Cardiac Physiology – Control of
Cardiac Output
Factors Controlling CO
Four factors control CO; heart rate, myocardial
contractility, preload, and afterload.
Heart rate and contractility are intrinsic factors,
characteristics of cardiac tissues, influenced by neural
and humoral mechanisms.
Preload and afterload depend on the characteristics of
both the heart and the vascular system.
Preload and CO relationships can be described in two curves:
cardiac function curve and vascular function curve.
The cardiac function curve is a characteristic of the heart and
is an expression of the Frank-Starling relationship
The vascular function curve defines the dependence of the
central venous pressure on the CO.
The Vascular Function Curve Relates
Central Venous Pressure to CO
The vascular function curve defines the
changes in central venous pressure evoked by
changes in CO (CVP is the dependant variable
and CO is the independent variable).
In contrast, with the cardiac function curve the
CVP is the independent variable and the CO is
the dependent variable.
How to Derive the Vascular Function
Curve
Assume that the entire heart is a single pump.
The high resistance microcirculation is the peripheral
resistance (20 mmHg/L/min).
Systen compliance is subdivided into the arterial
compliance (Ca) and the venous compliance (Cv).
Assume that the venous compliance is about 19 times
greater than the arterial compliance.
Assume Pa = 102 and Pv = 2 mmHg
Induce cardiac arrest.
Arteriovenous pressure gradient of 100 mmHg will
force a flow of 5 L/min through the peripheral
resistance of 20 mm Hg/L/min. (I=V/R)
Although CO is 0 L/min, the flow through the
microcirculation transiently is 5 L/min.
Gradually, the blood volume in the arteries
progressively declines and the blood volume in the
veins progressively increases until the pressure
gradient is 0.
When the pressure gradient is zero, flow ceases through the
microcirculatrion.
At zero flow, arterial and venous pressure equalizes and the
final pressure depends on the relative compliance of these
vessels.
Had the arterial and venous compliance been equal, the decline
in Pa would have been equal to the rise in Pv.
However, the veins are much more compliant than the arteries
and the transfer of blood from arteries to veins at equilibrium
would induce a fall in arterial pressure that is 19 X as great as
the concomitant rise in venous pressure.
The final pressure in the circulatory system in the absence of
flow is the mean circulatory pressure.
From this, two important points on the vascular function curve
have been derived.
Figure A represents the normal operating system (CO 5 L/min,
Pv 2 mmHg).
Then when flow was stopped (CO=0), Pv became 7 mmHg.
Next, the arrested heart is suddenly restarted, and begins
pumping at 1 L/min.
Blood is being moved from the veins at a rate of 1 L/min and
the arterial volume is increasing at the same rate.
Hence Pv begins to fall and Pa begins to rise.
Because of the difference in compliance, Pa will rise 19 times
faster than Pv will fall.
This will continue until the pressure gradient becomes 20
mmHg. This gradient will force a flow of 1 L/min through a
resistance of 20 mmHg/L/min. (V=IR)
You may have noticed the straight line on the curve.
At some critical maximal value of CO, sufficient fluid will be
translocated from the venous to the arterial side of the circuit
to reduce Pv below the ambient pressure.
The vessels will collapse when the intravascular pressure falls
below the extravascular pressure and obstruct venous return.
Hence, in this case, there is a limit on the maximal value of
CO to 7 L/min.
Effect of Blood Volume on the
Vascular Function Curve
The vascular function
curve shifts to the right
and left (no change in
slope) with increases and
decreases in blood
volume.
The maximal value of CO
becomes progressively
more limited as the total
blood volume is reduced.
This is why you can’t
drive up CO in a dry
patient with pressors.
Effect of Peripheral Resistance on the
Vascular Function Curve
Increases or decreases
in arteriolar tone do not
significantly alter the
mean circulatory
pressure.
Increased resistance
moves more blood from
the venous to arterial
side and decreases the
CVP for the same CO.
The opposite occurs in
vasodilation.
The Heart and Vasculature are
Coupled Functionally
The intersection
bewteen the vascular
and cardiac function
curve is homeostasis.
It is the point that the
system will return to
after any perturbations.
Consider a rise in Pv
from the equilibrium
point to point A.
The elevated Pv would increase CO (A to B) during the next systole
(Frank Starling).
The increased CO results in the transfer of blood from the venous to
the arterial side of the circuit, with a consequent reduction in Pv (B
to C).
Because of this reduction in Pv, the CO during the next beat
diminishes (C to D) by an amount dictated by the function curve.
Because point D is still above the intersection point, the heart will
pump blood from the veins to the arteries at a rate greater than that
at which the blood will flow across the peripheral resistance from
arteries to vein.
This process will continue, in diminishing steps with each heartbeat,
until the point of intersection is reached.
Myocardial Contractility
– Consider the equilibrium values for CO and Pv are
designated by point A.
– Cardiac sympathetic nerve stimulation would abruptly raise
CO to point B before Pv would change appreciably.
– However, this high CO would increase the net transfer of
blood from the venous to the arterial side of the circuit.
– Consequently, Pv would begin to fall (point C).
– CO would continue to fall until a new equilibrium point
(D) was reached.
Peripheral Resistance
– Predictions concerning the effects of changes in peripheral
resistance are complex because both the cardiac and
vascular function curves shift.
– With increased peripheral resistance, the vascular function
curve is moves counterclockwise.
– The cardiac function curve is also shifted downward
because (1) as peripheral resistance increases, arterial
pressure tends to rise; and (2) at any given Pv, the heart is
able to pump less blood against a greater afterload.
– Whether point B will fall directly below point A or will lie
to the right or left of point A depends on the magnitude of
the shift in each curve.
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