during diastole venous and atrial flow move into the ventricle unimpeded.
Although atrial displacement constitutes only 15% of the volume ejected by the ventricle
at each beat, the atrial effect makes possible four times the flow that would occur without
some mechanism to prevent the inertia of starting and stopping flow to the intermittent pump.
Atria, therefore, significantly minimize the inlet impedance to the pumps.
Clinical corollaries of an increased inlet impedance that reduces cardiac output include
mitral stenosis, venous obstruction, atrial fibrillation, nodal rhythm, cardiac tamponnade,
ventricular non-compliance, and extremely rapid heart rate. Clinical corollaries of
reduced inlet impedance with concomitant increase in cardiac output include arterial-venous
fistula that bypasses the compliant bed, and exercise, which uses muscle-vein pumps to
force fluid past inlet resistance points. So far, we have seen two determinants of cardiac
output: Mean vascular pressure, which has as its components fluid volume and system
compliance; and inlet impedance, which is a combination of resistance with a distensible
bed upstream from that resistance. We also confirmed that neither an increase
in rate nor strength of contraction increase the flow when I hand-crank the pump. But obviously rate is determining output now,
since the pump is stopped. At what point do increases in rate no longer cause increases
in output? To answer that question, you must first understand
that until this point we’ve been examining conditions where the pump is exerting excess
energy above what was used for circulation. In other words, an increase in mean vascular
pressure increased fluid flow into the ventricles, which increased cardiac output. But if a ventricle
has already filled completely, an increase in mean vascular pressure obviously could
not increase cardiac output, since the ventricle could not hold any more fluid.
Therefore, we must make a distinction between these two conditions. “Pump energy excess,” another new concept,
is that state where the pump is expending more energy than needed to eject the fluid
from the ventricles. It is this state that we’ve been examining
so far, in which we found the determinants of pump output to be mean vascular pressure
and inlet impedance. We know that human hearts in normal, day-to-day
living expend excess energy because propranalol, which in therapeutic dosage reduces heart
rate and strength of myocardial contraction, causes no decrease in output unless the ventricles
are in energy failure. “Pump energy failure,” not to be confused
with the term “congestive heart failure,” is that state where the pump is not expending
sufficient energy to prevent the ventricles from filling completely before the end of