Cardiac Output, Venous Return,

and Their Regulation

 LEARNING OBJECTIVES:
Define cardiac output and cardiac index
with their normal values in adults
Describe regulation of cardiac output
Describe causes of hypoeffective heart
Describe causes of hypereffective heart
Define venous return
Describe factors effecting venous return
 CARDIAC OUTPUT

Cardiac output is the quantity of blood

pumped into the aorta each minute by the
heart. This is also the quantity of blood
that flows through the circulation.

CO = SV x HR
 Normal Values for Cardiac Output at
Rest and During Activity
Cardiac output varies widely with the level
of activity of the body. The following
factors, among others, directly affect
cardiac output:
(1) The basic level of body metabolism,
(2) Whether the person is exercising,
(3) The persons age, and
(4) Size of the body
For young, healthy men, resting cardiac
output averages about 5.6 L/min.
For women, this value is about 4.9 L/min.
When one considers the factor of age as
wellbecause with increasing age, body
activity diminishes
The average cardiac output for the resting
adult, in round numbers, is often stated to
be almost exactly 5 L/min.
 Cardiac Index
Cardiac output per square meter of body
surface area.
70 kilograms, surface area of about 1.7 square
meters,
Average cardiac index for adults is about
3 L/min/m2 of body surface area.
Effect of Age on Cardiac Output.
Rising 4 L/min/m2 at age 10 years, the cardiac
index
Declines to about 2.4 L/min/m2 at age 80 years.
Depends on Overall bodily metabolic activity.
Cardiac Index
Under most normal unstressful conditions, the
cardiac output is controlled almost entirely by
peripheral factors that determine venous
return.

If the returning blood does become more than

the heart can pump, then the heart becomes
the limiting factor that determines cardiac
output
 Heart is not the primary controller of cardiac
output.
Instead, factors of the peripheral circulation
affecting venous return, are the primary
controllers.
The main reason peripheral factors are
usually more important than the heart itself in
controlling cardiac output is that the heart has a
built-in mechanism that normally allows it to
pump automatically whatever amount of blood
that flows into the right atrium from the veins.
 Regulation of Heart Pumping
Intrinsic regulation of heart pumping
The Frank Starling Mechanism

Extrinsic regulation of heart pumping

Role of autonomic nervous system

Effect ions on cardiac function

 Cardiac output is controlled by venous
return
Frank-Starling law of the heart
When increased quantities of blood flow into the
heart, the increased blood stretches the walls of the
heart chambers. heart rate.
Direct effect
Stretch of the sinus node in the wall of the right
atrium has a direct effect on the rhythmicity of the
node itself to increase heart rate as much as 10 to
15 per cent.
Nervous reflex called the Bainbridge reflex
passing first to the vasomotor center of the brain
and then back to the heart by way of the
sympathetic nerves and vagi, also to increase the
heart rate.
Cardiac output = stroke volume x heart
rate

CO (ml/min) = SV (ml/beat) x HR (beats/min)

SV = EDV-ESV
depends on the state
EDV depends on the rate of of the pacemaker,
filling (degree of balance of
relaxation, ventricular sympathetic
filling pressure and time and parasympathetic
between strokes) inputs.

ESV depends on the

contractility and afterload
Cardiac
Output
(CO)
 A combination of factors together determine
cardiac output. These include preload,
afterload, contractility and heart rate.
 Determinants of cardiac output
PRELOAD = Initial stretching of the cardiac myocytes
prior to contraction (related to sarcomere length)

AFTERLOAD = load that the heart must eject blood

against (related to aortic pressure)

CONTRACTILITY (INOTROPY) = Inherent ability of

myocardial cells to develop force at given muscle lengths
(related to Calcium)

HEART RATE autonomic nervous system

 Factors Effecting Cardiac Performance
Preload Total blood volume
( LV diastolic Venous tone (sympathetic tone)
volume) Body position
Intra thoracic / intra pericardial
Press.
Atrial contraction
Pumping action of skeletal muscle

After load Peripheral vascular resistance

(Impedance) L.V volume (preload, wall tension)
Physical characteristics of arteries
(e.g., elasticity of vessels or pressure
of outflow obstruction)
 Factors Affecting Preload
Posture

Blood volume

Intrinsic Venous Tone

Sympathetic neural tone to veins and vaso active drugs

Arterial Contraction

Muscular Activity

Intrapleural Pressure

Intrapericardial Pressure
 Factors Affecting End-diastolic
Volume

Ventricular performance
Ventricular EVD
Total blood Body Intrathoracic
volume position pressure

Atrial Intrapericardial
contrib. to STRETCHING OF MYOCARDIUM pressure
vent. filling ventricular
compliance
Pumping action Venous tone
to skeletal muscle
 Preload vs Afterload

Venules / veins Arterioles

Capacitance Resistance
vessels vessels

Affect preload Affect afterload

 Effect of Total Peripheral Resistance on the Long-
Term Cardiac Output Level
Under most normal conditions, the long-term cardiac
output level varies reciprocally with changes in total
peripheral resistance.
When the total peripheral resistance is exactly
normal, the cardiac output is also normal.
Then, when the total peripheral resistance increases
above normal, the cardiac output falls;
Conversely, when the total peripheral resistance
decreases, the cardiac output increases.
One can easily understand this by reconsidering one of
the forms of Ohms Law:
Cardiac Output =Arterial Pressure/Total Peripheral
Resistance
Cardiac sympathetic and parasympathetic nerves
 Innervations of Heart
Parasympathetic Sympathetic
 Regulation of heart rate
+25

0
mV
-25

-50

-75

Sympathetic nervous system

sympathetic nerves release norepinephrine
plus circulating epinephrine from adrenal medulla
both act on -receptors on sinoatrial node
increases slope of the pacemaker potential
increases heart rate = tachycardia
 Regulation of heart rate
+25

0
mV
-25

-50

-75

Parasympathetic nervous system

vagus releases ACh
acts on muscarinic receptors on sinoatrial node
hyperpolarizes cells and decreases slope of
pacemaker potential
decreases heart rate = bradycardia
Effect of sympathetic / parasympathetic on
cardiac output curves
Factors affecting Heart Rate
Heart rate increase by Heart rate slowed by
Decreased activity of Norepinephrine
Baroreceptor Increased activity of
Increased activity of Atrial Baroreceptor
stretch Expiration
Inspiration Fear
Excitement Grief
Anger Increased intracranial pressure
Painful stimuli
Hypoxia
Exercise
Epinephrine
Thyroid hormone
Fever
 Factors Effecting Cardiac Performance
Contractility Sympathetic nerve impulses
Circulating catecholamine
Digitalis, calcium, inotropic agents
Increased heart rate or
post extra systolic augmentation
Anoxia, acidosis
Pharmacologic depression
Loss of myocardium
Intrinsic depression

Heart Rate Autonomic nervous system

Temperature, metabolic rate
Ions( K+ and Ca++ )
 Effect of Bainbridge and Baroreceptor
Reflex on HR

Increased Bainbridg
Intravenou Stimulate
s infusion
right e reflex
atrial
atrial
receptors
pressure
Heart
rate

Increased Increased Barorecept

cardiac arterial or reflex
output pressure
HYPEREFFECTIVE HEART

Factors that can cause hypereffective heart

Only two types of factors usually can make the
heart a better pump than normal. They are
(1) Nervous stimulation
(2) Hypertrophy of the heart muscle.
 Effect of Nervous Excitation to Increase Heart
Pumping.
(1) Sympathetic stimulation
Greatly increases the heart rate-sometimes to
180 to 200 beats/min
Increases the strength of heart contraction
twice its normal strength.
(2) Parasympathetic inhibition
Increased Pumping Effectiveness
Caused by Heart Hypertrophy.
A long-term increased workload, but not
so much excess load that it damages the
heart, causes the heart muscle to increase
in mass and contractile strength in the
same way that heavy exercise causes
skeletal muscles to hypertrophy.
 HYPO EFFECTIVE HEART
Any factor that decreases the heart's ability to pump
blood causes hypoeffectivity. Some of the factors
that can do this are the following:
_ Coronary artery blockage, causing a "heart attack"
Inhibition of nervous excitation of the heart
Pathological factors that cause abnormal heart rhythm or
rate of heartbeat
Valvular heart disease
Increased arterial pressure against which the heart must
pump, such as in hypertension
Congenital heart disease
Myocarditis
Cardiac hypoxia
 Cardiac Output and Venous Return
Cardiac output is the quantity of blood
pumped into the aorta each minute by the
heart.
Most important factor we consider in
relation to the circulation.
Venous return is the quantity of blood
flowing from the veins into the right atrium
each minute.

The venous return and the cardiac output

must equal each other
 Venous Return
The venous return to the heart is the sum
of all the local blood flows through all the
individual tissue segments of the
peripheral circulation. Therefore, it follows
that cardiac output regulation is the sum of
all the local blood flow regulations.
Mean systemic filling pressure
It is the pressure measured everywhere in
the systemic circulation after blood flow
has been stopped by clamping the large
blood vessels at the heart, so that the
pressures in the systemic circulation can
be measured independently from those in
the pulmonary circulation.
 Venous Return

The greater the difference between the

mean systemic filling pressure and the
right atrial pressure, the greater becomes
the venous return.
Therefore, the difference between these
two pressures is called the pressure
gradient for venous return.
 Resistance to venous return.
Venous return can be calculated by the
following formula:
VR= Psf PRA/ RVR
in which VR is venous return, Psf is mean
systemic filling pressure, PRA is right atrial
pressure, and RVR is resistance to venous
return
 Factors Aiding Venous Return
Venous return is aided by
the:
Respiratory pump
pressure changes created
during breathing suck
blood toward the heart by
squeezing local veins
Muscular pump
contraction of skeletal
muscles milk blood
toward the heart
Valves prevent backflow
during venous return
MSFP
FACTORS RESISTING VENOUS
RETURN

Right Atrial Pressure

Resistance to blood flow

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