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    Physiology of Hemodynamics-1: Dr. Ghaleb Almekhlafi

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    GHALEB A. Almekhlafi
    1) The document describes basic hemodynamic diagrams including the vascular function diagram, cardiac function diagram, and ventricular pressure-volume loops. 2) It explains Guyton's experiments which showed that in steady state, venous return must equal cardiac output, and that venous return is driven by the pressure gradient between mean systemic filling pressure and right atrial pressure, divided by resistance to venous return. 3) Key factors that can affect venous return and cardiac output are then discussed, including blood volume, vascular compliance, intrathoracic and intra-abdominal pressures, and drug effects.

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    Physiology of Hemodynamics-1: Dr. Ghaleb Almekhlafi

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    GHALEB A. Almekhlafi
    31 views52 pages
    1) The document describes basic hemodynamic diagrams including the vascular function diagram, cardiac function diagram, and ventricular pressure-volume loops. 2) It explains Guyton's experiments which showed that in steady state, venous return must equal cardiac output, and that venous return is driven by the pressure gradient between mean systemic filling pressure and right atrial pressure, divided by resistance to venous return. 3) Key factors that can affect venous return and cardiac output are then discussed, including blood volume, vascular compliance, intrathoracic and intra-abdominal pressures, and drug effects.

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    HD PHYSIOLOGY

    Original Title

    hd PHYSIOLOGY PART1

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    1) The document describes basic hemodynamic diagrams including the vascular function diagram, cardiac function diagram, and ventricular pressure-volume loops. 2) It explains Guyton's experiments which showed that in steady state, venous return must equal cardiac output, and that venous return is driven by the pressure gradient between mean systemic filling pressure and right atrial pressure, divided by resistance to venous return. 3) Key factors that can affect venous return and cardiac output are then discussed, including blood volume, vascular compliance, intrathoracic and intra-abdominal pressures, and drug effects.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    31 views52 pages

    Physiology of Hemodynamics-1: Dr. Ghaleb Almekhlafi

    Uploaded by

    GHALEB A. Almekhlafi
    1) The document describes basic hemodynamic diagrams including the vascular function diagram, cardiac function diagram, and ventricular pressure-volume loops. 2) It explains Guyton's experiments which showed that in steady state, venous return must equal cardiac output, and that venous return is driven by the pressure gradient between mean systemic filling pressure and right atrial pressure, divided by resistance to venous return. 3) Key factors that can affect venous return and cardiac output are then discussed, including blood volume, vascular compliance, intrathoracic and intra-abdominal pressures, and drug effects.

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    of 52

    Physiology of

    HEMODYNAMICS-1
    DR. GHALEB ALMEKHLAFI
    OBJECTIVES
    TO DESCRIBE THE BASIC HEMIDYNAMIC DIAGRAMS
    • vascular function diagram
    • cardiac function diagram
    • Ventricular pressure-volume loops
    Introduction-why physiology?
    • The biologic system is complex
    • the organs cross-talk
    • disease disrupt function and interaction of organs
    • The organ interaction try to compensate-physiologic reserve
    • Derangement of function indicate failure of compensation
    • critically illness indicate organ failure
    • Knowing Physiology and pathophysiology Can help directing the
    management of complex situations
    Anatomy of the circulation
    arterial vs venous circulations
    Venous circulation Arterial circulation
    • function is to collect blood-reservoir • function is to distribute blood
    • contain ∼70% of blood volume
    Capacitance = volume / transmural pressure mmHg • 10%of blood volume
    • low pressure 0-10 mmhg • maintaining high pressure is a
    • The volume is primarily regulated ,not guarantee of perfusion-MAP
    tone • governed by laws of pressure
    • BF is governed laws of pressure difference
    difference
    MAP-RAP = CO x SVR
    The circulation dynamics
    The cardiac output
    Vascular function
    diagram
    “Obviously, except under momentary
    conditions the venous return and the
    cardiac output must be equal.” — Arthur
    Guyton

    Arthur Clifton Guyton


    (September 8, 1919 – April 3, 2003)
    The experiment
    • The invention of extracorporeal pumps allowed Guyton to control
    the heart function via the speed of a mechanical pump and separate
    pump effects from the vascular tree as the circuit.
    • He achieved maximum venous return with zero RAP.
    • Further increases in flow via increases in pump function were
    limited by collapse of the intrathoracic vessels.
    • When he increased RAP above zero (i.e., above atmospheric
    pressure), pump flow and therefore venous return would decline
    until flow ceased completely.
    • He termed the pressure at zero flow mean circulatory filling
    pressure (MCFP).
    • By influencing MCFP via volume expansion or epinephrine, he could
    increase venous return without changes in pump function (7,8,10).
    • From this, Guyton reasoned that in the steady state circulation,
    venous return (and therefore cardiac output in conclusion) was
    driven by the venous return driving pressure
    • (VRdP = MCFP minus RAP) divided by the resistance to venous
    return (RVR):
    Venous Return
    • rate at which blood is
    returned to the heart (in
    L.min-1).
    • driven by the pressure
    difference between MSFP
    and RAP
    VR=MSFP−RAP/RVR
    • At steady state, venous
    return is equal to cardiac
    output
    MSFP
    • In a circulatory standstill,
    pressure and volume
    equilibrate in the whole system
    at MCFP
    • Volume is distributed according
    to each segments compliances
    • The equilibrating pressure is
    related to blood volume and is
    independent of the hearts’
    function.
    mean systemic filling pressure [Pmsf]

    • The Pmsf is determined


    by

    1. venous blood volume


    • Filling volume
    • Stretching volume

    2-venous compliance
    2 volumes-Stressed and unstressed
    Stressed and unstressed vascular volume
    unstressed volume :
    fills the system without
    exerting tension in the
    vessel wall. P=0

    stressed volume:
    blood volume that creates
    positive transmural
    pressure via the elastic
    recoil of the vessel wall
    below –4 mm Hg,the veins collapse preventing any further
    increase in flow. Vascular waterfall= maximal flow
    independent of downstream pressure
    Venous return-normal

    Vascular
    waterfall
    Factors Affecting Venous Return
    VR=MSFP−RAP/RVR
    •MSFP
    • Volume
    e.g. Haemorrhage, resuscitation.
    • Compliance
    •RAP
    • Respiratory pump
    (Negative intrathoracic pressure reduces RAP, improving venous
    return.)
    • Positive pressure ventilation
    • Pericardial compliance
    • Constriction
    • Tamponade
    •Resistance to Venous Return
    • Posture
    • Vascular compression
    • Obesity
    • Pregnancy
    • Laparoscopy
    • Ascites, edema,ACS
    •Other factors affecting venous return
    • Skeletal muscle pump
    Contraction of leg muscles in combination with an intact venous
    system propels blood back towards the heart.
    • Venous valves
    MSFP-relevance to critical care
    practitioners
    Factors Affecting Venous
    Change in msfp

    Return
    VR=MSFP−RAP/RVR

    •MSFP Change in resistance to VR


    • Volume
    e.g. Haemorrhage,
    resuscitation.
    • Compliance

    resistance becomes infinite below –4 mm Hg, preventing any


    increase in flow above that present at –4 mm Hg.
    VR can only be zero if Pms – PRA is
    zero
    Prone effect on VR
    • prone position increase intra-
    abdominal pressure.
    • Increase PMS favors increase
    venous return.
    • variable effects upon the resistance
    to venous return depending on the
    patient’s underlying volume status.
    Prone Positioning Effects on Cardiac
    Function
    • Prone positioning reduces the compliance of the chest wall
    • the passive patient receiving mechanical ventilation will experience a relatively large increase in intra-
    thoracic pressure for a given tidal volume [16, 17]. Assuming that the intra-thoracic pressure is
    transmitted integrally to the pericardial space [18], the increased intra-thoracic pressure shifts the
    cardiac function curve rightwards relative to the systemic venous return curve [19]; to the extent that
    the cardiac function curve shifts rightwards relative to the right-shift of the MSFP, as elaborated above,
    there will be reduced cardiac output. Conversely, and less intuitively, the increase in intra-thoracic
    pressure will also reduce right ventricular afterload. The reason is that right ventricular afterload is
    determined by the distending pressure of the lung [i.e. the trans-pulmonary pressure] which is the
    pressure within the alveolar compartment less the pressure within the pleural compartment.
    Consequently, reduced chest wall compliance raises the pleural [or intra-thoracic] pressure relative to
    the alveolar pressure and this unloads right ventricular ejection [20-22]. Additionally, prone positioning
    recruits compressed dorsal lung [23] which lowers pulmonary vascular resistance [24], and improves
    oxygenation which releases hypoxemic vasoconstriction in the pulmonary bed [25]. Right ventricular
    afterload reduction is illustrated by an increase in the slope of the cardiac function curve [i.e. an up and
    to the left shift].
    • Gattinoni’s distinction pulmonary and extra-pulmonary ARDS
    • pulmonary ARDS is a consequence of direct pulmonary insult and leads to a
    profound reduction in pulmonary compliance, . less of the alveolar pressure is
    transmitted to the pleural space [28-30], therefore, trans-pulmonary pressure
    rises and right ventricular afterload is heightened This physiology favors
    enlargement of right ventricular volume and diminished cardiac output.
    • extra-pulmonary ARDS arises in the context of systemic unrest and results in
    severely diminished chest wall compliance. raised pleural pressure relative to
    alveolar pressure such that
    • trans-pulmonary pressure and right ventricular afterload are diminished; this
    favors diminution of right ventricular volume and improved cardiac output.
    • Hemodynamic Effects of Prone Positioning: Conclusions

    • Placing a patient in the prone position has important implications for both venous return and
    right ventricular function. While an increase in intra-abdominal pressure tends to raise the
    pressure head for venous return, improved venous return will only be realized in the absence of
    a contemporaneous rise in the resistance to venous return. Therefore, careful consideration
    should be paid to a patient’s volume status prior to initiating prone positioning. Additionally, the
    degree to which ventilator-applied airway pressure partitions into the alveolar space relative to
    the pleural space will determine to what extent the intra-thoracic milieu favors diminished right
    ventricular preload, afterload or some combination thereof. It follows that careful consideration
    should be given to underlying cardiac function as well as the relative contributions of the
    pulmonary and chest wall compliances to the overall compliance of the respiratory system.
    Integration of these multiple, co-varying physiological elements may explain conflicting
    hemodynamics both in ARDS and other mechanically-ventilated patient populations
    SELECTIVITY OF VASO ACTIVE
    DRUGS
    Predominant venous vasodilators like
    nitroglycerin reduce preload .
    Arterial vasodilators like hydralazine reduce
    afterload

    norepinephrine
    augment Pmsf,
    increase cardiac function,
    increasing the resistance to venous
    return and afterload
    leading to decreased VR and rt and
    down-shifting the cardiac function
    curve
    vasopressor
    CARDIAC FUNCTION DIAGRAM
    STARLING’S LAW
    By raising or lowering an artificial venous reservoir
    Starling showed that increased RAP resulted in increased SV
    STARLING’S LAW
    The curve status is defined by the existing
    conditions of
    • afterload
    • inotropy and
    • diastolic compliance
    Vascular function curve
    Dependant or independent-RAP,CO,VR
    Do the cardiac output and venous return depend
    on RAP?
    Does RAP depend on the cardiac output and
    venous return?
    The answer to both is yes!
    They all depend on each other.
    Both curves can be equal only at the single point
    where the two curves intersect.
    Only transient and small deviations in these two
    curves are possible unless either or both of the
    function curves change in shape.
    Momentary changes
    • CO and VR are equal (at 5 L/min) only when
    the CVP is 2 mm Hg.
    • If CVP decrease to 0 for any reason, CO
    would fall (to 2 L/min) but VR would
    increase (to 7 L/min).
    • Increase VR will return CVP back to the
    original level (2 mm Hg) in a very short time.
    • Conversely, in the same logic the similar
    thing would happen when CVP were to
    increase.
    • conclusion: CVS automatically adjusts to
    operate at the point where the cardiac and
    venous function curve intersect.
    Dynamics of the curves-matching
    Dynamics of the curves-
    matching
    high cardiac performance [Eh] low cardiac performance
    Eh is the slope of the
    Frank-Starling curve
    Eh=pmsf-pra
    Both curves increase
    or decrease by the
    msfp and RAP
    difference
    Starling did not consider the MSFP
    Function curves-clinical relevance
    Cardiac Cycle
    SAGAWA
    Ventricular pressure-
    volume loops
    clinical implications of
    vascular and cardiac
    function curves=part2
    Thank you

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