Download Increased HR →Decreased SV Increased Contractility → Decreased

External work states that a force must be applied to displace (move) the blood
from the ventricles towards the Aorta/Pulmonary trunk. However, Kinetic
energy of blood represents the energy which blood gains to increase its speed
through the blood vessels.
External work  Displacement
Kinetic energy  Speed
Since CO = SV x HR, any factor that affects either SV or HR will affect CO.
Venous Return (VR) affects EDV. EDV affects SV (Frank-Starling’s law)
ANS affects HR. HR affects the filling time
Increased HR Decreased SV
For example, increasing HR will decrease both systolic and diastolic periods;
with the diastolic period being the most affected one, hence decreasing the filling
time. Decreased filling time will decrease EDV. Lower EDV means lower SV. The
opposite is true.
Increased Contractility  Decreased ESV
Sympathetic stimulation has a positive inotropic effect on ventricles. This means
that the ventricular contractility will increase, thus increasing SV. EDV, however,
stays around its normal value. Since SV= EDV – ESV, a conclusion can be made:
ESV decreases.
Vascular resistance affects the afterload (diastolic pressure
in major vessels)
Assuming that the kinetic energy of blood remains constant, if vascular
resistance decreases, the afterload will decrease (i.e.; below 80mm Hg).
Semilunar valves will open earlier than normal and more blood will be ejected
from the ventricles, hence SV increases. ESV therefore decreases. EDV here
remains constant.
Venous Return Affects Diastolic Period
Increased VR will make blood press more on the SA node, generating Bainbridge
reflex, that is, increased HR. Increased HR will decrease diastolic
period.Hormones also affect HR, thus affecting the filling time.
Increased Preload  Increased SV
Increased preload increases the length of the cardiac sarcomere towards the
optimal length. This will increase the force of contraction. Increasing preload
also increases EDV. Consequently The SV will increase.
P.S.: this does NOT mean that increased preload will not affect ESV. It will, but to a
lesser extent.
Preload can increase due to:
1- increased venous blood pressure. (As blood will push more against the
ventricular walls).
2- decreased HR. (as filling time will increase)
As a consequence, increased preload will increase the force of contraction, SV,
and finally CO.
Q: Contractility vs. Force of Contraction, are they the same?
Contractility measures how much Ca++ is available INTRA-cellularly.
Force of contraction measures the length of the cardiac sarcomere and how close
it is to the optimal length. Inotropic change is thus related to contractility, not to
force of contraction.
So, we can conclude that contractility can be changed by any factor that changes
intracellular Ca++, such as hormones, ANS regulation, etc. On the other hand,
however, force of contraction is dependent mainly on preload.
The best way to measure contractility is via calculating the maximum change of
pressure per unit time, the dP/dT, back from the Ventricular pressure-volume
relationship curve. (Kindly, refer to the 5th slides pack, slide #34)
Elevated K+ levels decrease contractility.
Increased Afterload should decrease SV, unless we increase the kinetic energy
generated by the ventricular contraction. So, increased afterload – in general –
decreases CO. That’s why hypertensive patients’ ventricles undergo hypertrophy.
The ventricles must do more work to overcome the increased afterload.
Hypertensive patients are prone to develop ischemia, which could lead to MI,
because ventricles now do more work, which means they need more oxygen.
More oxygen means more blood, so if the patient has a Coronary Artery Disease,
he/she could develop ischemia.
Ventricular hypertrophy can be confirmed by echocardiography.
VENOUS RETURN
VR = amount of blood that returns to the heart per minute.
VR does NOT include the right side of the heart only, it also includes the left side.
VR = CO =△P/R (Ohm’s law, the most important law in CVS physiology)
VR = △P/R
= Venous pressure – Right atrial pressure/ Resistance to VR
What affects the VR?
1- △P (venous P- Rt. Atrial P):
VR increases if △P increases, i.e., if venous pressure increases.
Venous Pressure
Assuming the distance between the right atrium and lower extremities,
represented by one single non-partitioned vein, is 136cm, and the right atrial
pressure is zero mm Hg, the pressure in the lower end of the vein will be 136cm
of water, that is 10mm Hg (136/13.6; 13.6=density of Hg). This 10mm Hg is the
hypothetical venous pressure. This pressure is due to gravity.
However, the actual venous pressure is less than 10mm Hg. This is due to the
presence of venous valves. Those one-way valves allow the blood to move
upward towards the heart without allowing it to go back. Skeletal muscles
surround those valves from the outside. Contraction of those muscles squeezes
the blood found within two adjacent valves towards upward and downward
directions. The valves, however, are one-way valves. So, the lower valve will
prevent the squeezed blood (again, due to skeletal muscle contraction) from
moving downwards. The upper valve will allow the blood to pass through. As a
consequence, blood always moves toward the heart. (Remember: there is always
a degree of skeletal muscle contraction (tone)).
The numerous venous valves distributed along the veins draining blood from the
distal parts of the body toward the heart work as “Blocks” to partition the long
vein with high venous pressure to shorter, gated segments with much lower
venous pressure (that is because valves have decreased the height of the long
water column to multiple short columns).
Although there is always a pressure gradient between distal parts of the heart
and the right atrium, the presence of venous valves is a MUST, because the effect
of gravity on venous blood is much higher than the effect of pressure gradient.
Venous valves + skeletal muscle pump, both facilitate venous return.
Venous valves incompetency causes varicose veins.
2- Compressional factors:
Continuous increase in right atrial pressure tends to exert a backward effect, that
is, it compresses the blood coming towards the right atrium and forces it to move
away from the heart and to pool within the veins. This “pooling” increases
venous pressure. Since △P is the difference between venous and right atrial
pressures, both pressures will increase so △P decreases. Decreased △P means
decreased VR (according to Ohm’s law: VR = △P/R)
Increasing abdominal pressure also increases venous pressure (without affecting
the right atrial pressure). Consequently, VR increases.
CENTRAL VENOUS PRESSURE (CVP)
CVP is the right atrial pressure.
In cases of right heart failure (RHF), one must check the CVP if it is high or
normal. If CVP is high, pushing fluids into the patient’s circulation will kill him.
What does determine the CVP?
1- Pumping activity of the right atrium: ability of right atrium to pump blood out
of it.
2- Amount of blood flowing into the right atrium. (VR)
Increasing contractility increases emptying of the heart. This will decrease right
atrial pressure. Decreased right atrial pressure will increase △P, thus increasing
venous return. The effect of contractility allows the atrium to exert a “suction
effect” on the veins draining in it.
If we want to decrease CVP, we either increase venous pressure, or increase
contractility (decrease right atrial pressure).
 Factors that increase RAP (CVP):
1- Increased blood volume
2-Increased venous tone increased venous pressure  increased VR
3- Dilation of arteriolesflow into capillaries increases  increased
venous pressure  increased VR
4- Decreased cardiac functiondecreased contractility increased ESV
 increased CVP  decreased VR
Arterioles are the main resistant vessels in the circulation.
Considering the Total Peripheral Resistance (TPR), the most contributing factor
to its value is the arteriolar resistance. Venous resistance is very low, so it will
have a much smaller effect on TPR.
Resistance to VR is mainly due to resistance in the venous side, not in the arterial
one.
Right atrial pressure is an indicator of ESV in ventricles.
Explain the following:
Sympathetic stimulation increases Cardiac suction effect.
Sympathetic stimulation  positive inotropic effect  higher contractility 
more SV, less ESV  less CVP  more pressure gradient  more suction
towards right atrium.
What makes varicose veins dangerous?
Varicose veins will increase venous pressure. Blood flow will be slower, too.
Increased venous pressure will decrease pressure gradient. Decreased pressure
gradient means decreased VR.Besides,thrombi can ensue.
Venoconstriction, constriction of veins, increases venous pressure more than
venous resistance. This guarantees more blood flowing towards the heart.
Inhalation decreases pressure within the chest cavity. This will decrease the
pressure applied on the outer walls of the veins draining into the heart. Those
veins will expand. Decreased venous pressure in proximal regions of the heart
(i.e.; CVP) means more VR. The opposite is true.
Please refer to slides. Make sure you read slide #35 carefully.