Physiology of Cardiac Function
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Questions and Answers

What happens to tropomyosin as a result of TnT movement?

  • It covers the myosin binding site
  • It binds to myosin
  • It prevents actin-myosin overlap
  • It exposes the myosin binding site (correct)
  • What is the optimal sarcomere length for maximum tension development in skeletal muscle?

  • 1.65µm (correct)
  • 2.25µm
  • 1.25µm
  • 2.00µm
  • What is the effect of increasing sarcomere length on cardiac muscle?

  • Decreased Ca2+ sensitivity
  • Increased Ca2+ sensitivity (correct)
  • Force development becomes independent of [Ca2+]i
  • No change in Ca2+ sensitivity
  • What is the primary mechanism of length dependent activation in cardiac muscle?

    <p>Titin-mediated sensing of sarcomere length</p> Signup and view all the answers

    What happens to the distance between actin and myosin as sarcomere length increases?

    <p>It decreases</p> Signup and view all the answers

    What is the optimal [Ca2+]i for maximum force development in cardiac muscle?

    <p>1.0 mM</p> Signup and view all the answers

    At what sarcomere length is the force development in cardiac muscle maximally sensitive to [Ca2+]i?

    <p>2.0 microns</p> Signup and view all the answers

    What is the relationship between sarcomere length and Ca2+ sensitivity in cardiac muscle?

    <p>Increased sarcomere length increases Ca2+ sensitivity</p> Signup and view all the answers

    What is the effect of titin on the thin filament?

    <p>Increasing the sensitivity of troponin for Ca2+</p> Signup and view all the answers

    What determines CO at a given heart rate and contractility?

    <p>CVP</p> Signup and view all the answers

    What is the primary mechanism by which the heart maintains CO in the face of increased afterload?

    <p>The Frank-Starling mechanism</p> Signup and view all the answers

    What is the term for the strength of contraction of the heart?

    <p>Inotropy</p> Signup and view all the answers

    What regulates cardiac contractility?

    <p>Intracellular [Ca2+] in cardiac myocytes</p> Signup and view all the answers

    What is the effect of sympathetic stimulation on cardiac contractility?

    <p>Increasing cardiac contractility</p> Signup and view all the answers

    What is the result of an increase in RV output?

    <p>Increased filling of the LA</p> Signup and view all the answers

    What is the consequence of an increase in CVP on LV output?

    <p>Increased stroke volume and LV output</p> Signup and view all the answers

    What is the primary effect of blood loss on cardiac output (CO)?

    <p>Decreased CO due to decreased CVP</p> Signup and view all the answers

    What happens to CVP during sustained exercise?

    <p>CVP decreases due to progressive loss of fluid</p> Signup and view all the answers

    What is the effect of orthostasis on blood pressure?

    <p>BP decreases due to decreased CVP</p> Signup and view all the answers

    What percentage of blood is in the systemic veins at any given moment?

    <p>65%</p> Signup and view all the answers

    What is the effect of constriction of splanchnic veins by the SNS?

    <p>CVP increases and mobilizes blood into the heart</p> Signup and view all the answers

    What is the approximate amount of blood mobilized into the heart by constriction of splanchnic veins?

    <p>500-700 ml</p> Signup and view all the answers

    What percentage of blood is in the splanchnic veins?

    <p>20%</p> Signup and view all the answers

    What is the relationship between CVP and CO?

    <p>CVP increases CO</p> Signup and view all the answers

    What happens to the Frank-Starling curve in the case of heart failure?

    <p>The curve becomes flatter, indicating decreased contractility.</p> Signup and view all the answers

    Which of the following is NOT a compensatory mechanism activated by heart failure?

    <p>Increased heart rate due to decreased oxygen supply to the heart.</p> Signup and view all the answers

    What is the primary effect of increased sympathetic nervous system activity in response to heart failure?

    <p>Increased heart rate and contractility.</p> Signup and view all the answers

    What does the term "EDP" refer to in the context of heart failure?

    <p>End-diastolic pressure.</p> Signup and view all the answers

    Which of the following factors does NOT affect the Frank-Starling mechanism?

    <p>Heart rate.</p> Signup and view all the answers

    How does noradrenaline increase cardiac contractility?

    <p>By stimulating b1 adrenergic receptors.</p> Signup and view all the answers

    What physiological mechanism ensures that the cardiac output of the left ventricle (COLV) remains equal to the cardiac output of the right ventricle (CORV) over time?

    <p>The closed nature of the cardiovascular system, where the output of one ventricle must be equal to the input of the other.</p> Signup and view all the answers

    Which of the following accurately describes the concept of preload in relation to cardiac function?

    <p>The degree of stretch on the ventricular muscle fibers at the end of diastole.</p> Signup and view all the answers

    How does the Frank-Starling law of the heart contribute to maintaining a constant cardiac output (CO) over a range of afterloads?

    <p>By increasing the volume of blood ejected from the ventricle (stroke volume) in response to increased afterload, maintaining a constant CO.</p> Signup and view all the answers

    Which of the following factors can influence preload and affect cardiac output?

    <p>The volume of blood returning to the heart from the veins (venous return).</p> Signup and view all the answers

    How does the Anrep response differ from the Frank-Starling response in maintaining a constant cardiac output (CO) under varying afterloads?

    <p>The Anrep response involves an increase in contractility, whereas the Frank-Starling response involves an increase in preload.</p> Signup and view all the answers

    Which of the following accurately describes the relationship between end-diastolic volume (EDV) and ventricular function?

    <p>EDV and ventricular function have a complex relationship, where increased EDV can lead to improved function up to a certain point, beyond which it can become detrimental.</p> Signup and view all the answers

    Which of the following is NOT a factor that can affect heart rate (HR)?

    <p>The resistance of the blood vessels to blood flow (afterload).</p> Signup and view all the answers

    What is the primary mechanism by which changes in end-diastolic pressure (EDP) affect ventricular output?

    <p>Changes in EDP alter preload, as higher EDP leads to greater ventricular stretch and increased stroke volume.</p> Signup and view all the answers

    Study Notes

    Cardiac Output Control

    • Cardiac output (CO) must adjust to bodily tissue metabolic needs.
    • Systemic and pulmonary circulations are arranged in series; left and right ventricular outputs must be equal over time (COLV = CORV).
    • Venous return matches cardiac output, allowing for transient differences in specific situations, such as standing.

    Preload and Afterload

    • Preload refers to the initial stretching of the cardiac muscle before contraction, influenced by end-diastolic volume (EDV).
    • Afterload is the pressure against which the heart must work to eject blood during systole.
    • Changes in preload and afterload significantly impact cardiac performance and output.

    Frank-Starling Law

    • The Frank-Starling mechanism ensures stroke volumes of both ventricles are matched, stabilizing CO despite variations in afterload or contractility.
    • Increased ventricular filling leads to elevated stroke volume due to enhanced myocardial stretch linking to contractility through length-dependent activation.

    Contractility and Inotropy

    • Contractility is the inherent strength of heart muscle contraction, influenced by intracellular calcium levels in cardiac myocytes.
    • Sympathetic stimulation increases contractility via norepinephrine acting on β1 and β2 adrenergic receptors.
    • Several factors, including pH and pO2, also affect inotropic response.

    Cardiac Function and EDV/EDP

    • End-diastolic volume (EDV) and end-diastolic pressure (EDP) are critical in determining ventricular function and shaping cardiac function curves.
    • Cellular mechanisms relating EDV/EDP to output involve actin-myosin interactions and alterations in calcium sensitivity.

    Compensatory Mechanisms in Heart Failure

    • Heart failure occurs when CO is inadequate for metabolic requirements or maintained only at high EDP/volume levels.
    • Reduced CO activates compensatory responses, including fluid retention and increased heart rate.
    • Renin-angiotensin-aldosterone system is engaged in response to low blood pressure, promoting fluid retention and venoconstriction.

    Impacts of Blood Volume Changes

    • Decreases in central venous pressure (CVP) affect CO, particularly during hemorrhage or prolonged exercise.
    • Orthostatic changes lead to blood pooling, reducing CVP and subsequently decreasing CO and blood pressure.

    Venous System Role

    • Splanchnic vein constriction by the sympathetic nervous system can significantly increase CVP, mobilizing blood into the heart and arterial system efficiently without major impacts on venous return due to slow flow characteristics.

    Cellular Mechanisms and Length-Dependent Activation

    • Increased sarcomere length leads to enhanced actin-myosin overlap.
    • Titin protein affects myosin binding protein C, modifying troponin configuration, which heightens calcium sensitivity for contraction.

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    Related Documents

    Control Of Cardiac Output PDF

    Description

    This quiz covers the physiology of cardiac function, including preload, afterload, and ventricular function. It also explores the relationship between EDV/EDP and cardiac function, and drawing cardiac function curves.

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