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PHYSIOLOGY
Cardiac Output, Venous Return
and Their Regulation
Cardiac Output:
It is the quantity of blood pumped into the aorta
each minute by the heart or the quantity of blood that flows
through the circulation each minute.
Cardiac output = Heart Rate Stroke Volume
Venous return:
It is the quantity of blood flowing from the veins into
the right atrium each minute.
Venous Return = Cardiac Output
Physiology of Heart
Increase in Cardiac Output
The factors which increases the
cardiac output are:
 Heart
 Venous Return
 Arterio-Venous Fistula
 Blood Volume
Mean Systematic Filling Pressure
Metabolic Rate
 Exercise Rate
 Pathology
 Size of the body (Cardiac
Index)
Person’s age
Role Of Frank-Starling Mechanism
Frank-Starling Law:
It states that “ Within physiologic limits, the
heart pumps all the blood that returns to it by the
way of veins.”
Increased Venous Return
Cardiac muscles stretches to greater length
Ventricular muscle contracts with greater force
Increased Cardiac Output
EFFECTS
Stronger Contractions:
Increased heart volume stretches muscles and
causes stronger contraction.
Heart Rate:
Stretch increases heart rate as well.
S-A Node:
Direct effect on rhythmicity of the node to increase
heart rate as much as 10-15%.
Bainbridge Reflex:
It gives reflexes to the vasomotor center and then
back to the heart by the way of sympathetic nerves and
vagi, increases the heart rate.
Cardiac Output Regulation
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.
At each increasing level of
work output during
exercise, the oxygen
consumption and the
cardiac output increase in
parallel to each other.
To summarize, cardiac output is
determined by the sum of all the various
factors throughout the body that control
local blood flow. All the local blood flows
summate to form the venous return, and
the heart automatically pumps this
returning blood back into the arteries to
flow around the system again.
Physiology of Heart
Relation of Cardiac Output
and Stroke Volume
Stroke Volume:
Volume of blood that is
ejected by each ventricles during
systole is called Stroke Volume
Output.
 As the stroke volume increases the
cardiac output also increases.
 Stroke Volume depends upon
1. End diastolic Volume
2. Contractility
Limitations For The Cardiac Output
There are definite limits to the amount of blood that
the heart can pump, which is expressed quantitatively
in the form of cardiac output curves.
Normal:
The plateau level of this normal cardiac
output curve is about 13 L/min.
Hypoeffective:
The lowermost curves are for hypoeffective
hearts that are pumping at levels below normal.
Hypereffective heart plateau – 5 L/min
Hypereffective:
The uppermost curves are for
Hypereffective hearts that are pumping better
than normal. Hypoeffective heart plateau – 20
L/min
Hypoeffective Heart
In this the heart is pumping at a very slow
rate and the cardiac output decreases.
 Factors that can cause hypoeffectivity are following:
1. Increased Arterial Pressure
2. Inhibition of Nervous Excitation
3. Abnormal Heart Rhythm
4. Coronary Artery Blockage
5. Valvular Heart Disease
6. Congenital Heart Disease
7. Myocarditis
8. Cardiac Hypoxia
Hypereffective Heart
 In this the heart is pumping at a
high rate and the cardiac output
increases.
 Two type of factors can make the heart a
better pump than normal:
1. Nervous Stimulation:
It involves Sympathetic Stimulation and
Parasympathetic Inhibition.
2. Hypertrophy of The Heart
Muscles:
It involves the increased mass and
contractile strength due to exercise and
causing hypertrophy which allows increased
Pathologically High or Low
Cardiac Output
In healthy humans, the
average Cardiac Outputs are
surprisingly constant from one
person to another. However.
Multiple clinical abnormalities
can cause either high or low
cardiac outputs.
High Cardiac Output
 High cardiac output is mostly caused by
reduced total peripheral Resistance.
 Following are some of the conditions that
can decrease the Peripheral Resistance
and at the same time increase the Cardiac
Output to above the normal.
1. Beriberi
2.Arteriovenous Fistula
3.Hyperthyroidism
4. Anemia
Low Cardiac Output
There are two
factors that cause
Low Cardiac
Output:
B. Abnormalities
that cause the
Venous Return to
fall too low
A. Abnormalities
that cause
pumping
effectiveness of the
Heart to fall too low
A. Cardiac Factors:
Whenever the heart becomes severely
damaged, regardless of the cause, its limited level of
pumping may fall below that needed for adequate
blood flow to the tissues. Some examples of this include:
1. Severe Coronary Blood
2. Myocardial Infarction
3. Severe Valvular Heart Disease
4. Myocarditis
5. Cardiac Temponade
6. Cardiac Metabolic Derangements
B. Decreased Venous Return:
Anything that interferes with venous return also can
lead to decreased cardiac output. Some of these factors
are the following:
1.Decreased Blood Volume
2. Acute Venous Dilation
3. Obstruction of the Large Veins
4. Decreased Muscle Mass
5. Decreased Metabolic Rate
of the Tissues
THANK YOU
Any Questions???

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Physiology of Heart

  • 1. PHYSIOLOGY Cardiac Output, Venous Return and Their Regulation
  • 2. Cardiac Output: It is the quantity of blood pumped into the aorta each minute by the heart or the quantity of blood that flows through the circulation each minute. Cardiac output = Heart Rate Stroke Volume Venous return: It is the quantity of blood flowing from the veins into the right atrium each minute. Venous Return = Cardiac Output
  • 4. Increase in Cardiac Output The factors which increases the cardiac output are:  Heart  Venous Return  Arterio-Venous Fistula  Blood Volume Mean Systematic Filling Pressure
  • 5. Metabolic Rate  Exercise Rate  Pathology  Size of the body (Cardiac Index) Person’s age
  • 6. Role Of Frank-Starling Mechanism Frank-Starling Law: It states that “ Within physiologic limits, the heart pumps all the blood that returns to it by the way of veins.” Increased Venous Return Cardiac muscles stretches to greater length Ventricular muscle contracts with greater force Increased Cardiac Output
  • 7. EFFECTS Stronger Contractions: Increased heart volume stretches muscles and causes stronger contraction. Heart Rate: Stretch increases heart rate as well. S-A Node: Direct effect on rhythmicity of the node to increase heart rate as much as 10-15%. Bainbridge Reflex: It gives reflexes to the vasomotor center and then back to the heart by the way of sympathetic nerves and vagi, increases the heart rate.
  • 8. Cardiac Output Regulation 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. At each increasing level of work output during exercise, the oxygen consumption and the cardiac output increase in parallel to each other. To summarize, cardiac output is determined by the sum of all the various factors throughout the body that control local blood flow. All the local blood flows summate to form the venous return, and the heart automatically pumps this returning blood back into the arteries to flow around the system again.
  • 10. Relation of Cardiac Output and Stroke Volume Stroke Volume: Volume of blood that is ejected by each ventricles during systole is called Stroke Volume Output.  As the stroke volume increases the cardiac output also increases.  Stroke Volume depends upon 1. End diastolic Volume 2. Contractility
  • 11. Limitations For The Cardiac Output There are definite limits to the amount of blood that the heart can pump, which is expressed quantitatively in the form of cardiac output curves. Normal: The plateau level of this normal cardiac output curve is about 13 L/min. Hypoeffective: The lowermost curves are for hypoeffective hearts that are pumping at levels below normal. Hypereffective heart plateau – 5 L/min Hypereffective: The uppermost curves are for Hypereffective hearts that are pumping better than normal. Hypoeffective heart plateau – 20 L/min
  • 12. Hypoeffective Heart In this the heart is pumping at a very slow rate and the cardiac output decreases.  Factors that can cause hypoeffectivity are following: 1. Increased Arterial Pressure 2. Inhibition of Nervous Excitation 3. Abnormal Heart Rhythm 4. Coronary Artery Blockage 5. Valvular Heart Disease 6. Congenital Heart Disease 7. Myocarditis 8. Cardiac Hypoxia
  • 13. Hypereffective Heart  In this the heart is pumping at a high rate and the cardiac output increases.  Two type of factors can make the heart a better pump than normal: 1. Nervous Stimulation: It involves Sympathetic Stimulation and Parasympathetic Inhibition. 2. Hypertrophy of The Heart Muscles: It involves the increased mass and contractile strength due to exercise and causing hypertrophy which allows increased
  • 14. Pathologically High or Low Cardiac Output In healthy humans, the average Cardiac Outputs are surprisingly constant from one person to another. However. Multiple clinical abnormalities can cause either high or low cardiac outputs.
  • 15. High Cardiac Output  High cardiac output is mostly caused by reduced total peripheral Resistance.  Following are some of the conditions that can decrease the Peripheral Resistance and at the same time increase the Cardiac Output to above the normal. 1. Beriberi 2.Arteriovenous Fistula 3.Hyperthyroidism 4. Anemia
  • 16. Low Cardiac Output There are two factors that cause Low Cardiac Output: B. Abnormalities that cause the Venous Return to fall too low A. Abnormalities that cause pumping effectiveness of the Heart to fall too low
  • 17. A. Cardiac Factors: Whenever the heart becomes severely damaged, regardless of the cause, its limited level of pumping may fall below that needed for adequate blood flow to the tissues. Some examples of this include: 1. Severe Coronary Blood 2. Myocardial Infarction 3. Severe Valvular Heart Disease 4. Myocarditis 5. Cardiac Temponade 6. Cardiac Metabolic Derangements
  • 18. B. Decreased Venous Return: Anything that interferes with venous return also can lead to decreased cardiac output. Some of these factors are the following: 1.Decreased Blood Volume 2. Acute Venous Dilation 3. Obstruction of the Large Veins 4. Decreased Muscle Mass 5. Decreased Metabolic Rate of the Tissues