Physio Chapter 20
Saturday, January 19, 2013
5:14 PM
Cardiac Output, Venous Return, and Their Regulation
 Cardiac Output (CO) is the amount of blood pumped into the aorta each minute.
 Venous Return (VR) is the amount of blood flowing into the right atrium (RA) each minute.
 Normal Values for CO at rest and during activity
o Following factors affect CO
 Level of body metabolism
 Whether the person is exercising
 Age
 Size of body
o Cardiac out put increases roughly in proportion to the surface area of the body.
o Declining cardiac index is indicative of declining activity with age.
 Control of CO by VR - Frank-Starling Mechanism
o The heart itself is not the primary controller of CO, the VR is.
o The heart has a built in mechanism that allows it to pump out whatever it receives from the
body into the Right Atrium - Frank-Starling Mechanism.
 Increased blood flow into the RA increases muscles stretch, which causes the cardiac
muscle to contract with increase force.
 Increased stretch of the SA node also increases heart rate.
 Stretched RA also starts a nervous reflex (Bainbridge Reflex) which goes first to the
motor center of the brain and then back to the heart via sympathetics and vagi, to
increase heart rate.
o Under most normal conditions, the HR is controlled almost entirely by peripheral factors
that determine VR. The heart becomes the limiting factor in CO.
o Cardiac Output is the Sum of Blood Flow Regulation in all Local Tissues in Body - Tissue
Metabolism Regulates most Local Blood Flow
 In most tissues, blood flow increases in proportion to metabolism.
 All local blood flows summate to form the venous return.
 Effect of Total Peripheral Resistance on the Long-Term CO Level
 CO reciprocally varies with changes in total peripheral resistance (TPR).
 When the TPR increases above normal, the CO falls; likewise, when TPR
decreases, the CO increases.

𝐶𝑂 = 𝐴𝑟𝑡𝑒𝑟𝑖𝑎𝑙 𝑃𝑟𝑒𝑠𝑠𝑢𝑟𝑒 ÷ 𝑇𝑜𝑡𝑎𝑙 𝑃𝑒𝑟𝑖𝑝h𝑒𝑟𝑎𝑙 𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑇𝑃𝑅)
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o
Anytime the long-term level of TPR resistance changes, the CO will change
in exactly the opposite direction.
The Heart Has Limits for the CO That it Can Achieve
 Limits to amount of blood the heart can pump is shown by cardiac output curves.
 The normal human heart, working without any special stimulation, can pump up to 2.5
times the normal venous return before the heart becomes the limiting factor in CO.
 Factors that cause Hypereffective Effect (Hearts pumping better than normal)
 Nervous Stimulation
 Sympathetic Stimulation and Parasympathetic Inhibition greatly increases
heart rate and increases the strength of heart contraction (contractility) to
twice its normal strength.
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o
Hypertrophy of Heart Muscle
 Long-term increased heart workload, but NOT so much excess load that it
damages the heart, causes the muscle to increase in mass and contractile
strength in the same way that heavy exercise causes skeletal muscles to
hypertrophy.
 Factors affecting hypertrophy
 Any factor that decreases the heart's ability to pump blood causes
hypertrophy.
What is the role of the Nervous System in Controlling CO?
 Importance of Nervous System in maintaining Arterial Pressure When VR and CO
increase.
 When a dilating agent was applied to vessels, the Arterial Pressure was
maintained by the Nervous System, which allowed the CO to increase.
 Remember: 𝐶𝑂 = 𝐴𝑟𝑡𝑒𝑟𝑖𝑎𝑙 𝑃𝑟𝑒𝑠𝑠𝑢𝑟𝑒 ÷
𝑇𝑜𝑡𝑎𝑙 𝑃𝑒𝑟𝑖𝑝h𝑒𝑟𝑎𝑙 𝑅𝑒𝑠𝑖𝑠𝑡𝑎𝑛𝑐𝑒 (𝑇𝑃𝑅)

o
By decreasing TPR (vessel dilation) and maintaining Arterial
Pressure, CO increases reciprocally to TPR.
 If, on the other hand, a dilation agent is applied and the Nervous System
inhibited, this would cause and increase in TPR and a decrease in AP which
would cause CO to decrease.
 Effect of Nervous System to Increase AP during exercise
 Exercise = Increased Metabolism = Increased Vessel Dilation for More
Nutrients/Oxygen = Decreased TPR
 The nervous system compensates.
 Brain Activity that sends motor signals to muscles also sends signals into
ANS to excite circulatory activity, causing large vein constriction, increased
Heart Rate, and increased contractility of the heart.
 This increases AP to force more blood flow through active muscles.
Pathologically High and Low CO
 High CO Caused by Reduced TPR
 Beriberi: Insufficient vitamin thiamine (vB1) in diet.
 Causes disruption of metabolism which increases dilation and decreases
TPR.
 Levels of CO and VR often increase to twice the normal.
 Arteriovenous Fistula (shunt)
 Shunt of blood from major artery to major vein which decrease TPR.
Greatly increases CO and VR.
 Hyperthyroidism
 Increased Metabolism = Increased Oxygen Usage = Vasodilation =
Decreased TPR = Increased CO and VR to 40-80% above normal
 Anemia
 Reduced Viscosity of Blood and Diminished Delivery of Oxygen to Blood =
Increased Vasodilation = Decreased TPR = Increased CO and VR
 Low Cardiac Output
 Pumping Effectiveness of Heart Falls too low
 Severe Coronary Blood vessel blockage/MI, Severe valvular heart disease,
myocarditis, cardiac tamponade, cardiac metabolic derangements

o
When CO falls so low that tissues begin to have nutrient deficiency, the
condition is called cardiac shock
 Venous Return Falls too low
 Decreased Blood Volume: Most Common, resulting most often from
hemorrhage
 Loss of blood decreases filling of vascular system where there is not
enough blood to create peripheral pressures high enough to push
the blood back to the heart.
 Acute Venous Dilation
 Results when the SNS suddenly becomes inactive
 Blood pools in the vessels and does not return to the heart
 Obstruction of Large Veins
 Blood cannot flow back into heart
 Decreased Tissue Mass, especially decreased skeletal muscle mass
 Decreased muscle size decreases amount of blood needed which
decreases muscle blood flow and CO.
 These all can cause Circulatory Shock
Quantitative Analysis of CO Regulation
 Two primary factors concerned with CO regulation
 Pumping ability of heart - seen by Cardiac Output Curves
 Peripheral Factors that affect flow of blood from veins to heart - seen by Venous
Return Curves
 Cardiac Output Curves
 Effect of External Pressure Outside the Heart on CO Curves
 Normal External Pressure is equal to the normal intrapleural pressure
(pressure in the chest cavity), which is -4 mmHg.
 An increase in pressure outside makes it harder for the heart to
expand and therefore harder to pump.
 Factors that change intrapleural pressure and shift cardiac output curvees
 Cyclical changes of intrapleural pressure during respiration: about
±2 mmHg during resting and as much as ±50 mm Hg during
strenuous breathing.
 Breathing against a negative pressure: more negative pressure =
shift of curve to the left = easier to breath.
 Positive Pressure Breathing: shifts curve to the right (harder to
breathe)
 Opening the thoracic cage: increases intrapleural pressure to 0
mmHg and shifts curve to right = harder to breath.
 Cardiac Tamponade: Increase in fluid in pericardial cavity =
increased external cardiac pressure = shift in curve to the right =
harder to breath.
 Combinations of Different Patterns of Cardiac Output Curves
Final Cardiac Output Curve can change as result of changes in external

cardiac pressure and effectiveness of heart as a pump.
 Venous Return Curves
 Three principal factors affect VR:
 Right Atrial Pressure: exerts a backward force on veins to impede blood
flow
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Degree of filling of systemic circulation: forces blood towards heart
Resistance to blood flow: between peripheral vessels and RA.
Normal Venous Return Curve
 Curve relates VR to RA pressure.
 When heart pumping decreases and causes RA pressure to rise, the
backward force of rising atrial pressure on veins decreases VR.
 If all nervous effects are prevented, VR decreases to zero when RA
pressure reaches +7mm Hg.
 Mean Systemic Filling Pressure: +7mmHg or when the arterial and venous
pressures come to equilibrium and all flow in systemic circulation stops.
 Due to clamping of vessels mainly.
Plateau in VR Curve at Negative Atrial Pressures
 When the RA pressure falls BELOW zero VR virtually stops.
 Caused by collapse of veins entering the chest.
 Negative pressure in RA sucks the walls of veins together where
they enter the chest and pinch off the flow.
Mean Circulatory Filling Pressure: when blood flow stops and pressures
everywhere in the circulation become equal.
 Different from Msf because the heart actually stops.
 Effect of Blood Volume on Mean Circulatory Filling Pressure
 Greater the volume of blood = greater Mean Circulatory Filling
Pressure because extra blood volume stretches walls of vasculature
 Effect of SNS on Mean Circulatory Filling Pressure
 Strong SNS stimulation constricts all systemic blood vessels,
pulmonary blood vessels, and chambers of the heart.
 With constriction, the capacity of the system decreases so that at
each level of blood volume, the Mean Circulatory Filling Pressure
increases.
 If you decrease the space but not the fluid, the pressure
increases.
 Inversely, if you decrease SNS then the system relaxes and space
increases which decreases pressure.
Effect on VR Curve of changes in Mean Systemic Filling Pressure
 The greater the Mean Systemic Filling Pressure (means the greater the
"tightness" with which the system is filled with blood) the more the
venous return curve shifts upward and to the right.
 Opposite is also true, the less the Mean Systemic Filling Pressure the more
the curve shifts downward and to the left.
 Interpretation: the greater the system is filled, the easier it is for blood to
flow into the heart. The less the system is filled, the harder it is for blood
to flow into the heart.
Pressure Gradient for VR
 When RA pressure rises to equal Mean Systemic Filling Pressure, there is
no longer a pressure difference and so there is no flow.
 When RA pressure falls lower than Mean Systemic Filling Pressure, the
flow to the heart increases proportionately.
 The greater the pressure difference, the greater the VR.
Resistance to VR
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Most happens in veins, but some occurs in arterioles and small arteries.
When resistance in veins increases, blood begins to pool because the
veins are so distensible and pressure increases very little, overcomes little
resistance.
Even slight accumulation in ARTERIES raises the pressure greatly (30 times
as much) and this high pressure does overcome much of the increased
resistance.
𝑉𝑅 = (𝑃𝑠𝑓 − P𝑅𝐴) ÷ 𝑅𝑉𝑅
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o
VR: Venous Return, Psf: Mean Systemic Filling Pressure, PRA: Right
Atrial Pressure, RVR: Resistance to Venous Return
Effect of Resistance on Curve
 Decrease in resistance to one-half allows twice as much flow of
blood and rotates the curve upward to twice as great a slope.
 Increase in resistance to twice normal rotates the curve downward
to one-half as great a slope.
 When RA pressure equals Mean Systemic Filling Pressure, venous
return becomes zero and it doesn't matter when the RVR is. Flow is
still zero.
 Highest level to which RA pressure can rise is equal to Mean
Systemic Filling Pressure.
Analysis of CO and RA pressure, using simultaneous CO and VR Curves
 Predict CO and RA pressure:
 Determine pumping ability of heart and draw CO curve
 Determine state of flow from systemic circulation and draw VR curve
 Equate the curves
 Only one point will show that VR equals CO and where RA pressure is same for
both heart and systemic circulation.
 Effect of Increased Blood Volume on CO
 Sudden increase in volume of about 20% increases CO to 2.5 to 3 times
normal.
 Increased filling of system causes Mean Systemic Filling Pressure to
increase to 16 mm Hg, which shifts the curve to the right.
 Compensatory Effects in response to increased blood volume
 Greatly increased CO only lasts a few minutes because
 Increased CO increases capillary pressure which decreases VR
 Increased pressure in veins causes stress-relaxation which dilates
vessels/blood resevoirs and decreases VR.
 Excess blood flow causes autoregulatory increase in peripheral
resistance, which increases resistance to VR.
 Effect of SNS on CO
 Makes the heart a stronger pump
 Increases Mean Systemic Filling Pressure because of contraction of
peripheral vessels and increases resistance to VR
 Different degrees of SNS can increase CO to about twice normal for short
periods of time until other compensatory mechanisms occur.
 Effect of Opening a Large Arteriovenous Fistula
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o
Immediately after opening
 Large upward rotation of curve cause by large decrease in
resistance to VR
 Slight increase in CO curve because the fistula decreases peripheral
resistance.
 Net Result: Increase in CO and increase in RA pressure.
 One minute later
 Increase in Mean Systemic Filling Pressure because of vessel
constriction
 Further increase in CO due to SNS.
Methods for Measuring CO
 Fick Equation
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Mixed venous blood (Cv) can be measured from the Right Ventricle or
Pulmonary Artery
 Arterial Blood can be measured from any systemic artery in the body
 Rate of Oxygen Absorption (VO2) by the lungs is measured by rate of
disappearance of oxygen from respired air.
Indicator Dilution Method
 Dye, or indicator, is injected into a large systemic vein or preferrably, into
the right atrium.
 The concentration of dye is then measured after passing through the heart
and into a peripheral artery.
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