Cardiac Output and Stroke Volume Quiz
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Questions and Answers

What is the formula for calculating cardiac output?

  • CO = HR + SV
  • CO = SV / HR
  • CO = HR * SV (correct)
  • CO = HR - SV

    • Which of the following factors does NOT influence stroke volume?

  • Afterload
  • Contractility
  • Preload
  • Cardiac Cycle Duration (correct)

    • How does an increase in preload affect stroke volume according to the Frank-Starling mechanism?

  • It increases stroke volume (correct)
  • It does not affect stroke volume
  • It decreases stroke volume
  • It stabilizes stroke volume

    • What is the primary effect of increased afterload on stroke volume (SV)?

    <p>Decreases SV</p> Signup and view all the answers

    What occurs in a failing heart in terms of the Frank-Starling curve?

    <p>It becomes flat, leading to low output at high pressures</p> Signup and view all the answers

    Which mechanism describes the relationship between ventricular filling pressure and cardiac output?

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

    Which of the following factors can increase afterload?

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

    What role does contractility play in the cardiac output (CO) equation?

    <p>It enhances the force of contraction</p> Signup and view all the answers

    What does an increase in diastolic ventricular volume typically result in?

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

    Which of the following does NOT increase preload?

    <p>Increased arterial pressure</p> Signup and view all the answers

    Which condition would most likely lead to decreased CO due to increased afterload?

    <p>Pulmonary hypertension</p> Signup and view all the answers

    How does the Frank-Starling mechanism affect cardiac output?

    <p>Increased preload leads to increased ejection and output</p> Signup and view all the answers

    Which factor is likely to increase venous return?

    <p>Increased venous pressure</p> Signup and view all the answers

    What impact does a high heart rate have on preload?

    <p>Decreases preload if too high</p> Signup and view all the answers

    Which of these factors is NOT involved in affecting afterload?

    <p>Myocardial oxygen demand</p> Signup and view all the answers

    What happens to stroke volume and cardiac output if contractility increases?

    <p>Both increase</p> Signup and view all the answers

    Which condition is a major cause of Heart Failure with reduced Ejection Fraction (HFrEF)?

    <p>Coronary Artery Disease</p> Signup and view all the answers

    What is a primary characteristic of Heart Failure with preserved Ejection Fraction (HFpEF)?

    <p>Increased diastolic stiffness</p> Signup and view all the answers

    Which of the following factors is NOT typically associated with HFpEF?

    <p>Genetic cardiomyopathies</p> Signup and view all the answers

    In HFrEF, which of the following conditions is characterized by high End-Diastolic Volume (EDV)?

    <p>Low ejection fraction and high EDV</p> Signup and view all the answers

    What effect does fibrosis have on cardiac function in heart failure?

    <p>It leads to stiffer and less elastic hearts</p> Signup and view all the answers

    Which of the following is NOT a factor influencing the risk of developing heart failure?

    <p>Chronic hypotension</p> Signup and view all the answers

    What happens to cardiac output in heart failure (both HFrEF and HFpEF)?

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

    Which of the following correctly describes a hallmark of HFpEF?

    <p>Increased diastolic pressure</p> Signup and view all the answers

    What primarily determines the oxygen supply to the myocardium?

    <p>Coronary circulation flow</p> Signup and view all the answers

    What role does Ca++ play in the excitation-contraction coupling process?

    <p>It promotes the interaction between actin and myosin.</p> Signup and view all the answers

    How is myocardial energy demand primarily satisfied in the heart?

    <p>Via electron transport in mitochondria</p> Signup and view all the answers

    What happens to the contractility of the heart when b-blockers are administered?

    <p>It decreases calcium release, limiting contractility.</p> Signup and view all the answers

    During which phase is coronary blood flow significantly reduced?

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

    What effect does vasoconstriction have on coronary blood flow?

    <p>It decreases coronary flow and oxygen supply</p> Signup and view all the answers

    Which of the following statements about heart failure with reduced ejection fraction (HFrEF) is true?

    <p>It results in both reduced stroke volume and ejection fraction.</p> Signup and view all the answers

    Which mechanism is primarily responsible for the release of Ca2+ in smooth muscle contraction?

    <p>IP3 receptor activation on the sarcoplasmic reticulum</p> Signup and view all the answers

    What is the role of SERCA in cardiac muscle cells?

    <p>It pumps calcium back into the sarcoplasmic reticulum.</p> Signup and view all the answers

    How is ejection fraction (EF) mathematically defined?

    <p>EF = SV/EDV * 100</p> Signup and view all the answers

    What impact does activation of B-AR signaling have on calcium levels in cardiac tissue?

    <p>It increases calcium release through modulation of RyR and channels.</p> Signup and view all the answers

    What function does PLB serve in relation to SERCA?

    <p>PLB inhibits the action of SERCA.</p> Signup and view all the answers

    Which of the following correctly describes heart failure with preserved ejection fraction (HFpEF)?

    <p>Stroke volume is low, but EF remains normal.</p> Signup and view all the answers

    What initiates depolarization in phase 0 of the action potential?

    <p>Na+ influx</p> Signup and view all the answers

    What is the role of K+ channels during phase 2 of the cardiac action potential?

    <p>Remain open to facilitate repolarization</p> Signup and view all the answers

    Which statement about the differences between SA/AV node and ventricular action potentials is correct?

    <p>SA node shows a smaller Na+ influx compared to ventricular action potentials.</p> Signup and view all the answers

    What happens during phase 3 of the cardiac action potential?

    <p>Ca++ channels stop influx</p> Signup and view all the answers

    The resting membrane potential is established in which phase of the cardiac action potential?

    <p>Phase 4</p> Signup and view all the answers

    How do adrenergic signaling cascades affect heart rate in the SA node?

    <p>They enhance Na+ channel modification.</p> Signup and view all the answers

    What role does Na+/Ca++ exchange play in normalizing ion levels after action potentials?

    <p>It regulates the resting membrane potential.</p> Signup and view all the answers

    What is the consequence of disturbances or mutations in ion channels during action potentials?

    <p>Potential development of arrhythmias.</p> Signup and view all the answers

    Study Notes

    Cardiac Physiology Background

    • Lecture date: 12/11/2023
    • Course: BPS 337
    • Instructor: Richard T Clements

    Cardiac Physiology Refresher

    • Cardiac Cycle
    • Determinants of Cardiac Output (CO)
    • Pressure-Volume (PV) Loops
    • Mechanism of Cardiac Contraction/β-AR Modulation
    • Cardiac Function and Heart Failure (HF)
    • Coronary Circulation and O2 Supply/Demand
    • Cardiac Action Potential/β-AR Modulation

    Cardiac Cycle

    • Aortic valve opens
    • Isovolumic contraction
    • Ejection
    • Isovolumic Relaxation
    • Rapid Inflow
    • Mitral valve closes
    • Mitral valve opens
    • Diastasis
    • Atrial Systole

    Pressure-Volume Loops

    • Shows the relationship between left ventricular (LV) pressure and volume during the cardiac cycle.
    • Includes key points like End-Diastolic Volume (EDV), End-Systolic Volume (ESV), Stroke Volume (SV), End-Diastolic Pressure (EDPVR), End-Systolic Pressure (ESPVR)

    Multiple PV Loops Over Time

    • Multiple pressure-volume loops on graph demonstrates cardiac cycle variations over time.

    Cardiac Output

    • CO = HR * SV
    • Factors affecting SV: preload, afterload, contractility
    • Determinants of Cardiac Output: afterload, preload, contractility, and heart rate.

    Preload

    • The pressure that fills the ventricle.

    • Increases in preload increase stroke volume (SV) and cardiac output (CO).

    • Frank-Starling Mechanism: the more the ventricle wall is stretched, the more force is produced

    • Intrinsic properties of cardiac myocytes (stretch, tension) and Ca++ release machinery

    • Factors affecting preload: increased venous return, increased venous blood volume, increased venous pressure, decreased venous compliance, atrial inotropy, increased ventricular compliance

    Afterload

    • Pressure or resistance the heart has to actively work against.
    • High blood pressure = high afterload
    • Factors Affecting Afterload: blood pressure, vascular resistance, stiffness of the aorta, peripheral circulation
    • Increases in afterload decrease SV and CO

    Contractility

    • Force generated for a given sarcomere/fiber length
    • Modified by catecholamines, sympathetic/parasympathetic activity, inotropes, preload, afterload (Anrep Effect), HR (Bowditch Effect)

    ESPVR (Ees) and Contractility

    • End systolic pressure-volume relationship
    • Shows relationship of contractility to cardiac output (CO)

    Preload, Afterload, and Contractility

    • Interdependent: changes in one affect the others.

    Heart Rate

    • Increases cause an increase in CO (CO = HR * SV).
    • High heart rate = Impaired filling (decreased preload), decreased stroke volume and reduced heart rate.
    • High heart rate increases myocardial O2 demand and impairs contractility

    Summary: CO and SV

    • 4 Determinants (preload, afterload, contractility, and heart rate)
    • Frank-Starling Mechanism (heart responds to increased preload with increased ejection and CO)
    • ESPVR slope is contractility (Ees). Increased contractility increases CO. Increased afterload decreases CO.
    • PV loops useful to determine parameters regarding cardiac physiology

    Cardiac Contraction

    • All about Ca++
    • Cardiac Troponin-Tropomyosin complex inhibits myosin binding to actin.
    • Increases in cytosolic Ca++ bind to TnC allowing myosin and actin interaction, triggering contraction.
    • Relaxation occurs when Ca++ levels decrease.

    Excitation-Contraction (E-C) Coupling

    • Action potential causes Ca++ influx = depolarization.
    • Further Ca++ release from sarcoplasmic reticulum (SR).
    • Ca++ binds to troponin to initiate contraction.
    • Ca++ is removed to initiate relaxation.

    B1-AR PKA Activation Promotes Ca++ Release

    • PKA increases Ca++ release via RyR and external Ca++ channels.
    • pPLB inhibits SERCA to increase Ca++ stores.

    Summary Cardiac Contraction

    • Action potential depolarizes cell and activates PM Ca++ channels
    • Increased Ca++ causes Ca++ release from the SR.
    • Released Ca++ binds TnC to allow myosin:actin interaction and contraction
    • SERCA activates to restore Ca++ to SR and NCX expels Ca++ from the plasma membrane
    • Cell repolarizes.
    • B-AR activation causes PKA to increase RyR and SERCA activity. Increased intracellular Ca++ increases contractility

    Ejection Fraction and Heart Failure (HF)

    • Amount of blood ejected from the heart (stroke volume) divided by the amount in the heart at diastole (EDV) expressed as a percentage.
    • EF = SV/EDV*100
    • If SV is down, CO is down

    Heart Failure with Reduced Ejection Fraction (HFrEF)

    • Reduced contractility, causing decreased stroke volume (SV), and ejection fraction (EF).
    • Increased End-Diastolic Volume (EDV)

    Heart Failure with Preserved Ejection Fraction (HFpEF)

    • Impaired relaxation or stiffness of the ventricles.
    • Preserved Ejection Fraction (EF), but diastolic dysfunction
    • Increased End-Diastolic Volume Pressure (LVEDP)

    Causes of HFrEF

    • Structural abnormalities, Previous MI (myocardial infarction), Coronary artery disease, Diabetes, Metabolic syndrome, Lipids, Inflammation, O2 disruptions, etc.

    Causes of HFpEF

    • Not entirely clear mechanism, but factors like obesity, hypertension, CAD, diabetes, etc., are implicated.

    Fibrosis and Cardiac Remodeling

    • Fibrosis and ECM deposition are major components of cardiac remodeling (in addition to hypertrophy).
    • Deposition of ECM molecules promotes fibrosis. Fibrotic hearts are stiffer and less elastic, impairing contractile function.

    Coronary Circulation and Blood Flow

    • Highest oxygen demand in the body.
    • Coronary A-VO2 difference is the highest of any circulation (10-13 ml/100ml).
    • Coronary venous blood is VERY dark.
    • Flow changes dramatically due to metabolic demand (autoregulation and reactive hyperemia)
    • Flow is reduced during systole due to heart muscle contraction and increased coronary resistance. Majority of flow is during diastole.

    Myocardial Energy Demand

    • Balance of myocardial O2 supply and O2 demand.
    • Factors affecting supply: heart rate, oxygen content of blood, coronary perusion.
    • Factors affecting demand: heart rate, contractility, afterload, preload.
    • Oxygen consumption/demand is all electron transport in mitochondria.

    O2 Supply

    • Coronary circulation subject to vasoconstriction & vasodilation (same as peripheral circulation).
    • Vasodilation enhances coronary flow & O2 supply, vasoconstriction reduces.
    • Atherosclerosis impairs normal vasoregulation & reducing coronary flow.
    • Coronary flow is determined by pressure (MAP) and resistance (R).

    Molecular Basis of Smooth Muscle Contraction

    • Agonists activate receptors, leading to plasma membrane Ca++ channel opening.
    • Depolarization of smooth muscle with or without signaling causes Ca++ release from intracellular stores (via IP3 receptor).
    • Ca++ activates MLCK & phosphorylates MLC.
    • MLC phosphorylation causes myosin activation & contraction.

    Molecular Basis of VSMC Dilation

    • In endothelial cells: receptor activated pathways activate nitric oxide synthase (eNOS) releases NO.
    • NO (nitric oxide) diffuses to VSMC activating soluble guanylyl cyclase (SGC) converting GTP to cyclic GMP (cGMP).
    • SGC & cGMP cause a coordinated response to limit VSMC contraction
    • Decrease Ca++ influx/release
    • Decrease MLC phosphorylation
    • Increase K+ efflux
    • PKA activation inhibits PKG which limits MLC phosphorylation

    PKA and smooth muscle dilation

    • PKA has opposite effect on smooth muscle than on the heart.
    • PKA inhibits MLCK and activates MLCP to reduce contraction.

    Summary of VSMC Signaling

    • Vessels dilate/constrict dramatically changing flow.
    • Signalling mechanism of vessel contraction/dilation (signaling pathways & factors).
    • Mechanisms of dilation (Nitric oxide, cGMP, PKG).

    Summary Coronary Circulation

    • Coronary circulation provides O2 to the heart.
    • Factors that increase CO increase cardiac O2 demand (preload, afterload).
    • O2 supply in the coronary circulation can be modified by vasodilation and impaired contraction.

    Arrhythmia: Propagation of the Action Potential

    • SA nodal cells in atria initiate contraction.
    • Impulse travels through atria (P-wave).
    • Impulse travels from atria to ventricle (via AV node) (PR interval)
    • Conduction through Purkinjie system to ventricle .
    • Ventricular cardiomyocytes spread the action potential (QRS).
    • Cardiomyocytes repolarize (T wave)

    Action Potential and Ca++ Cycling

    Membrane Potential and Ionic Gradients

    • Resting membrane potential determined by differences in ion concentrations inside and outside the cell.
    • Large amounts of Na+ outside, K+ inside. Opening of ion channels cause rapid influx/efflux. Action potential changes dependent of these gradients.

    SA/AV Node Action Potentials

    • Na+ channel influx (funny current), Phase 4
    • Depolarization opens Ca++ channels, Phase 0
    • K+ channels open, causing efflux, Phase 3

    Sympathetic Stimulation of Heart Rate

    • Activation of β1 receptors increases Na+ current (funny current).
    • Increased positive charge allows Ca++ channels to open, increasing heart rate.
    • Parasympathetic stimulation decreases funny currents.

    ANS Effects Heart Rate

    • Increasing sympathetic stimulation or B-AR activation increases Na+ current (phase 4).
    • SA nodal cells reach threshold and Ca++ channels open earlier to increase heart rate. Vagal stimulation and Beta blockers have opposite effects on SNS.

    Cardiomyocyte Action Potential

    • Na+ channels open due to depolarization of neighboring cells.
    • K+ channels open (efflux) to repolarize the cell.
    • Ca++ channels open to assist with contraction.

    SA/AV Node and Ventricular action potentials

    • SA and AV node and ventricular action potentials differ greatly.

    Action Potential Ion Currents

    • Different proteins and channels contribute to phase based action potential depolarization & repolarization (0,1,2,3,4).
    • Disturbances can cause cardiac arrhythmia

    ECG Signal

    ECG Refresher of Intervals and Waves

    • ECG measures electrical activity in the heart.
    • Different waves (P, QRS, T) & intervals (PR, QRS, ST, QT) represent different stages of cardiac cycle.

    Action Potential/ECG Summary

    • Na+ high outside, K+ high inside.
    • Na channels open, positive charge inside
    • K+ and Ca++ channels balance & repolarize.
    • SA and AV node action potential propagation differ from cardiomyocytes.

    Summary: Things to Know This Lecture

    • Cardiac contraction mechanism
    • B-AR modulation of contractility
    • Vascular contraction mechanism
    • How A1-AR & other contractile agonists modulate contraction
    • Vascular dilation mechanism.
    • How Beta adrenergic agents increase HR.
    • SA/AV node modulation of cardiac action potential
    • PKA dependent modification of Na channels
    • Determinants of cardiac output
    • Do NOT worry about HF, PV loops, & O2 supply/demand for this test.

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    Cardiac_Vascular Physiology Review 2023 PDF

    Description

    Test your knowledge on cardiac output, stroke volume, and the factors affecting these concepts. This quiz covers key mechanisms such as the Frank-Starling principle and the impacts of preload, afterload, and contractility. Challenge yourself with questions about heart failure and cardiovascular physiology.

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