Tip:
Highlight text to annotate it
X
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 diastole.