6: Regulation of Cardiac Output
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Questions and Answers

How does an increase in central venous pressure affect ventricular preload?

  • It increases ventricular preload (correct)
  • It decreases ventricular preload
  • It has no effect on ventricular preload
  • It causes irregular heartbeats

    • Which factor positively influences ventricular compliance?

  • Increased myocardial stiffness
  • Increased blood volume (correct)
  • Decreased heart rate
  • Increased afterload

    • What is the relationship between stroke volume and ejection fraction as described by the Frank-Starling mechanism?

  • Ejection fraction decreases with decreased preload only
  • Ejection fraction decreases as stroke volume increases
  • Ejection fraction is unaffected by stroke volume
  • Ejection fraction increases with stroke volume up to a point of optimal preload (correct)

    • Which clinical condition is likely to increase afterload?

    <p>Aortic stenosis (D)</p> Signup and view all the answers

    What effect does increased atrial inotropy have on cardiomyocyte contraction during preload changes?

    <p>Increases the force of contraction (C)</p> Signup and view all the answers

    What does increased preload primarily affect in terms of volume in the heart?

    <p>Increases left ventricular end-diastolic volume (LVEDV) (D)</p> Signup and view all the answers

    Which statement accurately describes the Frank-Starling relationship?

    <p>Higher end-diastolic volume correlates with increased stroke volume. (A)</p> Signup and view all the answers

    What impact does increased afterload have on left ventricular end-systolic volume (LVESV)?

    <p>Increases LVESV (D)</p> Signup and view all the answers

    What is length-dependent activation in the context of cardiac function?

    <p>The increase in calcium binding to troponin C with sarcomere stretching (B)</p> Signup and view all the answers

    How does increased inotropy affect the heart's performance?

    <p>Increases the force of myocardial contraction (D)</p> Signup and view all the answers

    Which factor directly affects the compliance of the ventricles?

    <p>Thickness of the ventricular walls (A)</p> Signup and view all the answers

    What occurs when sarcomere length increases from 1.6 to 2.2 μm?

    <p>Enhanced muscle active tension during contraction (B)</p> Signup and view all the answers

    How does increased afterload affect stroke volume (SV)?

    <p>Decreases stroke volume (C)</p> Signup and view all the answers

    What happens to end-systolic volume (ESV) with decreased afterload?

    <p>Decreases end-systolic volume (A)</p> Signup and view all the answers

    What characterizes the family of Starling curves?

    <p>They reflect the afterload on the ventricle (C)</p> Signup and view all the answers

    Elevated afterload primarily affects which of the following?

    <p>Decreases ejection fraction (A)</p> Signup and view all the answers

    What does inotropy refer to in terms of cardiac muscle?

    <p>Ability to develop force independently of preload (B)</p> Signup and view all the answers

    How does increased afterload impact ejection velocity?

    <p>Decreases ejection velocity (A)</p> Signup and view all the answers

    What is the relationship between afterload and ventricular emptying?

    <p>Decreased afterload enhances ventricular emptying (B)</p> Signup and view all the answers

    What effect does increased afterload have on stroke volume and ejection fraction?

    <p>Decreases both stroke volume and ejection fraction (C)</p> Signup and view all the answers

    What mechanism causes the decrease in stroke volume as afterload increases?

    <p>Decreased velocity of fiber shortening and ejection (C)</p> Signup and view all the answers

    What effect does chronic dilation have on ventricular compliance?

    <p>Increases compliance (A)</p> Signup and view all the answers

    What is the relationship between ventricular compliance and stroke volume at a given end-diastolic volume (EDV)?

    <p>Higher compliance leads to higher stroke volume (C)</p> Signup and view all the answers

    What happens to left ventricular end-diastolic pressure (LVEDP) as preload decreases?

    <p>Decreases (D)</p> Signup and view all the answers

    Which of the following statements about decreased preload is correct?

    <p>It decreases left ventricular pressure development rate (B)</p> Signup and view all the answers

    What effect does decreased preload have on maximal ejection velocity (Vmax)?

    <p>Decreases Vmax (B)</p> Signup and view all the answers

    What is the relationship between stroke volume (SV) and ejection fraction (EF) with decreased preload?

    <p>Both SV and EF decrease (C)</p> Signup and view all the answers

    What is the primary definition of afterload in the context of cardiac physiology?

    <p>Tension required for shortening against a load (D)</p> Signup and view all the answers

    In terms of pressure-volume loops, a decrease in preload leads to which of the following?

    <p>Decreased stroke volume and decreased arterial pressure (A)</p> Signup and view all the answers

    What happens to the maximal rate of isovolumetric pressure development (dP/dtmax) when preload is decreased?

    <p>Decreases (D)</p> Signup and view all the answers

    Study Notes

    Cardiac Output Regulation

    • Cardiac output (CO) is the amount of blood pumped by the heart per minute.
    • CO = Stroke Volume (SV) × Heart Rate (HR)
    • Stroke volume (SV) is the volume of blood pumped per beat.
    • HR is the number of beats per minute.

    Learning Objectives

    • Describe how heart rate and stroke volume affect cardiac output.
    • Define ventricular preload, afterload, and inotropy.
    • Describe how changes in preload are affected by:
      • Central venous pressure
      • Blood volume
      • Ventricular compliance
      • Atrial inotropy
      • Heart rate
      • Inflow and outflow resistance
      • Afterload
      • Ventricular inotropy
    • Describe mechanisms by which preload changes alter cardiomyocyte force of contraction.
    • List clinical conditions that increase or decrease afterload.
    • Describe the Frank-Starling relationships and how preload, afterload, and inotropy affect stroke volume.
    • Draw ventricular pressure-volume loops depicting changes in preload, afterload, and inotropy, affecting end-diastolic volume (LVEDV), end-systolic volume (LVESV), stroke volume (SV), and ejection fraction (EF).
    • Describe receptor and intracellular mechanisms responsible for sympathetic and catecholamine regulation of cardiac muscle excitation-contraction coupling and relaxation.
    • Describe the interdependent effects of preload, afterload, and inotropy on LVEDV and LVESV using pressure-volume loops.

    Preload

    • Preload is the initial stretching of the cardiomyocyte sarcomere before contraction, related to end-diastolic volume.
    • Increased ventricular filling increases stroke volume.
    • The relationship between stroke volume (SV) and preload (measured as LVEDP or LVEDV) is called the Frank-Starling relationship or Starling's Law of the heart.
    • This relationship is length-dependent activation.

    Frank-Starling Relationship

    • Increased ventricular filling increases stroke volume.
    • The relationship between SV and preload (LVEDP or LVEDV) is called the Frank-Starling relationship or Starling's Law of the heart.
    • Length-dependent activation

    Mechanism of Length-Dependent Activation

    • Primary:
      • Changes in TN-C affinity for Ca²⁺
      • Sarcomere stretching increases Ca²⁺ binding to TN-C, increasing muscle active tension during contraction.
    • Secondary:
      • Changing actin-myosin filament overlap and active binding sites between actin and myosin.
      • Sarcomere stretching (1.6 to 2.2 μm) creates more available binding sites.

    Overview of Factors Determining Preload

    • Factors affecting preload include:
      • Atrial inotropy
      • Outflow resistance and afterload
      • Heart rate
      • Ventricular compliance
      • Venous pressure
      • Venous compliance
      • Total blood volume
      • Venous return

    How Ventricular Compliance Alters Sarcomere Length

    • Ventricular compliance (C = AV/∆P), inversely related to wall stiffness.
    • Altered by cardiac remodeling (chronic dilation or hypertrophy).
    • At a given EDP (green line), compliance ↑ (chronic dilation): EDV ↑ & sarcomere length ↑; compliance ↓ (hypertrophy): EDV ↓ & sarcomere length ↓.
    • At a given EDV (orange line), compliance ↑ (chronic dilation): EDP ↓; compliance ↓ (hypertrophy): EDP ↑.

    Afterload

    • Afterload is the force (tension) required for a cardiomyocyte to shorten against a load.
    • Afterload is related to the pressure the ventricle must generate to overcome aortic pressure and eject blood.

    Clinical Conditions Affecting Afterload

    • Hypertension
    • Ventricular dilation
    • Outflow tract obstruction
    • Ventricular hypertrophy

    How Afterload Affects Frank-Starling Relationship

    • At a given preload and inotropy, increased afterload decreases stroke volume (SV) by decreasing the velocity of fiber shortening and ejection.
    • Conversely, decreased afterload increases SV.
    • A family of Starling curves, each reflecting the afterload on the ventricle.

    Effects of Afterload

    • Increased afterload (aortic pressure) decreases stroke volume (SV) and ejection fraction (EF) by increasing end-systolic volume (ESV).
    • Conversely, decreased afterload decreases end-systolic volume (ESV) and increases SV and EF.

    Elevated Ventricular Afterload

    • Elevated ventricular afterload (primarily aortic pressure) decreases ejection velocity, stroke volume, and ejection fraction.
    • Ventricular emptying leads to increased end-systolic volume.

    Inotropy

    • Inotropy is the intrinsic ability of cardiac muscle to develop force independent of changes in preload.

    How Inotropy Affects Frank-Starling Relationship

    • At a given preload and afterload, increased inotropy increases stroke volume.
    • This is because increased inotropy increases the force of contraction and the velocity of fiber shortening and ejection.
    • Conversely, decreased inotropy decreases stroke volume.
    • A family of Starling curves reflects the inotropic state of the myocardium.

    Effects of Inotropy on P-V Loops

    • Increased inotropy decreases end-systolic volume (ESV) and increases stroke volume (SV).
    • Increases the ejection fraction (EF).
    • Conversely, decreased inotropy increases ESV and decreases SV.
    • Decreases the ejection fraction (EF).

    Regulation of Inotropy

    • Factors include:
      • Sympathetic adrenergic nerves
      • Circulating catecholamines
      • Parasympathetic nerves (atria)
      • Heart rate
      • Afterload

    Cardiac Sympathetic Mechanisms

    • Sympathetic nerves release norepinephrine (NE) that binds to β₁ and β₂ adrenoceptors (linked to Gs proteins).
    • ↑cAMP activates PK-A, phosphorylating intracellular sites to increase inotropy and heart rate.

    Intracellular Effects of PK-A Phosphorylation

    • ↑ opening of DHP Ca²⁺ channels
    • ↑ opening of ryanodine Ca²⁺ release channels
    • ↑ TN-C binding affinity for Ca²⁺
    • TN-I and myosin phosphorylation sites →↑ myosin ATPase activity.
    • ↑ SERCA activity. ↑ inotropy and lusitropy (relaxation rate.)

    Increased Ventricular Inotropy

    • Increased ventricular inotropy increases ejection velocity and stroke volume.
    • Augments ventricular emptying, decreasing end-systolic volume.
    • Increases ejection fraction.
    • Permits the heart to maintain its stroke volume when afterload is elevated.

    Interdependent Effects of Preload, Afterload, and Inotropy

    • Preload, afterload, and inotropy are interdependent changes in one usually result in secondary changes in others.

    Why Does Preload Change in Response to Changes in Afterload or Inotropy?

    • Changes in afterload or inotropy alter muscle shortening velocity and ejection velocity.
    • ESV decreases secondary to the decreased preload.
    • EF increases.

    Summary of Effects of Preload, Afterload, and Inotropy on Frank-Starling Curves

    • Increased preload increases stroke volume along the curve.
    • Decreased preload decreases stroke volume along the curve.
    • Increased afterload or decreased inotropy decrease stroke volume and increase preload.
    • Decreased afterload or increased inotropy increase stroke volume and decrease preload.

    Effects of HR on Pressures and Volumes

    • Increased HR (75→150 bpm): ↓ EDV, ↑ ESV, ↓ SV, ↓ EF, ↑ CO.
    • Decreased HR (75→50 bpm): ↑ EDV, ↓ ESV, ↑ SV, ↑ EF, ↓ CO.

    Regulation of Atrial Function

    • Atria respond to preload, afterload, and inotropic interventions similarly to ventricles, but vagal stimulation decreases atrial inotropy unlike ventricles.

    Summary

    • Ventricular preload is related to ventricular filling (EDV) and sarcomere length.
    • Increased preload increases contractile force and SV through the Frank-Starling mechanism.
    • Ventricular afterload is related to ventricular wall stress; higher afterload decreases SV.
    • Inotropy is myocyte's ability to develop tension independent of preload, influencing SV.
    • Preload, afterload, and inotropy are interconnected, and changes in any would cause secondary changes in the others.

    Q1: A Sudden Decrease in Venous Return

    • Decreases ventricular compliance.

    Q2: Reducing Afterload in Heart Failure

    • Muscle fiber shortening velocity is increased.

    Q3: Increasing Inotropy

    • Ventricular emptying increases.

    Q4: Sympathetic Activation of Heart

    • Increased release of calcium by sarcoplasmic reticulum.

    Answers (Referencing Previous Sections)

    • Q1 Answer A
    • Q2 Answer B
    • Q3 Answer B
    • Q4 Answer D

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    MPP2 2025 Lecture 07 Cardiac Output Regulation PDF

    Description

    This quiz explores key concepts in cardiac physiology related to preload, afterload, and contractility. It covers the Frank-Starling mechanism, ventricular compliance, and the effects of various factors on cardiac performance. Test your understanding of how these elements interact in the heart's function.

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