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    Control

    of

    Cardiac Output

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    Reading

    Klabunde, Cardiovascular Physiology

    Concepts

    Chapter 4 (Cardiac Function)

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    Basic Theory of

    Circulatory Function The blood flow to each tissue of the body is almost always

    precisely controlled in relation to the tissue needs

    The cardiac output is controlled mainly by the sum of allthe local tissue flows

    Frank-Starling Relationship is the predominant factor inmatching venous return and cardiac output

    In general, the arterial pressure is controlled independentlyof either local blood flow or cardiac output control

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    Definitions

    Cardiac Output

    The quantity of blood pumped into the aorta

    each minute

    Venous Return

    The quantity of blood flowing from the veinsinto the right atrium each minute

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    Cardiac Output

    CO = HR x SV

    SV = EDV ESV

    EDV

    ESVEDV

    EDV

    SVEF

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    End-Diastolic

    Volume

    End-Systolic

    Volume

    End-Diastolic Volume End-Systolic Volume = Stroke Volume

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    Cardiac

    Output

    Determinants of Cardiac Output

    Heart Rate Preload

    AfterloadContractility

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    CONTRACTILITY PRELOAD AFTERLOAD

    STROKE

    VOLUME

    HEART

    RATE

    CARDIAC

    OUTPUT

    (+)(+)

    (+) (+)

    (-)

    IMPORTANT RELATIONSHIPSIMPORTANT RELATIONSHIPS

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    Heart Rate

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    Heart Rate

    Changes in heart rate are generally more

    important quantitatively in producing

    changes in cardiac output than are changesin stroke volume

    Changes in heart rate alone inversely affectstroke volume

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    Heart Rate

    At low HR

    Increase in HR is greater than decrement in SV

    At high HR

    The decrease in SV is greater than the increase

    in HR (decreased filling time)

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    Effects of Heart Rate

    on Cardiac Output

    Heart Rate

    (Increased by Pacing)

    CardiacOutp

    ut

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    Stroke Volume= EDV-ESV

    EndDiastolicVolume

    Preload

    EndSystolicVolume

    Afterload

    Contractility

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    Preload

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    Preload

    Preload can be defined as the initial stretching ofthe cardiac myocytes prior to contraction. It isrelated to the sarcomere length at the end of

    diastole.

    Because we cannot measure sarcomere lengthdirectly, we must use indirect indices of preload.

    LVEDV (left ventricular end-diastolic volume) LVEDP (left ventricular end-diastolic pressure)

    PCWP (pulmonary capillary wedge pressure)

    CVP (central venous pressure)

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    Frank-Starling Mechanism

    When venous return to the heart is increased,

    ventricular filling increases, as does preload. This

    stretching of the myocytes causes an increase inforce generation, which enables the heart to eject

    the additional venous return and thereby increase

    stroke volume.

    Simply stated: The heart pumps the blood that is

    returned to it

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    Frank-Starling Curves

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    Effects of Afterload

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    Summary of Factors

    That Influence

    Cardiac Outputand

    Mean Arterial Pressure

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    Myocardial Oxygen

    Consumption

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    Factors Increasing

    Myocardial Oxygen Consumption

    Increased Heart Rate

    Increased Inotropy (Contractility)

    Increased Afterload

    Increased Preload Changes in preload affect myocardial oxygen consumption less

    than do changes in the other factors

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