CARDIOVASCULAR PHYSIOLOGY (Gloria Marie M. Valerio, MD) Outline:
1. 2. 3. 4. 5. 6. 7. 8. Functional Anatomy of the Heart Properties
of the Myocardial Cells Electrical Events Cardiodynamics
Characterics, Properties, Functions of the Different Types of Blood
Vessels Hemodynamics Microcirculation Mechanisms that Regulate
Cardiovascular Function
the different organs of the body. This is made possible by the
pumping 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 pCO2
Decrease pO2 Increase pCO2 Pulmonary capillary
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.
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
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 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.
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
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: 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
PHOTO: Four cardiac valves as viewed from the base of the heart.
Note how the leaflets overlap in the closed valves.
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Shannen Kaye B. Apolinario, RMT
however, when the papillary muscle contracts, it will pull the
chordae tendinae to prevent eversion or over-bulging of the AV
valves during ventricular contraction.
the leaflets. In insufficient or incompetent cardiac valve, the
leaflets do not close completely allowing back flow of the blood
either from the 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 Mitral Aortic
Heart Sounds Closing of the cardiac valves will produce the
normal heart 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 sound. Compared to the second
heart sound, closing of the AV valve is 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, 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 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 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 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
inspiration. During expiration, you will hear only one second heart
sound there is simultaneous closure of the aortic and pulmonary
valves. During inspiration, there is a physiological splitting of
the second sound with closing of the aortic valve occurring a
little ahead of the pulmonary valve and the sound produced by
closing of aortic valve is louder than that produced of the closing
of the pulmonary valve except in patients with pulmonary
hypertension. The pressure inside the thoracic cavity is negative
or below atmospheric pressure causing a suction effect on
structures that can be dilated. (In positive or above atmospheric
pressure, it will compress the structures in the thoracic cavity.)
The more negative the intra-thoracic 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 blood will
return from the systemic circulation. There will be an increase
volume of blood to the right heart causing a delay of the closing
of the pulmonary valve during inspiration. In children with thin
chest wall or patients suffering from left ventricular failure, a
third heart sound can be heard and that will coincide with filling
of blood in the ventricles. Rarely, there is a fourth heart sound
that can be heard and that will coincide with atrial contraction.
In some abnormal conditions, the third and fourth heart sounds may
be accentuated so that what you will hear in the stethoscope will
be triplets of sounds resembling the sound that is produced by
galloping horses called a gallop rhythm. Certain abnormal
conditions like an infection in the heart may damage the cardiac
valves and there are two types of lesions that may occur in the
cardiac valve: stenosis and incompetent cardiac valve. In stenosis,
the valve cannot open completely because of the hardening of 3
Shannen Kaye B. Apolinario, RMT
Type of lesion Stenosis Incompetent Stenosis Incompetent
Timing of murmur Diastole Systole Systole Diastole
Diastole ventricular relaxation Systole ventricular contraction
The Pericardium
Pericardial fluid Parietal pericardium Visceral pericardium The
heart is covered by a membrane which is made up of connective
tissue the pericardial sac or pericardium. This connective tissue
that makes up the pericardium is less distensible. Presence of this
will also prevent overstretching of the cardiac muscle when the
cardiac size increases. The pericardium is made up of two
membranes: visceral and parietal pericardium. The visceral
pericardium is the membrane directly attached to the anterior
surface of the myocardium. When the visceral pericardium is
reflected back, it forms the parietal pericardium. The space in
between the two membranes is filled with 30cc of pericardial fluid.
The importance of the pericardial fluid is to lubricate the heart
facilitating the movement of the heart when it contracts. (2)
Groups of Myocardial Cells 1. Automatic Cells An automatic cell is
a cell that is capable of spontaneously generating its own action
potential independent of extrinsic nervous stimulation. In the case
of myocardial cells, it is independent of automatic stimulation.
Aside from generating its own action potential, the cells of the
heart are capable of transmitting or conduction action potentials
throughout the heart. Structures that make up the hearts conduction
system: Synoatrial (SA) node = located at the junction of superior
vena cava and right atrium. Atrioventricular (AV) node = located
posteriorly on the right side of interatrial septum. It is divided
into three zones: o Atrionodal (AN) zone most proximal zone, a
transitional zone between the right atrium and AV node o Nodal (N)
zone - middle
o
Nodal His (NH) zone most distal, connects with the bundle of
His
1
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.
0 4
2
-90 mv
3
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.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.
Intracellular Increase K+ Negatively charged proteins Decrease
Na+ Decrease Cl-
Extracellular Decrease K+ Increase Na+ 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 Properties of Myocardial Cells 1st Property: Automaticity
generation of action potentials 4 Shannen Kaye B. Apolinario, RMT
-60 mv
3
4
250-300 milliseconds hyperpolarization Action potential of an
automatic cell- SA node
Difference from the AP of skeletal muscle: Duration is longer
250-300 millisecond 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. 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 Na
leakage, Decrease K -40 mv -50 mv -60 mv 250-300 milliseconds
Action potential of an automatic cell (same thing happens in SA
node, AV node, bundle of HIS) With parasympathetic or vagal
stimulation, the neurotransmitter released (NTA) released is
acetylcholine (Ache). When Ache binds with muscarinic 2 receptors
in the SA node, it increases permeability to K+, allowing more K+
efflux. Parasympathetic or vagal stimulation will hyperpolarize the
SA node. If it is hyperpolarized, it is less excitable and the
duration of the membrane pre-potential is longer or delayed
generation of action potential. In parasympathetic or cholinergic
stimulation, SA node is inhibited, heart rate decreases. The
opposite happens with sympathetic stimulation, 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. Hyper: prolonged opening of K
channels
Non-automatic Fiber Action Potential (ventricular muscle)
PHOTO: Action potential in the ventricle (250-300
milliseconds)
Activation of slow (inclined) voltage gated long lasting Ca++
channels allowing Ca influx with some Na influx = MP will become
less negative
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) Peak of the spike Na channels closes,
K channels open. Ca++ channels are still open Phase 1 initial phase
of repolarization brought about mainly by slow voltage gated K+
channels 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 Ca++ channels will close leaving only the K+
channels open that will bring about the final phase of
repolarization Phase 3 final phase of repolarization Phase 4 - -90
RMP is re-established. The increase membrane permeability to
potassium is responsible for the -90 mv RMP. No hyperpolarization
Although the K+ channels can remain open for a long time, because
of the plateau, it is open for a long period of time thus it does
not reach hyperpolarization Similarities and differences with the
action potential of skeletal and cardiac muscles: Similarities: -90
mv RMP, fast-paced depolarization Differences: repolarization, no
hyperpolarization, duration
PHOTO: Action potential of the SA node
PHOTO: Action potential of the atrium
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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
ARP RRP
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. Duration Action potential ARP RRP Heart rate of 75
beats per min 0.25 sec 0.20 sec 0.05 sec Heart rate 200/min 0.55
sec 0.13 sec 0.02 sec Skeletal muscle 0.005 sec 0.004 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
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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.
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: basal.
Conduction Speed in Cardiac Tissue SA node Atrial muscle AV node
Bundle of His Purkinje fibers Ventricular muscle Conduction rate
(m/sec) 0.05 1 0.05 1 4 1 antero-basal apex postero-basal
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.
The part of the heart that will depolarize last is the
postero-
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
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: 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
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 reentry 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 thats
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.
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).
PHOTO: AV blocks. A, First-degree block; the PR interval is 0.28
second (normal: AP atr. systole inc. VF vent. systole atr. diastole
inc. VP dec. AP 20% VF 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. From the AV node, the impulse will now be transmitted to
the ventricular conduction system (VCS) or Purkinje system and that
will cause ventricular depolarization in the ECG recorded as the
QRS complex. The response of the ventricular muscle to
depolarization is to contract so following ventricular
depolarization will be ventricular systole. When the ventricles
contract, the ventricular pressure increases. Simultaneous with
ventricular depolarization is atrial repolarization and no ECG wave
represents atrial repolarization. The response of the atrial muscle
to repolarization is to relax so atrial diastole happens. Since the
atria is relaxed, there will be a decrease in the atrial pressure.
When the ventricular pressure exceeds atrial pressure, there will
be a pressure 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 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 are contracting,
there is increase in ventricular pressure and this is called
isovolumic or isovolumetric contraction phase of the cardiac cycle.
When the ventricles are contracting, ventricular pressure still
increases and this high pressure may push the AV valves to bulge
into the atria and that will cause a slight increase in atrial
pressure which is now called the C wave. But remember that the AV
valves does not over-bulge into the atria when the ventricular
pressure is increased because when the ventricles contract, the
papillary muscles will contract pulling the chordae tendinae which
will prevent over-bulging of the AV valves into the atria resulting
to only a slight increase in the atrial pressure. When ventricular
pressure exceeds 80 mmHg, this will push 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 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 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 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 collecting
blood so that little by little, there will be atrial filling. The
ventricles will undergo repolarization so this is the S-T interval
in the ECG. The response of the ventricular muscle to
repolarization is to relax so there will be ventricular diastole
therefore 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 now exceeds ventricular pressure, this
will close the semilunar valves and that will produce the second
heart sound. But there is a short interval of time between
ventricular diastole and closure of SL valves which is called
protodiastole. There will be a condition again wherein the SL
valves are now closed, the AV valves are still closed so there is
no change in ventricular volume but since the ventricles are in a
relaxed state, ventricular pressure decreases and this is called
isovolumic relaxation. At the same
close AV valves (1st heart sound)
isovolemic contractions: slight inc. AP (C wave) VP > 80 mmHg
open SL valves rapid ejection reduced ejection; atrial filling
vent. repo vent. diastole dec. VP (S-T interval) AP > VP
protodiastole close SL valves (2nd heart sound) isovolemic
relaxation; inc. atr. filling; inc. AP (V wave) AP > VP open AV
valves rapid inflow diastasis reduced inflow of blood to the
ventricles atr. atrial AV - antrioventricular AVN atrioventricular
node dec. - decrease depo depolarization inc. - increase repo
repolarization SAN sinoatrial node SL - semilunar vent.
ventricular/ventricle VF- ventricular filling VP ventricular
pressure
At the beginning of one cardiac cycle, before an impulse is
generated from the sinoatrial (SA) node, the atrium and ventricles
are all relaxed atrial systole and ventricular diastole. The
semilunar (SL) valves are closed but the atrioventricular (AV)
valves are open so that 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 are in a relaxed state.
It is not needed for the atria to contract to have ventricular
filling because its contraction is weak primer pump, so whenever
the AV valves are open, there is 80% of ventricular filling. 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
open SL valves close 2nd heart sound ***Atrial pressure curve
yellow dotted line 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 sound 14 AV
valves open
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 c
v
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 ventricles after contraction
PHOTO: Pressure-volume loop
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. Phase IV the volume of blood is still
50 mL but the pressure is decreasing and decreasing. This is
isovolumic relaxation. I can do EVERYTHING through Him who gives me
strength -Philippians 4:13 GOD BLESS YOU!
16
Shannen Kaye B. Apolinario, RMT