CARDIAC PHYSIOLOGY PHYSIOLOGY: Midterms Lec 2.

1
Cardiac 1 – Functional Anatomy of the Heart DR. GLORIA VALERIO |SEPT 20, 2021

GENERAL OUTLINE 3. Blood vessels → through which blood flows;

I. Functional Anatomy and properties of the Myocardial cells composed of:
II. Cardiac cycle
III. Cardiodynamics
IV. Electrocardiography
V. Characteristics, Properties, and Functions of the Vascular
System and Hemodynamics
VI. Microcirculation and Regulation of Cardiovascular System

LECTURE OUTLINE
I. Functions of the Cardiovascular System (CVS)
II. Three Major Components of CVS
III. Functional Anatomy of the Heart
A. Normal Anatomical Position
B. Human heart
C. Oxygenated and Deoxygenated Blood
D. Systemic and Pulmonary Circulation of Blood
E. Chambers of the Heart
F. Elastic Tissues in Atrial/ Ventricular Wall
V. Other Important Structures in the Heart
VI. Myocardial Cells
A. Automaticity
B. Rhythmicity
C. Conductivity
D. Contractility
References:
[1] Dra. Valerio’s 2021 Lecture

I. FUNCTIONS OF THE CARDIOVASCULAR SYSTEM

A. Major Function
• To service the needs of the tissues
o To transport to the tissues substances that are a. Arterial System
essential for normal cellular metabolism: ▪ high pressure area
▪ Oxygen ▪ arterial walls are thick and strong so
▪ Nutrients (glucose, fatty acids, amino acids) that the volume of blood inside will have
▪ Transport of Electrolytes to exert greater force to stretch the
▪ Transport of Hormones and Enzymes to areas of arterial wall
the body where they are needed ▪ Arteries are called “DISTRIBUTING
o Transport AWAY from the tissues non-essential VESSELS” because their main function
substances (products of cellular metabolism) is to distribute oxygenated blood under
▪ CO2 high pressure to all organs of the body
▪ Excess electrolytes
▪ Metabolites b. Venous System
• Creatinine ▪ Low pressure area
• Uric Acid ▪ Same volume of blood that can be
o Participates in the thermoregulation, as well as the accommodated in a vein
maintenance of the balance of different fluid ▪ Venous walls are thin so that the same
compartments in the body volume of blood will exert little force and
that will already stretch the venous wall
II. THREE MAJOR COMPONENTS OF THE CVS ▪ Called “CAPACITANCE VESSELS”
1. Heart → functions as a pump because they have greater capacity to
2. Blood → serves as a medium by which essential accommodate a large volume of blood
and non-essential substances can be transported with little increase in pressure
to and from tissues ▪ Also called “COLLECTING VESSELS”
because they collect deoxygenated

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

blood from the different organs of the ▪ Located at the 5th

body. Also return blood to the heart Intercostal Space Left
Midclavicular Line or 5
c. Blood Vessels (Microciculation) ICS LMCL (yellow dot or
▪ “EXCHANGE VESSELS” purple dot)
▪ In between arterial and venous systems
▪ In direct contact with the tissues:
• Venules
• Arterioles
• Capillaries
B. Human Heart (4-chambered, double pump)
▪ Capillary wall: thin and fenestrated or
• Right Heart/ Pump
porous (“may mga butas”)
o Right Atrium
• Can allow exchange of fluids and
o Right Ventricle
some solutes between
• Left Heart/ Pump
intravascular fluid or plasma and
o Left Atrium
interstitial fluid
o Left Ventricle
• Interatrial Septum –
Important to Remember!
band of connective
• Arteries → Distributing Vessels tissues that separates
• Veins → Capacitance and Collecting Vessels 2 ventricles
• Capillaries → Exchange Vessels • Mass of connective
tissue separates the
III. FUNCTIONAL ANATOMY OF THE HEART 2 atria from ventricles
A. Normal Anatomical Position of the Heart
• This is the normal position of the heart inside the thoracic C. Oxygenated VS. Deoxygenated Blood
cavity in relation to the right and left lungs • Oxygenated Blood
• It is TILTED TO THE LEFT, POINTING DOWNWARDS o Many O2, low CO2
• VEINS – blue structures o Essential/ needed by organs
• ARTERIES – red structures • Deoxygenated Blood
• DIAPHRAGM – o Has products of cellular metabolism
below the heart, o Low O2, High CO2
separates the o Removed from tissues
thoracic cavity from
the abdominal cavity D. Blood Flow
• APEX – lower • Systemic/ Peripheral/ Grater Circulation
part that point o 70-130 mmHg (high pressure area)
downwards o Blood flow from left heart to all organs except lungs
• BASE – upper o Lungs → pulmonary vein → LA → mitral valve →
part LV → Aorta
• CARDIAC o Pulmonary vein: ONLY vein in the entire body that
MUSCLE FIBERS – carries OXYGENATED or ARTERIAL BLOOD
have spiral o Aorta: largest artery in the body that divides into
arrangement → when the heart contracts, it will rotate several distributing arteries the distribute oxygenated
slightly to the right (“naintindihan niyo section A?”) blood under high pressure to all organs of the body
o Pag-ikot niya to the right, that will expose more the EXCEPT for the lungs
contracting cardiac apex and vibrations produced by ▪ CNS, cardiac muscles, GIT, GUT, skin, endo- and
the contractions of cardiac apex can be transmitted to exocrine glans, etc.
the chest wall • Pulmonary Circulation
▪ When you place the BELL of the stethoscope on o 4-25 mmHg (low pressure area)
the chest wall, that is where you will hear the o Deoxygenated blood coming from systemic circulation
heartbeat loudest (Remember: “BELLow”) will be collected by venules, emptied into bigger
▪ APEX BEAT or POINT OF MAXIMUM IMPULSE veins, then into vena cava

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

o SVC/ IVC → RA → tricuspid valve → RV → ➔ Cardiac output = Venous return

pulmonary artery → lungs E. Chambers of the Heart
o Pulmonary Artery: only artery in the body that • 2 Atria
carries venous blood o Covered by the atrial wall made up of cardiac
o Lungs: where exchange of gases occur muscle cells (Myocardium)
o Atrial wall is thinner than the ventricular wall
o Alveoli: functional unit of the lungs
▪ Because of this, when the atria
▪ When inhale atmospheric air which contains many contracts, they do not contract as
oxygen enters the lungs and will reach the alveoli forcefully as the ventricles
▪ Alveoli air - high in O2, low in CO2 o Functions mainly as primer pumps in the heart
▪ Deoxygenated blood from pulmonary artery will • 2 Ventricles
flow into arterioles, until it reaches the pulmonary o Covered by the ventricular wall made up of
capillaries cardiac muscle cells (Myocardium)
o Has thicker walls
▪ Pulmonary capillaries – level where exchange of
o Functions as major pumps in the heart
gases takes place between alveolar air and LV>RV o Left ventricular wall
pulmonary capillary blood across the respiratory afterload
workload ▪ Thicker than the right ventricular wall
membrane P ▪ Measures about 1.2-1.5cm thickness
Force of contraction
wall thickness o Right ventricular wall
▪ Respiratory membrane – separates alveoli from
pulmonary capillaries LV=RV ▪ Thinner; Measures only 0.3-0.5 cm
EDV/preload
▪ Exchange of gases take place by simple SV ▪ Pumps blood to the pulmonary
ESV
CO circulation (low pressure area)
diffusion brought about by pressure gradient
(HPA → LPA) Why is the left ventricle thicker than the right ventricle?
• O2 diffuses from alveoli to pulmonary
capillaries
➔ Left ventricle pumps blood to the systemic circulation,
• CO2 diffuses from pulmonary capillaries to which has a high-pressure area
alveoli to be eliminated during exhalation ➔ Right ventricle pumps blood to the pulmonary
▪ Oxygenated blood in pulmonary capillaries will be circulation, which is a low-pressure area
collected by pulmonary venules, emptied into
The opposing force or resistance to the left ventricle contraction
pulmonary vein, then to the left atrium again is greater than that of the right ventricle. In order for the left
ventricle to eject blood, it has to contract more forcefully. If the
Important to Remember! left ventricle will have a stronger contraction, the cardiac muscle
cell wall will be thicker (hypertrophy)
[Pulmonary Circulation]: SVC/ IVC → RA → tricuspid
valve → RV → pulmonary artery (deoxygenated/ venous The right ventricle will pump blood to the pulmonary circulation,
blood) → [Systemic Circulation]: lungs → pulmonary vein there is a weaker opposing force or resistance to right ventricular
contraction. Will have a weaker contraction for blood to be
(oxygenated/ arterial blood) → LA → mitral valve → LV ejected, there will be no hypertrophy of the cardiac muscle cells.
→ aortic valve → aorta → all organs in the body (except
the lungs) Although the opposing force to left ventricular contraction is
greater than the right;
Although the workload of the left ventricle is higher to that of the
right;
Although the peak left intraventricular pressure is higher
compared to that of the right;
Although the left ventricle contracts more forcefully compared to
the right;
Although the wall of the left ventricle is thicker than that of the
right;

-------- OUTPUT OF THE 2 VENTRCLES IS THE SAME ------

So that means, If the left ventricle can pump 5 liters of blood per
Blood from the Pulmonary Circulation will go to the left heart min or 70ml of blood per contraction, so can the right.
Blood from the Systemic Circulation will go to the right heart Only difference is that in order for the left ventricle to be able to
pump 5 liters of blood per min or 70ml of blood per contraction,
it needs to have a stronger contraction since the opposing force
Although the circulatory system is divided into to, it is actually a
is strong.
CLOSED SYSTEM.
➔ Whatever the amount or volume of blood that is ejected
by the heart per minute (Cardiac output), is equal to the
amount or volume of blood that will return in the heart per
minute (venous return)

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

The right can pump 5 liters of blood per min or 70ml of
blood per contraction even if the contraction is weaker
since the opposing force is weaker.
F. Elastic Tissues in Atrial/ Ventricular Wall
• Also present in the atrial and ventricular walls are fair
amounts of elastic tissues
• Enable to stretch the ventricular wall and atrial wall
o In order to accommodate a large volume of
blood with little increase in pressure
• The 4 chambers can also function as a blood reservoir
There are no valves between the atria and veins
So that, when the atria contract, there is a small amount
of blood that can backflow to the veins. Because when
the atria contracts, it is not that strong, and because of
inertia, when it contracts, the tendency is to push blood
to the ventricles.
Also, when the atria contract, the orifice of the vena
cava and pulmonary vein become smaller. So even if
there is backflow, it will only be a small amount.

V. OTHER IMPORTANT STRUCTURES IN THE HEART

TWO SETS OF CARDIAC VALVES

1. Atrioventricular valves
o Located between the atria and ventricles
2. Semilunar valves
o Located between the ventricles and arteries

A. Atrioventricular Valves
1. Tricuspid valve – right side
o Between the right atrium and right ventricle
2. Mitral (Bicuspid) valve – left side
o Between the left atrium and left ventricle

C. Structure of the Valves

• Each cardiac valve is made up of cup like or triangular
structures → CUSPS
o Main component of the cusps is connective
tissue
• 3 cusps each for pulmonic, aortic and tricuspid valves
• 2 cusps for mitral valve

B. Semilunar Valves
1. Pulmonary or Pulmonic valves – right side
o Between the right ventricle and pulmonary
artery
2. Aortic valve – left side
o Between the left ventricle and aorta

• The base of the AV valves is thin and weak

o In order to hold the AV valves in place, the
cusps should be supported by strong ligaments
known as CHORDAE TENDINAE
▪ The chordae tendinae are attached to
the papillary muscle arising from the
ventricular wall

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

• When the ventricles contract, the papillary muscles will
also contract and that will pull the chordae tendinae,
preventing eversion or over-bulging of the AV valves into
the atria when the ventricles are contracting
D. Function of Cardiac Valves
• Each cardiac valve has an opening
o Opening is covered by leaflets made up of
loose fibrous tissues hence freely movable
o When the leaflets open, they allow blood to flow
o When the leaflets close, there is extensive
overlapping of leaflets and this will prevent
backflow or regurgitation of the blood

1. When they open, blood flows

2. When they close, that will prevent backflow or
regurgitation of blood

• Hence, these cardiac valves ensure a unidirectional

flow of blood in the heart
o Atrium → ventricle → artery
• AV valves have a bigger opening than semilunar valves
• The size of the opening is related to the velocity of blood
flow → inversely related
o AV valves = bigger opening = decrease velocity
of blood flow
o Semilunar valves = smaller opening = increase
velocity of blood flow
• Opening and closing of cardiac valves are passive
The semilunar valves -- Pulmonary and Aortic Valves do processes brought about by 2 types of pressure
not have chordae tendinae gradient:
1. Forward pressure gradient
o Will open up the cardiac valves and allow
• The base of the semilunar valve is thick and strong. blood to flow
o The base is already embedded within the wall of
the aorta Example:
o The base of the pulmonary valve is embedded When the atria contract = high pressure;
in the wall of the pulmonary artery When the ventricle is relaxed = low pressure
So, there is pressure gradient; Atrium is higher than the
ventricle, that is a forward pressure gradient that will
AV VALVES SEMILUNAR VALVES open up the AV valves that will allow the blood to flow
Thin and weak base Thick and strong base from the atria to the ventricles
They have supporting No supporting chordae
chordae tendinae tendinae
Bigger opening Smaller opening In semilunar valves, when the left ventricle contracts, it
has a higher pressure than the aorta. So it is a forward
pressure gradient, that will open up the aortic valve
allowing blood to be ejected from the left ventricle to the
aorta.

2. Backward pressure gradient

o This will close cardiac valves
o To prevent backflow or regurgitation of
blood
Example:
When the atria are relaxed = lower pressure
When the ventricle is contracted = high pressure
AV valves will close and there is no backflow of blood

The blood is ejected to the aorta= higher pressure

Left ventricle relaxes = lower pressure
When aortic pressure is greater than left ventricular
pressure, there is backward pressure gradient, AV valves
will close and there is no backflow of blood

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
E. Heart Sounds
• Produced when the cardiac valves close
• Usually, 4 heart sounds but only 2 are heard
• First and second heart sounds described as “lubb dubb”
First Heart Sound (S1)
• Closing of atrioventricular valves
• Marking the end of ventricular relaxation and beginning
of ventricular contraction
o Tricuspid Valve – sound produced when close
is heard on the 5th INTERCOSTAL SPACE
LEFT PARASTERNAL MARGIN (5 ICS LPSM)
(lateral or border of left side sternum)
o Mitral (Bicuspid) Valve – sound prodiced
when close is heard best on the 5th
INTEROSTAL SPCE LEFT MIDCLAVICULAR
LINE (5 ICS LMCL)
SECOND HEART SOUND (S2)
• Closing of semilunar valves
• Marking the end of ventricular contraction and beginning
of ventricular relaxation
o Pulmonary Valve – sound produced when
close is heard at the 2nd INTERCOSTAL SPCE
LEFT PARASTERNAL MARGIN (2 ICS LPSM)
o Aortic Valve – sound produced when close is
heard best at the 2nd INTERCOSTAL SPACE
RIGHT PARASTERNAL MARGIN (2 ICS
RPSM)
• The nature of the S2 can be influenced by the
respiratory phase
o EXPIRATION
▪ Only one S2 sound can be heard
▪ Simultaneous closure of the aortic and
pulmonary valves
o INSPIRATION
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▪ Physiologic splitting of the S2
▪ Wherein the aortic valve closes first
that the pulmonary valve and the
sound produced by the closing of aortic
valve is louder than that produced of
the closing of the pulmonary valve
except in patients with pulmonary
hypertension (paradoxical splitting od
S2)
Intrathoracic Pressure
• Pressure in thoracic cavity
• No direct communication between the atmosphere and
the thoracic cavity (normally air does not enter the
thoracic cavity)
• If chest wall has a hole, penetrating stab wound; air
comes in the thoracic cavity
• Normally, intrathoracic pressure is negative (below
atmospheric pressure). When inspiring, intrathoracic
pressure becomes more negative so there will be
distension at the lungs, heart, and blood vessels
o If right heart is distended blood coming from the
peripheral organs will increase; increasing also
the pressure in the right heart and decreasing
the pressure gradient slows down the closure of
the pulmonary valves
• If intrathoracic pressure is positive, equal or above the
atmospheric pressure, the lungs, heart, and blood
vessels will compress and eventually collapse
Which has a higher-pressure gradient between the atria
and the ventricles or between the ventricles and the
arterial system?
✓ Between the ventricle and arterial system
Which has the longer duration between the S1 and S2?
✓ S1
✓ AV valves closes slower since the pressure
gradient is lower between the atria and the
ventricles
Recap!
CLOSING OF CARDIAC VALVES against the PRESSURE GRADIENT
↑ pressure gradient = faster the cardiac valve to close
↓ pressure gradient = slower the cardiac valves to close
Normally, ↓pressure in the pulmonary circulation, but
↓↓ pressure in the right heart especially when it is relaxed
INSPIRATION
➔ Pressure in the thoracic cavity becomes more negative (if
negative, there is a suction effect to structures in the thoracic
cavity meaning there is distention of lungs, heart, and blood
vessels)
➔ If the heart is distended, there will be an increase blood flow in
peripheral circulation back to the right heart causing an
increase volume of blood in the right heart; increasing the
pressure
➔ Pressure difference between the right heart and the pulmonary
circulation decreases
Pressure difference of the ventricles and aorta is greater since the
pressure in the aorta is high so the valves close faster
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

• In fact, when semilunar valve close, they close is a ventricle increasing the left
SNAP position ventricular pressure and
distention of left ventricular
THIRD HEART SOUND (S3) wall causing left ventricular
• Coincides with rapid ventricular filling or filling of failure
blood in the ventricles o Incompetent or Insufficient Cardiac Valves
• Heard in some normal individuals and even in children ▪ Exemplified by prolapse mitral valve
with thin chest wall and also to patients suffering from ▪ Normally, if left ventricle contracts,
left ventricular failure mitral valve is closed to prevent
backflow
FOURTH HEART SOUND (S4) ▪ In prolapse, leaflets do not close
• Coincides with atrial contraction and can also be heard completely allowing backflow so there
in normal individuals will be a decrease ejection like in
stenosis
Normal • If the valve is stenotic, the opening becomes narrower
➔ PHYSIOLOGIC SPLITTING increasing the velocity of blood flow making it a
➔ Aortic valve closes first than the pulmonary valve turbulent blood flow and there will be an abnormal
sound. If the valve, on the other hand, in incompetent,
ABNORMAL backflow of blood also creates an abnormal sound or
➔ PARADOXICAL SPLITTING MURMUR
➔ Pulmonary valve closes first than the aortic valve
Damaged valve Type of lesion Timing of murmur
➔ Patients with PULMUNARY HYPERTENSION
AV valve (either Stenosis Diastole
Tricuspid/ Mitral Incompetent Systole
S1 and S2 valve)
• Usually heard Semilunar valve Stenosis Diastole
• But S4 can also be heard before S1 and S2 (either pulmonary/
aortic valve) Incompetent Systole

Accentuated S3 and S4 * diastole = ventricular relaxation

Systole = ventricular contraction
• Abnormal condition wherein there will be triplets of
sounds resembling the sound produced by horses called
Pericardium
gallop rhythm
Pericardial sac
Pathologic Heart Conditions • Made up of
connective
• Like infection in the heart that may damage the cardiac
tissue covering
valves
the membrane
• 2 types of lesions occurring in the cardiac valves:
of the heart
o Stenosis
• Less distensible
▪ The valves cannot open completely
because of the hardening of leaflets • Presence of this
▪ Compromising the blood flow entering will prevent the
and amount of blood to be ejected overstretching or sudden distention of the cardiac
▪ In the left heart, it compromises the muscle when the cardiac size increases
amount of blood to be ejected in the o Visceral Pericardium
peripheral circulation (compromised ▪ Membrane directly attached to anterior
perfusion of peripheral organs); there surface of the myocardium
will be pooling of blood in the left o Parietal Pericardium
atrium; increasing the left atrial ▪ When the visceral pericardium is
pressure and distention of left atrial reflected back
wall occurs • Pericardial Fluid – space
• Left atrial pressure increases between the two
and there will be pooling of membranes filled with 30cc
blood also in the pulmonary fluid that lubricates the
circulation since blood coming heart facilitating the
from the pulmonary circulation movement of the heart
enters the left atrium causing
pulmonary edema or
congestion
• In aortic stenosis, blood is
also compromised to
peripheral organs; there will
be pooling of blood in the left
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
V. MYOCARDIAL CELLS
• We have 2 myocardial cells
o Automatic Cells – capable of generating their own
action potential even without autonomic stimulation
o Non-automatic Cells
A. Automatic Cells (Structure Overview)
• Automatic: impulse generation and conduction
o Sinoatrial Node (SA Node)
▪ Aka Node of Keith and Flack
▪ Located at the junction of the superior vena cava
(SVC) with the membrane of the right atrium
(RA)
o Atrioventricular Node (AV Node)
▪ aka Node of Kent and Tawara
▪ located posteriorly on the right side of the
interatrial septum (separates RA and LA)
▪ Divided into 3 zones:
• Atrionodal zone (AN ZONE) – most proximal
• Nodal zone (N ZONE) - middle
• Nodal His zone (NH ZONE) – most distal;
attached to the bundle of His
Important to Remember!
Most DELAY in the transmission of impulses in the AV
node occur between the AN and N Zones.
Most of the AV BLOCK– block of transmission of AV
Node impulses occurs in N zone.
• Purkinje System
o Made up of: Bundle of His and Purkinje Fibers.
o BUNDLE OF HIS
▪ Located at the interventricular septum. Branches
out.
▪ Right Bundle Branch
▪ Left Bundle Branch: subdivides into left posterior
and left anterior fascicles.
▪ Tips of the Right bundle branch and left anterior
and posterior fascicles connect with the Purkinje
fibers mostly located at the cardiac apex but are
also present all throughout the ventricles.
Important to Remember!
SA NODE → AV NODE → BUNDLE OF HIS → RIGHT
AND LEFT BUNDLE BRANCHES → PURKINJE FIBERS
= AUTOMATIC CELLS OF THE HEART. ELECTRICAL.
• 3 Internodal Tracks
o Located between the SA node and AV node.
Facilitates the transmission of impulses between
the SA node and AV node
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▪ Internodal Tract
of Bachman
(Anterior)
▪ Internodal Tract
of Wenckebach
(Middle)
▪ Internodal Tract
of Thorell
(Posterior)
B. Autonomic Cells: Impulse Generation and
Conduction
• Impulse generation and conduction. Hearts Conduction
system.
• Capable of spontaneously generating its own action
potential independent of extrinsic nervous stimulation
• Are MODIFIED myocardial cells, it is independent of
automatic stimulation.
Characteristics of modified cardiac muscle cells
1. They contain fewer striations
2. Boundaries between cells are indistinct (hard to
separate sarcomere from the other sarcomere)
3. Fewer Mitochondria (Not specialized for
contraction).
In a normal heart, all action potentials are generated by the
Sinoatrial node (SA NODE).
So, all impulses that determine the heart rate and heart
rhythm is from the SA NODE. The SA NODE is referred as
the Primary pace maker of the heart. Because it has the
highest frequency of discharge of action potentials (60-
100 action potentials per minute)
SA NODE: 60-100 per minute
AV NODE: 40 - <60 per minute
Purkinje Fibers: 15 - <40 per minute
Overdrive Suppression
• Increase frequency of discharge of an action potential
from an automatic cell will diminish the automaticity of
other automatic cells.
“Pakinggan Mabuti. Intindihin”
Examples:
• The automaticity of cell B (AV node) diminishes when it
receives impulses from cell A (SA node) at a frequency
that is greater than its own).
• During complete AV block, there will be no impulses
from the SA node that will generate impulses to the
ventricles and this will remain quiescent for 5-20
seconds after which it will escape to suppression and the
Purkinje fibers will be activated and will generate its own
impulses.
Normal Sinus Rhythm (NSR) – the Rhythm determined by
the SA Node.
Potential / Latent Pacemakers – Other automatic cells (AV
Node, Bundle of His, Purkinje Fibers) in NORMAL conditions
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
they DO NOT generate action potentials or impulses. In
SOME ABNORMAL conditions, they can be activated to
create their own impulse or action potential.
C. Non-Autonomic Cells: Contraction
• Atrial muscle (wall)
• Ventricular muscle (wall)
Q: If you cut the autonomic nerve of the atrial and ventricular muscle,
will the heart stop beating?
A: No, because the automatic cell will generate its own action
potential. The role of Autonomics is to regulate the activities of both
automatic and non-automatic cells. JUST TO REGULATE.
VII. PROPERTIES OF MYOCARDIAL CELLS
A. 1ST PROPERTY: AUTOMACITY (Generation of
Action Potential)
• 2 Types of Action Potentials Generated in the Heart:
o Fast Response – AP generated in the atrial
ventricular muscle, Bundle of His, and Purkinje
Fibers
o Slow Response – AP generated in the SA
node and AV node (both automatic cells)
B. Overview of Characteristics of Slow Response
1. Long duration – occurs in 200-300 ms. (In comparison
to the action potential of skeletal muscles which is only
5-30 ms)
2. Phase 4 – Resting membrane potential (RMP) wherein
the cell is less negative (-60mv). Unstable and not
completely rested; wherein there is a presence of slow
rise in membrane potential; Phase 4 is called Pre-
potential OR Pacemaker potential OR Slow diastolic
depolarization.
3. Phase 0 – Actual depolarization. Also, not a straight
line and is inclined. Depolarization in an automatic cell
occurs SLOWLY.
4. Peak is not pointed / No spike – No involvement of
Fast voltage gated sodium channels.
5. Repolarization – There is no Phase 1; instead, the initial
phase of repolarization occurs in Phase 2 followed by
Phase 3.
6. Hyperpolarization – RMP goes below
-60mv.
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C. IONIC BASIS FOR THE DIFFERENT PHASES OF
THE AUTOMATIC CELLS
• RMP is less negative (-60mv)
o Membrane is less permeable to potassium
(less K efflux)
o Amount Potassium efflux determines the
electronegativity of the RMP; the more
permeable it is to K the more K to go out
and RMP will become more negative
• Slow rise to membrane potential
o Membrane is more permeable (leaky) to
Sodium
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
are more Na leak channels, membrane potential
increases.
• When it reaches -50 mv, opening of transient
calcium-sodium channels: making the MP more
negative
• When it reaches -40 mv (CRITICAL FIRING
LEVEL), opening of long-lasting calcium-sodium
channels; main factor responsible for SLOW
PHASE 0 of depolarization
Phase 0
• Depolarization. Somewhat inclined, depolarization
occurs slowly
• No spike because fast voltage gated sodium
channels have no
role and also because of SLOW LONG LASTING CALCIUM
SODIUM CHANNEL (main factor)
Phase 2 and 3
• Repolarization. Inclined, occurs slowly, there is also
hyperpolarization like in the skeletal muscle
• Ca influx and K efflux
• Phase 2: The amount of K efflux > Ca Influx;
tendency is still to repolarize but it is slow
• Not pronounced plateau (Ca that goes in is less than
the K efflux)
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

• At the end of Phase 2, K channels remains open and F. Non-Automatic Cardiac Muscle Fiber AP
causes the start of Phase 3 (final phase of • Aka Fast Response Action Potential
repolarization)
• K channels remain open for a long time the (K keeps
going out) the membrane potential becomes more
negative than RMP which results to
Hyperpolarization.
• When the voltage gated potassium channels close,
the RMP will be restored (-60 mv). But it is unstable
of the slow rise in membrane potential

It is called Slow response because of its slow

depolarization at phase 0. Its phase 0 depends on the
opening of the LONG-LASTING VOLTAGE GATED
CALCIUM CHANNELS.

Post repolarization refractoriness

• The duration is the same of that of the slow
response action potential

Why is that they have the same duration but different

action potential?
• In slow response, there is both slow
depolarization and repolarization
• In non-automatic fiber action potential,
depolarization is rapid, but repolarization is
slower.
Proper stimulus intensity can re-excite the membrane but, for
G. Difference between Skeletal and Cardiac Muscle
the automatic cell we have this something we call post
repolarization refractoriness, this means that even if it is
already repolarized it is still difficult to re-excite. (Puwede
mastimulate pero mahirap)

D. Parasympathetic/ Cholinergic/ Vagal Stimulation

• Originating from the medulla oblongata
• Cranial Nerve X
• NTA released is Acetylcholine (ACh)
• Vagus with release Ach binds with muscarinic 2
(M2) receptors in SA node resulting to
• ↑cAMp ↑K conductance =
HYPERPOLARIZATION/ INHIBITORY
• There is hyperpolarization, prolonged duration of
pre-potential, and decreased slope of AP, hence,
will elicit inhibitory responses

E. Sympathetic Stimulation
• Coming from T3, T4, and T5 • Similarities:
• NTA release is Norepinephrine (NEP) o Both have RMP that is about -90 mV
• NEP will bind to Beta 1 receptor in the SA node o Both have Phase 0 Depolarization that is a
resulting to straight line (rapid)
• Differences:
• ↑cAMp ↑Ca conductance = EXCITATORY
o There is a big difference between the
• Membrane potential is less negative, shortened repolarization and the duration
duration of the pre-potential, quickly depolarizes
• The slope of the AP became more steep
→ EXCITATORY/ STIMULATORY

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
H. Ionic Bases
Recap:
• The RMP is stable at -90 mV like in the skeletal
muscle (straight line) membrane is highly
permeable to potassium and slightly permeable to
sodium
• Phase 0: Depolarization
o Straight line; occurs rapidly due to opening
of fast voltage gated Na channels. Na
influx reaches threshold voltage of -65
mV (CFL) resulting to depolarization and
when it reaches -20 mV, it will open up
slow, long lasting L voltage gated Ca
channels → Ca influx (main factor for
depolarization in Na influx)
o Has spike (Na channels closes, K
channels open, Ca channels are still open)
• Phase 1: Initial phase of repolarization
o Prominent; initial phase of repolarization
brought about by slow voltage gated K
channels
• Phase 2
o More flat plateau and prolonged
compared to that of the SA node
o The amount of K+ that goes out is
equal to the amount of Ca++ that goes
in.
o No electrical activity (Isopotential)
o 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
o No hyperpolarization because
repolarization is long
o Although the K+ channels remain open for
a long time, because of the plateau, it is
open for long period of time thus it does
not reach hyperpolarization
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• Phase 4
o -90 RMP is re-established/ restored
o The increase membrane permeability to
potassium is responsible for the -90 mV
RMP
• Upon stimulation, there are some fast voltage-gated
sodium channels that will open allowing sodium influx
• The membrane potential will be less negative, until it
reaches -65 mv → the critical firing level
• When -65 mv is reached, it will open up more fast voltage-
gated sodium channel that will allow large amount of
sodium to enter for it to depolarize rapidly
• But before the membrane completely depolarizes, at -20
mv, the L-voltage gated calcium channels open again
• Though the main factor responsible for the fast
depolarization is the sodium influx, at -20, the calcium
channels still open
• At the peak of the spike, the fast voltage-gated sodium
channels will close, with the L-voltage-gated calcium
channels still open. Slow voltage-gated potassium
channels will now open, this will bring about Phase 1, the
initial phase of repolarization
• However, repolarization is slow because of the opened
long lasting calcium channels at -20 mv.
• At Phase 2, there is equal calcium influx and potassium
efflux. The plateau is flatter and longer in duration. As
compared with automatic cell at Phase 2, there is more
potassium efflux than calcium influx that is why its plateau
is less flat and shorter in duration.
• At the end of Phase 2, only then the long-lasting calcium
channels will close leaving only the potassium channels
open allowing potassium efflux.
• Since the potassium channels have been open since the
start of the peak, it no longer reaches hyperpolarization
and eventually closes. This restore the RMP of -90 mv.
• In the figure A and C, the ventricular and atrial
muscle have both fast responses. The main
difference is the plateau in Phase 2. The
musculature of the atrial wall is thinner compared
to the ventricular wall. Thus, the calcium influx is
greater in the ventricle the force of contraction is
stronger compared to the atria.
• Figure B is for the automatic cells.
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

I. Periods of Refractoriness • Unlike the skeletal muscle, it needs to be

completely depolarized before it contracts. In the
cardiac muscle, once it starts to depolarize, the
contraction also begins.
• The peak of contraction corresponds to Phase 2
where there is still calcium influx.
• The relaxation begins at Phase 3, the final phase
of repolarization.
• When you apply a 2nd stimulus to the cardiac
muscle cell where it is beginning to contract, no
action potential or 2nd contraction will occur
because the membrane is still in absolute
refractory period
• From the beginning of depolarization until the end
• When you apply a 2nd stimulus at the peak of
of Phase 2, the membrane of the cardiac muscle
contraction, still no 2nd action potential or 2nd
cell is absolute refractory. No amount of stimulus
contraction will occur because the membrane is
intensity will be able to re-excite and already
still in absolute refractory period
excited cardiac muscle cell membrane because the
• A 2nd action potential or 2nd contraction will occur
voltage-gated sodium channels are already open.
when the muscle is relaxing.
You cannot re-open or re-activate voltage-gated
• One property of the skeletal muscle is tetanization,
sodium channels that are already open.
successive stimuli with increasing frequency is
• In Phase 1 and Phase 2, the voltage-gated sodium
applied. The individual twitches will fuse together.,
channels are already close, why can’t it be re-
there will be sustained or tetanic contraction. In a
opened? → Because these are voltage-gated
normally functioning heart, even if you apply
channels that can be activated at a certain voltage
successive stimuli of increasing frequency, there
that is near the CFL which is -65 mv.
will be no sustained or tetanic contraction because
• The beginning of Phase 3 until the -90 mv RMP is
of the very long duration of period of refractoriness.
restored is the relative refractory period. Wherein a
stronger stimulus intensity will now be able to re-
excite a cardiac muscle cell membrane.
• In Phase 3, the voltage is near the CFL (-65 mv),
so you can now re-open the voltage-gated sodium
channels.
• The period of refractoriness is from the beginning
of the depolarization until the end of Phase 3.

•
When the HR is 75/min, the duration of the action
potential is 0.25 sec or 250 milliseconds. In the
skeletal muscle, the duration is very short. There is
also a huge difference between the duration of the
ARP and RRP of the cardiac muscle and skeletal
muscle. Even if the HR is increased to 200 bpm,
there will still be no tetanic contraction because
there is still a long duration of refractoriness.
• Importance of long period of refractoriness
o One important factor that determines the force of
ventricular contraction is how much ventricular
• The white line is the entire duration of wall is stretched before it contracts.
refractoriness (absolute and relative), the red line is o More stretched = Stronger force of contraction =
the mechanical response of the cardiac muscle. Greater output
• Upward is contraction; downward is relaxation. o The amount of blood that is present in the
ventricle will stretch the ventricular wall. The
ventricles fill with blood when they are in the
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

relaxed state. So longer period of refractoriness,
longer relaxation period, so more blood will fill the
ventricles, the ventricular wall will be stretched
more, there will be stronger force of contraction
and greater output.
o The main source of energy for cardiac muscle
contraction is oxidative metabolism. Oxygen is
required because the contraction is continuous.
The coronary arteries will supply blood with
oxygen to the cardiac muscles (perfusion).
o Coronary arteries are embedded in the thick wall
of ventricles. When the ventricles contract, the
coronary arteries are compressed. That is why
during systole, the perfusion in the cardiac
muscles is poor.
o The duration of diastole is longer, the ventricular
muscle is relaxed for an extended period, the
period of refractoriness is also extended, so the
perfusion and oxygen flow is good during diastole.
B. 2ND PROPERTY: RHYTHMICITY
• in a normally functioning heart, the heart rate and
rhythm are determined by the SA node (normal
sinus rhythm)
• SA node - generates impulses at regular intervals
• ECG – measures/ records the electrical activities of
the heart (depolarization and repolarization of the
atria and ventricles) all are recorded in an ECG
paper
P wave – represent atrial depolarization
QRS complex – represents ventricular depolarization
T wave – represents ventricular repolarization
• Look at the NSR first (figure A). Look at the highest
wave (R) and count the number of squares of each
successive wave
• In figure A, there are 7 or 8 squares between each
successive tall waves
• To determine that if the rhythm is determined by
the SA node is it should be regular--the distance
between each successive tall waves should be the
same
• Figure B. The interval between tall waves
shortened (5 waves)
• Increase in rate, however, the distance between
tall waves is the same = regular rhythm
• The rate and rhythm is still determined by the SA
node. But since the rate increased, it is called
sinus tachycardia (happens where there is
sympathetic overstimulation)
• Figure C. Vagal Overstimulation.
• Increased distance and still has the same number
of squares in between tall waves
• Decrease in rate, rhythm is still regular, hence still
determined by the SA node, it is called sinus
bradycardia

Sick Sinus Syndrome (SSS)

• Sinus Tachycardia
• Sinus Bradycardia

Arrythmia – abolished normal sinus rhythm (rate and

rhythm are no longer determined by the SA node)

C. 3RD PROPERTY: CONDUCTIVITY

• We will now trace the direction of impulse
transmission in the heart

Conduction Pathway:
1. SA node - heart rate and rhythm are determined. where
impulses are generated. Located at the junction of superior
vena cava membrane of RA. Impulses are then transferred
to…

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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
2. AV node - located posteriorly on the right side of the
interatrial septum. Facilitated by the presence of three
internodal tracts:
a. Anterior internodal tract of Bachmann
b. Middle internodal tract of Wenckebach
c. Posterior internodal tract of Thorell
There is direct transmission of impulses from the SA
node to the right atrium
3. Transmission of impulses from right atrium to the left
atrium and is facilitated by the presence of many gap
junctions (when impulse travels from SA node to the AV
node, the right and left atria will depolarize)
Will the right and left atria depolarize at the same
time or will one atrium depolarize and contract a little
ahead to the other atria?
The RIGHT ATRIUM will depolarize a little ahead simply
because there is a direct impulse transmission from the
SA node to the right atrial muscle cells the direction of the
depolarization in atria will be from the base where SA
node is located to the AV node and the direction of
repolarization in atria will follow that of the flow of
depolarization in the atria
• THE FIRST PART TO DEPOLARIZE WILL BE
THE FIRST PART TO REPOLARIZE
• THE LAST PART TO DEPOLARIZE WILL BE
THE LAST PART TO REPOLARIZE)
• When impulse reaches the AV node, there will be
slowing down in the velocity of impulse conduction
called the AV NODAL DELAY which take place
between the AN and N zones of AV node
• Reasons for AV nodal delay:
o Presence of small fiber diameter
o Fewer gap junctions
o Increase resistance to impulse conduction
o Slow Depolarization – opening of the voltage
gated Ca channels (the impulse does not quickly
go to the ventricles, it stops temporarily in the AV
node)
• Importance of AV nodal delay:
o ensures that the atria and ventricle will not
contract at the same time
o Allow more time for better ventricular filling (for
ventricles to remain at a relaxed stated)
➔ Because of the slow impulse conduction at the AV
node, most of the HEART BLOCKS or AV
BLOCKS (not referring to the heart blocks that
decreases the blood supply in coronary arteries but
the blocks in impulse conduction) occurring in the
AV NODE particularly between the atrionodal (AN)
and nodal (N) zones
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• From the AV node, the impulse will travel to the
bundle of His, located in the interventricular septum
(left to right bundle branches) → Purkinje fibers
present mostly at the cardiac apex → Ventricular
depolarization
Will the two ventricles depolarize and contract at the
same time?
No, LEFT VENTRICLE will depolarize first followed by
Right.
The two ventricles will CONTRACT at the same time also
because of the SYNCITIAL ARRANGEMENT of the
ventricular muscle fibers
The RIGHT VENTRICLE will eject blood first before the
left ventricle because the right ventricle will pump blood
against a LOWER RESISTANCE to the pulmonary
circulation than the left ventricle which will pump blood
against a HIGHER RESITANCE to the systemic
circulation
The transmission of impulses in the ventricles will not stop
at the cardiac apex but will continue to the Postero-Basal
part of the ventricles (order of depolarization: Antero-basal
to apex to postero-basal)
• THE LEFT WILL DEPOLARIZE AHEAD OF
THE RIGHT
• THE TWO CONTRACTS AT THE SAME TIME
• THE RIGHT VENTRICLE WILL EJECT BLOOD
FIRST BEFORE THE LEFT
*Only small difference
Will repolarization follow the direction of depolarization in
the ventricle just like in the atria?
No, OPPOSITE DIRECTION (order of repolarization:
postero-basal to apex to antero-basal)
In the ventricles,
• THE FIRST PART TO DEPOLARIZE IS THE
LAST PART TO REPOLARIZE
• THE LAST PART TO DEPOLARIZE WILL BE
THE FIRST PART TO REPOLARIZE
This is due to the thickness of ventricular walls. When
ventricles contact, the conduction system also
compresses so the free part will be the one to repolarize.
A. Conduction Speed in Cardiac Tissue
Conduction Rate
(meters/ sec)
SA node 0.05
Atrial muscle 1
AV Node 0.05
Bundle of His 1
Purkinje System 4
Vent muscle 1
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
• Conduction speed is SLOWEST at the AV node
(not the same as SA node since SA node functions
to generate impulses and AV node function
primarily to conduct impulses like the Purkinje
fibers)
• Conduction speed is FASTEST in the Purkinje
fibers (opposite to AV node) because of larger
fiber diameter and more gap junctions so there is
LOWER RESISTANCE to impulse conduction
Important to Remember: Remember the location of the AV
node. It is through only the AV node that impulses from the
SA node can reach the ventricles. If the impulses transmitted
from the AV node is blocked, the impulse from the SA node
will no reach the ventricles.
1st DEGREE HEART BLOCK: INCOMPLETE HEART BLOCK
• Each P wave is still followed by a QRS complex so
it also 1:1 but has longer PR segment
• Atrial contraction is equal to ventricular contraction
but the ASVS interval is long
• All impulses from the SA node are still transmitted
to the ventricle so that the ration of atrial to
ventricular contraction is still 1:1
• Only problem here is the prolonged duration of the
PR segment or the ASVS interval
• Also called ASVS interval
2ND DEGREE HEART BLOCK: INCOMPLETE HEART BLOCK
• PPQRSP PPQRSP
• Atria will contract twice while ventricle contract once
• Not all impulses from the SA node will reach the
ventricles
• But since there are impulses that can reach the
ventricles, it can be still called incomplete heart
block
• The ration of atrial to ventricular depolarization/
contraction is 2:1 or 3:1
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3rd DEGREE HEART BLOCK: COMPLETE HEART BLOCK
• No impulses from the SA node will reach the
ventricles
• The atria will contract normally in response to
impulses generated from the SA node but there will
be no impulses in the ventricles for 5-20 seconds,
there will be no contraction in
the ventricles
• No suppression to Purkinje fibers since there are
no impulses
from the SA node reaching the ventricles causing
the activation of Purkinje fibers after 20 seconds
and it will generate its own impulses
• Atria will contract in response to impulses
generated from the SA node (normal rate and
rhythm) while the ventricles will also contract in
response to impulses generated from Purkinje
fibers but only 15-40 impulses per minute
whereas the SA node is 70-80 impulses per
minute
• 5-20 seconds is very important because in some
individuals this
5-20 seconds that the ventricles will not contract,
no cardiac output, no blood flow to brain will cause
light headedness, fainting and eventually loss of
consciousness called the STOKES- ADAMS
SYNDROME
D. 4th PROPERTY: CONTRACTILITY
Characteristics of Cardiac Muscle Cell:
1. Involuntary
• The activities of cardiac muscle cells are not
regulated by the cortex. It is instead regulated by the
autonomic nervous system.
2. Smaller
• Compared to the skeletal muscle cell it is smaller in
size.
3. Mononucleated/ Binucleated
• Skeletal muscle cell is multinucleated.
4. Striated (Functional Syncytium)
Just like skeletal muscle. Muscle fibers are
individually separated from one another. Each muscle fiber
is surrounded by the sarcolemma. In the sarcoplasm, you
have many nuclei complete with all the other intracellular
organelles. The functional unit is still the sarcomere.
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

Contractile Proteins
Proteins seen in the skeletal muscle cell are also present in
the cardiac muscle cell.
• Myosin
• Actin, Tropomyosin, Troponin
• Meromyosin, C Protein
• Nebulin
• Alpha Actinin
• Tropomodulin
• Titin
What differentiates the cardiac muscle cell from the
skeletal muscle cell is that: 5. Elastic Tissue
In the cardiac muscle, the sarcolemma or • That’s why atrial and ventricular wall can be
membrane branches out to reconnect with the membrane of stretched.
the next muscle fiber. So that if the cardiac muscle cells are
arranged in bundles and there’s a connection in the 6. Connective Tissue
sarcolemma when one muscle force generated in one Presence of this in the pericardial sac prevents
muscle fiber it can be transmitted to the other muscle fibers overstretching of the cardiac muscle.
as well. 7. More mitochondria and active capillaries
The main source of energy for cardiac muscle contraction is
⮕The blue lines are the Z line. In the cardiac muscle cell,
oxidative metabolism.
present at your Z line is your intercalated disks.
8. Sarcopalsmic Reticulum Transverse Tubular System
• The sarcoplasmic reticulum is not as well
developed as in the skeletal msucle. SR in cardiac
muscle cannot store large amounts of calcium ions
that can provide for maximum muscle contraction.
There has to be another source of calcium which is
the extracellular fluid but the main source is still the
sarcoplasmic reticulum.
• The transverese tubular system here is well-
developed.

⮕Intercalated disks provide mechanical connection,

electrical connection between individual msucle cells. It’s
mechanical connection is in the form of tight junction.
Example, if you pull one muscle fiber it can also pull the next
because they are connected in the Z line. Electrical
connection in the presence of many gap junctions. Gap
junctions are channels that will allow ions to flow freely from
one muscle fiber to the next.
Active capillaries needed in cardiac muscle for
⮕If you have a bundle of cardiac muscle fibers when an oxygen supply.
action potential is generated anywhere in a bundle it can be
readily transmitted in all directions and that will cause the
whole bundle to depolarize, to contract as a single unit. That
is what we call a syncytium.

⮕In the cardiac muscle, you can’t observe individual

twitches like in skeletal muscle because there is a syncytial
arrangement of the cardiac muscle fibers so when it contract
it is by bundle. Like when the two atrias or two ventricles
contract, they are synchronous.
On the right side is the sarcolemma, the
Importance: If they contract synchronously, the force of
invaginations, and T-tubules (orange structure)
contraction is stronger.
Synchronous contraction = Synchronous relaxation

⮕Myocardial tissue is anatomically striated but it is a

functional syncytium.
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART
Excitation-Relaxation Coupling
⮕Present on the Sarcolemma:
• Sodium-Potassium pump- pump 3 Na ions out and
2 K ions in. The energy directly comes from
hydrolysis of ATP, this is called Primary Active
transport.
• Calcium pump- a uniport. Pumps calcium out. The
energy directly comes from hydrolysis of ATP, this
is called primary active transport.
• Sodium-Calcium exchanger- Sodium’s activity will
come first releasing 3 Na out and 2 K in that will
create a concentration gradient for Na (marami sa
labas, konti sa loob). This will fuel the actvity of Na-
Ca exchanger. 3 Na in, 1 Ca out. Since this will
depend on Na-K pump it is secondary active
transport.
⮕ Invagination in the sarcolemma will form the T-tubules.
Na-Ca exchanger is also present. We also have the
dihydropyridine receptors.
• What will activate and what will happen if they are
stimulated?
o Stimulated if there is a change in the
membrane potential (electrical) and when
stimulated it will open up the voltage-gated
long lasting Ca channels that will allow Ca
influx.
⮕ Inside are:
• Sarcoplasmic reticulum that will store and release
Ca ions. Presence of ryanodine receptor on its
membrane. The relationship of DHPR and RYR is
electrical-mechanical. Stimulation of DHPR will
cause conformational change stimulating RYR.
Electrical-chemical, when DHPR is stimulated there
will be a Ca influx then the Ca will bind to RYR. Only
then will this Ca-gated channels on the membane of
SR will open to allow Ca stored to be released into
the cytoplasm.
• SERCA (Ca pump) – SER Ca ATPase; it will
actively transport Ca back into the SR. Energy is
directly provided by hydrolysis of ATP, it is called
primary active transport.
• Phospholamban- function is to inhibit SERCA
• Myofilaments that contain contractile proteins
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⮕ Excitation
• An impulse is generated from the SA node.
Transmitted to the cardiac muscle in the atrial wall
ventricular wall.
• RMP = -90 mv
• When action potential is received, Voltage-gated Na
channels will open, Na influx, until the membrane
potential reaches the critical firing level which is -65
mv. When reached, more Voltage-gated Na
channels will open, more Na influx, the more the MP
will become less negative.
• When it reached -20mv, DHPR will be stimulated in
the T-tubule. Long lasting voltage-gated Ca
channels will open, Ca influx. Some Ca will bind
immediately to Tropnin C. Some will bind with RYR
on the SR membrane that will open up Ca gated Ca
channels that will allow stored Ca to move out and
will also bind with Troponin C.
• High Calcium-Troponin C complex will initiate the
process of cardiac muscle contraction. The
mechanism of which is exactly the same as that with
the skeletal muscle. Ca-TropC will remove
Troponin-Tropomyosin complex that initially covers
the active site of actin that will now form cross
bridges with the myosin head. One myosin head has
ATPase activity, there will be a breakdown of ATP,
then powerstroke, detachment, myosin head will
reattach to next active site of actin, powerstroke,
detachment. There is a repeated attachment-
powerstroke-detachment that will cause the thick
filament to slide against the thick filament causing
increased overlapping of thick and thin filaments.
Meaning the cardiac muscle contracted. Same as
skeletal the only difference is the relationship of
DHPR and RYR.
• Following depolarization is contraction,
depolarization is followed by repolarization,
repolarization is followed by muscle relaxation. For
it to relax, you have to remove Ca from Trop C. So
that troponin can bind again a tropomyosin and
cover the active site of actin.
• Acidification of medium of cytosome will decrease
the affinity of Ca with Trop C. Some Ca will be
actively trasnported back into the SR by the action
of SERCA. Some will be actively transported out into
the ECF by the activity of Ca pump in the
sarcolemma.
• To restore –90mv, Na-K pump will release 3 Na out
and 2 K in creating a concentration gradient for Na
that will now fuel the activity of Na-Ca exchanger
that will pump 3 Na in and 1 Ca out. Muscle will now
relax.
Take note: There are a lot of factors that will make Ca go out
the sarcolemma, Ca pump and Na-Ca exchanger.
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 CARDIAC PHYSIOLOGY: FUNCTIONAL ANATOMY OF THE HEART

⮕ In the cardiac muscle cell membrane although the affinity

of Ca to Ca pump is higher compared to Na-Ca exchanger
there are more Na-Ca exchanger that Ca pump in the
sarcolemma. So that the main means by which Ca is
extruded out of the myocardial cell is through the activity of
the Na-Ca exhanger. Although there are 2 sources of Ca, the
main source is still SR. Although lacking and will not go out
if there’s no Ca coming from the ECF that will bind with RYR.

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