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Cardiac Physiology – Control of Cardiac Output

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Cardiac Physiology Control of Cardiac Output Factors Controlling CO Four factors control CO; heart rate, myocardial contractility, preload, and afterload. – PowerPoint PPT presentation

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Title: Cardiac Physiology – Control of Cardiac Output


1
Cardiac Physiology Control of Cardiac Output
2
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.

3
  • 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.

4
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.

5
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

6
  • 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. (IV/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.

7
  • 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.

8
  • 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 (CO0), Pv became 7
    mmHg.

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10
  • 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.
    (VIR)

11
  • 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.

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13
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 cant drive up CO in a dry
    patient with pressors.

14
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.

15
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.

16
  • 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.

17
  • 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.

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  • 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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