Cardiodynamics Correlation of SV, EDV, ESV with the Ejection Loop

(Gloria Marie M. Valerio, MD)

From point D to point A, the volume of blood increases in the
Definition of Terms: ventricles with little increase in pressure, this is the ventricular filing
time. At point A, the atrioventricular (AV) valves will close so that
Cardiac Output (CO) whatever amount of blood will be present in the ventricles before closure
- is the amount/quantity/volume of blood ejected by each of the AV valves, that is now the end diastolic volume (EDV) which is a
ventricle per minute little less than 150 mL, average of 130 mL.
- CO = SV x HR
- Normal Value: 5 L/min From point A to point B, the ventricles will now start to
5, 000 mL/min contract, but since all the valves are closed, there will be no change in
ventricular volume.
* Although the left ventricle will pump blood against a higher pressure of
resistance in the systemic circulation compared to the right ventricle, From point B to C, that is the period of ejection of blood from
although the workload of the left ventricle is greater than that of the right the ventricles so the EDV will be decreased and the amount that will be
ventricle, although the left ventricular wall or musculature is thicker than ejected is the stroke volume. At point C, the semilunar (SL) valves will
that of the right ventricle, the output of the two ventricles are the same. close, the ventricles will start to relax and the volume of blood that is now
in the ventricles is the end systolic volume (ESV).
Heart Rate (HR)
- the number of contractions/heart beats/cardiac cycles per Stroke volume is equal to EDV minus ESV or ESV + SV will be
minute the EDV.
- Normal Value (normal resting adult): 75 beats per min.
CO = SV x HR
* In a normally functioning heart, the heart rate and rhythm are
determined by the activity of the SA node. EDV ESV

Stroke Volume (SV) Whatever factor that will affect EDV and ESV will also affect the
- is the amount/quantity/volume of blood ejected by each SV. Whatever factor that will affect the SV and HR will affect the CO. As
ventricle per contraction/per heartbeat/per cardiac cycle for the SV, this is determined mainly by the force of myocardial
- SV = EDV ESV contraction. So if the force of myocardial contraction increases, the SV
- Normal Value: 70 mL will increase. On the other hand, if the force of myocardial contraction
decreases, the SV will also decrease. We can therefore say that the HR, SV
The stroke volume of the left ventricle is the same of that of the right as a reflection of the force of myocardial contraction are factors intrinsic
ventricle. to the heart that will affect the cardiac output. But aside from factors
intrinsic to the heart, there are also factors outside the heart called
End Diastolic Volume (EDV) peripheral factors that may also affect the cardiac output.
- is the amount/quantity/volume of blood in the ventricles at
the end of diastole, before systole = PRELOAD What are the factors outside the heart that may affect the
- Normal Value: 110-130 mL cardiac output?
1. Total blood volume
* Whatever amount of blood that will be present in the ventricles after 2. Status of the venous sytem that will deter blood back to the
the ventricular filling time, before contraction of the ventricle; that is the heart
end diastolic volume. It is the EDV that will exert force on the ventricular 3. Status of the arterial system which is the opposing force to
wall stretching the ventricular wall before it contracts thus it is called ventricular contraction
preload or the load of the ventricle that is needed to be ejected. All of these factors make up the vascular or circulatory system
so that means that the activity of the heart is dependent on the status of
End Systolic Volume (ESV) the vascular system and vice versa the status of the vascular system is
- is the volume of blood in the ventricles at the end of systole also dependent on the activity of the heart. The heart and the vascular
- Normal Value: 45-50 mL system are actually inter-dependent and that is because of the close
nature of the cardiovascular system.
* ESV is the amount/quantity/volume of blood remaining in the
ventricles after contraction. No matter how strong the force of ventricular End Diastolic Volume (EDV)
contraction is, there will always be a certain amount of blood that will
remain in the ventricles. What are the factors that will influence the EDV? EDV is the
volume of blood in the ventricles after the relaxation phase, before
contraction.

PHOTO: Preload

1 Shannen Kaye B. Apolinario, RMT|

 Take note of where the black arrows are directed. These black Both of the equations are true but there is a range of heart rate.
arrows represent the EDV. It is directed towards the ventricular wall so The horizontal axis on the graph represents heart rate while the vertical
the greater the volume or EDV, the greater the force that will be exerted axis represents cardiac output. Based on the graph, when the heart rate
on the ventricular wall. If the force exerted on the ventricular wall is increases from 060 beats per minute, there is a corresponding increase
greater, that will now stretch the ventricular wall and if the ventricular in cardiac output. They are directly related because when the heart rate
wall is stretched, that will now increase the force of myocardial increases from 0-60, the duration of filling time is not yet compromised
contraction. So in other words, the greater the EDV, the more the because the normal heart rate is 75 beats per minute so that means that
ventricular wall is stretched, the greater will be the force of contraction. the ventricles can still be filled with blood adequately so the cardiac
And if the force of contraction is increases, stroke volume increases, output increases. In the first phase, sympathetic stimulation increases the
cardiac output increases. So EDV is directly related to cardiac output. heart rate. Sympathetic stimulation increases not only the heart rate but
also the force of contraction. When the heart rate increases, the stroke
Factors Affecting EDV volume increases therefore the cardiac output increases.

1. Effective filling time When the heart rate increases from 60-180 beats per minute,
the duration of the filling time is quite affected but still, the ventricles can
Filling time refers to the duration of the diastolic or relaxation still be filled with blood because from 60-180 beats per minute, the
phase because that is when the ventricles are filled with blood. increase in heart rate is equal to the decrease in stroke volume so that the
cardiac output is maintained at a constant level.
FT EDV SV CO
When the heart rate increases from 180 beats per minute and
If the duration of filling time increases, there will be enough above, the duration of the filling time is now severely compromised. And
time for the ventricles to accommodate a larger volume of blood so the sympathetic stimulation can no longer compensate on the very short
EDV increases. Again, if the EDV is greater, the greater the ventricular duration of filling time. So the increase in heart rate is now less than the
wall is stretched, the greater the force of contraction so the SV as well as decrease in stroke volume so the cardiac output will now decrease. There
the CO increases. All are directly directed. is a range wherein the cardiac output will start to decrease with an
increase in heart rate.
HR FT EDV SV CO
If you will recall, if the heart rate is 75 beats per minute, the
One factor that will influence the duration of the filling time is duration of one cardiac cycle is 0.8 sec, the duration of the systolic phase
heart rate. When the heart rate increases, the duration of the filling time is 0.27 sec, and much longer is the duration of the diastolic phase which is
will decrease less time for ventricular filling so the EDV will decrease 0.53 sec. The longer duration of the diastolic phase is important because
and so will the SV and CO. it is during the diastole that the ventricles are filled with blood and at the
same time, it is during diastole that perfusion of oxygen supply to the
HR FT EDV SV CO cardiac muscle is better.

The reverse is also true that when the HR decreases, the Cardiac Cycle Duration with Heart Rate
duration of the filling time will increase, more EDV, SV and CO. Duration Heart Rate Heart Rate
75 beats/min 200 beats/min
Increased HR decreases the CO and decreased HR increases the Cardiac cycle 0.80 sec 0.30 sec
CO but going back to the formula: CO = SV x HR, heart rate is directly Systole 0.27 sec 0.16 sec
related to CO, meaning to say that an increase in HR will increase the CO. Diastole 0.53 sec 0.14 sec
Which among the formula is true?
When the heart rate increases to 200 beats per minute, the
In the formula, it is directly related and of course that is true. If duration of cardiac cycle will decrease from 0.8 to only 0.3 sec but if you
the HR increases, there will be an increase in the frequency of will compare the decrease in the duration of systole and diastole, diastole
depolarization on the sarcolemma of the cardiac muscle cell. So the more is more affected (bigger decrease in duration of diastole) from 0.53 to
the cardiac muscle is depolarized, the more Ca++ enters the cell and if 0.14 sec which means that the filling time is really compromised and the
more Ca++ enters the cell, the greater the force of contraction, the more EDV is severely decreased.
the stroke volume increases, increased cardiac output. That is how an
increase in HR will increase the CO. What about the other equation? 2. Effective filling pressure

EFP = CVP ITP

EFP - effective filling pressure

CVP central venous pressure
ITP intra-thoracic pressure

Aside from the duration of the filling time, another factor that
may influence the diastolic volume is the effective filling pressure or
transmural pressure - pressure difference between the inside and
outside of the heart. Pressure inside the heart is the central venous
pressure while outside is the intra-thoracic pressure. The greater the
difference between the pressure inside and outside of the heart, the
greater the effective filling pressure. And when the effective filling
pressure is greater, that will now distend the ventricles, allowing the
ventricles to accommodate a larger EDP. The intra-thoracic pressure is
always negative or below atmospheric pressure and that will enable the
heart as well as the other dilatable structures in the thoracic cavity to be
distended so it can accommodate greater volume.

2 Shannen Kaye B. Apolinario, RMT|

3. Myocardial compliance Within physiologic limits, the force of myocardial contraction
will be determined by the initial muscle length that means resting length
All elastic structures have the property of compliance and that of the cardiac muscle or length of the cardiac muscle before it contracts.
is the measure of distensibility or stretchability of an elastic structure.
The force of contraction will depend on the length of the
C=V cardiac muscle before it contracts so what will stretch the cardiac muscle
P before it contract ? The force that will be exerted by the EDV. the greater
the EDV, the greater will be the force exerted on ventricular wall, the
Compliance is equal to change in volume over change in more the ventricular wall will be stretched and that will now increase the
pressure. For a structure to have an increase in compliance, the change in force of contraction and this is called heterometric autoregulation.
volume should be higher or greater compared to the change in pressure. Autoregulation means that the heart itself can regulate its own force of
And this is true for the ventricles, remember that the ventricles can contraction. Metric is the length. Hetero - changes. So the change in the
accommodate a large volume of blood with little increase in pressure and length of cardiac muscle will enable the heart to regulate its own force of
that is because of the presence of the elastic tissue in the cardiac muscle contraction. Remember that this only happens within physiologic limits
that will enable the ventricles to distend. it does not stretch continuously when the EDV is increasing and more and
more powerful the force contraction becomes. There is a limit because
4. Venous return when the cardiac muscle is overstretched or distended, there will be less
overlapping between thin filaments and thick filaments so there will be
VR = CO less myosin length that will bind on the actin active site so when it
5 L/min contracts, it becomes weak.

The most important factor that determines the EDV is the Actin filament
volume of blood returning to the heart per minute and that is venous Myosin filament
return. Because of the closed nature of the cardiovascular system,
whatever volume of blood that will return to heart per minute, will be
effectively ejected or pumped by the heart per minute so that means But remember that overstretching or overdistention of the
venous return is equal to cardiac output. The average venous return is cardiac muscle does not occur in the first place because of the presence of
also 5 L or 5,000 mL per minute. connective tissue. The connective tissue on the cardiac muscle and on the
pericardium prevents overdistention when the cardiac size increases
End Systolic Volume (ESV) because connective tissue is less distensible while the elastic tissue
allows distension.
What is the major factor that will affect the volume of blood
remaining in the ventricles after contraction or ESV? It is the force of Factors that affect cardiac muscle length:
contraction. So if the force of myocardial contraction increases, SV will
increase, ESV will decrease. If the force of myocardial contraction Stronger atrial contraction. Remember that most of the
decreases, SV will decrease, ESV will increase. In other words, force of ventricular filling will take place when the ventricles as well as
myocardial contraction is inversely related to the end systolic volume the atria are in a relaxed state. But during atrial systole, there
(ESV). is an additional amount of blood that will be ejected to the
ventricles so the EDV increases. If the force of contraction in
the atria is greater, there will be more than the 20% that will
be added in the ventricular filing, the EDV will be more
increased.

Increased total blood volume. Total blood volume is actually

one factor that will affect venous return. So if the total blood
volume increases, venous return will increase, EDV will also
increase so that will stretch the ventricular wall.

Increased venous tone. One property of smooth muscle cells

present in the vascular wall as well as in the visceral wall is the
tone. For example, the stomach and the small intestinal wall
have a tone, the same is also true with blood vessels, arteries
and veins - their wall has a tone.

When the smooth muscle layer in the veins contract,

there will be veno-constriction, the blood cannot go back to the
heart. The veins are called capacitance vessels because the
smooth muscle layer is thin and it has elastic tissue so the
venous wall is highly distensible so it can accommodate large
The normal systolic volume (red line) is about 70 mL but if the volume of blood. If the venous wall is in a relaxed state, the
force of myocardial contraction increases, SV increases so the remaining blood in the veins cannot go back to the heart. So what is
part becomes smaller. venous tone? Tone means state of partial contraction. One
Since the force of myocardial contraction will affect the ESV, property of smooth muscle is they can remain partially
what now are the factors that will influence the force of myocardial contracted for a long time. If the wall of the veins is partially
contraction? What is the EDV and the relationship between EDV and force contracted, there will be less capacity to accommodate blood
of myocardial contraction is reflected in the Frank starlings Law. so the blood will go back to the heart thus increasing venous
return and EDV and that will stretch the cardiac muscle cell.
Factors Affecting ESV
Increased pumping of skeletal muscle. When you remain in
a. Force of myocardial contraction a standing position for a long time, blood pools in the veins of
the lower extremities. So again, if there is pooling of blood in
1. Frank Starlings Law the veins of the lower extremities, the venous return will
decrease, EDV will decrease, and the cardiac muscle will not be

3 Shannen Kaye B. Apolinario, RMT|

 stretched. But once you move, the skeletal muscle will contract
and that will compress the veins. When the veins are But that is not the end of sympathetic effects. It does not allow
compressed, that will open up the venous valves. The opening Ca++ to always enter the cell because when it always depolarizes, more
of the valves is directed toward the heart. So when the veins Ca++ will enter the cell.
are compressed by skeletal muscle contraction, venous valves
will open and blood will return to the heart. But hidni dun nagtatapos ang sympathetic effects. Hindi lang
basta nagpapapasok ng ca kasi malimit magdepolarize, mas madaming ca
* The three factors: increased total blood volume, increased venous tone na papasok
and increased pumping of the skeletal muscle will first influence venous
return. Venous return will then influence EDV, EDV is the one that will Another action of sympathetics is when norepinephrine and
exert force on the ventricular muscle to stretch the ventricular muscle. epinephrine bind with 1 receptors in the heart, this will cause activation
of G-proteins. Activated G-proteins will activate the enzyme system -
Increased negative intrathoracic pressure. Increased adenylyl cylcase that will lead to the formation of an intracellular ligand
negative intrathoracic pressure allows the ventricles to or a second messenger that is cyclic AMP (cAMP). As a second
distend, so that will stretch the ventricular muscle. messenger, cAMP will mediate the actions of catecholamines on the
cardiac muscle cell and one action of cAMP is to cause activation of
All of these are factors will affect cardiac muscle length before another intracellular enzyme that is protein kinase A (cAMP-PK). One
contraction. So if these factors will increase, cardiac muscle length will action cAMP-PK is to phosphorylate the Ca++ channels on the
increase before contraction so that during contraction, the force of sarcolemma. When it is phosphorylated, that will allow more Ca++ to
myocardial contraction will increase. enter that will increase the force of myocardial contraction.

But take note that sympathetic stimulation will increase not

2. Autonomics only the force of contraction; it will also facilitate relaxation of the cardiac
muscle by the action of cAMP-PK. So another action of cAMP-PK is to
Aside from cardiac muscle length another factor that will phosphorylate troponin I so that troponin cannot bind with Ca++. If
influence the force of myocardial contraction is the autonomic troponin cannot bind with Ca++, the muscle will relax because troponin-
innervations: sympathetic that will release catecholamine, tropomyosin complex will go back to cover the active site of actin due to
norepinephrine, epinephrine; and parasympathetic that will release absence of troponin-Ca++ complex.
acetylcholine.
Another action of cAMP-PK is to phosphorylate an intracellular
Sympathetic stimulation will increase the force of contraction protein called phospholamban. The normal action of phospholamban is
of both the atria and ventricles primarily because norepinephrine binds to inhibit the Ca++ pump on the sarcoplasmic reticulum. If the Ca++ pump
with 1 receptors will increase membrane permeability to calcium is inhibited, Ca++ will not return it will remain bound to troponin C so
allowing more Ca++ to enter myocardial cell and that will increase the there will still be muscle contraction. But once phosphorylated by cAMP-
force of contraction. But aside from this, sympathetic stimulation can also PK, the inhibitory effect of phospholamban will decrease so the Ca++
increase the heart rate so the more frequent the myocardial cell is pump will be activated and when activated, it will actively transport Ca++
depolarized, again, the more Ca++ will enter the myocardial cell and that back to the sarcoplasmic reticulum so there will be no Ca++ that is
will increase the force of contraction. attached to troponin and the muscle will relax. So again, aside from
increasing the force of myocardial contraction, sympathetic stimulation
In contrast, vagal or parasympathetic stimulation by releasing can also facilitate relaxation of the cardiac muscle.
acetylcholine will decrease the force of atrial contraction. It has no direct
effect on the force of ventricular contraction because there is very little, if
any parasympathetic or vagal innervation to the ventricles. 3. Calcium

Another important factor that will affect the force of

myocardial contraction will be the amount Ca++ available that will bind
with troponin C. In contrast to the skeletal muscle, there are two sources
of Ca++ for myocardial contraction: sarcoplasmic reticulum and ECF. That
means that the plasma Ca++ level will have an effect on the force of
myocardial contraction.

4. Adequate coronary flow

Another factor is adequacy of the coronary arteries. Remember

that the coronary arteries supply blood and oxygen to the cardiac muscle
itself. So when there is an obstruction (e.g. thrombus or embolus) in one
of the branches of coronary arteries, there will be an area of that
myocardium that will be deprived of oxygen supply so the area will be
ischemic. If the ischemic area is not corrected, it will cause necrosis to the
tissue developing an infarct and that infarcted area cannot contract
anymore. Since there is an area in the myocardium that is not contracting,
the overall force of contraction will decrease and that will predispose to
ventricular or heart failure.

5. Heart rate
PHOTO: Schematic diagram of the movement of calcium in excitation-contraction
coupling in cardiac muscle. Influx of Ca++ from interstitial fluid during excitation The force of myocardial contraction can also be influenced by
triggers release of Ca++ form the sarcoplasmic reticulum (SR). The free cytosolic Ca++ heart rate. It is mentioned earlier that when the heart rate increases, the
activates contraction of the myofilaments (systole). Relaxation(diastole) occurs as a depolarization of cardiac muscle will be more frequent and remember
result of uptake of Ca++ by the SR, by extrusion of intracellular Ca++ by the 3 Na+-1 that with each depolarization, it allows more Ca++ to enter and that will
Ca++ antiporter, and to a limited degree by the Ca++-ATPase pump. R, -adrenergic increase the force of contraction.
receptor: cAMP-PK, cAMP-dependent protein kinase.

4 Shannen Kaye B. Apolinario, RMT|

Factors that influence or regulate heart rate: 7. Afterload

Autonomics. The most important factor. Sympathetic nerves Afterload is the aortic pressure load, opposing force to left
innervating the SA node and the effect of norepinephrine is to ventricular contraction. Why in the aortic artery only and not in
increase membrane permeability to Na+ and Ca++ that will pulmonary artery? Because remember that there is low/no pressure area
make the SA node more excitable so the heart rate will in the pulmonary circulation, not much resistance to right ventricular
increase. On the other hand, parasympathetic or vagal contraction unless there is pulmonary hypertension. More of the
stimulation will make the SA node more permeable to K+ so resistance happens in the left ventricle because there is high pressure
that will hyperpolarize the SA node making it less excitable, area in the arterial system. So when we say afterload, it is the pressure in
decreasing the heart rate. the aorta.

Hormones. Aside from the neurotransmitters released by the

autonomic nerves, heart rate can also be affected by several
hormones one of which is cortisol - corticosteroids from the
adrenal cortex. The effect of cortisol is to potentiate the effect
of epinephrine so that means increased corticosteroids may
increase the heart rate.

Other hormones are T3 and T4 thyroid hormones.

Thyroid hormones directly stimulate the SA node so that one
clinical manifestation of hyperthyroidism is tachycardia.

Neural reflexes. Heart rate can also be influenced by neural

reflexes that are centered on the medulla and that will include
reflexes that actually regulate arterial blood pressure: the
baroreceptor reflex and the chemoreceptor reflex. These
reflexes that regulate arterial blood pressure can also regulate
heart rate. PHOTO: Afterload

Bainbridge reflex. This time, when venous return increases, Remember the photo on preload, the arrows are directed on
the volume of blood in the right atrium will increase and that the ventricular wall because the EDV exerts force on the ventricular wall
will stretch the right atrial wall where you have the SA node. to increase the force of contraction.
When the right atrial wall is stretched, the SA node is
stimulated and that will increase the heart rate. So this When the ventricles contract, the blood or EDV goes in the
Bainbridge reflex is sensitive to an increase in blood volume aorta so the direction is directed towards the aorta but the pressure in
that will return to the right atrium. the aorta counteracts the EDV so when the pressure is greater on the
aorte, EDV will have a hard time to go out. So if the aortic pressure
Exercise. During exercise, heart rate increases for two increases, stroke volume decreases, end systolic volume increases and
reasons: increased metabolism and increased sympathetic this is shown on the photo below:
stimulation.

Excitement and anxiety. Emotions like excitement and

anxiety will also increase the heart rate partly because of
increased sympathetic stimulation.

Temperature. Increased environmental temperature can also

increase the heart rate. Not only environmental temperature
but also body temperature so when there is fever, heart rate
increases.

6. Cardiac glycosides

Cardiac glycosides are given to patient suffering from

congestive heart failure. The main purpose of giving cardiac glycosides is
to increase the force of myocardial contraction.

When the muscle is relaxed, the Na-K pump is activated. Na-K

pump will extrude 3 Na+ in exchange for 2 K+ transported into the cell
creating a concentration gradient for Na that will now activate the Na+-
Ca++ pump. If the Na+-Ca++ pump is activated, 3 Na+ will go inside and
Ca+ will go outside decreasing the concentration of Ca+ inside the cell and
that is not ideal if there is congestive heart failure. It is needed for the
Ca++ to remain inside the cell to have an increased force of contraction. The normal stroke volume is still represented by the red line.
So what the cardiac glycosides do is to inhibit the Na-K pump so there will When the aortic pressure increases, the tendency of the ventricles is to
be no concentration for Na+ and that will not activate the Na-Ca pump. If increase its contraction because the pressure against it is stronger. Thats
the Na-Ca pump is not activated, there will be no increase concentration why the pressure in the ventricles is increasing and increasing but
of Ca++ that will go out of the cell or Ca++ will remain inside the cell so because the opposing force is greater, stroke volume is decreased and the
the force of contraction is increased. end systolic volume is increased.

So what is the consequence of that? There is much left so in

every venous return, what will happen in the EDV? There is much left but

5 Shannen Kaye B. Apolinario, RMT|

even if there is less amount that goes out, some will still go back to the To summarize the factors that will determine the cardiac
heart, so what will happen to the EDV? EDV will increase because there is output, there are factors intrinsic to the heart and there are factors
much [blood] left and there was an additional amount added during the outside the heart. Factors intrinsic to the heart will include the heart rate
relaxation phase. When the EDV is increased, the ventricular wall will be and the force of myocardial contraction. Factors outside the heart or
stretched; its contraction will be increased. But even if the contraction is peripheral/coupling factors will include the preload (factors that will
increased but there is persistent increase in aortic pressure, less will still affect EDV) and afterload or aortic pressure load. These are the major
be ejected so that eventually there will be pulling of blood in the left factors that will determine cardiac output
ventricle and that will cause the left ventricle to dilate. Since the SV is less,
eventually the venous return will also be lessened because there is a
decrease in the amount ejected so less will go back or return to the heart.
Effects of Various Conditions on Cardiac Output

Increase:

- Anxiety or excitement (50-100%) partly because of

sympathetic stimulation.

- Eating (30%) eating increases blood flow to the

gastrointestinal tract. Increase in blood flow increases venous
return and increases cardiac output.

- Exercise (up to 700%) increased metabolism, sympathetic

stimulation.

- Increased environmental temperature

- Pregnancy due to increased blood volume that will increase

venous return.

- Epinephrine

Decrease:

- Sitting or lying down from a standing position (20-30%)

- Rapid arrhythmias heart rate of 200 beats per minute that

will severely compromise the duration of the filling time so
that will decrease the cardiac output.

- Heart diseases examples are congestive heart failure,

myocardial infarction, cardiac valve diseases, arrhythmias,
chronic hypertension all of these factors that will decrease the
force of myocardial contraction.
PHOTO: Pressure-Volume Loop. Cardiac output is the volume of blood pumped by the
heart each minute. In the steady state the output from both the right and left ventricles
No change
is the same. The pressure-volume loop for the left ventricle is depicted here. The
cardiac output is calculated as: Cardiac output = Heart rate x stroke volume
where: stroke volume = end-diastolic volume end systolic volume - Sleep
Increases in venous return (increased preload) increase the stroke volume and thus
cardiac output. Increases in arterial pressure (increased afterload) decrease stroke - Moderate change in environmental temperature
volume and thus cardiac output (lower panel).

Ejection Fraction (EF)

8. Stenosis
- Percentage of the EDV is ejected by the left ventricle per
Another condition that will increase aortic pressure is stenotic contraction
aortic valve. If the aortic valve hardens, even if the ventricular pressure is - EF = SV x 100
greatly increased, the SV and cardiac output will still be diminished. EDV
Blood will again accumulate in the left ventricle and eventually, the left - Normal value: 65-70%
ventricle will dilate so the force contraction will decrease.
The volume of blood that should be ejected per contraction
should be 65-70% of 130 mL that is why the average stroke volume is 70
Determinants of Cardiac Output mL.
Cardiac factors: Coupling factors: In patients suspected of having congestive heart failure, one
Heart rate Preload procedure that is requested is 2-D echocardiogram to determine the
ejection fraction (EF). Because if the EF falls below what is normal, it
means that the SV is decreased and it is decreased because the
Cardiac Output ventricular contraction is weak.

Myocardial Afterload
contractility

6 Shannen Kaye B. Apolinario, RMT|

Cardiac Index

- Cardiac output per square meter or body surface area

- Normal value: 3L/min/m2 of body surface area

Another factor that may influence cardiac output is body

surface area and the normal cardiac index is 3L/min/m2. It means that in
the elderly where the physical activity is less, the skeletal muscles
atrophy so the body surface area decreases and the cardiac output and
cardiac index is decreased. Compared to the athletes who have well-
developed muscles, they have a bigger body surface area so the CO and
cardiac index is increased because what happens is that when there is
increased need (bigger muscles) to be supplied with blood, the heart
compensates so the CO increases.

Cardiac Reserve

- Maximum percentage that cardiac output can increase above

normal (300-600%)

In certain conditions, the CO may be increased from 5L to 13-

15 L per minute and that is called a hypereffective heart. Hypereffective
because the heart can pump blood a volume that is greater than what is
normal. Hypereffective heart happens if there is sympathetic stimulation
and parasympathetic inhibition, during moderate to heavy exercise or
during athletic activities that will involve endurance (e.g. marathon
races). The opposite is a hypoeffective heart the heart pumps blood
that is less than normal and that is brought about by cardiac diseases (e.g.
congestive heart failure, rapid arrhythmia, cardiac valvular diseases).

Ask and it will be given to you; seek and you will f ind; knock and
the door will be opened to you. For everyone who asks receives; he
who seeks finds; and to him who knocks, the door will be opened.
-Matthew 7:7-8

GOD BLESS YOU

7 Shannen Kaye B. Apolinario, RMT|