Chapter 20
Sunday, December 02, 2012
4:10 PM
Cardiac Output, Venous Return, and Their Regulation

Venous return - quantity of blood flowing from the veins into the R atrium each minute
 Cardiac Output - quantity of blood pumped thru aorta each min by the heart; quantity of blood that flows
thru circulation
o Factors directly affecting output
 Basic level of body metabolism
 Whether the pt is exercising
 Age
 Declining cardiac index - declining activity or declining muscle mass w/age
 Cardiac index declines to ~ 2.4 L/min/m2 at age 80
 Body size
o Resting cardiac output averages
 Young, healthy men = 5.6ml/min
 Women = 4.9ml/min
 Adult = 5ml/min
o Cardiac index = cardiac output per square meter of body surface area
 normal = 3L/min/m2
 Control of Cardiac Output
o Controlled by venous return (VR)
o Frank-Starling Law of the Heart - heart has built-in mech that allows it to pump automatically whatever
flows into R atrium
 Inc. quantities of blood flow into heart -> Inc. blood stretches walls of the chambers -> muscle
contracts w/Inc. force in order to empty extra blood that has entered from the systemic
circulation
o Stretching the heart causes the heart to pump faster - Inc. HR
o Bainbridge reflex - stretched R atrium initiates an Inc. HR
o Normal non-stressful conditions - output controlled almost entirely by peripheral factors that determine
VR
o Cardiac output is determined by the sum of all the various factors thruout the body that control local
blood flow
o Long term cardiac output level varies reciprocally w/changes in total peripheral resistance (arterial
pressure unchanged)
o Cardiac output = arterial pressure/total peripheral resistance
 Total peripheral resistance inc above normal -> cardiac output falls
 Total peripheral resistance dec below normal -> cardiac output rises
o Cardiac Output Curves
 Normal heart - can pump VR up to ~2.5 times normal before heart becomes a limiting factor
 Hypereffective hearts - pumping better than normal
 Factors:
 Nervous stimulation
 Hypertrophy of heart muscle
 Nervous Excitation to Inc. HR
 Combination of sym stim and parasym inhibition
 Inc. HR a lot
 Inc. heart contractility 2X normal, can raise plateau level of cardiac output curve
to almost 2X normal
 Inc. pumping effectiveness - caused by hypertrophy
 Long-term inc in workload -> inc in muscle mass and contractile strength
 Marathon runners -> inc mass by 50-75%
Allows the heart to pump greater cardiac output
 Marathon runners -> pump as much as 2.5X average (most important in
determining running time)
 Hypoeffective hearts - pumping at levels below normal
 Factors:
 Inc arterial pressure (i.e. hypertension)
 Inhibition of nervous excitation of the heart
 Path factors -> abnormal heart rhythm or rate of heartbeat
 Coronary artery blockage -> heart attack
 Valvular heart dz
 Congenital heart dz
 Myocarditis
 Cardiac hypoxia
NS Control of Cardiac Output
 Dinitrophenol
 With ANS control
inc metabolism of all tissues 4X -> intense dilation of peripheral vessels

 No change in arterial pressure b/c of NS
 Cardiac output inc 4X
 After ANS blocked
 No circulatory reflexes to maintain arterial pressure
 Vasodilation -> fall in arterial pressure
 Cardiac output inc 1.6X
 Normal arterial pressure maintenance by nervous reflexes essential to achieving high cardiac
outputs
 Inc arterial pressure in exercise
 Intense inc in metabolism in skeletal muscles -> relaxes muscle arterioles -> dec total
peripheral resistance
 normally would dec arterial pressure BUT...
 NS compensates; sends simultaneous signals to the brain
 Large vein constriction
 Inc HR
 Inc contractility of the heart
 These effects -> inc arterial pressure above normal -> forces more blood flow thru active
muscles
Reduction in Total Peripheral Resistance causes High Cardiac Output
 Beriberi
 Caused by insufficient quantity of vitamin thiamine (vitamin B1)
 Diminished ability of tissues to use some nutrients
 Local tissue blood flow mech -> compensatory peripheral vasodilation
 Long -term levels of venous return and cardiac output rise
 Arteriovenous fistula (shunt) - AV shunt
 b/w major artery and major vein
 Dec total peripheral resistance -> inc venous return and cardiac output
Hyperthyroidism

 Metabolism of most tissues inc
 Oxygen usage inc, vasodilator products released from tissues -> dec total peripheral
resistance
 Venous return and cardiac output often inc to 40-80% above normal
 Anemia
 Reduced viscosity of blood - dec [RBCs]
 Diminished delivery of oxygen to tissues -> local vasodilation

o
o
o
o
 Both inc cardiac output greatly
Low Cardiac Output
 Two categories
 Pumping effectiveness of heart falls too low
 Caused by cardiac factors - heart damage causes limited pumping
 Severe coronary blood vessel blockage -> MI
 Severe valvular heart dz
 Myocarditis
 Cardiac tamponade
 Cardiac metabolic derrangments
 Cardiac shock = cardiac output falls so low that the tissues thruout the body begin to
suffer nutritional deficiency
 Venous return falls too low
 Caused by non-cardiac factors
 Decreased blood volume - most common factor
 Most often from hemorrhage
 Not enough blood in peripheral vessels to create peripheral vascular
pressures high enough to push blood back to the heart
 Acute venous dilation
 Most often when SNS suddenly becomes inactive
 Fainting often results
 Dilation -> dec filling pressure of the vascular system -> blood volume
cannot create adequate pressure causing blood to "pool" in vessels
instead of returning to the heart
 Obstruction of the large veins
 Rare - large veins become obstructed
 Decreased tissue mass (esp skeletal muscle mass)
 Dec total oxygen consumption and blood flow needs of muscles
 Dec in skeletal muscle blood flow and cardiac output
 Dec metabolic rate of the tissues
 i.e. prolonged bed rest
 Oxygen and nutrition needs will be lower
 Dec blood flow to tissues -> reduced cardiac output
 Circulatory Shock = cardiac output falls below that level required for adequate
nutrition of the tissues
 Lethal w/in a few min/hours
Cardiac Output Curves (Look at graphs in textbook)
 External Pressure
 Normal external pressure = normal intrapleural pressure (-4mmHg)
 Intrapleural pressure (-2mmHg) - extra R atrial pressure required to overcome inc pressure
on outside of heart
 Intrapleural pressure (+2mmHg) - even more R atrial pressure required
 Factors:
 Cyclical changes of intrapleural pressure during respiration
 2 in normal breathing
 50 in strenuous breathing
 Breathing against a negative pressure
 Shifts to more negative R atrial pressure
 Positive pressure breathing
 Shifts curve to right
 Opening the thoracic cage
 Inc intrapleural pressure to 0
 Shifts the cardiac output curve to the right

o
Cardiac tamponade
 Accumulation of a large quantity of fluid in the pericardial cavity
 Results in inc in external cardiac pressure, shifts curve to the right
 Pattern Combos of Curves
 Final curve change b/c
 External cardiac pressure
 Effectiveness of the heart as a pump
 Combo of hypereffective heart and inc intrapleural pressure -> inc max level of cardiac
output due to inc pumping capability of heart but curve shifts to the right (to higher atrial
pressures) due to inc intrapleural pressure
Venous Return Curves
 Principal factors:
 R atrial pressure
 Exerts backward force on veins to impede flow of blood from veins to R atrium
 Degree of filling of systemic circulation (measured by mean systemic filling pressure)
 Forces systemic blood toward heart
 Resistance to blood flow
 b/w peripheral vessels and R atrium
 Normal Curve
 When heart pumping capability goes down, R atrial pressure rises -> decreased VR
 Slight rise in atrial pressure -> drastic decrease in VR
 Blood dams in systemic system while R atrial pressure rises causing venous stasis, pumping
decreases
 Mean systemic filling pressure = when both arterial and venous pressures come to
equilibrium
 Plateau:
 When R atrial pressure falls below 0 (below atm pressure) -> inc venous return almost
ceases
 Plateau caused by collapse of veins entering chest
 Neg pressure in R atrium sucks walls of veins together -> prevents flow from
peripheral veins
 Even very neg pressures in R atrium cannot increase VR
 Heart pumping stopped by shocking heart - flow everywhere ceases a few sec later, when flow
pressures everywhere become equal = mean circulatory filling pressure
 Effect of blood volume
 Greater the volume in circulation, the greater is the mean circulatory filling pressure
 Blood volume @ 4000ml, mean circulatory filling pressure close to zero b/c
unstressed volume (inc linearly)
 Effect of SNS
 Strong sym stim constricts all systemic blood vessels, larger pulmonary blood vessels,
and chambers
 Capacity of the system dec, mean circulatory filling pressure is inc for each volume
level (2.5X)
 Complete inhibition of SNS relaxes both vessels and heart, dec mean circulatory filling
pressure
 Mean Systemic Filling Pressure (Psf)
 Pressure measured everywhere in the systemic circulation after blood flow has been
stopped
 Almost always nearly equal to the mean circulatory filling pressure
 Venous Return/Mean Systemic Filling Pressure
 Greater the Psf, the more the VR curve shifts upward and to the R
 Lower the Psf, more the VR curve shifts downward and to the L
 *the greater the system is filled, the easier it is for blood to flow into the heart*
 *the less the filling, the more difficult it is for blood to flow into the heart*
Pressure Gradient for Venous Return
 No pressure gradient = no venous return (Psf = R atrial pressure)
 R atrial pressure falls progressively lower than Psf, the flow to the heart inc
proportionately
 The greater the difference b/w the Psf and the R atrial pressure, the greater becomes
venous return
 Resistance to Venous Return
 Most occurs in veins (2/3), some in arterioles and small arteries (1/3)
 When resistance in veins inc, blood begins to dam up mainly in veins (pressure rises
little b/c of distensibility) -> blood flow into R atrium dec drastically
 When arteriolar and small artery resistances inc, blood accumulates in arteries
(capacitance only 1/30 veins) slight accumulation raises pressure greatly -> high
pressure overcomes inc resistance
 Venous Return = Psf-R atrial pressure/resistance to venous return
 VR = Psf-PRA/RVR
 Healthy Pt: venous return = 5L/min, Psf = 7mmHg, R atrial pressure = 0mmHg
 Effect of Resistance to Venous Return on VR Curve
 Dec in resistance to 1/2 normal allows twice as much flow - rotates curve upward to
2X slope
 Inc in resistance to 2X normal rotates curve downward to 1/2 slope
 When R atrial pressure rises to equal Psf -> VR becomes 0 at all levels of resistance
b/c no pressure gradient to cause flow (flow = 0)
 Highest level the R atrial pressure can rise is equal to the Psf
Simultaneous Cardiac Output/Venous Return Curves
 Venous return must equal cardiac output
 R atrial pressure is the same for both heart and systemic circulation
 Can predict cardiac output and R atrial pressure
 Determine momentary pumping ability of heart - cardiac output curve
 Determine momentary state of flow from systemic circulation into heart - venous return
curve
 Equate these curves
 Effect of Inc Blood Volume -> inc cardiac output, inc Psf, shifts VR curve right, distends vessels,
dec VR resistance
 Last only a few mins
 Compensatory effects:
 Inc cardiac output inc the capillary pressure -> fluid transudes out capillaries into
tissues
 Inc pressure in veins cause continued distention by "stress-relaxation" (esp causing
reservoirs to distend) -> reducing mean systemic pressure
 Excess blood flow thru peripheral tissues causes autoregulatory inc in peripheral
vascular resistance -> inc resistance to VR
 Cardiac output returns to normal (almost) w/in 10-40min
 Effect of Sym Stim
 Makes heart a stronger pump (by ~ 100%) - cardiac output rises but R atrial pressure hardly
changes
 Inc mean systemic filling pressure b/c peripheral vessel contraction (esp veins)
 Inc resistance to VR
 Effect of Sym Inhibition
 Total Spinal Anesthesia or Hexamethonium - block transmission of nerve signals thru the
autonomic ganglia
 Mean systemic filling pressure falls
 Effectiveness of heart as a pump dec to ~80% of normal

o


 Cardiac output dec to ~60%
AV Fistula
 Immediately after opening fistula
 VR curve goes upward - large dec in resistance to VR
 Slight inc in level of cardiac output curve - dec peripheral resistance allows acute fall
in arterial pressure
 Net Result: inc in cardiac output, inc in R atrial pressure
 1 min later
 Sym nerve reflex have restored the arterial pressure almost to normal, which causes:
 Inc in mean systemic filling pressure b/c constriction of vessels
 Further elevation of cardiac output curve b/c sym nervous excitation of the
heart
 Cardiac output rises, R atrial pressure rises
 Several weeks later
 Blood volume inc b/c slight reduction in arterial pressure and sym stim have reduced
kidney output of urine
 Mean systemic filling pressure risen
 Prolonged inc workload on heart has caused heart muscle to hypertrophy slightly,
raising level of cardiac output and R atrial pressure
Measuring Cardiac Output
 Indirect methods
 Oxygen Fick method
 Cardiac Output (L/min) = O2 absorbed per min by the lungs
(ml/min)/arteriovenous O2 difference (ml/L of blood)
 Mixed venous blood usually obtained thru catheter inserted up brachial vein of
forearm, thru subclavian vein, down to R atrium, and into R ventricle or
pulmonary artery
 Systemic arterial blood obtained from any systemic artery
 Rate of oxygen absorption measured by rate of disappearance of O2 from the
respired air
 Indicator dilution method
 Small amount of indicator (i.e. dye) injected into a large systemic vein or into R
atrium
 Concentration of dye is recorded as the dye passes thru one of the peripheral
arteries
 Cardiac Output (ml/min) = (milligrams of dye injected X 60) / ((avg conc of dye
in each ml of blood for duration of the curve)x(duration of the curve in sec))
 Echocardiography - US waves from transducer on chest wall or in esophagus to
measure chamber size
 Stroke volume calculated from velocity of blood flowing into aorta and aorta
cross-sectional area
 Cardiac output calculated from product of the stroke volume and HR
 Pulsatile Output of Heart measured by electromagnetic or ultrasonic flowmeter
 Blood flow rises rapidly to peak during systole
 Reverses for fraction of a sec at the end of systole
 Reverse flow causes the aortic valve to close