Regulation of the Cardiac Output I and II Flashcards Preview

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Flashcards in Regulation of the Cardiac Output I and II Deck (15):

Preload and Afterload

  • Preload
  • Afterload
  • Factors contributing to afterload
  • Effect of increasing afterload on preload

  • Preload
    • Pressure stretching the ventricle after passive filling & atrial contraction
    • Major factor that augments cardiac output via the Frank-Starling mechanism
    • Heart can contract more with greater ability to stretch/contract
    • Increased by the same factors that increase venous return
  • Afterload
    • Mean tension produced by a chamber of the heart in order to eject blood
    • Force that must be overcome to eject blood from the ventricle
    • Total peripheral resistance (TPR): main determinant of afterload
    • Hypertension --> increased pressure --> more afterload --> heart has to work harder
  • Factors contributing to afterload
    • Aortic pressure: an increase in peripheral resistance increases afterload
      • Aortic valve closes earlier during the cardiac cycle, cardiac output is reduced, & end systolic volume increases
    • Aortic valve stenosis increases ventricular stiffness
  • Effect of increasing afterload on preload
    • Increasing afterload increases preload
    • Increased end systolic volume is added to normal venous return
    • Increase in preload activates the Frank-Starling mechanism to compensate for the reduction in stroke volume caused by the increase in afterload


Treatment following a heart attack where the left ventricle is damaged

  • Vasodilator drugs
    • Augment stroke volume by decreasing afterload
    • Reduce ventricular preload
  • When arterial pressure is reduced, ventricle can eject blood more rapidly
    • Increases troke volume
    • Decreases end-systolic volume
    • Ventricle won't fill to same end-diastolic volume before the afterload reduction
    • Higher stroke volumes can be sustained by weaker ventricular contractions
    • Diminishes risk of congestive heart failure


Intrinsic and extrinsic factors that influence cardiac output

  • Intrinsic factors
    • Heart rate
    • Contractility (end systolic pressure-volume relationship)
  • Extrinsic factors
    • Preload (end diastolic volume)
      • If preload increases, CO increases w/o any changes in HR & contractility
    • Afterload (end systolic pressure / mean arterial pressure)
      • If afterload increases, CO decreases unless HR & contractility also increase


Influence of heart and vasculature on cardiac output

  • Vascular function curve (venous return curve)
  • Cardiac function curve
  • Assumptions
  • Equations
  • Significance

  • Vascular function curve (venous return curve)
    • Considers how changes in vasculature (flow, cardiac output) affects systemic venous pressure (pressure in the circulation, atrial pressure)
  • Cardiac function curve
    • Considers how changes in systemic venous pressure affects cardiac output
  • Assumptions
    • Cardiac output = venous return
    • Central venous pressure = right atrial pressure
  • Equations
    • Pa = systemic arterial pressure
    • Pv = systemic venous pressure
    • R = 20 mmHg / L/min
    • Q = CO = 5 L/min
    • R = ΔP / Q = (Pa - Pv) / Q
    • Pa = 100 mmHg + Pv
  • Significance
    • Systemic arterial pressure is 100 mmHg greater than Pv


Systemic filling pressure (Psf)

  • Definition
  • Value
  • Compliance & pressure

  • Systemic filling pressure (Psf)
    • Effective pressure head in the systemic circulation pushing the blood back into the heart
    • Equal pressure in the veins & arteries when the heart is stopped
  • Pv = 2 mmHg, Pa = 102 mmHg --> Psf = 7 mmHg
    • Psf is closer to venous pressure than arterial pressure b/c venous compliance is ~19x higher than arterial compliance
  • Compliance & pressure
    • C = ΔV/ΔP
    • ΔVa = ΔVv when the heart is stopped
    • CaΔPa = CvΔPv
    • Cv = 19Ca
    • ΔPa = 19ΔPv
    • The change in arterial pressure is 19x larger than the change in venous pressure when the heart is stopped


Vascular function curve (venous return curve)

  • Equations
  • Cardiac factors
  • Vascular factors

  • Equations
    • Pv = Psf - (R*Ca / Ca+Cv)*Q
    • Pa = Psf + (R*Cv / Ca+Cv)*Q
  • Cardiac factors
    • Venous pressure (Pv) = right atrial pressure
    • Flow through the vascular system (Q) = venous return = cardiac output
  • Vascular factors
    • Peripheral resistance (R)
    • Arterial & venous compliance (Ca & Cv)
    • Systemic filling pressure (Psf)


Relationship b/n right atrial pressure & venous return (cardiac output)

  • Relates venous return (cardiac output) to right atrial pressure
  • When right atrial pressure = Psf, venous return (or cardiac output) is 0 since there's no pressure difference to drive blood flow
  • As right atrial (venous) pressure increases, venous return (cardiac output) decreases
  • As right atrial (venous) pressure decreases, flow through the CV system (venous return or cardiac output) increases
  • Little additional venous return b/n right atrial pressure of 0 & -8 mmHg
    • Negative right atrial pressure tends to suck together the walls of the large veins near the heart, limiting further increase in blood flow


Resistance to vascular return (RVR) & its relation to the vascular function curve

  • Resistance to movement of blood through the vasculature
    • Total peripheral resistance + consideration of compliance & vasculature
    • RVR = (R*Ca / Ca+Cv) = (Psf - Pv) / Q = 1mmHg / L/min
  • Slope of vascular function curve = 1 / RVR
    • As RVR increases, slope decreases
    • Higher RVR
      • A given change in right atrial/venous pressure causes smaller changes in cardiac output/venous return
      • Max cardiac output / venous return is lower


Circulatory blood volume

  • Unstressed volume
  • Stressed volume
  • Circulatory blood volume vs. Psf

  • Unstressed volume = 4L
    • At a circulatory blood volume of 4L, Psf = 0
    • Volume is insufficient to contribute to pressure b/c there's insufficient stretch of the vessel walls
  • Stressed volume > 4L
    • Any additional volume inside the CV system above the unstresed volume
  • Small change in circulatory blood volume --> huge change in Psf
    • --> vascular function curve shifts up & to the right
    • --> at a particular right atrial pressure, cardiac output & venous return are much larger
    • When circulatory blood volume increases, it's easier for the heart to fill w/ blood, & cardiac output increases


Cardiac function curve

  • Definition
  • Right atrial pressure vs. cardiac output
  • Heart rate vs. cardiac output
  • Hypereffective vs. hypoeffective ventricle

  • Cardiac function curve
    • Effects of right atrial pressure on cardiac output
    • Effects of changing preload on cardiac output & blood pressure
  • Right atrial pressure vs. cardiac output
    • Low right atrial pressure --> cardiac output = 0
      • Too little blood in cardiac chambers to generate pressure during systole
    • Right atrial pressure > 4 mmHg --> cardiac output = max
      • Ventricle fills maximally & can't accommodate more blood
  • Heart rate vs. cardiac output
    • Modest increases in HR facilitate cardiac output despite shorter ventricular filling time due to the Bowditch effect
    • Large increases in HR shorten filling time so much that cardiac output plummets
  • Hypereffective vs. hypoeffective ventricle
    • Hypereffective ventricle: when SNS activity is high or ventricle is hypertrophied, muscle mass has increased, & afterload increases
    • Hypoeffective ventricle: when SNS activity is low or ventricle is damaged, afterload decreases


Equilibrium Point

  • Definition
  • Normal
  • Increased blood volume
  • SNS stimulation
  • Exercise

  • Equilibrium point: where vascular function & cardiac function curves intersect
    • Indicates cardiac output, venous return, & right atrial pressure at this physiological condition
  • Normal
    • Right atrial pressure = 0 mmHg
    • Cardiac output & venous return = 5 L/min
  • Increased blood volume
    • Psf increases
    • Shifts vascular function curve up
    • Doesn't affect cardiac function curve
  • SNS stimulation
    • Cardiac function shifts up & to the left
    • Vascular function curve shifts up & to the right
    • Due to...
      • Increased cardiac contractility
      • Increased heart rate
      • Decreased venous compliance
      • Increased total peripheral resistance
    • Increased afterload opposes this shift so cardiac output only rises a little
  • Exercise
    • Afterload decreases as arterioles dilate
    • Skeletal muscle pumping --> increase venous return --> increase cardiac output


Pressure volume relationship: external work, diastolic & systolic pressure curves

  • External work (EW): funcitonal pressure-volume curve
  • Diastolic pressure curve: end diastolic pressure-volume relationship (EDPVR)
    • Below 150ml: diastolic pressure doesn't increase greatly w/ increased volume in noncontracting ventricles
    • Above 150ml: diastolic pressure increases rapidly b/c the ventricle is fully filled & the heart tissue can't stretch anymore
  • Systolic pressure curve: end systolic pressure-volume relationship (ESPVR)
    • Represents the max pressure at a particular ventricular volume
    • During ventricular contraction, systolic pressure increases & reaches a maximum at a ventricular volume of 150-170ml
    • As volume increases further, systolic pressure decreases b/c the actin & myosin of cardiac muscle are pulled apart to suboptimal lengths


Pressure-volume loops

  • Aortic valve closure
  • Slope of ESPVR
  • Effect of increasing cardiac output on MAP & afterload

  • Aortic valve closure: upper left corner of pressure-volume curve
    • Pressure at this poitn is nearly MAP
    • ESPVR shows mean arterial pressure generated at different ventricular volumes
  • Slope of ESPVR: dependent on ventricular contractility
    • Under sympathetic stimulation, slope steepens so that at a particular ventricular volume, pressure is greater
  • Increasing cardiac output increases MAP & afterload
    • Increasing contractility facilitates & opposes increasing cardiac output
    • Increases in cardiac output are thus relatively modest


Stroke volume vs. afterload and preload

  • Effects of increased afterload on stroke volume
  • Effects of increased preload on stroke volume
  • Factors that contribute to an increase in preload
    • Venous compliance (venoconstriction)
    • Resistance to venous return (RVR)
    • Blood volume
    • Intrathoracic pressure
    • Heart rate
    • Ventricular stiffness
    • Posture
    • Skeletal muscle pumping

  • Effects of increased afterload on stroke volume
    • Alpha-receptor agonist increases afterload
    • Ventricular pressure must increase for aortic valve to open
    • Valve closes earlier
    • Stroke volume is reduced
    • Effects are ameliorated when contractility increases w/ afterload
  • Effects of increased preload on stroke volume
    • More filling of ventricle during diastole
    • Stroke volume increases w/ additional filling due to the Frank-Starling effect
  • Factors that contribute to an increase in preload
    • Decreased venous compliance (venoconstriction)
    • Decreased resistance to venous return (RVR)
    • Increased blood volume
    • Negative intrathoracic pressure
    • Decreased heart rate (more time for ventricle to fill)
    • Decreased ventricular stiffness
    • Supine posture
    • Increased skeletal muscle pumping


Effects of cardiomyopathy and myocardial infarction on the pressure-volume relationship

  • Cardiomyopathy
    • Causes scarring & stiffening of the left ventricle
    • EDPVR curve shifts up
    • Pressure inside ventricle increases quickly as fluid enters the chamber
    • Filling is limited before intraventricular pressure matches atrial pressure
    • EDV decreases --> SV decreases
  • Myocardial infarction
    • Causes scarring of the ventricular wall
    • Loss of contractility
    • SV decreases