CARDIOVASCULAR PHYSIOLOGY (Gloria Marie M. Valerio, MD) the different organs of the body.
the different organs of the body. This is made possible by the pumping
Outline:
1. Functional Anatomy of the Heart
2. Properties of the Myocardial Cells
3. Electrical Events
4. Cardiodynamics
5. Characterics, Properties, Functions of the Different Types of
Blood Vessels
6. Hemodynamics
7. Microcirculation
8. Mechanisms that Regulate Cardiovascular Function
Functional Anatomy of the Heart
The normal position of the heart inside the thoracic cavity is
slightly tilted to the left, pointing downwards.
When the heart contracts, it has a wringing action, meaning to
say, when the heart contracts, it rotates slightly to the right and that will
now expose the cardiac apex, so that when you place the diaphragm of
the stethoscope over the chest wall particularly on the fifth intercostal
space, left mid-clavicular line, that is where you will heartbeat the loudest
called apex beat or point of maximum impulse.
Fifth intercostal space: Start palpating below the clavicle and
first rib – the second intercostal space, and move three spaces down. The
midclavicular line: left of the left clavicle, take note of the mid-point then
move five spaces below. In males, it is easily located because it is exactly
below the left nipple. In females, the location may be variable so you need
to palpate.
PHOTO: Schematic diagram of the parallel and series arrangement of the vessels
composing the circulatory system. The capillary beds are represented by thin lines
connecting the arteries (on the right) with the veins (on the left). The crescent-shaped
thickenings proximal to the capillary beds represent the arterioles (resistance vessels).
The cardiovascular system consists of the heart at the center
and the different blood vessels which are arranged in parallel and in
series with each other. The red are the arteries, the blue are the veins,
and the capillaries are the smallest vessels in the body.
The major function of the cardiovascular system is to transport
nutrients including oxygen to the different organs of the body and to
remove the waste products of metabolism including carbon dioxide from
1 Shannen Kaye B. Apolinario, RMT
action of the heart, so when the heart contracts, it will pump blood to the
arteries. The arteries in turn will distribute blood at a high pressure to
the different organs of the body. And from the different organs of the
body, blood then will be collected by the veins and returned to the heart.
So the arteries are distributing blood vessels while the veins are
collecting blood vessels. The capillaries will allow the exchange of fluid
and solutes between intravascular and interstitial fluid compartments.
The human heart is divided into two pumps: right and left and
they are connected in series. The left heart pumps blood to the systemic
or peripheral circulation by way of the aorta. The right heart pumps
blood to the pulmonary circulation by way of the pulmonary artery.
Systemic or peripheral circulation includes blood flow to all
organ systems of the body except for the lungs. When the cells of the
systemic or peripheral circulation are metabolizing, they consume oxygen
and produce carbon dioxide that will now be collected by the veins and
will have a low oxygen tension and a high carbon dioxide tension called
unoxygenated/deoxygenated/venous blood. This blood will be
emptied by way of vena cava to the right side of the heart. When the right
heart contracts, this same blood will be ejected to the pulmonary
circulation by way of pulmonary artery. Unlike the other arteries of the
body, the pulmonary artery carries deoxygenated or venous blood. This
same blood will then reach the pulmonary capillaries and this is where
exchange of gases will take place between the alveoli in the lungs and
blood in pulmonary capillary across respiratory membrane. The blood
from the pulmonary capillaries will come from the right side of the heart
– low oxygen tension, high carbon dioxide tension. The opposite is true
with regards to air in alveoli - increase oxygen tension, low carbon
dioxide tension. Movement or transport of these gases across the
respiratory membrane is a passive process. It occurs by simple diffusion
brought about by pressure gradient. So the transport of movement of
oxygen will take place from alveoli to pulmonary capillary, the carbon
dioxide goes in opposite direction. So the blood that will enter the
Alveoli Increase pO2 Decrease pO2 Pulmonary capillary
Decrease pCO2 Increase pCO2
pulmonary vein is already oxygenated. Unlike the other veins in the body,
the pulmonary vein carries oxygenated or arterial blood which will then
be emptied on the left side of the heart which means the left heart pumps
blood to the systemic circulation and receives blood from the pulmonary
circulation while the right heart pumps blood to the pulmonary
circulation and receives blood from the systemic circulation.
The circulatory system is a closed system – whatever amount
of blood will be pumped by the blood per minute will be equal to the
volume of blood that will return to the heart per minute.
Structures of the Human Heart
The heart is divided into two pumps: the right and the left. The
two pumps in turn are made up of two chambers: atrium and ventricle.
The right heart is made up of the right atrium and right ventricle while
the left heart is made up of the left atrium and left ventricle.
 The two atria are separated by a band of connective tissue
forming the interatrial septum. The two ventricles are also separated by
a band of connective tissue forming the interventricular septum. The
two atria are separated from the two ventricles by a mass of connective
tissue. The four chambers of the heart are separated by connective
tissues.
The wall of the atria and ventricles is made up of cardiac
muscle. The atrial wall/musculature is thinner compared to the
ventricular wall or musculature. The two atria functions as a primer
pumps for the ventricles and as conduits of blood from veins to ventricles.
It is therefore the ventricles with the thicker wall that are the major
pumps in the heart with the left ventricular wall thicker than the right
ventricular wall. The left ventricular wall is thicker because it pumps
blood to the systemic circulation with an average pressure of 70-130
mmHg. On the other hand, the right ventricle will pump blood to the
pulmonary circulation with an average pressure of only 4-25 mmHg. The
left ventricle will have to pump blood against a higher pressure resistance
in the systemic circulation compared to the right ventricle that will pump
blood against a lower pressure in the pulmonary circulation. Since the
opposing force is higher in the left ventricle, the tendency is to contract
more forcefully because of increased workload resulting to hypertrophy
of the muscle fibers. Although the left ventricular wall is thicker, contract
more forcefully, higher workload and higher opposing force than the
right, the output of the two ventricles is the same. Whatever amount will
be ejected by the left ventricle per minute is the same with the amount of
blood ejected by the right ventricle per minute.
Aside from the cardiac muscles, the atrial and ventricular wall
also contains a fair amount of elastic tissues that will enable the
different chambers of the heart to dilate when the volume of the blood
inside increases. Also present in the atrial and ventricular wall is a fair
amount of connective tissue and this connective tissue in turn will
prevent overstretching or distension of cardiac muscles when the cardiac
size increases.
PHOTO: Four cardiac valves as viewed from the base of the heart. Note how the leaflets
overlap in the closed valves.
2 Shannen Kaye B. Apolinario, RMT
Other important structures in the heart are the valves and
there are two sets of cardiac valves. Between the atria and ventricles are
the atrioventricular valves - tricuspid valve on the right side and
mitral valve on the left side. The tricuspid valve is between the right
atrium and right ventricle while the mitral valve is between the left
atrium and left ventricle. The other sets of cardiac valves are between the
ventricles and the arteries – the pulmonary valve between the right
ventricle and pulmonary artery; the aortic valve between the left
ventricle and aorta. Functions of the valves: first, when they open, they
allow blood to flow from one chamber of the heart to another – when the
atrioventricular valves are open, blood flow from the atria to the
ventricles and when the semilunar valves are open, blood ejects from the
ventricles to the arteries. When they close, they will prevent regurgitation
or backflow of blood. However, there are no cardiac valves between the
atria and veins so when there is atrial contraction, small amount of blood
backflows to the veins. There is only small amount of backflow because
when the atria contracts, there is increase in pressure and the tendency is
to push blood downwards to the ventricles and at the same time, when it
contracts, the orifice of the veins becomes smaller.
Structure of Cardiac Valves
PHOTO: Drawing of a heart split perpendicular to the interventricular septum to
illustrate the anatomic leaflets of the atrioventricular and aortic valves.
The three cardiac valves – tricuspid, pulmonary and aortic
contains three cusps. It is only the mitral valve that contains only two
cusps. For the atrioventricular valve, the cusps are attached by strong
ligaments called chordae tendinae to the papillary muscle and the
papillary muscle arises from the ventricular wall. Mitral valve has two
cusps attached by the chordae tendinae to the papillary muscle. The
semilunar valve – aortic valve has no chordae tendinae. Tricuspid valve
has chordae tendinae attached to the papillary muscle and arises from the
ventricular wall.
Each cusp has an orifice or opening covered by leaflets which
are made up of loose fibrous tissue. One end of the leaflets is attached to
the border of the orifice while the central part is freely movable. Since it
is thin and freely movable, it can open. However when they close, they
close completely because there is extensive overlapping of the leaflets
that cover the orifice of the cusp. Opening and closing of the cardiac valve
is a passive process brought about by pressure differences between the
two chambers of the heart. In the case of tricuspid valve for example, if
the right atrium is contracting, the right ventricle is in a relaxed state.
When the right atrium is contracting, the pressure increases and that will
push open the tricuspid valve so that blood will flow from the right
atrium and right ventricle. On the other hand, if it now the right ventricle
contracting and the right atrium is relaxed, the high pressure in the right
ventricle will close the tricuspid valve to prevent back flow of blood to the
right atrium. It is also a passive process due to the pressure gradient.
Same things happen with regards to the mitral valve as well as to the
semilunar valves. When the ventricle is contracting, the papillary muscle
also contracts but the contraction of the papillary muscle is not essential
in closing the atrioventricular valves. Remember that when the ventricle
is contracting due to the thick musculature, the pressure is high. So the
high pressure will tend to push the AV valves to bulge into the atria
however, when the papillary muscle contracts, it will pull the chordae the leaflets. In insufficient or incompetent cardiac valve, the leaflets do
tendinae to prevent eversion or over-bulging of the AV valves during not close completely allowing back flow of the blood either from the
ventricular contraction. ventricles to the atria or from the arteries to the ventricles.

In normal mitral valve, when the left atrium is contracting, that

is the amount of blood that will be ejected to the left ventricle. In stenotic
mitral valve, even if the left atrium is contracting, there will be less
amount of blood that will be ejected to the left ventricle. There will be
now pooling of blood in the left atrium causing the left atrium to dilate. In
stenotic aortic valve, the leaflets hardened so that during contraction, the
amount of blood ejected in the aorta will be decreased. There will be
pooling of blood in the left ventricle causing the left ventricle to dilate.

An example of an insufficient or incompetent cardiac valve is a

prolapsed mitral valve. When the left ventricles contract, it does not
close even if there is blood ejected in the aorta, it will be lessened because
of the backflow of blood in the left atrium.

Presence of a stenotic or an incompetent cardiac valve will

produce abnormal heart sounds called a murmur.

PHOTO: Mitral and aortic valves (the left ventricular valves)

Valve Type of lesion Timing of murmur
Mitral Stenosis Diastole
Heart Sounds Incompetent Systole
Aortic Stenosis Systole
Closing of the cardiac valves will produce the normal heart Incompetent Diastole
sounds. The first heart sound is at the onset of ventricular contraction
with closing of AV valve. That closing of AV valve produces the first heart Diastole – ventricular relaxation
sound. Compared to the second heart sound, closing of the AV valve is Systole – ventricular contraction
said to be louder and longer in duration. The sound produced by the
closing of the tricuspid valve is heard best on the fifth intercostal space, The Pericardium
left of the sternum while the sound produced by closing of the mitral
valve is heard best on the fifth intercostal space at the cardiac apex - left
mid-clavicular line. The second heart sound occurs at the onset of
ventricular relaxation with closing of the semilunar valves. And because Pericardial fluid
of the pressure in the arterial system, when the semilunar valves close,
they close abruptly and that will make the duration of the heart sound Parietal pericardium
shorter. The sound produced by the closing of the pulmonary valve is
heard best on the second intercostal space left of the sternum while the Visceral pericardium
sound produced by the closing of the aortic valve is heard best on the
second intercostal space right of the sternum. The quality of the second
heart sound can be affected by respiratory phase – expiration and The heart is covered by a membrane which is made up of
inspiration. During expiration, you will hear only one second heart sound connective tissue – the pericardial sac or pericardium. This connective
– there is simultaneous closure of the aortic and pulmonary valves. tissue that makes up the pericardium is less distensible. Presence of this
During inspiration, there is a physiological splitting of the second sound will also prevent overstretching of the cardiac muscle when the cardiac
with closing of the aortic valve occurring a little ahead of the pulmonary size increases. The pericardium is made up of two membranes: visceral
valve and the sound produced by closing of aortic valve is louder than and parietal pericardium. The visceral pericardium is the membrane
that produced of the closing of the pulmonary valve except in patients directly attached to the anterior surface of the myocardium. When the
with pulmonary hypertension. visceral pericardium is reflected back, it forms the parietal pericardium.
The space in between the two membranes is filled with 30cc of
The pressure inside the thoracic cavity is negative or below pericardial fluid. The importance of the pericardial fluid is to lubricate
atmospheric pressure – causing a suction effect on structures that can be the heart facilitating the movement of the heart when it contracts.
dilated. (In positive or above atmospheric pressure, it will compress the
structures in the thoracic cavity.) The more negative the intra-thoracic (2) Groups of Myocardial Cells
pressure is, the more the heart and lungs are dilated. When the heart is
dilated, it allows more blood to return especially to the right heart – more 1. Automatic Cells
blood will return from the systemic circulation. There will be an increase An automatic cell is a cell that is capable of spontaneously
volume of blood to the right heart causing a delay of the closing of the generating its own action potential independent of extrinsic nervous
pulmonary valve during inspiration. stimulation. In the case of myocardial cells, it is independent of automatic
stimulation. Aside from generating its own action potential, the cells of
In children with thin chest wall or patients suffering from left the heart are capable of transmitting or conduction action potentials
ventricular failure, a third heart sound can be heard and that will coincide throughout the heart. Structures that make up the hearts’ conduction
with filling of blood in the ventricles. Rarely, there is a fourth heart sound system:
that can be heard and that will coincide with atrial contraction. In some
abnormal conditions, the third and fourth heart sounds may be  Synoatrial (SA) node = located at the junction of superior vena
accentuated so that what you will hear in the stethoscope will be triplets cava and right atrium.
of sounds resembling the sound that is produced by galloping horses
called a gallop rhythm.  Atrioventricular (AV) node = located posteriorly on the right side
of interatrial septum. It is divided into three zones:
Certain abnormal conditions like an infection in the heart may o Atrionodal (AN) zone – most proximal zone, a transitional
damage the cardiac valves and there are two types of lesions that may zone between the right atrium and AV node
occur in the cardiac valve: stenosis and incompetent cardiac valve. In o Nodal (N) zone - middle
stenosis, the valve cannot open completely because of the hardening of

3 Shannen Kaye B. Apolinario, RMT

 o Nodal His (NH) zone – most distal, connects with the bundle
of His
 Purkinie system/ventricular conduction system = made up of
bundle of HIS and purkinje fibers
o Bundle of HIS – located at the interventricular septum. The
bundle of HIS forms right and left bundle branches. The left
bundle branch will divide to form the posterior and anterior
fascicles. The left posterior and anterior fascicles as well as the
right bundle branch will then connect with the Purkinje fibers
that are present mostly at the apex of the heart.
PHOTO: The cardiac conduction system
All of these cells are automatic cells and can generate own
action potential. But in a normally functioning heart, all action potentials
are generated by the sinoatrial (SA) node and is referred as the primary
pacemaker of the heart while the other automatic cells are latent
pacemakers. They are called latent pacemakers because although they do
not normally generate action potential, in some abnormal conditions,
they can be stimulated to generate their own action potential.
The primary pacemaker of heart is the one that determines the
heart rate – number of heart beats per minute. The average heart beats
per minute is 75-80 beats per minute. The SA node is the primary
pacemaker of the heart because it is the fastest that can generate an
action potential. Overdrive suppression is the increase frequency of
discharge of an action potential from an automatic cell will diminish the
automaticity of other automatic cells. The SA node will fire at a high rate
of 75-80 beats per minute with each action potential that will depolarize
other automatic cells. With each depolarization, a certain amount of
sodium ions will enter the cell that will create a concentration gradient
for sodium that will activate the Na-K exchange pump. The Na-K pump
will extrude sodium ions. The more frequent the other automatic cells are
depolarized, the more sodium ions will enter the cell, the more Na-K
pump will be activated, the more sodium ions will be extruded from the
cell that would cause the cell to be hyperpolarized. If the other automatic
cells are hyperpolarized, they will become less excitable. When the
overdrive stops, the activity of Na-K pump will not stop immediately; it
will remain active, continuing to extrude sodium ions, the more the other
automatic cells will become hyperpolarized, the more they will become
less excitable, and the more their automaticity will be diminished. (44m)
2. Non-automatic cells
Non-automatic cells cannot generate own AP and are specialized
mainly for contraction. The presence of non-automatic cells in the heart,
even if you cut the automatic innervation to the cardiac muscle, it can still
contract. Non-automatic cells are the cardiac muscle cells present in the
atrial wall and ventricular wall.
Properties of Myocardial Cells
1st Property: Automaticity – generation of action potentials
4 Shannen Kaye B. Apolinario, RMT
1
2
0
4 3
-90 mv
Skeletal muscle action potential: 5-30 millisecond
Phase 4 – Resting Membrane Potential (-90mv) – membrane is highly
permeable to potassium because of the presence of many potassium leak
channels. Since there are many potassium leak channels on the
membrane of the skeletal muscle and there is a concentration gradient for
potassium, the tendency is for potassium to move out – decreasing the
amount of positively charged ions inside. Also present inside the cell are
negatively charged molecules including proteins which are large
molecules so they remain inside. The main extracellular cation is sodium,
there is a concentration gradient for sodium but the membrane is only
slightly permeable to sodium ions because of there are only few sodium
leak channels – most sodium will remain outside. The membrane is
permeable to chloride at rest, it allows the chloride ions to move in but
because of the presence of the negatively charged ions inside the cell,
chloride will eventually get out. To maintain the concentration of Na and
K inside the cell, you have the activity Na-K pump (3 Na out, 2 K in). These
things stabilize the RMP of the cell to -90mv.
Intracellular Extracellular
Increase K+ Decrease K+
Negatively charged proteins
Decrease Na+ Increase Na+
Decrease Cl- Increase Cl-
Resting Membrane Potentials:
 Neurons = -70mv
 Skeletal muscle = -90 mv
 SA node = -60mv
 Ventricular muscle = -90mv
 Gastrointestinal smooth muscle = -60mv
The resting membrane potential is different in each cells because of
the potassium leak channels. The more potassium leak channels present
on the membrane, more K+ will move out of the cell, making the
membrane potential more negative and vice versa.
Phase O – depolarization – opening of fast voltage gated Na+ channels
Phase 1,2,3 – repolarization – re-establishing the RMP, brought about by
the closure of fast voltage gated Na channels and opening of slow voltage
gated K channels. Since these K channels are slow, they remain open for a
long time allowing K+ to continuously move out so that at some point, the
MP will go below the resting level = hyperpolarization. When the K+
gated are closed, the RMP will be restored
Automatic Fiber Action Potential
1
0 2
4 3 4
-60 mv
250-300 milliseconds hyperpolarization
Action potential of an automatic cell- SA node
Difference from the AP of skeletal muscle: Non-automatic Fiber Action Potential
 Duration is longer – 250-300 millisecond (ventricular muscle)
 RMP is less negative - -60 mv

Phase 4 – slow rise in membrane potential and is unstable. The slow rise
in membrane potential is called the pre-potential or slow diastolic
depolarization. There is more Na leak channels, membrane potential
increases.

Phase 0 – Depolarization. Somewhat inclined, depolarization occurs

slowly

Phase 1,2,3 –Repolarization. Inclined, occurs slowly, there is

hyperpolarization like in the skeletal muscle

 The increase in sodium leakage and a decrease in the

membrane permeability to potassium will account for the
automaticity of the SA node.
Activation of slow (inclined)
voltage gated long lasting Ca++
channels allowing Ca influx with
some Na influx = MP will become
less negative
Voltage gated K channels will
open allowing K efflux. But
repolarization cannot occur
rapidly because of the long
lasting Ca channels are still open.
Ca influx and K efflux
Midway of repo: Ca
channels close, K
channels open
PHOTO: Action potential in the ventricle (250-300 milliseconds)
RMP - -90, straight line, it is stable
Phase 0 – depolarization, straight line. Occurs rapidly due to opening of
fast voltage-gated Na channels = Na influx then reaches the threshold
voltage of -60 mv resulting to depolarization. When the membrane
potential reaches -20 mv, it will open up slow, long lasting voltage gated
Ca channels = Ca influx. (The main factor responsible for depolarization is
Na influx)

-40 mv Peak of the spike – Na channels closes, K channels open. Ca++ channels
Na leakage, are still open
Decrease K Hyper: prolonged
opening of K
-50 mv channels Phase 1 – initial phase of repolarization – brought about mainly by slow
voltage gated K+ channels
-60 mv
Phase 2 – plateau – the amount of K+ that goes out is equal to the amount
of Ca++ that goes in. no electrical activity. At the end of the plateau, the
250-300 milliseconds Ca++ channels will close leaving only the K+ channels open that will bring
about the final phase of repolarization
Action potential of an automatic cell
(same thing happens in SA node, AV node, bundle of HIS) Phase 3 – final phase of repolarization

Phase 4 - -90 RMP is re-established. The increase membrane permeability

With parasympathetic or vagal stimulation, the to potassium is responsible for the -90 mv RMP.
neurotransmitter released (NTA) released is acetylcholine (Ache). When
Ache binds with muscarinic 2 receptors in the SA node, it increases No hyperpolarization –Although the K+ channels can remain open for a
permeability to K+, allowing more K+ efflux. Parasympathetic or vagal long time, because of the plateau, it is open for a long period of time thus
stimulation will hyperpolarize the SA node. If it is hyperpolarized, it is it does not reach hyperpolarization
less excitable and the duration of the membrane pre-potential is longer or
delayed generation of action potential. In parasympathetic or cholinergic Similarities and differences with the action potential of skeletal and
stimulation, SA node is inhibited, heart rate decreases. cardiac muscles:
 Similarities: -90 mv RMP, fast-paced depolarization
The opposite happens with sympathetic stimulation,
 Differences: repolarization, no hyperpolarization, duration
norepinephrine released by sympathetic nerves will bind with the B1
receptor in the SA node resulting to an increased permeability to Na and
Ca causing hypopolarization of the SA node, making it more excitable and
the heart rate increases.

PHOTO: Action potential of the SA node

PHOTO: Action potential of the atrium

5 Shannen Kaye B. Apolinario, RMT

Similarities and differences between the ventricle and atrium:
 Similarities: same, RMP, depolarization, phase 1
 Differences:
o phase 2 – plateau. In the atrium, the membrane is
more permeable to K+ than to Ca++. More K+
conductance than Ca++ conductance that will make
the duration of the plateau shorter and not
sustained as compared to that of the ventricle.
o Repolarization phase is shorter in atrium than in the
ventricle
Periods of Refractoriness
The importance of prolonged duration of refractoriness is for
the ventricles to be filled with blood resulting to a more effective
pumping action, no fatigue, no tetanic contractions. One cannot elicit
successive action potentials or contractions without tetanic or sustained
contractions in the cardiac muscle = allow more time for ventricular
filling. The musculature of the ventricle is thick so when it contracts, it
compresses the coronary arteries. The coronary arteries supply blood
and oxygen to the cardiac muscle thus when it is compressed, there is
poor perfusion of cardiac muscle and less oxygen supply, this happens if
there is tetanic contractions but in the cardiac muscle, there are no
tetanic contractions. There is longer period of relaxation, when the
ventricles are relaxed, there will be better perfusion of the cardiac
muscle.

ARP RRP Duration Heart rate of 75 Heart rate Skeletal muscle

beats per min 200/min
Action potential 0.25 sec 0.55 sec 0.005 sec
ARP 0.20 sec 0.13 sec 0.004 sec
RRP 0.05 sec 0.02 sec 0.001 sec

In Absolute or Effective Refractory Period (ARP), no

amount of stimulus intensity will be able to re-excite the membrane of
that cell. It covers the whole of depolarization until 1/3 of the
repolarization phase. At phase 0, it is absolute refractory because all the
voltage gated sodium channels are open and it is not able to re-open the
already open sodium channels. In phases 1 and 2, the Na channels are
already close but it is still absolute refractory because Na channels are
voltage gated and they only open at a certain voltage or membrane
potential near the critical firing level of about -60mv more so if the
membrane potential is at its resting level. It is far from the CFL.
In Relative Refractory Period (RRP), its level is near the
critical firing level and resting level, the membrane becomes more
excitable so that a stronger than threshold stimulus can be able to open
up the voltage gated sodium channels and elicit a second action potential.
PHOTO: Changes in action potential amplitude and upstroke slope as action potentials
are initiated at different stages of the relative refractory period of the preceding
excitation
As the membrane potential reaches the relative refractory
period as well as the RMP, if there is stimulus later in the RRP, that will
open up more and more voltage gated Na channels so that its
depolarization increases its amplitude, same thing happens in the SA
node.
2nd Property: Rhythmicity

It is said that the SA node generates the action potentials at

regualr intervals. Even if the heart rate increases, if the impulses are still
generated at regular intervals, that is still called the sinus rhythm.

Photo: Normal sinus rhythm

PHOTO: Relationship between action potential and contraction in the ventricle

A contraction cannot be elicited unless the ventricle is almost

completely relaxed.
Photo: Normal ECG

6 Shannen Kaye B. Apolinario, RMT

P wave – represents atrial depolarization
QRS complex – represents ventricular depolarization
When seeing a normal sinus rhythm, take note of the interval
between successive P waves – regular interval, take note of the interval
between successive QRS complex – regular interval.
Photo: Sinus tachycardia
The heart rate may increase with sympathetic stimulation,
during moderate to heavy exercise, and increase temperature during
fever. In these three conditions, the heart rate will increase but if the
impulses are generated at regular intervals, that is still sinus rhythm. But
since the rate will increase, it is now called sinus tachycardia.
Photo: Sinus bradycardia
On the other hand, in cold temperatures or if there is vagal
over stimulation that inhibits the SA node, the rate of firing will decrease
but if the impulses are generated at regular intervals, that is still sinus
rhythm but this time, it is now called sinus bradycardia.
If there is no rhythm or if it is irregular, it is now called
arrhythmia.
3rd Property: Conductivity
Photo: Transmission of the cardiac impulse through the heart, showing the time of
appearance (in fractions of a second after initial appearance at the sinoatrial node) in
different parts of the heart.
All impulses from a normal functioning heart will come from
the SA node. From the SA node, the impulse will be transmitted to the AV
node and transmission of impulses from the SA node to the AV node is
facilitated by means of three internodal tracts: anterior internodal tract of
Bachmann, middle internodal tract of Wenckeback and posterior
internodal tract of Thorel. Take note that the tips of the fibers of the SA
node are directly connected to the right atrial muscle cells so there is
direct transmission of impulses from the SA node to the right atrium.
7 Shannen Kaye B. Apolinario, RMT
With regards to the right and left atrium, transmission of
impulses can occur locally through gap junctions. When the impulse
reaches the AV node, there is a delay in the transmission of impulses so
the velocity of conduction decreases at the AV node and this is called the
AV nodal delay. Most of the delay will take place between the AN and N
zones of the AV node. There is a delay in the transmission of impulses in
the AV node because it has a small fiber diameter and few gap junctions –
spaces or channels between the membranes of the muscle fibers that will
allow ions to flow freely from one muscle fiber to the next. The smaller
fiber diameter and fewer gap junction causes increased resistance to
impulse conduction - the AV nodal delay. The importance of AV nodal
delay is for the ventricles to remain in a relaxed state for a longer period
of time allowing more time for the ventricular filling and to ensure that
the atria and ventricles will not contract simultaneously.
From the AV node, the impulse will then travel to the bundle of
His then to the left and right bundle branches then to the Purkinje fibers
then it would stop (from antero-basal  apex  end).
Transmission of impulse in heart: antero-basal  apex  postero-basal
The part of the heart that will depolarize last is the postero-
basal.
Conduction Speed in Cardiac Tissue
Conduction rate (m/sec)
SA node 0.05
Atrial muscle 1
AV node 0.05
Bundle of His 1
Purkinje fibers 4
Ventricular muscle 1
Conduction speed is lowest in the AV node (not in the SA node
because it is generation). Fastest is in the Purkinje fibers because of the
large fiber diameter. In the atria and ventricles, conduction of impulses
may occur locally through gap junctions.
Reentry
Photo: The role of unidirectional block in re-entry. In A, an excitation wave traveling
down a single bundle (S) of fibers of continues down the left (L) and right (R)
branches. The depolarization wave enters the connecting branch (C) from both ends
and is extinguished at the zone of collision. In B, the wave is blocked in the L and R
branches. In C, a bidirectional block exists in branch R. in D, a unidirectional block
exists in branch R. the antegrade impulse is blocked, but the retrograde impulse is
conducted through and re-enters bundle S.
A – Normal direction. Coming from the SA node to the AV node to the
bundle of His. From the bundle of His, the impulse will be transmitted to
the left and right bundle branches. From the left and right bundle
branches to the apex of the heart but there is a connecting fiber between
the right and left bundle branches.
B – Both left and right bundle branches are blocked so there is no impulse
transmission to the apex of the heart as well as to the connecting fiber.
C – Only one bundle branch is blocked (right bundle branch). The impulse
that is supposed to go the right bundle branch is blocked but the left
bundle branch goes to its normal route – to the apex and to the
connecting fiber. The one that goes to the connecting fiber can now go to
the apex but can also go back to the area that is blocked; this is called re-
entry or circus movement.
D – Since the right bundle branch is blocked, the transmission of impulse
is blocked while that coming from the left will re-enter the area where the
impulse came from, it goes round and round that’s why it is called circus
movement. Reentry or circus movement is possible because the distance
travelled by this impulse is longer compared to other one which is
blocked so it becomes refractory. Since the distance is longer, when it
reaches the area that is blocked, it becomes out of refractory/out of
refractoriness so it can go back. Because of this phenomenon, this is the
path that is responsible for atrial or ventricular fibrillation/flatter. In
the synchronised contraction, the whole atria or the whole ventricle,
there is an area that will contract and there is an area that will relax.
Ectopic Tachycardias
Atrial contraction
Ventricular contraction
AV nodal delay
Most of the blocks takes place in the AV node so that it will
produce the 1st degree, 2nd degree and 3rd degree heart block, all of
these are abnormal conditions. The normal ratio between atrial and
ventricular depolarization is 1:1, so that during atrial and ventricular
contraction, if the atria will contract three times, the ventricles will also
contracts three times but atrial contraction happens first than ventricular
contraction causing an AV nodal delay.
PHOTO: AV blocks. A, First-degree block; the PR interval is 0.28 second (normal: <0.20
sec). B, Second-degree block (2:1). C, Third-degree block; note the dissociation between
the P waves and the QRS complexes
8 Shannen Kaye B. Apolinario, RMT
1st degree heart block – Incomplete heart block. All impulses from the SA
node can still be transmitted to the ventricles. Based on the spacings in
the photo, there is atrioventricular depolarization happening. The ratio of
ventricular depolarization is still 1:1. So that when it contracts – three
contractions in the atria, there will also be three contractions in the
ventricles. The difference from the normal is that it has a longer duration
of the AV nodal delay.
2nd degree heart block – Not all impulses from the SA node will reach the
ventricles. What happens is P-P-QRS, P-P-QRS. This time, the ratio of the
atrial to ventricular depolarization is 2:1 or 3:1. Not all the impulses
reach the ventricles but since there are impulses that can reach the
ventricles, this is still an incomplete heart block.
3rd degree heart block – Complete heart block. No impulses from the SA
node will be able to reach the ventricles. What happens is P-P-P-P. The
atria will be contracting normally at a rate that is dictated by the SA node;
that is 75 beats per minute. Initially, the ventricle will not contract
because no impulses will reach the ventricles but there are pacemaker
cells in the ventricles – the bundle of His and Purkinje fibers. The two are
latent pacemakers and they are also automatic cells. For 20 seconds,
there will be no impulse coming from the SA node, the latent pacemaker
in the ventricle specifically the Purkinje fibers will be activated, it will
escape from the overdrive suppression and this is called the ventricular
escape. When activated, the Purkinje fibers will generate its own impulse
causing the ventricles to contract at a rate that is dictated by the Purkinje
fibers. If the contraction in the atria is 75 beats per minute, in the
ventricle, it is 30-40 beats per minute. The firing of Purkinje fibers is
slower than the SA node.
Another abnormal condition is the presence of a premature
contraction or an extrasystole wherein another contraction happens in
response from an impulse that will not come from the SA node. For
example, there is atrial contraction that is initiated by the impulse from
the SA node, other parts of the atria will be activated, and there will be an
ectopic fossi – impulse coming from other sources. So when it contracts, if
there is another impulse, there will be another contraction and this is
premature contraction or extrasystole.
PHOTO: Frequency summation and tetanization
In wave summation in the skeletal muscles, if three maximal
stimuli is applied successively, the magnitude of the 2nd contraction is
higher than the first because in the muscle, calcium ions have not yet
returned to the sarcoplasmic reticulum and when another stimuli is
applied, there will be more releasing of calcium ions that will increase the
force of contraction.
In cardiac muscle, the magnitude of the 2nd contraction is lower
than the first. Take note that extrasystole can only be elicited during the
mid or late diastole. It is not able to elicit an extrasystole during systole or
early diastole because of the long duration of the Absolute Refractory
Period. Another contraction can be produced only during the mid or late
diastole when the muscle is almost completely relaxed (Note: “almost”
but not yet relaxed).
 Remember that one of the important factors that will
determine the force of cardiac muscle contraction is the volume of blood
that will stretch the muscle before contraction. The longer the relaxation
phase, the more blood will be filled in the ventricles, the greater the
stretch of the cardiac muscle will be and the greater the force of
contraction will be.
There is a decrease in the magnitude of the 2nd contraction
because the relaxation phase is not yet complete so the filling of the blood
is less resulting to less stretch of the muscle and less force of contraction.
4th Property: Contractility
 Nebulin – forms the scaffold of the thin filament
 α actinin – will connect the thin filament to the Z line
 Titin – connects the thick filament to the Z line
 Tropomodulin – regulates the length of the thin filament
 Elastic tissue. Fair amount of elastic tissue that will enable the
chambers of the heart to dilate to accommodate a greater volume of
blood.
 Connective tissue. Presence of connective tissue that will prevent
over distension or overstretching of a cardiac muscle when the
cardiac size increases.

Important characteristic of a cardiac muscle:  More mitochondria and active capillaries. Compared to the skeletal
muscle, there are more mitochondria as well as active capillaries in
 Involuntary. Activity of the heart is not controlled by the cerebral the cardiac muscle and that is important because the main source of
cortex, it is controlled by the autonomic nervous system although energy for cardiac muscle contraction is oxidative metabolism.
there are automatic cells present in the heart.
 Sarcoplasmic reticulum. The sarcoplasmic reticulum in the cardiac
 Smaller. Compared to skeletal muscle cell, the cardiac muscle cell is
muscle is less well developed. Meaning to say, it can’t store large
smaller quantities of calcium ions that will provide for full contraction so
there has to be another source of Ca++ for the cardiac muscle
 Either binucleated or mononucleated contraction and that is the extracellular fluid (ECF). And because the
transverse tubular system in the cardiac muscle is more developed –
 Striated. Just like the skeletal muscle cell, the cardiac muscle is it has a bigger diameter; it can allow more Ca++ from the ECF to
striated. Striated means that the muscle fibers are distinctly enter the cardiac muscle cell.
separated from one another. What separates the individual muscle
fibers is the Z line that is why the area between two Z lines will form
a sarcomere. The difference between the skeletal and cardiac muscle
cell is that the membrane of the cardiac muscle branches out to
reconnect with the membrane of the next muscle fiber so that the
force generated with one muscle fiber can be transmitted to the
other muscle fibers as well.

PHOTO: “Syncytial,” interconnecting nature of cardiac muscle fibers.

 Presence of the intercalated disk. The intercalated disk is present on

the Z line. Its function is to separate one muscle fiber from another
but at the same time, to connect one muscle fiber to another by
means of gap junctions. Present in the intercalated disk are channels
that will allow ions to flow freely from one muscle fiber to the next
so that when an action potential is generated anywhere in a bundle,
it can be transmitted rapidly causing the whole bundle to be
depolarized at the same time and to contract as a single unit and this
is called a syncytial type of arrangement of muscle fibers. The
cardiac muscle cell anatomically is striated but functionally or
physiologically, it is a syncytium. The syncytial arrangement of
muscle fibers is important because it will provide synchronized
contraction of the atria and ventricles that is important for the
pumping action of the heart. It will also provide synchronized
relaxation of the atria and ventricles that is important for filling of PHOTO: Cardiac muscle (panel A) has high resistance to stretch when compared with
skeletal muscle (panel B). When either cardiac or skeletal muscle is stretched, there is
blood in the different chambers of the heart. an increase in resting tension (RT). If the muscle is then stimulated to contract
maximally, it generates more tension (termed total tension – TT). The difference
 Contractile proteins present: between total tension and resting tension at any given length is the force produced by
 Thick filament - myosin contraction (e.g. active tension – AT). The bell-shaped dependence of active tension on
 Thin filament – actin, troponin, tropomyosin muscle length is consistent with the sliding filament theory of cardiac and skeletal
muscle. It is, however, difficult to stretch cardiac muscle beyond its optimal sarcomere
 Meromyosin, C protein – forms the scaffold or suport of the
length, as evidenced by the rapid rise in resting tension in the middle of the bell-shaped
thick filament AT curve.

9 Shannen Kaye B. Apolinario, RMT


Above is a graph that shows the importance of the presence of
elastic tissue in the cardiac muscle. The blue line represents the resting
tension – tension that develops in the muscle before contraction. The red
line represents active tension – tension that develops in the muscle
during contraction. Because of the many elastic tissue in the cardiac
muscle, even in the resting state or resting length, passive tension
increases in the muscle and it can dilate so that when the cardiac muscle
fiber contracts, the difference between active and passive tension is
smaller compared to skeletal muscle. The importance of that is the
different chambers of the heart can accommodate a large volume of blood
with little increase in pressure.
Excitation-Contraction Coupling
PHOTO: Excitation-contraction coupling in the heart requires Ca++ influx
through L-type Ca++ channels in the sarcolemma and T tubules.
Present on the membrane or sarcolemma is a calcium pump,
calcium-sodium exchange pump, sodium-potassium exchange pump and
the last two are antiporters. Invagination of the sarcolemma will form the
T-tubules. Present on the membrane of the T-tubules are voltage-gated
calcium channels. Inside the cell, there are myofilament and sarcoplasmic
reticulum (SR). On the membrane of the sarcoplasmic reticulum is
another calcium pump. Also on the membrane of SR are ryanodine
receptors and these receptors are calcium-gated calcium channels.
What happens is when a membrane is depolarized, this will
activate the voltage-gated calcium channels of the membrane of the T
tubule and that will allow Ca++ to enter from the extracellular fluid (ECF)
to the inside of the cardiac muscle cell. Some of this Ca++ will
immediately bind with troponin C forming the calcium-troponin C
complex that will initiate muscle contraction but some of the Ca++ will
bind with the ryanodine receptors on the membrane of SR activating the
calcium-gated calcium channels that will allow Ca++ to move out from the
SR to the cytoplasm to bind with troponin C. The difference of this from
the skeletal muscle is that the Ca++ from the SR will not move out unless
there is a trigger that will cause the Ca++ to move out. The trigger is also
Ca++ from the ECF that will bind with ryanodine receptors hence it is
called calcium-gated calcium channels. It needs Ca++ from ECF to trigger
movement of Ca++ from SR into the cytoplasm. That is why it has two
sources of Ca++ compared to skeletal muscle – the SR and ECF. If there
are already many Ca++, the force of contraction is stronger. With
repolarization, it is expected that the muscle will relax but for the muscle
relax; Ca++ has to be removed. Ca++ is removed by the activity of calcium
pump on the membrane of the SR that will actively transport Ca++ back
into the SR. Another means to remove Ca++ is through the activity of the
calcium pump on the sarcolemma that will actively transport Ca++ back
into the ECF. But the most important means by which calcium is extruded
from the cardiac muscle cell is through the activity of the sodium-calcium
antiporter. Initially, with repolarization, the sodium-potassium pump is
activated that will pump three sodium ions out in exchange for two
10 Shannen Kaye B. Apolinario, RMT
potassium ions pumped into the cell so that it will create a concentration
gradient for sodium – increased concentration outside, low concentration
on the inside. That will now activate the sodium-calcium exchange pump
that will pump three Na+ in, in exchange for one Ca++ that is pumped out
of the cell and that is the main means by which Ca++ is extruded from the
cardiac muscle cell.
In patients suffering from heart failure, the main problem is
poor force of contraction of the ventricle. This poor force of contraction
has to be made strong by giving cardiac glycosides (e.g. digitalis). The
main mechanism of action of cardiac glycosides is to inhibit the sodium-
potassium pump. If this pump is inhibited, Na+ will not be extruded so
that will not create a concentration gradient for Na+. If there is no
concentration gradient for Na+, nothing will activate the sodium-calcium
pump so Ca++ will remain inside the cell and that can be utilize to
increase the force of ventricular contraction.
Arrangement of Muscle Fibers
When the heart contracts, it rotates slightly to the right and
that will expose the cardiac apex. The heart can rotate when it contracts
because of the arrangement of muscle fibers. The arrangement of muscle
fibers is synospiral and bulbospiral.
Autonomic Innervation of the Heart
How does the Autonomic Nervous System (ANS) regulates the
cardiac activity?
Sympathetic:
SA node
T3 AV node
T4 Norepinephrine + β1 receptor Purkinje system
T5 Atrial muscle
Ventricular muscle
First, the sympathetic nerves that innervate the heart originate
from T3, T4, and T5 segments (T = thoracic). Pre-ganglionic fibers from
T3, T4 and T5 will synapse with the sympathetic ganglia and this is called
the sympathetic chain. Post-ganglionic fibers from the sympathetic
chain will bind with β1 receptors in the heart and the neurotransmitter
agent (NTA) released by these sympathetic nerves is norepinephrine
(NE). The effect of NE at the myocardial cells is to increase membrane
permeability to Ca++ and Na+ so that will make the myocardial cell more
excitable and therefore increased cardiac activity. Sympathetic nerves
innervate ALL structures in the heart either automatic and non-automatic
so that will include the sinoatrial (SA) node, atrioventricular (AV) node,
ventricular conduction system or the Purkinje system as well as the atrial
and ventricular muscle.
Parasympathetic:
SAN
CN 10 Acetylcholine + M2 AVN
Atrial muscle
On the other hand, parasympathetic innervation to the heart is
carried by the vagus nerve which originates from the medulla. So the
vagus nerve will bind with muscarinic 2 receptors in the heart and the
NTA released is acetylcholine (Ache). The effect of Ache on the
myocardial cells is to increase membrane permeability to K+ so that will
hyperpolarize the myocardial cells inhibiting them or decreasing cardiac
activity. The structures in the heart that receive parasympathetic or vagal
innervation are the SA node, AV node, only the proximal part of the
bundle of His, atrial muscle, and there is very little, if any, vagal
innervation to the ventricles.
Chronotropic regulation:
Sympathetic Increased frequency of discharge of the SA node
Increased the heart rate
Parasympathetic Decreased frequency of discharge by the SA node
Decreased the heart rate
 Lead I represent electrical potential difference between
In relation to this, let’s look at how the autonomics regulate electrodes that are placed on the right arm and on the left arm. In lead I,
cardiac activity: First, regulation of heart rate is called chonotropic the electrode that is on the right arm is the negative electrode that of the
regulation. The sympathetic nervous system will increase the activity of left arm is the positive electrode.
the SA node so that this stimulation will increase the frequency of
discharge of action potentials from the SA node, increasing the heart rate. Lead II represents electrical potential difference between
On the other hand, parasympathetic or vagal stimulation will inhibit the electrodes that are placed on the right arm and on the left leg. The
SA node, decreasing the heart rate. electrode of the right arm is designated as the negative electrode that of
the left leg as the positive electrode.
Dromotropic regulation
Sympathetic Increased velocity of conduction Lead III represents electrical potential difference between
Decreased duration of AV nodal delay electrodes that are placed on the left arm and on the left leg. The
Parasympathetic Decreased velocity of conduction electrode of the left arm is designated as the negative electrode that of the
Increased duration AV nodal delay left leg as the positive electrode.

Regulation of the velocity of conduction of impulses in the

heart is called dromotropic regulation. Sympathetic stimulation will
increase the velocity of conduction of impulses in the heart so it will
decrease the duration of the AV nodal delay. In contrast, parasympathetic
stimulation decreases the velocity of conduction of impulses in the heart
prolonging the duration of the AV nodal delay.

*** In parasympathetic or VAGAL stimulation, buma-VAGAL ang heart

rate and velocity of conduction. 

Inotropic regulation
Sympathetic Increased force of atrial and ventricular contraction
Parasympathetic Decreased force of atrial contraction

Regulation of the force contraction of the myocardial cells or

inotropic regulation is by increasing membrane permeability to Ca++.
Sympathetic stimulation increases the force of contraction of both the
atria and ventricles. As for parasympathetic stimulation, it decreases the
force of atrial contraction and it has no direct effect on the force of
ventricular contraction. It has no direct effect but it has an indirect effect,
that is, parasympathetic stimulation will prolong the duration of the AV
nodal delay allowing more time for ventricular filling so the more the
ventricles are filled with blood, the more the ventricular wall is stretched,
and the greater will be the force of ventricular contraction.

Cardiac Cycle

Cardiac cycle is the sequence of events - electrical and

mechanical events taking place in the heart from the beginning of one
heart beat initiated by an impulse from the SA node to the beginning of
the next heart beat also initiated by an impulse from the SA node.

Electrical events – depolarization, repolarization of the atria and PHOTO: Einthoven triangle illustrating the electrocardiographic connections for
standard limb leads I, II, and III.
depolarization and repolarization of the ventricle

Mechanical events – contraction or relaxation of the atria and ventricles The electrode that is placed on the right arm is always negative
and on the left leg, it is always positive. In one lead, the electrode is
Electrical events positive when it is located nearer on the apex of the heart. Lead II will
approximate the direction of impulse transmission in the heart. So that
The electrical events will precede the mechanical events. All when asked to measure the duration of the different ECG waves, the
the electrical events taking place in the heart can be recorded by the amplitude of the different ECG waves, it is preferable to use lead II
electrocardiogram (ECG). To get an ECG tracing, electrodes are placed because it approximates the direction of impulse transmission in the
on the four extremities of the subject as well as on different locations on heart – right arm is negative, left leg is positive (from base to apex).
the chest wall. This electrodes act as sensors so that it will be able to pick
up electrical potentials produced by the myocardial cells so that what is
seen on the ECG tracing will represent electrical potentials and electrical
activities of the myocardial cell. Right arm
(negative)
By placing electrodes particularly on the four extremities,
bipolar limb leads are formed or standard limb leads. There are three
bipolar limb leads – Lead I, II and III. These leads will represent electrical
potential difference between two electrodes placed on two different
extremities. In order to have an electrical potential difference between
two electrodes, one electrode is arbitrarily designated as the negative
electrode and the other one is the positive electrode. Left leg
(positive)

Lead II

11 Shannen Kaye B. Apolinario, RMT


P-R segment S-T segment
(isoelectric) (isoelectric)
PHOTO: Important deflections and intervals of a typical scalar ECG.
Above is an example of an ECG tracing that shows electrical
events in the heart in one cardiac cycle. The P wave represents atrial
depolarization, QRS wave or complex represents ventricular
depolarization, and T wave represents ventricular repolarization.
ECG Rules:
Depolarization (+) electrode = upward
Depolarization away from (+) electrode = downward
Repolarization (+) electrode = downward
Repolarization away from (+) electrode = upward
Why is there an upward or positive deflection and a downward
or negative deflection? The rule in ECG is that if depolarization will move
towards a positive electrode, it is recorded as an upward or positive
deflection. On the other hand, if depolarization will move away from a
positive electrode, it is recorded as a downward or negative deflection. In
repolarization, if the electrode moves toward a positive electrode, it is
recorded as negative or downward deflection and if repolarization will
move away from a positive electrode, it is recorded as an upward or
positive deflection. Remember that in lead II, the positive electrode is on
the left leg.
P wave
P wave - atrial depolarization, it is a positive deflection.
Remember that the impulse is generated from the SA node transmitted to
the AV node so the direction of impulse transmission in the atria is it
moves towards a positive electrode. That is why the P wave is recorded
as an upward deflection.
There is no ECG wave that represents atrial repolarization
because atrial repolarization occurs simultaneously with ventricular
depolarization. If ever there is an ECG wave that will represent atrial
12 Shannen Kaye B. Apolinario, RMT
repolarization, it will appear as a downward or negative deflection
because the direction of repolarization in the atria follows the direction of
depolarization – repolarization is toward a positive electrode. This means
that in the atria, the first part to depolarize is also the first part to
repolarize and the last to depolarize is also the last part to repolarize.
When the impulse reaches the AV node, there will an AV nodal
delay ad that is represented by the straight line called a P-Q or P-R
segment. The P-R segment starts at the end of P up to the beginning of
the QRS complex. It is a straight or isoelectric line because of the delay on
the impulse transmission at the AV node.
From the beginning of P to the beginning of the QRS complex is
the P-R interval. The P-R interval will cover the P wave representing
atrial depolarization and the P-R segment that represents AV nodal delay.
PHOTO: Depolarization of interventricular septum from the left to right bundle branch
QRS complex will represent ventricular depolarization. It is a
complex made up of three waves. In the QRS complex, there is an initial
negative or downward deflection that represents depolarization of the
interventricular septum which will occur from left bundle branch to right
bundle branch. The positive electrode is in the left leg [it is moving from
the left to right bundle branch] so it is moving away from a positive
electrode that is why the Q wave which represents the depolarization of
the interventricular septum and is recorded as a downward or negative
deflection.
R wave is a very high positive deflection that represents
depolarization of the cardiac apex that is definitely towards a positive
electrode.
Then there is a second downward deflection which is the S
wave. So which part of the heart will depolarize last? Usually it goes from
the anterobasal  apex  posterobasal so when the wave of
depolarization moves from the apex to posterobasal part, again it is
moving away from a positive electrode so the S wave which represents
depolarization of the posterobasal part of the ventricle is recorded as
negative or downward deflection.
T wave is only a part of ventricular repolarization because
ventricular repolarization starts at the end of QRS complex. So from the
end of S wave to the beginning of T wave, there is an isoelectric line or the
S-T segment. Recall the action potential generated in the ventricle, the
phase of repolarization that represents the S-T segment is the plateau or
phase II. There is a straight line because of the equal conductance of Ca+
and K+; there is no change in membrane potential.
The T wave will represent only the phase III of repolarization
or the final phase of repolarization and it is a positive or upward
deflection. In the ventricles, the repolarization does not follow the
direction of depolarization, unlike in the atria. Repolarization will occur
in the opposite direction: from posterobasal  apex  anterobasal. It is
moving away from a positive electrode because from the apex, it will go
up hence it is recorded as an upward or positive deflection. So in the
ventricles the first part of the ventricles that will depolarize is the last
part to repolarize and the last part to depolarize will be the first part to
repolarize. So when it is said ventricular repolarization, it is actually the
S-T interval, from the end of S to the end of T, not just the T wave.
Mechanical events
Following depolarization, the atrial and ventricular muscles
will contract and it is called the systole. During systolic phase of the
cardiac cycle, blood is ejected from the different chambers of the heart.
Following repolarization, the muscles will relax and it is called diastole.
During diastolic phase, there will be filling of blood in the different
chambers of the heart.
The average duration of one cardiac cycle is 0.8 second. The
duration of the systolic phase is 0.27 second and that of the diastolic
phase is longer which 0.53 of a second and this happens at the heart rate
of 75 beats per minute. When the heart rate increases, the duration of the
cardiac cycle will decrease so the duration of the systole and diastolic
phases is also decreased. But there is a greater decrease in the duration of
the diastolic phase and there is a constant duration in the systolic phase
when the heart rate increases.
Correlation of the Electrical and Mechanical Events in the Heart in
One Cardiac Cycle
SAN
atr. depo atr. systole 20% VF
(P wave) inc. AP (a wave)
An impulse will be generated from the SA node transmitted to
the AV node. Transmission of the impulse from the SA node to the AV
node is facilitated by the three internodal tracts: Bachman, Wenckeback
and Thorel. In the process, the atria will undergo depolarization recorded
in the ECG as the P wave. The response of the atrial muscle to
depolarization is to contract so there will be atrial systole. When the atria
contracts, although it is a weak pump, there is still blood ejected to the
ventricles and that will account for only 20% of ventricular filling. When
the atria are contracting, atrial pressure increases and remember that
there are no cardiac valves between the atria and veins so that any
increase in atrial pressure can be transmitted to the veins so that in the
recording of the jugular venous pressure curve will show increase atrial
pressure during atrial systole and this is called A wave. A wave is not an
ECG tracing, it is only a label to the increase atrial pressure during atrial
systole.
When the impulse reaches the AV node, there will be a delay
called the AV nodal delay, in the ECG that is recorded as the P-R segment.
The importance of the AV nodal delay is that it will provide more time for
ventricular filling.

AVN delay inc. VF From the AV node, the impulse will now be transmitted to the
(P-R segment) ventricular conduction system (VCS) or Purkinje system and that will
cause ventricular depolarization in the ECG recorded as the QRS complex.
VCS vent. depo vent. systole inc. VP The response of the ventricular muscle to depolarization is to contract so
(QRS) following ventricular depolarization will be ventricular systole. When the
atr. repo atr. diastole dec. AP ventricles contract, the ventricular pressure increases. Simultaneous with
ventricular depolarization is atrial repolarization and no ECG wave
VP > AP close AV valves (1st heart sound) represents atrial repolarization. The response of the atrial muscle to
repolarization is to relax so atrial diastole happens. Since the atria is
isovolemic contractions: slight inc. AP (C wave) relaxed, there will be a decrease in the atrial pressure. When the
ventricular pressure exceeds atrial pressure, there will be a pressure
VP > 80 mmHg gradient and that will now close the AV valves therefore the first heart
sound will be heard. There will be a condition wherein the SL are still
open SL valves closed and the AV valves are now closed, there is no change in ventricular
volume because all the cardiac valves are closed but since the ventricles
rapid ejection are contracting, there is increase in ventricular pressure and this is called
isovolumic or isovolumetric contraction phase of the cardiac cycle.
reduced ejection; atrial filling
vent. repo vent. diastole dec. VP When the ventricles are contracting, ventricular pressure still
(S-T interval) increases and this high pressure may push the AV valves to bulge into the
AP > VP atria and that will cause a slight increase in atrial pressure which is now
protodiastole called the C wave. But remember that the AV valves does not over-bulge
close SL valves into the atria when the ventricular pressure is increased because when
(2nd heart sound) the ventricles contract, the papillary muscles will contract pulling the
chordae tendinae which will prevent over-bulging of the AV valves into
isovolemic relaxation; inc. atr. filling; the atria resulting to only a slight increase in the atrial pressure.
inc. AP (V wave)
When ventricular pressure exceeds 80 mmHg, this will push
AP > VP open the SL valves and following the opening of the SL valves is the
period of rapid ejection of blood from the ventricles to the arteries: aorta
open AV valves and pulmonary arteries. But when it is ejecting more and more blood, the
volume of the blood in the ventricles as well as ventricular pressure will
rapid inflow start to decrease. So the period of rapid ejection will now be followed by a
period of reduce ejection of blood from the ventricles to the arteries and
diastasis – reduced inflow of blood to the ventricles at the same time, the blood that is contained in the aorta will drop off to
the arteries to the different organs of the body and the veins are also
atr. – atrial repo – repolarization collecting blood so that little by little, there will be atrial filling.
AV - antrioventricular SAN – sinoatrial node
AVN – atrioventricular node SL - semilunar The ventricles will undergo repolarization so this is the S-T
dec. - decrease vent. – ventricular/ventricle interval in the ECG. The response of the ventricular muscle to
depo – depolarization VF- ventricular filling repolarization is to relax so there will be ventricular diastole therefore
inc. - increase VP – ventricular pressure ventricular pressure will start to decrease. Pressure in the aorta or in the
arterial system is always high so that when arterial or aortic pressure
At the beginning of one cardiac cycle, before an impulse is now exceeds ventricular pressure, this will close the semilunar valves and
generated from the sinoatrial (SA) node, the atrium and ventricles are all that will produce the second heart sound. But there is a short interval of
relaxed – atrial systole and ventricular diastole. The semilunar (SL) time between ventricular diastole and closure of SL valves which is called
valves are closed but the atrioventricular (AV) valves are open so that protodiastole.
will allow blood to flow from the atria to the ventricles. In fact, 80% of
ventricular filling (VF) takes place when all four chambers of the heart There will be a condition again wherein the SL valves are now
are in a relaxed state. It is not needed for the atria to contract to have closed, the AV valves are still closed so there is no change in ventricular
ventricular filling because its contraction is weak – “primer pump”, so volume but since the ventricles are in a relaxed state, ventricular
whenever the AV valves are open, there is 80% of ventricular filling. pressure decreases and this is called isovolumic relaxation. At the same

13 Shannen Kaye B. Apolinario, RMT

time as isovolumic relaxation, the atrial filling increases which will again
increase atrial pressure and is called the V wave.
When atrial pressure exceeds ventricular pressure, this will
now open the AV valves which will be followed by a period of rapid
inflow of blood to the ventricles and this event will account for the 80% of
ventricular filling. When there is more blood filled in the ventricle, it will
be slightly stabilized so that the period of rapid inflow will be followed by
a period of reduced inflow of blood to the ventricles called diastasis.
From that, there will be another impulse from the SA node beginning
another cycle. All of these events take place in the heart for 0.8 second.
Cardiac Cycle
Ventricular pressure is initially low. It will increase slightly
during atrial systole because of the additional volume of blood that will
be ejected by the atria to the ventricles. Ventricular pressure will actually
increase during isovolumic contraction and still high during the period of
ejection of blood. But as the volume of blood in the ventricles decreases,
ventricular pressure will also decrease. It will continue to decrease
during the period of isovolumic relaxation. It will remain low during the
periods of rapid inflow of blood to the ventricles and diastasis. Again,
slight increase with atrial systole because of the additional volume of
blood ejected from the atria to the ventricles.
Closing of the AV valves will mark the onset of isovolumic
contraction. Remember that in isovolumic contraction, all the cardiac
valves are closed so there will be no change in the volume of ventricles.
So that means at that point, the first heart sound will be heard.

Opening of the AV valves mark the end of isovolumic relaxation

so there will be period of ventricular filling.

What will happen at the end of isovolumic contraction? There

will be opening of the SL valves. While at the beginning of isovolumic
relaxation, the SL valves close so the second heart sound will be heard.

Atrial Pressure Curve

incisura

Phases: as – atrial systole

ic – isovolumic contraction
ejection – rapid and reduced ejection phase
ir – isovolumic relaxation
R inflow – rapid inflow of blood to the venticles
diastasis
as – atrial systole

The period of ventricular systole covers from the beginning of

isovolumic contraction until the end of the ejection phase while the
ventricular diastole will start with isovolumic relaxation up to the end of
atrial systole.

Ventricular Pressure Curve

SL valves SL valves close – ***Atrial pressure curve – yellow dotted line

open 2nd heart sound
Aortic pressure or arterial pressure is always high. It will
continually increase during the period of rapid ejection because of the
increased volume that will be ejected from the ventricle to the aorta. So if
the volume of blood in the aorta is greater, there will be greater force
exerted by that volume of blood on the aortic wall.

During the period of reduced ejection, the aortic pressure

decreases because there will be peripheral run-off blood, meaning to say,
blood that is contained in the aorta will now be distributed to the arteries,
to the arterioles, and to the different organs of the body so the volume of
blood in the aorta will decrease and that will now cause the aortic wall to
recoil. When the aortic wall recoils, there is a slight vibration of blood
inside so there will be slight increase again in aortic pressure which is
called a dichotic notch or incisura.

All throughout the period of ventricular diastole, the aortic

pressure is stable and is slightly low but it is still higher compared to the
ventricular pressure.

The pressure difference between the aorta and the ventricles

will cause the closing of the SL valves when aortic pressure exceeds
ventricular pressure.
*** Ventricular pressure curve – green line
1st heart AV valves
sound open

14 Shannen Kaye B. Apolinario, RMT

Ventricular Volume Curve The 3rd heart sound heard in abnormal conditions is due to
ventricular filling. There is an increase in ventricular filling coinciding
with the appearance of the 3rd heart sound.

At the start, there is additional increase in volume with atrial

systole – additional 20% of ventricular filling. During isovolumic
contraction, all cardiac valves are closed so there is no change in the
ventricular volume. During period of rapid ejection, blood is ejected from
the ventricles so the ventricular volume will decrease. In the period of
isovolumic relaxation, all cardiac valves are closed so there is no change
in ventricular volume. During the period of rapid inflow, there is a very
high increase in ventricular volume. It is somewhat stabilized in diastasis
and a slight increase again during atrial systole.

Atrial Pressure or Central Venous Pressure (CVP) Curve

a c v
c

PHOTO: Left atrial, aortic, and left ventricular pressure pulses correlated in time with
aortic flow, ventricular volume, heart sounds, venous pulse, and the electrocardiogram
for a complete cardiac cycle.

Ventricular Volume Pressure Curve (Ejection Loop)

A wave is increase in atrial pressure during atrial systole. C

wave is slightly increased in atrial pressure during isovolumic
contraction when the increased ventricular pressure pushes the AV
valves to bulge into the atria. The V wave is increase atrial pressure
during isovolumic relaxation where it is simultaneous with the increase
in atrial filling.

Heart Sounds

The 1st heart sound is due to closure of the AV valves. Closure

of the AV valves will mark the onset of the period of isovolumic
contraction so when seen at the ventricular volume curve, it is a straight
line – no change in ventricular volume.

The 2nd heart sound is due to the closure of the SL valves that
will now mark the onset of the period of isovolumic relaxation. Again,
there is no change in the ventricular volume.

15 Shannen Kaye B. Apolinario, RMT

 PHOTO: Relationship between left ventricular volume and intraventricular pressure
during diastole and systole. Also shown by the heavy red lines is the “volume-pressure
diagram,” demonstrating changes in intraventricular volume and pressure during the
normal cardiac cycle. EW, net external work.

Reduced ejection Rapid ejection

Volume of blood
remain on
PHOTO: Pressure-volume loop
ventricles after
contraction

The vertical axis will represent changes in ventricular

pressure, the unit is mmHg. The horizontal axis represents changes in
ventricular volume and the unit is either cc or mL.

In relation to changes in ventricular volume and pressure, the

cardiac cycle is divided into four phases. The letters represent each point.

Point A - ventricular volume is 50 mL. This 50 mL is actually the volume

of blood remaining in the ventricles after contraction. At 50 mL, the
pressure is low – a little above 0 mmHg. At point A, the atrioventricular
valves open.

Phase I – from 50 mL, the volume of blood in the ventricles increased to

120 or 130 mL but there is little increase in pressure. Phase I is
ventricular filling.

Point B - the volume of blood is 130 mL. There is closing of the AV valves
so the first heart sound is heard.

Phase II – the volume of blood is 130 mL and the pressure continues to

increase. At phase II, there is period of isovolumic contraction.

Point C – opening of SL valves. When the SL valves open, the ventricular

pressure still increases but the volume is already decreasing. From C
prime, it is the period of rapid ejection.

Phase III – in the latter part of Phase III – the volume decreases and the
pressure decreases, this is now the reduced ejection.

Point D – closing of the SL valves so the second heart sound is heard.

“ I can do EVERYTHING through Him who gives me strength”
Phase IV – the volume of blood is still 50 mL but the pressure is -Philippians 4:13
decreasing and decreasing. This is isovolumic relaxation.
GOD BLESS YOU! 

16 Shannen Kaye B. Apolinario, RMT

Cardiodynamics
(Gloria Marie M. Valerio, MD)
Definition of Terms:
Cardiac Output (CO)
- is the amount/quantity/volume of blood ejected by each
ventricle per minute
- CO = SV x HR
- Normal Value: 5 L/min
5, 000 mL/min
* Although the left ventricle will pump blood against a higher pressure of
resistance in the systemic circulation compared to the right ventricle,
although the workload of the left ventricle is greater than that of the right
ventricle, although the left ventricular wall or musculature is thicker than
that of the right ventricle, the output of the two ventricles are the same.
Heart Rate (HR)
- the number of contractions/heart beats/cardiac cycles per
minute
- Normal Value (normal resting adult): 75 beats per min.
* In a normally functioning heart, the heart rate and rhythm are
determined by the activity of the SA node.
Stroke Volume (SV)
- is the amount/quantity/volume of blood ejected by each
ventricle per contraction/per heartbeat/per cardiac cycle
- SV = EDV – ESV
- Normal Value: 70 mL
The stroke volume of the left ventricle is the same of that of the right
ventricle.
End Diastolic Volume (EDV)
- is the amount/quantity/volume of blood in the ventricles at
the end of diastole, before systole = PRELOAD
- Normal Value: 110-130 mL
* Whatever amount of blood that will be present in the ventricles after
the ventricular filling time, before contraction of the ventricle; that is the
end diastolic volume. It is the EDV that will exert force on the ventricular
wall stretching the ventricular wall before it contracts thus it is called
preload or the load of the ventricle that is needed to be ejected.
End Systolic Volume (ESV)
- is the volume of blood in the ventricles at the end of systole
- Normal Value: 45-50 mL
* ESV is the amount/quantity/volume of blood remaining in the
ventricles after contraction. No matter how strong the force of ventricular
contraction is, there will always be a certain amount of blood that will
remain in the ventricles.
1 Shannen Kaye B. Apolinario, RMT|
Correlation of SV, EDV, ESV with the Ejection Loop
From point D to point A, the volume of blood increases in the
ventricles with little increase in pressure, this is the ventricular filing
time. At point A, the atrioventricular (AV) valves will close so that
whatever amount of blood will be present in the ventricles before closure
of the AV valves, that is now the end diastolic volume (EDV) which is a
little less than 150 mL, average of 130 mL.
From point A to point B, the ventricles will now start to
contract, but since all the valves are closed, there will be no change in
ventricular volume.
From point B to C, that is the period of ejection of blood from
the ventricles so the EDV will be decreased and the amount that will be
ejected is the stroke volume. At point C, the semilunar (SL) valves will
close, the ventricles will start to relax and the volume of blood that is now
in the ventricles is the end systolic volume (ESV).
Stroke volume is equal to EDV minus ESV or ESV + SV will be
the EDV.
CO = SV x HR
EDV – ESV
Whatever factor that will affect EDV and ESV will also affect the
SV. Whatever factor that will affect the SV and HR will affect the CO. As
for the SV, this is determined mainly by the force of myocardial
contraction. So if the force of myocardial contraction increases, the SV
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
as a reflection of the force of myocardial contraction are factors intrinsic
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
peripheral factors that may also affect the cardiac output.
What are the factors outside the heart that may affect the
cardiac output?
1. Total blood volume
2. Status of the venous sytem that will deter blood back to the
heart
3. Status of the arterial system which is the opposing force to
ventricular contraction
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
the vascular system and vice versa – the status of the vascular system is
also dependent on the activity of the heart. The heart and the vascular
system are actually inter-dependent and that is because of the close
nature of the cardiovascular system.
End Diastolic Volume (EDV)
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
 Take note of where the black arrows are directed. These black
arrows represent the EDV. It is directed towards the ventricular wall so
the greater the volume or EDV, the greater the force that will be exerted
on the ventricular wall. If the force exerted on the ventricular wall is
greater, that will now stretch the ventricular wall and if the ventricular
wall is stretched, that will now increase the force of myocardial
contraction. So in other words, the greater the EDV, the more the
ventricular wall is stretched, the greater will be the force of contraction.
And if the force of contraction is increases, stroke volume increases,
cardiac output increases. So EDV is directly related to cardiac output.
Factors Affecting EDV
1. Effective filling time
Filling time refers to the duration of the diastolic or relaxation
phase because that is when the ventricles are filled with blood.
FT  EDV  SV  CO
If the duration of filling time increases, there will be enough
time for the ventricles to accommodate a larger volume of blood so the
EDV increases. Again, if the EDV is greater, the greater the ventricular
wall is stretched, the greater the force of contraction so the SV as well as
the CO increases. All are directly directed.
HR  FT  EDV  SV  CO
One factor that will influence the duration of the filling time is
heart rate. When the heart rate increases, the duration of the filling time
will decrease – less time for ventricular filling so the EDV will decrease
and so will the SV and CO.
HR  FT  EDV  SV  CO
The reverse is also true that when the HR decreases, the
duration of the filling time will increase, more EDV, SV and CO.
Increased HR decreases the CO and decreased HR increases the
CO but going back to the formula: CO = SV x HR, heart rate is directly
related to CO, meaning to say that an increase in HR will increase the CO.
Which among the formula is true?
In the formula, it is directly related and of course that is true. If
the HR increases, there will be an increase in the frequency of
depolarization on the sarcolemma of the cardiac muscle cell. So the more
the cardiac muscle is depolarized, the more Ca++ enters the cell and if
more Ca++ enters the cell, the greater the force of contraction, the more
the stroke volume increases, increased cardiac output. That is how an
increase in HR will increase the CO. What about the other equation?
2 Shannen Kaye B. Apolinario, RMT|
Both of the equations are true but there is a range of heart rate.
The horizontal axis on the graph represents heart rate while the vertical
axis represents cardiac output. Based on the graph, when the heart rate
increases from 0–60 beats per minute, there is a corresponding increase
in cardiac output. They are directly related because when the heart rate
increases from 0-60, the duration of filling time is not yet compromised
because the normal heart rate is 75 beats per minute so that means that
the ventricles can still be filled with blood adequately so the cardiac
output increases. In the first phase, sympathetic stimulation increases the
heart rate. Sympathetic stimulation increases not only the heart rate but
also the force of contraction. When the heart rate increases, the stroke
volume increases therefore the cardiac output increases.
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
still be filled with blood because from 60-180 beats per minute, the
increase in heart rate is equal to the decrease in stroke volume so that the
cardiac output is maintained at a constant level.
When the heart rate increases from 180 beats per minute and
above, the duration of the filling time is now severely compromised. And
sympathetic stimulation can no longer compensate on the very short
duration of filling time. So the increase in heart rate is now less than the
decrease in stroke volume so the cardiac output will now decrease. There
is a range wherein the cardiac output will start to decrease with an
increase in heart rate.
If you will recall, if the heart rate is 75 beats per minute, the
duration of one cardiac cycle is 0.8 sec, the duration of the systolic phase
is 0.27 sec, and much longer is the duration of the diastolic phase which is
0.53 sec. The longer duration of the diastolic phase is important because
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
cardiac muscle is better.
Cardiac Cycle Duration with Heart Rate
Duration Heart Rate Heart Rate
75 beats/min 200 beats/min
Cardiac cycle 0.80 sec 0.30 sec
Systole 0.27 sec 0.16 sec
Diastole 0.53 sec 0.14 sec
When the heart rate increases to 200 beats per minute, the
duration of cardiac cycle will decrease from 0.8 to only 0.3 sec but if you
will compare the decrease in the duration of systole and diastole, diastole
is more affected (bigger decrease in duration of diastole) from 0.53 to
0.14 sec which means that the filling time is really compromised and the
EDV is severely decreased.
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.
3. Myocardial compliance
All elastic structures have the property of compliance and that
is the measure of distensibility or stretchability of an elastic structure.
C=∆V
∆P
Compliance is equal to change in volume over change in
pressure. For a structure to have an increase in compliance, the change in
volume should be higher or greater compared to the change in pressure.
And this is true for the ventricles, remember that the ventricles can
accommodate a large volume of blood with little increase in pressure and
that is because of the presence of the elastic tissue in the cardiac muscle
that will enable the ventricles to distend.
4. Venous return
VR = CO
5 L/min
The most important factor that determines the EDV is the
volume of blood returning to the heart per minute and that is venous
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
venous return is equal to cardiac output. The average venous return is
also 5 L or 5,000 mL per minute.
End Systolic Volume (ESV)
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
contraction. So if the force of myocardial contraction increases, SV will
increase, ESV will decrease. If the force of myocardial contraction
decreases, SV will decrease, ESV will increase. In other words, force of
myocardial contraction is inversely related to the end systolic volume
(ESV).
The normal systolic volume (red line) is about 70 mL but if the
force of myocardial contraction increases, SV increases so the remaining
part becomes smaller.
Since the force of myocardial contraction will affect the ESV,
what now are the factors that will influence the force of myocardial
contraction? What is the EDV and the relationship between EDV and force
of myocardial contraction is reflected in the Frank starling’s Law.
Factors Affecting ESV
a. Force of myocardial contraction
1. Frank Starling’s Law
3 Shannen Kaye B. Apolinario, RMT|
Within physiologic limits, the force of myocardial contraction
will be determined by the initial muscle length that means resting length
of the cardiac muscle or length of the cardiac muscle before it contracts.
The force of contraction will depend on the length of the
cardiac muscle before it contracts so what will stretch the cardiac muscle
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
more the ventricular wall will be stretched and that will now increase the
force of contraction and this is called heterometric autoregulation.
Autoregulation means that the heart itself can regulate its own force of
contraction. Metric is the length. Hetero - changes. So the change in the
length of cardiac muscle will enable the heart to regulate its own force of
contraction. Remember that this only happens within physiologic limits –
it does not stretch continuously when the EDV is increasing and more and
more powerful the force contraction becomes. There is a limit because
when the cardiac muscle is overstretched or distended, there will be less
overlapping between thin filaments and thick filaments so there will be
less myosin length that will bind on the actin active site so when it
contracts, it becomes weak.
Actin filament
Myosin filament
But remember that overstretching or overdistention of the
cardiac muscle does not occur in the first place because of the presence of
connective tissue. The connective tissue on the cardiac muscle and on the
pericardium prevents overdistention when the cardiac size increases
because connective tissue is less distensible while the elastic tissue
allows distension.
Factors that affect cardiac muscle length:
 Stronger atrial contraction. Remember that most of the
ventricular filling will take place when the ventricles as well as
the atria are in a relaxed state. But during atrial systole, there
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
volume of blood. If the venous wall is in a relaxed state, the
blood in the veins cannot go back to the heart. So what is
venous tone? Tone means state of partial contraction. One
property of smooth muscle is they can remain partially
contracted for a long time. If the wall of the veins is partially
contracted, there will be less capacity to accommodate blood
so the blood will go back to the heart thus increasing venous
return and EDV and that will stretch the cardiac muscle cell.
 Increased pumping of skeletal muscle. When you remain in
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
the veins of the lower extremities, the venous return will
decrease, EDV will decrease, and the cardiac muscle will not be
 stretched. But once you move, the skeletal muscle will contract
and that will compress the veins. When the veins are
compressed, that will open up the venous valves. The opening
of the valves is directed toward the heart. So when the veins
are compressed by skeletal muscle contraction, venous valves
will open and blood will return to the heart.
* The three factors: increased total blood volume, increased venous tone
and increased pumping of the skeletal muscle will first influence venous
return. Venous return will then influence EDV, EDV is the one that will
exert force on the ventricular muscle to stretch the ventricular muscle.
 Increased negative intrathoracic pressure. Increased
negative intrathoracic pressure allows the ventricles to
distend, so that will stretch the ventricular muscle.
All of these are factors will affect cardiac muscle length before
contraction. So if these factors will increase, cardiac muscle length will
increase before contraction so that during contraction, the force of
myocardial contraction will increase.
2. Autonomics
Aside from cardiac muscle length another factor that will
influence the force of myocardial contraction is the autonomic
innervations: sympathetic that will release catecholamine,
norepinephrine, epinephrine; and parasympathetic that will release
acetylcholine.
Sympathetic stimulation will increase the force of contraction
of both the atria and ventricles primarily because norepinephrine binds
with β1 receptors will increase membrane permeability to calcium
allowing more Ca++ to enter myocardial cell and that will increase the
force of contraction. But aside from this, sympathetic stimulation can also
increase the heart rate so the more frequent the myocardial cell is
depolarized, again, the more Ca++ will enter the myocardial cell and that
will increase the force of contraction.
In contrast, vagal or parasympathetic stimulation by releasing
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.
PHOTO: Schematic diagram of the movement of calcium in excitation-contraction
coupling in cardiac muscle. Influx of Ca++ from interstitial fluid during excitation
triggers release of Ca++ form the sarcoplasmic reticulum (SR). The free cytosolic Ca++
activates contraction of the myofilaments (systole). Relaxation(diastole) occurs as a
result of uptake of Ca++ by the SR, by extrusion of intracellular Ca++ by the 3 Na+-1
Ca++ antiporter, and to a limited degree by the Ca++-ATPase pump. βR, β-adrenergic
receptor: cAMP-PK, cAMP-dependent protein kinase.
4 Shannen Kaye B. Apolinario, RMT|
But that is not the end of sympathetic effects. It does not allow
Ca++ to always enter the cell because when it always depolarizes, more
Ca++ will enter the cell.
But hidni dun nagtatapos ang sympathetic effects. Hindi lang
basta nagpapapasok ng ca kasi malimit magdepolarize, mas madaming ca
na papasok
Another action of sympathetics is when norepinephrine and
epinephrine bind with β1 receptors in the heart, this will cause activation
of G-proteins. Activated G-proteins will activate the enzyme system -
adenylyl cylcase that will lead to the formation of an intracellular ligand
or a second messenger that is cyclic AMP (cAMP). As a second
messenger, cAMP will mediate the actions of catecholamines on the
cardiac muscle cell and one action of cAMP is to cause activation of
another intracellular enzyme that is protein kinase A (cAMP-PK). One
action cAMP-PK is to phosphorylate the Ca++ channels on the
sarcolemma. When it is phosphorylated, that will allow more Ca++ to
enter that will increase the force of myocardial contraction.
But take note that sympathetic stimulation will increase not
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
phosphorylate troponin I so that troponin cannot bind with Ca++. If
troponin cannot bind with Ca++, the muscle will relax because troponin-
tropomyosin complex will go back to cover the active site of actin due to
absence of troponin-Ca++ complex.
Another action of cAMP-PK is to phosphorylate an intracellular
protein called phospholamban. The normal action of phospholamban is
to inhibit the Ca++ pump on the sarcoplasmic reticulum. If the Ca++ pump
is inhibited, Ca++ will not return – it will remain bound to troponin C so
there will still be muscle contraction. But once phosphorylated by cAMP-
PK, the inhibitory effect of phospholamban will decrease so the Ca++
pump will be activated and when activated, it will actively transport Ca++
back to the sarcoplasmic reticulum so there will be no Ca++ that is
attached to troponin and the muscle will relax. So again, aside from
increasing the force of myocardial contraction, sympathetic stimulation
can also facilitate relaxation of the cardiac muscle.
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
The force of myocardial contraction can also be influenced by
heart rate. It is mentioned earlier that when the heart rate increases, the
depolarization of cardiac muscle will be more frequent and remember
that with each depolarization, it allows more Ca++ to enter and that will
increase the force of contraction.
Factors that influence or regulate heart rate: 7. Afterload

 Autonomics. The most important factor. Sympathetic nerves
innervating the SA node and the effect of norepinephrine is to
increase membrane permeability to Na+ and Ca++ that will
make the SA node more excitable so the heart rate will
increase. On the other hand, parasympathetic or vagal
stimulation will make the SA node more permeable to K+ so
that will hyperpolarize the SA node making it less excitable,
decreasing the heart rate.
Afterload is the aortic pressure load, opposing force to left
ventricular contraction. Why in the aortic artery only and not in
pulmonary artery? Because remember that there is low/no pressure area
in the pulmonary circulation, not much resistance to right ventricular
contraction unless there is pulmonary hypertension. More of the
resistance happens in the left ventricle because there is high pressure
area in the arterial system. So when we say afterload, it is the pressure in
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,
the volume of blood in the right atrium will increase and that
will stretch the right atrial wall where you have the SA node.
When the right atrial wall is stretched, the SA node is
stimulated and that will increase the heart rate. So this
Bainbridge reflex is sensitive to an increase in blood volume
that will return to the right atrium.
 Exercise. During exercise, heart rate increases for two
reasons: increased metabolism and increased sympathetic
stimulation.
Remember the photo on preload, the arrows are directed on
the ventricular wall because the EDV exerts force on the ventricular wall
to increase the force of contraction.
When the ventricles contract, the blood or EDV goes in the
aorta so the direction is directed towards the aorta but the pressure in
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
increases, stroke volume decreases, end systolic volume increases and
this is shown on the photo below:

 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. That’s
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
heart, so what will happen to the EDV? EDV will increase because there is
much [blood] left and there was an additional amount added during the
relaxation phase. When the EDV is increased, the ventricular wall will be
stretched; its contraction will be increased. But even if the contraction is
increased but there is persistent increase in aortic pressure, less will still
be ejected so that eventually there will be pulling of blood in the left
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.
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
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
Increases in venous return (increased preload) increase the stroke volume and thus
cardiac output. Increases in arterial pressure (increased afterload) decrease stroke
volume and thus cardiac output (lower panel).
8. Stenosis
Another condition that will increase aortic pressure is stenotic
aortic valve. If the aortic valve hardens, even if the ventricular pressure is
greatly increased, the SV and cardiac output will still be diminished.
Blood will again accumulate in the left ventricle and eventually, the left
ventricle will dilate so the force contraction will decrease.
Determinants of Cardiac Output
Cardiac factors: Coupling factors:
Heart rate Preload
Cardiac Output
Myocardial Afterload
contractility
6 Shannen Kaye B. Apolinario, RMT|
To summarize the factors that will determine the cardiac
output, there are factors intrinsic to the heart and there are factors
outside the heart. Factors intrinsic to the heart will include the heart rate
and the force of myocardial contraction. Factors outside the heart or
peripheral/coupling factors will include the preload (factors that will
affect EDV) and afterload or aortic pressure load. These are the major
factors that will determine cardiac output
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.
No change
- Sleep
- Moderate change in environmental temperature
Ejection Fraction (EF)
- Percentage of the EDV is ejected by the left ventricle per
contraction
- EF = SV x 100
EDV
- Normal value: 65-70%
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
mL.
In patients suspected of having congestive heart failure, one
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
ventricular contraction is weak.
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 find; 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|

Circulatory or Vascular System
(Gloria Marie M. Valerio, MD)
The Circulatory System or Vascular System is made up of
different types of blood vessels that are arranged either parallel or in
series with one another forming a closed system of conduits or tubes that
will transport blood to and from the heart. Take note that the blood
vessels are not rigid tubes, they are distensible. The primary function of
the circulatory system is to service the needs of the tissues that is - by
transporting blood, it will transport essential substances like oxygen and
nutrients to the tissues and at the same time it will transport the waste
products of metabolism away from the tissues.
As what we have learned from the previous lecture, the
circulatory system is divided into two – pulmonary and systemic
circulation. The pulmonary circulation receives unoxygenated or
venous blood from the right heart and supplies blood to the lungs. On the
other hand, the systemic circulation receives arterial or oxygenated
blood from the left heart and supplies blood to almost all organs of the
body except for the lungs. Since the systemic circulation will supply blood
to almost all organs of the body, it is also called peripheral or greater
circulation.
Blood Vessels
PHOTO: Schematic diagram of the parallel and series arrangement of the vessels
composing the circulatory system. The capillary beds are represented by thin lines
connecting the arteries (on the right) with the veins (on the left). The crescent-shaped
thickenings proximal to the capillary beds represent the arterioles (resistance vessels).
On the right is the arterial system or distributing vessels. On
the left is the venous system or collecting vessels.
When the left ventricle contracts, blood is ejected to the aorta
and from the aorta to the arteries. The wall of the aorta and arteries is
strong and thick so it is able to transport oxygenated blood under high
pressure to the different organs of the body and we call the blood volume
that is contained in the arterial system as stressed blood volume. One
important characteristic of the aortic as well as arterial wall is that it
contains more elastic tissue than smooth muscle fibers. So that will make
the aortic and arterial wall highly distensible so during ventricular
systole, when blood is ejected to the aorta, the aortic wall will distend to
accommodate the large volume of blood. On the other hand, during
ventricular diastole, the aortic and arterial wall will recoil on the
contained blood.
1 Shannen Kaye B. Apolinario, RMT|
In the different organs of the body, the arteries will divide into
smaller branches forming the arterioles. This time, the wall of the
arterioles contains more smooth muscle fibers than elastic tissue. In fact,
among all the different types of blood vessels, the arteriolar wall has the
thickest muscular layer so that when the smooth muscle layer of the
arteriolar wall contracts or if there is vasoconstriction, that will decrease
tremendously blood flow to the capillaries and to the tissues. On the other
hand, when the smooth muscle layer of the arteriolar wall relaxes or if
there is vasodilatation, that will now increase tremendously blood flow to
the capillaries and to the tissues. So one important function of the
arterioles is to regulate blood flow to the capillaries and to the tissues and
also because of its thick muscular layer, resistance to blood flow is
highest in the arterioles so the arterioles are called resistance vessels.
The smallest blood vessels are the capillaries. The capillary
wall is thin and porous - it allows exchange of fluids and some solutes
between intravascular and interstitial fluid compartments. The capillaries
are known as exchange vessels.
From the capillaries, blood will be collected by the venules
which will then coalesce to form the bigger veins. Comparing the wall of
the vein to that of an artery, the venous wall is thinner and more
distensible that is why the veins can accommodate a large volume of
blood with little increase in pressure and the volume of blood that is
contained in the veins is what we call unstressed blood volume because
of the low pressure area of the venous system. It means that the vascular
capacity is bigger and veins are also called capacitance vessels. There
are two functions of veins: one is to act as blood reservoir and another
one is to return blood back to the heart.
In the veins of the limbs or extremities, there are venous valves
present with openings of which are directed towards the heart. So that
when you move your limbs and the skeletal muscles contract that will
open up the venous valves and facilitate venous return.
Layers of the Blood Vessel
1. Tunica intima
2. Tunica media
3. Tunica adventitia
Except for the capillaries, the wall of the different blood vessels
is made up of the same structure. There are three layers of the vascular
wall. The innermost layer is the tunica intima which is made up of the
endothelium and basement membrane. The middle layer is the tunica
media which is made up of smooth muscle fibers. The outermost layer is
the tunica adventitia which is made up of connective tissue. Just like in
the heart, the presence of connective tissue in the vascular wall will
prevent overstretching or over distension of the vascular wall when
blood volume as well as blood pressure increases.

Properties and Characteristic of the Vascular Smooth Muscle
2 types of Smooth Muscle
1. Multiunit
2. Single unit
PHOTO: Control systems of smooth muscle. Contraction (or inhibition of
contraction) of smooth muscles can be initiated by (1) the intrinsic activity of
pacemaker cells, (2) neutrally released transmitters, or (3) circulating or locally
generated hormones or signalling molecules. The combination of a neurotransmitter,
hormone, or drug with specific receptors activates contraction by increasing cell Ca++.
The response of the cells depends on the concentration of the transmitters or
hormones at the cell membrane and the nature of the receptors present. Hormone
concentrations depend on diffusion distance, release, uptake, and catabolism.
Consequently, cells lacking close neuromuscular contacts will have a limited response
to neural activity unless they are electrically coupled so that depolarization is
transmitted from cell to cell. A. Multiunit smooth muscles resemble striated muscles in
that there is no electrical coupling and neural regulation is important. B. Single-unit
smooth muscles are like cardiac muscle, and electrical activity is propagated
throughout the tissue. Most smooth muscles probably lie between the two ends of the
single unit-multiunit spectrum.
There are two types of smooth muscles in the body: multi-unit
smooth muscle and single unit smooth muscle. In the visceral wall as well
as the vascular wall, the type of smooth muscle fibers present is mostly
the single unit type.
Characteristics of Smooth Muscle
1. Smaller. Compared to the skeletal muscle cell, the smooth muscle
cell is smaller
2. Involuntary. The activity of the vascular smooth muscle is not
regulated by the cerebral cortex.
3. Resting Membrane Potential. The RMP is less negative, it is also
unstable. It ranges from -50 to -60 mv. The action potential
generated is brought mainly by opening of slow calcium channels so
that will make the duration of the vascular smooth muscle action
potential longer than that in the skeletal muscle. So that the duration
of the contraction-relaxation cycle in the vascular smooth muscle is
also longer.
4. Tonic contraction. Another important property of the vascular
smooth muscle - it can remain partially contracted for a long time
with little expenditure of energy and that is what we call tonic
contraction.
5. Sarcolemma. The vascular smooth muscle cell is also surrounded
by the sarcolemma and present on the sarcolemma are voltage-
gated as well as ligand-gated calcium channels. Also present is a
calcium pump, a sodium-potassium anti-porter, and a sodium-
calcium anti-porter. However, invaginations of the sarcolemma will
not form the T-tubules; instead the invaginations will form cave-like
2 Shannen Kaye B. Apolinario, RMT|
structures which are called calveolae. However, this calveolae are
actually analogous to the T-tubules.
6. Few mitochondria. There are fewer mitochondria in the smooth
muscle and the main source of energy for contraction is glycolysis.
7. Sarcoplasmic Reticulum. The sarcoplasmic reticulum is less well-
developed so that means it is not able to store large quantities of
calcium ions just like in the cardiac muscle cell so in order to
contract, there has to be another source of calcium ions and that is
the extracellular fluid (ECF). Also present on the membrane of the
sarcoplasmic reticulum are ryanodine receptors that will bind with
calcium coming from the ECF and there is also a calcium pump.
8. Contractile Proteins. Contractile proteins are also present that will
include actin, myosin and tropomyosin but there is no troponin so in
order to contract, calcium will bind with another protein and that is
calmodulin so you have a calcium-calmodulin complex that will
initiate vascular smooth muscle contraction.
9. Stimuli. Stimuli that will cause contraction of the vascular smooth
muscle. Remember that in the skeletal muscle, the primary stimulus
will be neural or nervous. You have an action potential for a somatic
nerve transmitted to the skeletal muscle cell that will depolarize the
skeletal muscle cell and that will now initiate the excitation-
contraction coupling. In vascular smooth muscle, there are different
types of stimuli that can stimulate the vascular smooth muscle:
a. Neural. First is again neural so we have autonomic innervation
and the vascular smooth muscle is innervated mainly by the
sympathetic nervous system so you have sympathetic
adrenergic and sympathetic cholinergic. Sympathetic
adrenergic nerves innervate the blood vessels in the skin and
viscera while sympathetic cholinergic nerves innervate the
blood vessels in the skeletal muscle.
The neurotransmitter agent that is released by
sympathetic nerves is norepinephrine. You also have
norepinephrine and epinephrine from the adrenal medulla so
that when either norepinephrine or epinephrine binds with
alpha-1 receptors that will cause contraction of the vascular
smooth muscle so there will be vasoconstriction. On the other
hand, when either norepinephrine or epinephrine binds with
beta-2 receptors, that will cause relaxation of the vascular
smooth muscle so there will be vasodilatation. Remember in
relation to beta-2 receptors, epinephrine has a greater effect
than norepinephrine.
In sympathetic cholinergic, you have acetylcholine
binding with muscarinic receptors that will also relax the
vascular smooth muscle in the skeletal muscle so there will be
vasodilatation.
b. Hormones. Aside from neural, the vascular smooth muscle can
also be stimulated by circulating hormones which could either
be vasoconstrictors or vasodilators. Among the circulating
vasoconstrictors are angiotensin 2 and vasopressin or
antidiuretic hormone (ADH). Among the circulating
vasodilators are bradykinin and histamine.
c. Stretch. Stretch of the muscle will initiate a reflex action. For
example, when the blood volume and blood pressure
increased, that will now stretch the arterial wall that will
initiate a reflex action that will cause vasoconstriction.
d. Local factors. Local factors for example actively metabolizing
tissue so there will be oxygen consumption and production of
carbon dioxide. So that oxygen tension (pO 2) will decrease and
pO2
pCO2
carbon dioxide tension (pCO 2) will increase, these two factors
will also cause vasodilatation.
pH = H+
 Other local factors that will cause vasodilatation will
include a decrease in plasma pH so increase hydrogen, increase
lactic acid concentration. Increase potassium, increase
adenosine, all of these will produce vasodilatation.
There are several factors that can either stimulate or
inhibit the vascular smooth muscle.
Contraction-Relaxation Cycle
PHOTO: Regulation of smooth muscle myosin interactions with actin by Ca++-
stimulated phosphorylation. In the relaxed state, cross-bridges are present as high-
energy myosin-ADP-Pi complex in the presence of ATP. Attachment to actin depends on
phosphorylation of the cross-bridge by a Ca++-calmodulin-dependent myosin-light-
chain kinase (MLCK). Phosphorylated cross-bridges cycle until they are
dephosphorylated by myosin phosphatase. Note that cross-bridge phosphorylation at a
specific site on a myosin regulatory light chain requires ATP in addition to that used in
each cyclic interaction with actin.
Depolarization
Ca + calmodulin
Myosin light-chain kinase
Phosphorylation of myosin
Increased ATPase
M+A contraction
If the membrane is depolarized, that will allow Ca++ to enter the vascular
smooth muscle cell. When the Ca++ enters, it will bind with calmodulin
which will now initiate the contraction process. What happens is that the
calcium-calmodulin complex will activate an intracellular enzyme that
is myosin light chain kinase. When activated, myosin light chain kinase
will cause phosphorylation of myosin which will then increase the
activity of ATPase. With increased activity of ATPase, myosin will now
form cross bridges with actin and that will bring about contraction.
3 Shannen Kaye B. Apolinario, RMT|
Latch-Bridge Mechanism
Repolarization
Ca++  out
Myosin phosphatase
Dephosphorylation of myosin  relax
M+A
On the other hand, with repolarization, Ca++ will be removed
either through the activity of the Ca++ pump on the sarcoplasmic
reticulum, Ca++ pump on the sarcolemma or Ca++-Na+ antiporter. In the
skeletal muscle as well as in the cardiac muscle, once Ca++ is unbound
from troponin, it is expected to relax but in this case, even if Ca++ is
removed from calmodulin, the vascular smooth muscle will remain
contracted that is why it is capable of tonic contraction with little
expenditure of energy. It will take some time before the muscle will relax
by activation of another intracellular enzyme called myosin
phosphatase. When activated, myosin phosphatase will cause
dephosphorylation of myosin. When myosin is dephosphorylated, it will
be unbound from actin and that will bring about relaxation and this is
called the latch-bridge mechanism.
Smooth Muscle Fiber
PHOTO: Apparent organization of cell-to-cell contacts, cytoskeleton, and
myofilaments in smooth muscle cells. Small contractile elements functionally
equivalent to a sarcomere underlie the similarities in mechanisms between smooth
and skeletal muscle. Linkages consisting of specialized junctions or interstitial fibrillar
material functionally couple the contractile apparatus of adjacent cells.
Smooth muscle is non-striated. There is no regular
arrangement of the actin and myosin filaments so that when you observe
the smooth muscle under the microscope, alternating thick and thin
filaments and alternating light and dark bands will not be seen. The
structure of a smooth muscle fiber is usually arranged in bundles.
Another characteristic, there is no Z line, instead of the Z line,
there are dense bodies attached to the membrane of the smooth muscle
which will also provide an attachment between the membrane of the
individual muscle fibers. So that force generated in one muscle fiber can
be transmitted to other muscle fibers as well.
Also, there are gap junctions present in the membrane
allowing ions to flow freely from one muscle fiber to the next so that
when an action potential is generated anywhere in a bundle, it can be
transmitted readily and that will cause the whole bundle to depolarize
and to contract as a single unit and that arrangement of the muscle fiber
is called synctitium. That is why the type of the smooth muscle is single-
unit smooth muscle.
 Attached to the dense bodies are the actin filaments and capillaries which is slower because it is numerous and smaller and that is
interspersed within the actin filaments are the myosin filaments. And the why the velocity is inversely related to the cross-sectional area.
myosin filaments here form what we call side-polar crossbridges –
myosin on one side is attached to actin and it is attached to actin on the As to radius, the vena cava actually has a bigger radius than the
other side. When activated, that means myosin can pull the actin filament aorta but the aorta has the thickest wall. Composition of the vascular wall
on one side in one direction at the same time pulling the other actin you have elastin, smooth muscle, collagen. Elastin and collagen
filament on the other side in the opposite direction. component is highest in the aorta but take note the smooth muscle
component is most abundant in arterioles. The capillary wall has no
elastin, no smooth muscle, and no collagen.
Differentiation of the Blood Vessels
As for transmural pressure, this is difference in the pressure
Char. Aorta Arteriole Capillary Venules Vena between the inside and outside of a blood vessel and the transmural
cava pressure is highest in the aorta, lowest in the vena cava. It is mentioned
Number earlier that the arterial system is a high pressure area while the venous
in body 1 109 1010 3 x 108 2 system is a low pressure area.

Cross-
sectional 4.5 300 5,000 4,000 18
area
Radius
(mm) 12 0.010 0.004 0.02 17

Wall
thickness 2 0.02 0.001 0.002 1.5
(microns)

Elastin +++ + 0 + +

Smooth
muscle ++ +++ 0 + ++

PHOTO: Internal diameter, wall thickness, and relative amounts of the

Collagen +++ + 0 + + principal components of the vessel walls of the various blood vessels that compose the
circulatory system. Cross sections of the vessels are not drawn to scale because of the
Trasmural huge range from the aorta and venae cavae to capillary.
pressure 110 70 20 10 5
(mmHg)
Peak
velocity 50 0.3 0.017 0.02 4.6
(cm/s)

Let us now differentiate the blood vessels that make up the

circulatory system so you have the aorta, arterioles, capillaries, venules
and vena cava. Number in the body: there is only 1 aorta, 2 vena cava –
superior and inferior, millions of arterioles, millions of venules, and
billions of capillaries.

As to cross-sectional area, you will notice that although the

aorta is the biggest artery in the body, its cross-sectional area is small.
Compare it to the smallest blood vessel in the body which is the capillary,
it has the biggest cross-sectional area. What does cross-sectional area
mean? If you put the blood vessels side by side, there is one aorta, two
vena cava and billions of capillaries and if you spread all of those, which
among those blood vessels would occupy the most space. When we say
cross-sectional area, that is not the size of the blood vessel - you put the
blood vessels side by side then spread it, which among the blood vessels
will occupy the biggest space and of course that will be the most
numerous even though it is the smallest and that will be the capillaries.
Correlate it with the velocity of the blood flow. When we say
velocity of blood flow, that is the distance travelled by a volume of blood
per unit of time. As you can see, cross-sectional area is inversely related
to velocity. The aorta which has a small cross-sectional area has the
highest velocity of blood flow, in contrast, the capillaries with the biggest
cross sectional area has the lowest velocity of blood flow. Why did that
happen? You will learn later on that again because of the closed nature of
the circulatory system, blood flow is equal to cardiac output equal to
venous return so that means the blood flow in every blood vessel per unit
of time is the same. So if blood flow is 5L/min, in a big blood vessel like
the aorta, it can easily fill up 5 L. What about the capillaries? It is small
and numerous, it is slower to fill up the 5L so although the volume is the
same in both, the blood flow in the aorta is faster compared to the
PHOTO: Phasic pressure, velocity of flow, and cross-sectional area of the
systemic circulation. The important features are the inverse relationship between
velocity and cross-sectional area, the major pressure drop across the small arteries
and arterioles, and the maximal cross-sectional area and minimal flow rate in the
capillaries. AO, aorta; ART, arterioles; CAP, capillaries; LA, large arteries; LV, large
veins; SA, small arteries; SV, small veins; VC, venae cavae; VEN, venules.
This graph will show you again the relationship between cross-
sectional area and velocity of blood flow. So to summarize, cross-sectional
area increases from the aorta to the capillaries, it decreases from the
capillaries to the vena cava. For the velocity of blood flow, it is highest in
the aorta so it decreases from the aorta to the capillaries; it increases
from the capillaries to the vena cava. As to pressure, again, pressure is
high in the arterial system, highest in the aorta and then it progressively
decreases towards the vena cava but the biggest drop in pressure is in the
arterioles.

4 Shannen Kaye B. Apolinario, RMT|

Velocity  How much quantity of blood that can be stored in a given portion
V=D the circulation for each millimeter of mercury pressure rise.
T
The formula for velocity is distance over time and the unit is How come that the venous system can accommodate large
centimetres per second. As said earlier, when we say velocity, that is the volume of blood with little increase in pressure? When we say compliance
distance that is travelled by a volume of blood in a blood vessel. or vascular capacity or capacitance, that is the measure of the degree of
stretching or distensibility of an elastic structure. So a structure can be
V=Q distensible because of the presence of elastic tissue and compliance is
X equal to change in volume over change in pressure or how much blood
Where: Q = blood flow can be accommodated in a blood vessel for every mmHg increase in
X = area pressure.

What is the difference between velocity and blood flow

because the two are directly related? Velocity is equal to blood flow over
cross-sectional area. The two are directly related so if the blood flow is
increased, velocity is also increased. When you say velocity, again, that is
the distance that a volume of blood will travel per unit of time in a blood
vessel (unit: cm/s). But when you say blood flow that is the
volume/quantity/amount of blood that will pass through a blood vessel
per unit of time (unit: mL/unit of time). And again, the two are directly
related. We already explained why velocity is inversely related to cross-
sectional area.
Distribution of Blood Volume
Vascular Distensibility
Which of the two will have more elastic tissue, artery or vein?
Arteries have more elastic tissue and the elastic tissue is responsible for
the distensibility of a blood vessel.
Which is more distensible, artery or vein? It is supposed to be
the artery but the arteries are 8x less distensible than the veins. So how
did that happen? The artery has more elastic tissue so we expect it to be
more distensible than the vein but how come that it is 8x less distensible?
The veins has higher vascular capacity, it can accommodate a large
volume of blood compared to the artery. There are more elastic tissue in
the arterial wall than in the venous wall but the venous wall is thinner.
Meaning to say, if you have an artery and a vein of the same size, both can
accommodate the same volume of blood but in order to stretch the
arterial wall which is thick and strong, that volume of blood will exert a
greater pressure or force. Compare it to the same volume of blood in the
vein, whose wall is thin and also distensible so the same volume of blood
will exert less force or pressure to distend the venous wall. So the venous
wall being thinner that also has elastic tissue, it is more distensible, it can
accommodate a large volume of blood with little increase in pressure.

 Arteries are 8x less distensible than the veins i.e. a given increase in
pressure causes about 8x as much increase in blood in a vein as in
on artery of comparable size.
Veins = increase V
little P
Arteries = increase V
higher P
In the case of the veins, increase in volume but there is only
little increase in pressure. In the arteries, same volume and increase in
pressure. So the compliance is higher in veins.

PHOTO: Distribution of blood (in percentage of total blood) in the different parts of
the circulatory system.

Percentage Parts of circulatory system

39 % Large veins
25 % Small veins and venules
8% Large arteries
5% Small arteries
2% Arterioles
5% Capillaries
7% Heart
9% Pulmonary circulation

At any point in a cardiac cycle, about 65% of the blood is

contained in the venous system, 13% in the arteries, 2% in the arterioles,
5% in the capillaries, 7% in the heart and 9% in the pulmonary
circulation.

Vascular Compliance or Capacitance

C=ΔV
ΔP
Where: Δ V = change in volume
Δ P = change in pressure
5 Shannen Kaye B. Apolinario, RMT|
 PHOTO: A to D, When the arteries are normally compliant, blood flows through the
capillaries throughout the cardiac cycle. When the arteries are rigid, blood flows
through the capillaries during systole, but flow ceases during diastole.
At the top, is a normal artery or aorta. Below, you have a rigid
aorta or artery. Still we are discussing compliance or stretchability of the
arterial or aortic wall.
A - During ventricular systole, blood will be ejected to the aorta so that
the volume of blood in the aorta will increase and under normal
conditions, the aortic wall will distend. At the same time, during
ventricular systole, that volume of blood will be transported under high
pressure to the arteries, to the arterioles, capillaries and therefore to the
tissues.
B - Now, during ventricular diastole (ventricles are not ejecting), the
aortic wall being distensible, it can now recoil on the contained blood.
And because of the recoil of the aortic wall, that will still push blood to the
arteries, arterioles, capillaries and to the tissues so that means although
the ejection of blood from the ventricles to the arterial system is pulsatile,
the transport of blood to the tissues is continuous so there is still
transport of blood to the tissues during diastole.
C - What will happen if the arterial wall becomes rigid for example there
is atherosclerosis which is common in the elderly. So that will make the
arterial wall less distensible. During ventricular systole, blood will be
ejected to the aorta, it can still be transported under high pressure to the
arteries, arterioles, capillaries and to the tissues but as you can see here,
it is not distended anymore. . .
D - So that during ventricular diastole, because the walls are already rigid,
it can no longer recoil. Nothing will push the blood towards the arteries,
arterioles, capillaries and tissues so that means if the arterial wall
becomes rigid i.e. atherosclerosis, that will already compromise blood
supply to the tissues during ventricular diastole.
Laplace equation
PHOTO: Diagram of a small blood vessel to illustrate the law of Laplace: T = Pr, where
P = intraluminal pressure, r = radius of the vessel, and T = wall tension as the force per
unit length tangenital to the vessel wall. wall tension acts to prevent rupture along a
theoretical longitudinal slit in the vessel.
T=Pr
Where: T = tension on the wall
P = transmural pressure (pressure inside blood vessel)
r = radius of the vessel
Laplace equation that is wall tension is equal to the product of
distending pressure and radius of a blood vessel. Tension is tension on
the wall and pressure is inside a blood vessel. So they are directly related.
How come a small blood vessel like a capillary is less prone to rupture
while in large vessel i.e. artery or aorta is more prone to rupture.
T
P = distending pressure
P T = wall tension
T vein because no blood will flow. So that means that when the blood
6 Shannen Kaye B. Apolinario, RMT|
Large artery Capillary
In the case of the capillary, there is less tension on the wall so
that means less pressure is needed to balance the tension on the wall so
its transmural pressure is also less. That is why the capillary wall is not
prone to rupture. Compare it to a large artery, its wall is strong, so the
wall tension is high so that the pressure needed to balance the wall
tension is also high so that will make the transmural pressure high also
that is why a large blood vessel like an artery or aorta is more prone to
rupture.
Blood Flow
 Volume of blood that passes through a specific point in the
circulatory system per minute
 Approximately equal to CO and VR
Blood flow is the amount/quantity/volume of blood that will
pass through a specific point in the circulatory minute per minute. It is
equal to cardiac output and venous return so that means the average
blood flow is 5,000 mL or 5L/min.
Ohms Law
Volume flow = Δ Pressure
Resistance
According to Ohms law, blood flow is equal to pressure
gradient over resistance.
A B
Let’s say this (above) is a blood vessel with point A and point B.
So for blood to flow from point A to point B, there has to be difference in
pressure between point A and point B. the greater the difference in
pressure, the greater will be the blood flow so that if the pressure in point
A is equal to that in point B, there will be no blood flow, it becomes
stagnant.
As for resistance, that is the impediment to blood flow and
there are two types of resistance depending on the arrangement of the
blood vessels. For example, there are blood vessels arranged in series or
arranged in parallel with one another.
Series:
artery arteriole capillary venule vein
TR =
resistance
In in series arrangement, let’s say you have an artery
connected to an arteriole, connected to a capillary and then you have a
venule and finally a vein. If the arteriole will constrict, resistance to blood
flow will increase and so will resistance in the capillaries, venules, and
vessels are arranged in series, the total resistance is equal to the sum of
all the resistances in individual blood vessels.
Parallel: resistance
TR <
On the other hand, an artery will give rise to several arterioles
arranged in parallel with one another. Each arteriole can function
independently of the others so that if one arteriole will constrict, the
resistance will increase only in this (arrow) arteriole so the total
resistance this time will become less than the resistance in one blood
vessel.
One type of blood flow is laminar flow wherein blood flows at
a constant rate. When we say laminar flow, the layer of blood that is in
close contact with the vascular wall hardly moves. The next layer which is
a little farther away from the vascular wall will flow at a low velocity. The
next layer will move at a higher velocity. That means the highest velocity
will be at the center and that will be the direction, that will be the rate
along a blood vessel meaning to say, when the blood reaches the end of
the blood vessel it cannot be that the one in contact with the blood vessel
wall will have the highest velocity and the one at the center will have the
lowest velocity. The direction is straight at a constant rate so that laminar
flow is also called stream line and this type of blood flow is silent, it
creates no sound.
2. Turbulent Flow

The sum of all the resistances to blood flow in the systemic or

peripheral circulation is what we call total peripheral resistance (TPR).

Factors that will increase resistance to blood flow:

Poiseuille’s Equation
When blood flows in different directions, it creates a sound and
Resistance = Length x Viscosity x 8
that is what we call a turbulent flow and the sound that is produced by
Π r4
turbulent flow is a bruit. In the heart, the abnormal sound is a murmur;
in the blood vessel it is called a bruit.
Factors that will increase resistance to blood flow are expressed in
Poiseuille’s equation. So resistance is directly related to length of a blood
What are the conditions that will predispose to a turbulent
vessel. The longer the blood vessel is, the higher the resistance to blood
type of blood flow?
flow. It also related to blood viscosity. Remember that blood is 3-4x more
viscous than water and there are two factors that make blood viscous:
1. If the velocity of blood flow increases.
haematocrit/concentration of red blood cells and concentration of plasma
proteins. In polycythemic patients, there is increase RBC production,
2. If the blood passes over a rough surface. Remember that
increase RBC count, increase haematocrit that will make blood more
endothelial lining of a blood vessel is smooth. But if there will
viscous so resistance to blood flow is increased. On the other hand, the
an injury on the blood vessel wall or if there will be
opposite is true to anaemic patients, decrease RBC count, decrease
atherosclerotic plaques deposited on the blood vessel wall, that
haematocrit that will make blood less viscous so that the rate of blood
will make the endothelial lining rough and when blood passes
flow increases.
over a rough surface, the direction of blood flow is disturbed.
Another important factor related to resistance but this time
3. If there is an obstruction. So along a blood vessel, blood flows
inversely related is the radius of a blood vessel and not just the radius,
laminar then suddenly there is a thrombus, that will again
radius to the 4th so that will make it a very important factor. Meaning to
change the direction and the rate of blood flow will be
say, during vasoconstriction, if the lumen of a blood vessel will decrease
disturbed
twice its normal size, that means blood flow will decrease 4x. or if during
vasodilatation, the lumen or the radius of a blood vessel will increase
4. When the blood vessel makes a sharp angle, that will again
twice its normal size, that means blood flow will increase 4x normal. So
predispose to a turbulent type of blood flow.
the radius of the blood vessel is very important in regulating resistance to
blood flow.

Reynold’s Number
2 Types of Blood Flow
Re = Diameter x Velocity x Density
1. Laminar Flow Viscosity

The factors that will increase the tendency of blood flow to

become turbulent are expressed in Reynold’s number. The factors that
are directly related to the Reynold’s number are diameter of blood vessel,
velocity of blood flow, and density of the fluid or medium whereas blood
viscosity is inversely related to the Reynold’s number.

When will turbulent flow occur? If the Reynold’s number is

below 2,000, blood flow is laminar and there is very little turbulence but
it will easily die out. Between 2,000 to 3000 is the transition from laminar
to turbulent flow but above 3000, blood flow is definitely turbulent

0 1 2
Velocity Venous Return
PHOTO: When flow is laminar, all elements of the fluid move in streamlines that are
parallel to the axis of the tube; the fluid does not move in a radial or circumferential
direction. The layer of fluid in contact with the wall is motionless; the fluid that moves  Volume of blood that goes back to the heart per minute
along the central axis of the tube has the maximal velocity.  5,000 mL/min

7 Shannen Kaye B. Apolinario, RMT|

 Venous return is the amount/quantity/volume of blood that
will return to the heart per minute. It is equal to cardiac output and equal
to blood flow so it is 5,000 mL or 5L/min.
Factors that Regulate Venous Return
long time, there will be pulling of blood on the lower
extremities. Since the venous return cannot be facilitated
because of the damaged venous valves, the accumulation of
blood in the lower extremities will now cause stretching or
distension on the wall of the veins and that will cause
varicosities.

VR = MCSFP – CVP 5. Negative intra-thoracic pressure. A negative intra-thoracic

RV
Where: MCSFP = Mean Circulatory Static Filling Pressure
CVP = Central Venous Pressure
RV = resistance in veins
Venous return is equal to mean circulatory static filling
pressure (MCSFP) – the measure of the degree of filling of the systemic
or circulatory system. Meaning to say, when blood blow in the systemic
circulation stops the pressure exerted by the volume of blood in the
systemic circulation is what we call MCSFP – how much blood is present
in the systemic circulation when blood flow stops. It is actually directly
related to the total blood volume (TBV).
MCSFP = TBV
VC
Where: TBV = total blood volume
VC = vascular capacity
So increase in the total blood volume will increase the MCSFP
and therefore increase the venous return but it is inversely related to
vascular capacity. Remember there is increase capacitance if the venous
wall is in a relaxed state because the veins will accommodate a large
volume of blood and that blood will not return to the heart so with
sympathetic stimulation, you increase the tone of the venous wall that
will now increase the veins vascular capacity and therefore increase
venous return. So, sympathetic stimulation increase venous tone,
decrease vascular capacity, and increase venous return.
CVP is central venous pressure or more specifically pressure
in the right atrium which is normally 0 mmHg. For venous return to
increase, CVP should be lower than the pressure in the venous system.
When will the right atrial pressure or CVP increase? There are
factors:
1. Rate of venous return increases. When the rate of venous
return increases above normal so that will easily fill up the
right atrium so that is increased volume blood in the right
atrium will increase the CVP.
pressure that will allow the veins and the heart to dilate so that
will facilitate venous return and allow more blood to be
accommodated in the heart.
Arterial Blood Pressure
 Force exerted by the volume of blood on the arterial wall
When you get your BP: 120/80, what does that mean? What do
you mean by arterial blood pressure? That is the force exerted by the
volume of blood on the arterial wall. It is expressed as systolic pressure
over diastolic pressure.
Blood Pressure:
Systolic Pressure (SP) = is the highest pressure in the aorta at systole
Systolic pressure is the highest pressure recorded in the aorta
during ventricular systole. Why will the pressure in the aorta increase
during ventricular systole? Because when blood is ejected into the aorta,
the volume of blood in the aorta will increase and that will exert pressure
on the aortic wall to distend the aortic wall. in the elderly, systolic
pressure is usually high (higher than normal – 130, 140 and the average
is 120 mmHg) because of atherosclerosis that will cause hardening of the
aortic wall so the volume of blood ejected by the left ventricle will have to
exert a greater force to stretch the already rigid aortic wall.
Diastolic Pressure (DP) = is the lowest pressure in the aorta at diastole
Diastolic pressure is the lowest pressure recorded in the aorta
during ventricular diastole. Why will pressure in the aorta decease during
ventricular diastole? Because there is no more ejection of blood from the
ventricles and the volume of blood that is present in the aorta will drop
off to the arteries, arterioles, capillaries and tissues and the aortic wall
will recoil.

2. Pumping capacity of heart. The other factor is the pumping

ability of the heart. If the pumping ability of the heart is
normal, the volume of blood in the right atrium will be ejected
to the right ventricle and on to the pulmonary circulation.
What if there is right-sided heart failure? So the pumping
ability of the right heart is depressed so the blood in the right
atrium will back up in the venous system and that will now
increase the venous pressure so that one clinical manifestation
of right-sided heart failure will be distension of the neck veins.

3. Resistance in veins. Next is resistance in the veins which is

quite low because remember that the veins are low pressure
area but resistance may increase if the intra- abdominal
pressure increases because for example during pregnancy or if
there is tumor in the abdominal cavity or if there is ascites
(accumulation of fluid in the abdominal cavity), that will now
compress the veins so the resistance in the veins will increase
and that will decrease venous return. PHOTO: Arterial systolic, diastolic, pulse, and mean pressure. Mean arterial pressure
(Pa) represents the area under the arterial pressure curve.
4. Venous pump. Other factors that may influence venous return
will be the venous pump or activity of the venous valves. We all Pulse Pressure = SP – DP
know that when you move your limbs, the venous valves will
open and that will facilitate venous return. What will happen Where: SP = systolic pressure
when the venous valves are damaged? When you stand for a DP = diastolic pressure

8 Shannen Kaye B. Apolinario, RMT|

 The difference between the systolic pressure and diastolic recoils, the volume of blood is still high and that will increase the diastolic
pressure is the pulse pressure. Again, in the elderly with atherosclerosis, pressure.
what will happen to the pulse pressure? It will increase because the
systolic pressure, the diastolic pressure will not change so that will now
increase the pulse pressure. Factors that Affect ABP

What about during moderate to heavy exercise? The
sympathetic nervous system is stimulated so that will increase the heart
rate, increase the stroke volume, and increase the cardiac output. When
the cardiac output increases, the systolic pressure increases. What
happens to the diastolic pressure? During exercise, with increased
metabolism, there is increase heat production. Increase heat production
will cause vasodilatation decreasing the total peripheral resistance (TPR).
With a decrease in TPR, diastolic pressure decreases so that will widen
the pulse pressure.
The pulse pressure can actually be influenced by two factors:
one is stroke volume – greater stroke volume, increase systolic pressure,
no change in diastolic pressure so that will increase the pulse pressure.
The other factor is compliance of the arteries. So again, when the arterial
wall becomes rigid, its compliance will decrease and that will again
increase the systolic pressure, no change in diastolic pressure so that will
widen the pulse pressure.
Another condition is in hyperthyroidism. Thyroid hormones
can directly stimulate the SA node and the myocardial cell so increase
heart rate, increase stroke volume, increase cardiac output, increase
systolic pressure. But at the same time, thyroid hormones can increase
intracellular metabolism. Again, that will increase heat production,
vasodilatation, decrease TPR, decrease diastolic pressure. So in
hyperthyroidism, you have an increase systolic pressure, decrease
diastolic pressure that will widen or increase the pulse pressure. So
hyperthyroid patients are prone to what we call high cardiac output
failure.
To summarize, here are the factors that affect the arterial
blood pressure:
1. Blood volume. How come we always say that if there is
hypervolemia, there is hypertension or if there is hypovolemia,
there is hypotension? If blood volume increases, that will
increase initially the MCSFP. When increased, MCSFP will
increase venous return. The effect of an increased venous
return on the heart increases the following parameters: end
diastolic volume that will stretch the ventricular wall, increase
force of contraction, increase stroke volume, increase cardiac
output, and increase blood pressure.
2. Compliance of arteries. When the compliance of the arteries
decreases, it increases mainly systolic pressure.
3. Cardiac output. Increase in cardiac output will increase
mainly systolic pressure.
4. Total peripheral resistance. Vasoconstriction that will
increase TPR will increase mainly diastolic pressure.

Mean Arterial Pressure (MAP)

MAP = DP + 1/3 (SP-DP)

Where: MAP = mean arterial pressure

DP = diastolic pressure
SP-DP = pulse pressure

The average pressure in the circulatory system in one cardiac

system is the mean arterial pressure (MAP). Remember that this is not
the average of systolic and diastolic pressure. This is the average pressure
in the circulatory in one cardiac cycle. And it is equal to the diastolic
pressure plus one third of the pulse pressure. Why diastolic pressure?
Because 60% of the cardiac cycle is diastole, only 40% is systole.

ABP = CO x TPR

Where: ABP = arterial blood pressure

CO = cardiac output
TPR = total peripheral resistance

The formula for arterial blood pressure (ABP) is cardiac

output (CO) times total peripheral resistance. If for example TPR is
normal, CO increases, which will be affected more, will it be the systolic
pressure or diastolic pressure? Systolic pressure because if the stroke
volume increases, increase CO, increase volume of blood in the aorta that
will exert a greater force on the aortic wall.

Now, if the TPR increases, which will be affected more? It is

diastolic pressure but why? What causes an increase in TPR?
Vasoconstriction. Remember that during diastole, supposed to be there is “Trust in the Lord with all your heart and lean not on your own
peripheral run off blood to decrease the volume of blood in the aorta and understanding; in all your ways acknowledge him, and he will make
the aortic wall will recoil. What if there is vasoconstriction? Increase TPR, your paths straight.”
blood cannot runoff to the capillaries, to the tissues etc. so there will be -Proverbs 3:5-6
pulling of blood in the arterial system so that when the arterial wall
GOD BLESS YOU 

9 Shannen Kaye B. Apolinario, RMT|