Cardiac Output Overview and Mechanisms
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Questions and Answers

What is the relationship described by Starling's Law regarding the heart's contraction?

  • Increased venous pressure decreases the stroke volume.
  • Heart contraction is independent of end diastolic volume.
  • The more the heart fills, the harder it contracts, up to a limit. (correct)
  • The more the heart fills, the weaker it contracts.
  • How does sympathetic nerve stimulation affect myocardial contractility?

  • It decreases myocardial contractility.
  • It increases myocardial contractility. (correct)
  • It causes a variable effect depending on other factors.
  • It has no effect on myocardial contractility.
  • What affects the difficulty of ejecting blood during ventricular contraction?

  • Heart rate alone.
  • The amount of blood returning to the heart.
  • End diastolic volume only.
  • Aortic impedance, primarily determined by total peripheral resistance. (correct)
  • What happens to stroke volume if arterial pressure falls?

    <p>Stroke volume rises. (A)</p> Signup and view all the answers

    What role do baroreceptors play in heart rate control?

    <p>They sense arterial pressure and send signals to the medulla. (A)</p> Signup and view all the answers

    How does a rise in venous pressure affect stroke volume?

    <p>Stroke volume rises. (C)</p> Signup and view all the answers

    What mechanism is primarily responsible for cardiac output increase when arterial pressure falls?

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

    What triggers the release of vasopressin in response to decreased systemic blood pressure?

    <p>Activation of central baroreceptors. (B)</p> Signup and view all the answers

    What is the relationship between total peripheral resistance (TPR) and arterial pressure when TPR falls and cardiac output remains unchanged?

    <p>Arterial pressure falls and venous pressure rises (A)</p> Signup and view all the answers

    What factors influence stroke volume?

    <p>Preload, afterload, and inotropic state (B)</p> Signup and view all the answers

    How does an increase in cardiac output (CO) affect arterial and venous pressure assuming TPR remains unchanged?

    <p>Arterial pressure rises, venous pressure falls (A)</p> Signup and view all the answers

    What physiological response occurs when local vasodilators are released after eating a meal?

    <p>Arterial pressure falls due to decreased TPR (D)</p> Signup and view all the answers

    What best describes the relationship between venous pressure and ventricular filling?

    <p>Higher venous pressure allows for greater ventricular filling (B)</p> Signup and view all the answers

    What occurs in the heart during systole?

    <p>Blood is ejected into the arteries (B)</p> Signup and view all the answers

    What happens to venous pressure when cardiac output decreases and TPR remains constant?

    <p>Venous pressure rises (C)</p> Signup and view all the answers

    Which factor is considered part of the control of cardiac output?

    <p>Heart rate (B)</p> Signup and view all the answers

    Flashcards

    Stroke Volume

    The volume of blood pumped out of the heart with each beat.

    Afterload

    The pressure against which the heart must eject blood.

    Preload

    The amount of blood in the ventricle at the end of diastole, just before contraction.

    Inotropic State

    The force of contraction of the heart muscle. It determines how much blood is ejected with each beat.

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    Total Peripheral Resistance (TPR)

    The total resistance that the blood faces as it circulates throughout the body.

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    Cardiac Output

    The volume of blood pumped by the heart per minute.

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    Systolic Pressure

    The pressure in the arteries during the heart's contraction phase.

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    Diastolic Pressure

    The pressure in the arteries during the heart's relaxation phase.

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    Starling's Law

    The relationship between the amount of blood filling the ventricle (end-diastolic volume) and the force of contraction. Increased filling leads to a stronger contraction.

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    End-Systolic Volume

    The volume of blood remaining in the ventricle after contraction (systole).

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    Aortic Impedance

    The resistance the heart encounters when ejecting blood into the aorta.

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    Myocardial Contractility

    The ability of the heart muscle to contract forcefully, influenced by factors like sympathetic/vagal nerve activity and medications.

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    Autonomic Control of Heart Rate

    The control of heart rate by signals from the nervous system (autonomic outflow).

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    Vasopressin

    A hormone released by the pituitary gland in response to low blood pressure. It causes vasoconstriction, leading to increased blood pressure.

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    Compensatory Mechanisms

    The mechanisms that work to compensate for changes in blood pressure, such as increased heart rate, contractility, and vasoconstriction.

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    Study Notes

    Cardiac Output Overview

    • Cardiac output is the product of stroke volume and heart rate.
    • Arterial and venous pressures influence both.

    Stroke Volume

    • Determined by the interaction of preload, inotropic state, and afterload.
    • Preload: the amount of blood in the ventricles before contraction.
    • Inotropic state: the force of ventricular contraction.
    • Afterload: the resistance the ventricles must overcome to eject blood.
    • Stroke volume is the difference between end diastolic volume and end systolic volume.
    • The heart fills in diastole.

    Ventricular Filling

    • Ventricles fill until intraventricular pressure equals venous pressure.
    • Venous pressure directly affects ventricular filling.
    • A relationship exists between venous pressure and ventricular volume, known as the ventricular compliance curve.

    End Diastolic Volume and Force of Contraction

    • Starling's Law of the heart: the more the heart fills, the harder it contracts. The stronger the contraction the larger the stroke volume.
    • Rises in venous pressure automatically increase end diastolic volume.

    Myocardial Contractility

    • Myocardial contractility (inotropic state) is influenced by sympathetic and vagal nerve activity, drugs, and receptors.
    • Sympathetic stimulation increases contractility.
    • Vagal stimulation decreases contractility.

    End Systolic Volume

    • Determined by the force of ventricular contraction and the difficulty of ejecting blood (aortic impedance).
    • Force of contraction is influenced by end diastolic volume (Starling's Law) and contractility.
    • Contractility is increased by sympathetic stimulation.
    • Aortic impedance, or the resistance to blood ejection from the ventricle, is largely determined by the TPR (total peripheral resistance).

    Direct Effects of Arterial and Venous Pressures on Stroke Volume

    • Increased venous pressure leads to increased stroke volume.
    • Decreased arterial pressure leads to increased stroke volume.

    Control of Heart Rate

    • Heart rate is controlled by autonomic outflow to the heart, including baroreceptors, and signals from the carotid sinus.
    • The carotid sinus senses arterial pressure.
    • Signals are sent to the medulla to regulate the heart.
    • Falls in arterial pressure increase heart rate by reducing parasympathetic activity and increasing sympathetic activity.
    • Increases in heart rate increase contractility via increasing sympathetic activity.

    Total Peripheral Resistance (TPR) Changes

    • TPR affects both arterial and venous pressure.
    • If TPR falls and cardiac output remains constant, arterial pressure falls, and venous pressure rises.
    • If TPR rises and cardiac output remains constant, arterial pressure rises, and venous pressure falls.

    Changes in Demand for Blood

    • Total peripheral resistance (TPR) is inversely proportional to the body's need for blood.
    • Metabolic changes affect TPR and generate signals in the form of changes in arterial and venous pressure.
    • For example, eating a meal increases blood flow to the gut. This is signaled by local vasodilators and leads to decreased TPR.

    Demand-Led Pumping

    • If the body needs more blood, the heart needs to pump more to meet the 'demand'.
    • Demand is expressed as changes in arterial and venous pressures.
    • The heart responds to these changes (falls in arterial pressure and rises in venous pressure) by increasing its pumping action.

    Control of Cardiac Output Summary

    • Cardiac output is influenced by stroke volume (preload, inotropic state, afterload), and heart rate.
    • Both arterial and venous pressure affect these parameters, and in turn cardiac output.

    Compensatory Mechanisms of Blood Pressure

    • Decreased systemic blood pressure stimulates central baroreceptors
    • This triggers the release of vasopressin from the pituitary gland to increase peripheral vascular resistance (vasoconstriction) to increase blood pressure.

    Summary

    • Falls in arterial pressure increase cardiac output via increased stroke volume and heart rate.
    • Rises in venous pressure lead to increased heart rate and increased stroke volume.

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    Description

    This quiz explores the key concepts surrounding cardiac output, including its definition and components such as stroke volume and heart rate. It delves into the physiological factors influencing stroke volume and examines the principles of ventricular filling, compliance, and Starling's Law. Test your understanding of these critical cardiovascular principles.

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