Lecture 1:

• If there is no troponin-tropomyosin —> no

calcium binding to troponin C
• Smooth muscle = gut tube, bladder, blood
vessels

• Don’t have troponin C &

tropomyosin
• When you contract a smooth
muscle it pulls in from di erent
sides
• When it’s activated the dense
bodies move closer together
• Green line = sphincters —> have high force —> contracted • When skeletal muscle isn’t functioning —>
• Food in —> sphincter relax & open up —> food goes in —> re-contract it’s relaxed
for it to come back again • Some smooth muscle have tone —> their
• Blue line = Blood vessels —> partially contracted —> you can either normal state is to be contracted —> i.e
relax it or contract it blood vessel
• Contract —> to decrease blood ow in a particular area • Blood vessels are always contracted —>
• Red line = esophagus & bladder —> when food enters the esophagus blood vessels can relax & dilate
—> it stimulates contraction of smooth muscle above the bolus to push • Sphincters in the digestive system —> i.e
it down lower esophageal sphincter is highly
• Esophagus is normally relaxed but when food enters it contracts —> & contracted to prevent the contents of the
relaxes again to allow the next bite to come down stomach (acidic) from back ow —> can
• Purple line = stomach & intestines —> phasically active —> intestines cause heartburn if it’s forced up
contract & relax —> segmentation —> helps break it down into smaller • The normal function of the sphincter is to
pieces —> greater surface area for digestive enzymes to work on be relaxed when you need it to

• Skeletal muscle —> Ca comes in & binds to

troponin C
• Smooth muscle —> Ca comes in & changes
smth which lead to muscle contraction

• In smooth muscle we have sarcoplasmic reticulum which is full of high Ca conc —> good Ca store
• If we depolarize smooth muscle —> Voltage dependent channels will open —> Ca can come in —> & cause contraction
• RYR channel on SR —> Ca binds to RYR channel on smooth muscle —> opens it & release more Ca —> process known
as Ca induced Ca release
• Depolarizes cell —> open voltage dependent channels —> Ca comes in —> stimulate SR to release more Ca —> elevate
Ca levels
• We can also have agonist bind to its receptor & activate the G protein —> cause production of IP3 —> IP3 stimulate the
Ca channel on SR to open —> Ca moves out —> increase Ca concentration inside the cell
• In summary, we can elevate Ca through major mechanisms:
1. Via Ca channels on the membrane
2. Via Ca induced Ca release from SR
3. Via mechanisms such as IP3 which open the Ca channels on the SR
 • MLCK is found in myosin —> activates myosin

• Ca binds to a protein in the cell called

Calmodulin —> binds to Ca &
modulate the functions of the smooth
muscle
• Calmodulin activates myosin light
chain kinase

• MLCK phosphorylates the regulatory

light chain
• Myosin regulatory regulates whether
you’re regulate or not

• When you din’t have activation of this light

chain —> the binding sites of the myosin are
head are covered —> you can’t bind
• Skeletal muscle = the heads are energized the
actin that has binding sites that are covered
• Smooth muscle = there is no troponin &
tropomyosin
• The amount of myosin light chains or the
amount of myosin molecules whose light • When the light chain is phosphorylated it then
chains have been phosphorylated depends opens up the actin binding sites —> & then myosin
on the concentration of myosin light chain can bind to the actin
kinase • If it’s not phosphorylated —> the actin binding sites
• The amount of MLCK depends on Ca will not open / not available to bind to actin
• Ca comes in —> Ca binds to Calmodulin —> elevates MLCK —> MLCK phosphorylates myosin leading to —>
contraction

• Relaxation = less actin binding sites

on the myosin heads available —>
less actin-myosin interaction —>
which causes relaxation —> less force
produced

• If we de-phosphorylate it —> get red of the phosphate —> changes

the conformation —> actin-binding sites are no longer available to
bind to actin
 • Enzyme MLC phosphatase
dephosphorylates the myosin —> it
will then shift myosin-p to simple
myosin —> will cause simple
relaxation

• More phosphorylated myosin —>

more actin-binding sites on the
myosin head able to bind —> more
cross-bridges moving —> more
force

• MLCK amount can be changed by

elevating Ca levels
• MLC phosphatase takes the phosphate o the myosin —>
causes relaxation
• If we inhibit MLC phosphatase (less relaxation force) —> will
take less phosphates o myosin —> more myosin
phosphorylated —> more contraction
• Increasing the amount of Rho —> inactivates myosin
phosphatase —> less myosin phosphatase —> more binding
sites available —> more binding —> greater force —>
contraction

• Increase MLCK —> Increase contraction

• Decrease MLCK —> decrease contraction &
increase relaxation
• Increase MLCP —> Increase relaxation
• Decrease MLCP —> Decrease relaxation &
increase contraction

• Shut the channels —> No

Ca coming in —> less ca
stimulating Ca release
from the SR —>
decreases the
intracellular Ca levels —>
less Ca2+/calmodulin —>
less activated MLCK —>
less contracted muscle
• L-type ca channel —> activated by voltage —> if it is stimulated —> Ca comes in —> elevated Ca levels —> also stimulates
Ca release from the SR —> Ca released from SR can be stimulated by increase in IP3 —> Increase in IP3 is stimulated by
release of Gq-R —> Ca binds to Calmodulin —> increase levels of Calmodulin —> activate MLCK —> leads to
phosphorylation of the myosin head —> contraction
• Agonist binds to its receptor —> Activation of cAMP inhibits MLCK—> less phosphorylation —> relaxation
• Another way of inhibiting is by NO —> produces cGMP —> activates MLCP —> more MLCP —> more relaxation
Recitation:

• Cardiac Muscle —> pumping

blood
• Glycogen —> energy —> ATP
for contractions
• When a cardiac muscle
contracts it shortens

Cardiac muscle has:

• lots of sarcomeres joined together
• Lots of mitochondria —> to produce energy

• The cells are connected together by intercalated discs —> coordinated

contraction
• When a single cardiac muscle cell contracts —> it pulls on its neighbor
& pull on the intercalated discs —> the heart gets smaller —> pushes
the blood out
• Gap junctions: ions & uid go through the gaps
• When you depolarize one cardiac muscle the ions move through the
gap junctions to the next muscle
• Gap junctions allow depolarization to move from cell to cell

• Sacromeres —> thick & thin laments, Z lines

• Has troponin C & tropomyosin
• Ca comes in & binds to troponin C & moves it away —> muscle contraction
• Ca goes down & cause Ca release from the SR
• More mitochondria in cardiac muscle —> because cardiac muscle uses aerobic respiration to produce ATP
• A lot of blood supply to the heart muscle —> to supply the oxygen to produce ATP —> because the heart uses a lot of
ATP —> contracting all the time
• There is no physical connection between the voltage dependent Ca channel & RYR
• What you need for the cardiac muscle to contract is for the Ca to come from outside (ECF)
• When you open the channel —> the Ca comes in through the channel —> Binds to RYR channel —> opens & Ca
comes rushing in
• This is known as Calcium induced calcium release
• Wave of depolarizations comes through by two ways:
1. Electrical Conducting system of the heart
2. From its neighbor through gap junctions
• Depolarization moves along down the T-tubule —> open the voltage dependent Ca channels —> Ca comes in RYR
channel opens
• Ca has to come in which means you must need extracellular Ca
• The more Ca that comes in —> the more Ca that gets released from the SR —> the greater the contraction
• Cardiac muscle has Na-Ca exchanger & Ca pump
• When Na-K pump is inhibited —> builds up Na inside the cell —> inhibit the Na-Ca exchanger —> excreting less
Ca —> Ca stays in the cell & builds up in SR —> increases the heart pumps
 c

• The greater the force of

contraction —> the more blood
you pump

• If we increase the amount of blood in the heart we stretch the heart —> heart contract with more force
• Ventricular end-diastolic volume: volume in ventricle prior to the ventricle contracting
• If you increase myosin overlap between the thick & thin lament —> you will get a greater force of contraction
• Straight volume: amount of blood you pump out in each beat
• More forceful contraction —> amount of blood pumped increases
• Greater the force —> greater the blood you pump
• As we increase stretch (stretch the heart muscle) —> we increase the force we produce (why?) —> because we have better
myo lament overlap & greater force of contraction
• At rest the heart is lled with approx. 135 ml of blood
• If you put more blood in to the heart & stretch it —> it’s going to increase force of contraction —> push more blood out —> force
it around the body
• When you exercise —> the amount of blood pumped through increases —> the blood returning to the heart increases
• More blood returning to the heart —> your heart gets bigger —> heart contracts harder —> more blood out
a

• With any given amount of stretch,

norepinephrine present —> producing
force & ejecting more blood
• Norepinephrine: more Ca —> more active
sites —> more interaction —> more force
—> contractility
• When you increase the force of contraction
—> you’re increasing the intracellular Ca
levels —> this is called increase in
contractility
Lecture 2:

• Cardiovascular physiology —>

pressure & blood ow
• By controlling blood pressure
you’re controlling blood ow
• Vascular = blood vessels

• Red —> oxygenated blood

• Blue —> deoxygenated blood
• Left ventricle pumps blood out of the aorta & it travels through the circulatory system to all parts of the body including
head & down to areas such as stomach, liver intestine & lower limb
• The blood becomes deoxygenated once it passes through capillaries
• Capillaries —> exchange of blood
• When muscles are active about 75-80% of oxygen being supplied is used
• The blood then travels up & goes to the right side of the heart —> right ventricle pumps it to the lungs
• In the lungs you will get the movement of oxygen from the alveoli into the pulmonary capillaries
• Pulmonary capillary —> reoxygenate blood & the blood will make it’s way back to the left atria & left ventricle —> pumped
through the system again
• In order to force the blood to move around we need —> pressure
• Circulatory shock —> when there isn’t
enough pressure to drive the blood
through the system
• No adequate blood supply to cells —>
deoxygenated —> cells will die
• Without oxygen —> cells are hypoxic —>
decrease in the pH —> can’t produce
energy —> cells will eventually die
 • Pressure gradient will drive the ow
• Blood will move from an area of high pressure to an area
of low pressure

• Pump —> generates the pressure

• Pressure gradient —> comes from
the pump —> which is the heart

• Left & right ventricle —> pump

• Heart has 2 ventricles
• Left ventricle is a pump that generates the pressure that drives the blood ow from the left ventricle all the way back to the
right ventricle
• Right ventricle is a pump that generates enough pressure to drive the blood from the right ventricle all the way from the
lungs back to the left side of the heart
• Left ventricle pumps harder —> thicker walls
• Right pumps at lower pressure —> thinner walls
• The pressure that goes from the blood being pumped out the left ventricle into the major arteries is: 120/80
• 120 = Maximum pressure
• 80 = Diastolic pressure
• Main arterial pressure = 93 —> an average pressure coming out of the left ventricle of the blood of 93 mmHg
• When we get to our veins —> the pressure is about 10 mmHg
• Veins have valves which help return the blood & prevent back ow
• By the time we reach the right atrium the pressure of the blood is about 0 —> it changes as you breathe
• Breathing in: increase volume in cavity —> decreases pressure in thoracic cavity —> decrease pressure in right atrium —>
there is a better gradient to put the blood into the right atrium
• Pressure in right ventricle 25/8 mmHg —> main arterial pressure = 15 —> this is enough to get the blood through the lungs
to the pulmonary veins (8 mmHg) —> to the left atrium = 2mmHg
 • Aortic pressure —> the lower it gets is
80 —> we have blood in the aorta
• When the ventricle contracts it ejects 70
ml of blood into the aorta —> aorta
stretches out due to increase in pressure
—> aorta pushes down again — you get
a steady push of blood through the
circulatory system
• This e ect is called windkessel e ect
• Right atrium pressure = 0

The diagram shows the:

• pressure of the aorta over four contractions of the ventricle
• Pressure of the ventricle after four contractions of the ventricle
• Pressure of the large arteries after four contractions of the large arteries
• Pressure in systemic circulation is much higher than the pressure in the pulmonary circulation

• Left ventricle pressure goes from 0 to 120

• Aortic pressure goes from 80 to 120 (why?) —> because blood remains in the aorta
• Blood remain in ventricle however after it contracts it relaxes fully
• Why do we need the pressure to go back to 0 in the ventricle? Because we need a pressure gradient for the blood to enter
into the ventricle

• The pressure seems to drop the most in the small arteries & arterioles & capillaries
• What’s causing the pressure to drop? Resistance
• If we increase the resistance of blood to ow in our system —> the blood pressure that we need to drive the blood
through increases
• If arteries are narrowed —> the resistance in the arteries increases —> the heart must pump blood harder & increase
pressure
• High pressure —> ventricle has to go back to 0 —> needs to get blood from atrium
 • If a ventricle is going to generate pressure —> you have a set
volume of blood in the ventricle —> ventricle starts contracting —>
valves are shut
• Since valves are closed there is no way for the blood to go when the
ventricular muscle is contracting because the valves back to the
atria shut & the valves connected the aorta & pulmonary artery shut
—> so there is no way for the blood to go —> pressure increases
• When the ventricle contracts —> increases pressure of the blood
• What happens if the mitral valve is leaky when the ventricle is
contracting & generating pressure? Back ow of blood into the right
atria
• The valves must be shut when the ventricles are contracting but
once the ventricle produces enough force to be greater than the
pressure in the aorta —> aortic valve open —> push blood out
• Once you push some of the blood out —> the ventricle starts
relaxing & the pressure in the ventricle decreases —> aortic valve
shut

• When mitral valve is open —> blood can ow from the

atria into the ventricle
• Whenever pressure in the atria is greater than pressure in
the ventricle —> valve is open & blood will ow through
• As soon as the ventricle starts to contract & the pressure
in the ventricle becomes greater than the pressure in the
atria —> mitral valve shuts —> lub
• Mitral valve shutting —> lub
• Aortic valve shutting —> dub
• When muscle contracts —> pushes down on the blood —> Pressure increases —> blood will increase until the
pressure in the ventricle becomes higher than the pressure in the aorta
• As soon as you get to 80 mmHg —> the aortic valve opens & you start ejecting blood
• Pressure in ventricles become higher until the atrium opens

• When ventricle contracts it must squeeze

from bottom to top —> so blood is forced
out of the aorta 🫀
Lecture 3:

• The signal starts at the sinoatrial node —> travels through electrical bers & transmit action potential
• The AV node connects the atria to ventricles electrically
• Everytime a signal comes from the sinoatrial node to the AV node it will lead to the depolarization of the ventricle —> cause
ventricular contraction
What happens in the AV node?
• You slow down the signal —> so it allow time for the atria to contract prior to the ventricle contracting —> because as soon
as the ventricle contract it increases the pressure & the tricuspid valve shuts
• Ventricle pressure > atria —> tricuspid valve shuts

• Sinoatrial node cells cause ventricular contraction —> via the signal traveling through the electrical conducting
system of the heart
• If we want to make our heart beat faster —> send signals to SA node to make it beat faster —> have more
action potential over a short period of time —> Sympathetic nervous system does that
• Sympathetic nervous system —> release neurotransmitter (norepinephrine) —> re faster —> ventricles
contract more —> heart rate increases
• The information from the SA node passes through the atria —> specialized electrical cells depolarize the cells
around them —> muscle cells
• Muscle cells depolarized
• One cell contraction below internodal pathways cause the contraction of neighboring cells —> coordinated
contraction of heart
• The signal waits in the AV node in the bundle of his before passing into the ventricle —> waits to allow the atria
to contract
• Then the signal passes through —> depolarization of the septal muscle which will lead to the contraction —>
the bottom part of the heart contracts next —> followed by the sides & pushing up —> pushing the blood down
the aorta from the left side —> out of the pulmonary artery
• 0.00 —> associated with the stimulation of the SA
node
• The other times indicate where the di erent areas
of muscle are getting depolarized
• After they get depolarized —> they contract
• Any access blood in atrium gets pumped to
ventricles —> the signal travels down the septum &
into other areas of the heart
• Muscle of the heart is well innervated by electrical
bers —> you get a very rapid depolarization —>
give us a coordinated contraction

• Septum contracts —> pulls in the chambers from

either side —> tissue in bottom of the heart starts
contracting & pushing up —> the sides start
contracting as well —> forcing the blood up through
the valves into the pulmonary artery in the aorta
 • SA re by themselves —> due to leaky
membranes —> leaky to Na
• The open channels —> called funny channels —>
open at negative membrane potential —> Na
steadily coming into the cell —> the membrane
potential increases
• These cells don’t have a resting membrane
potential because soon as they repolarize these
Na channels allow Na to come back in again —>
slowly depolarizing it until you reach threshold —>
you get an action potential

• Pacemaker potential —> because it controls the pace of your heartbeat

• Action potential cause ventricular contraction —> repolarizes & comes down —> instead of staying at rest the
membrane potential slowly rises
• As it rises due to Na coming through the funny channels —> reaches threshold —> open the other Na dependent
channels —> you get another response
In summary:
• Membrane potential slowly rises —> once you reach threshold all these voltage dependent Ca channels open —> Ca
comes rushing into the cell —> depolarization —> Ca channel shuts —> K channels open —> repolarize —> potential
goes up since funny channels are open —> Na comes in —> depolarizes the cell
• If we want to make the heart beat faster —> make the pacemaker potential steeper —> reach threshold at an earlier
stage
• Ventricular muscle —> has a resting membrane potential —> when its depolarized —> you get a rapid in ow of Na+
—> due to Na channels opening
• As soon as you reach threshold you get rapid depolarization —> due to na channels opening
• Plateau period —> goes on longer to maintain contraction & calcium coming in —> maintain high depolarization
• Na channels cause the rapid depolarization & depolarization is maintained by Ca ions coming in
• At the same time Ca ions are coming in —> some K ions are leaving out
• Depolarization maintained —> Ca channels are kept open —> muscle contraction continuing on
Two reasons we have a long action potential:
1. To get the Ca coming through the voltage dependent Ca channels —> to maintain the Ca release from the SR —>
to maintain & produce contraction
2. Have a long refractory period —> you can’t have high frequency contractions of the cardiac muscle
 • The diagram shows the pressure changes in the ventricle (red), atria (bottom dotted line), aorta - left ventricle
(top dotted line)
• Those pressure changes will determine which valves are open & where the blood is owing
• Vol of ventricle (blue line): ventricle lls —> ejects the blood —> re lls —> eject the blood again
• Heart sounds are associated with the closing of the valves
First heart sound —> mitral valve closing (Lub)
Second heart sound —> aortic valve closing (Dub)

• Closing of valves —>

pressure change
determines if the valve
is open

• First period:
1. Where the atria is about to contract
2. High volume of blood in the ventricle
3. Aortic pressure is high —> blood in the aorta —> pressure in the aorta drop to 80
4. Pressure in ventricle is 0

• First stage: Aorta pressure drops to 80 —> pressure in atria is greater than pressure in ventricle —> mitral valve open —> blood
will ow from atria to the ventricle —> atrial contraction —> pressure in the atria increases & you pump blood into the ventricle
—> increases volume in ventricles —> aortic valve shut - pressure in the aorta > pressure in the ventricle
• Second stage (isovolumic contraction): Ventricle begins to contract —> Pressure in ventricles greater than the pressure in
atria —> AV valve shut —> aortic valve shut - pressure in ventricle < pressure in aorta —> all valves shut —> vol of ventricles
stays same but pressure in it increases —> causes blood ow to aorta
• Third stage: Slowly as the pressure rises —> pressure in ventricle > pressure in aorta —> AV open —> Volume of blood in
ventricle decreases - ventricle is ejecting its blood into the aorta —> atrial pressure is slowly increasing —because blood needs
to return to the atria —> atria start lling with blood —> increase pressure in atria
• Isovolumic relaxation stage: pressure in ventricle < pressure in aorta —> ventricle relaxing —> pressure in ventricle > pressure
in the atria —> AV & mitral valve are shut —> no movement of blood —> volume constant —> isovolumic relaxation state
This phase will continue as long as pressure in ventricle > pressure in atria
• Rapid in ow ( rst stage of re lling the ventricle): rapid lling of ventricle initially —> because pressure in the atria increased &
when the pressure in the ventricle decreases it drops below that —> greater pressure gradient —> i.e pressure in ventricle <
pressure in atria —> mitral valve open & blood will move in —> AV shut

• Pressure in ventricle > pressure in aorta —> Aortic valve —> blood ows out of the ventricle into the aorta
• Pressure in ventricle is less than aorta —> aortic & mitral valve is shut —> no blood ow

• Pressure in ventricle > pressure in atria —> mitral valve shuts

• Pressure in ventricle < pressure in atria —> mitral valve opens
 Recitation:

• Any change away from the baseline means —> There is

some charge di erence on the surface of the cardiac heart
muscle
• We are measuring charge di erence happening on top of
the cardiac muscle
• If all positive charges on top of membrane —> no charge
di erence
• If all negative charges —> no charge di erence
• Straight lines —> no charge di erence
• If you depolarize a cell —> cell going through action
potential —> + charge is going into the cell & the cell is
becoming + on the inside of the membrane
• P wave is caused by —> atrial depolarization —> some
cells in the atria which are negative on the outside (some
are yet to be depolarized)—> you’re going to have negative
on the outside & positive on outside —> & when they meet
you’re going to produce an electrical signal

• When it becomes 0 (graph) — end of P wave—> completely depolarized —> all

negative charge on the outside of the atria —> no charge di erence —> at line
in graph
• Remain at until charge is depolarized
• QRS signal —> ventricular depolarization —> at the beginning the septum cells
start to depolarize —> end is when most cells depolarize
• Why is signal much bigger for the ventricle than the atria? Ventricle has thicker
walls —> more cells —> greater border between the - & + —> you’ll see a
bigger response
• T wave—> ventricular repolarization —> di erent charges because the cells
don’t repolarize at the same time —> therefore there is a charge di erence
• Why don’t we see atrial repolarization? It’s too small & gets obliterated by the
ventricular depolarization
• ST signal —> no charge di erence (why?) —> there all the same charge —>
plateau period —> all the ventricular muscle is depolarized —> all negative
charge on the outside —> no charge di erence
• Lead I —> measuring between the right arm
& the left arm —> horizontal plane —>
looking at how the movement of the
electrical charges relate to that horizontal
plane
If it’s moving towards the left —> positive
de ection
If it’s moving towards the left —> negative
de ection
• The wave of depolarization in lead I —> is
mainly going to be positive
• Lead II —> measuring between the right arm
& the left leg
• Lead III —> measuring between left arm to
left leg

• At lead I —> If the wave of depolarization is moving

directly towards the left arm —> biggest response
• If it’s moving slightly away (downwards) —> smaller
response
• If it’s moving perpendicular —> 0
 • Left bundle branch is faster to depolarize than right
bundle branch
• Depolarization comes from the bundle of his —> down
the bundle branches
• Septum is the rst part of the heart to get depolarized
• The left side gets depolarizes rst because —> the
electrical conducting system on the left side is a little bit
faster
• The surface of septum will be negative while the rest will
be + (hasn’t been depolarized yet) —> charge di erence
• The vector will point towards the - electrode —> because
the overall signal is moving towards the - it’s going to be
slightly - —> so ECG will be moving down
• Q wave goes down

• Now all the septum has depolarized —> the wave of

conduction is at bottom —> the information has traveled
down the bundle branches into the purkinje bers —> all
that area is going to be - on the outside —> since it’s all
depolarized
• White stu is yet to be depolarized —> there is going to be
a whole heap of negative & positive interactions —> more
interactions in the left (thicket muscle wall) —> the vector
will be pointing towards the + electrode —> the ECG
pointing upwards — positive value —> positive de ection
—> the R wave
• Now the whole ventricle is depolarized except the
top part —> yet to depolarize
• Movement to the left in the right ventricle
• Movement to the right in the left ventricle —> more
depolarization in that direction (left-thicker walls)
—> more charge interaction —> towards A —>
positive de ection
• Are the interaction between the cells the same at
the bottom? No there will be less interaction —>
since its on the top —> not a big muscle —> the
magnitude of the vector is going to be smaller than
it was before —> de ection is going to be less
• It is still going to be positive —> shows
depolarization moving towards the + electrode —>
but it is not as much —> so moves back down to 0

• P-wave —> already depolarized most of the the right

atrium & depolarized about half to 3/4 of the left atrium
• The depolarization moving - —> + moving towards left
arm —> positive de ection
Why does the P wave sit upright?
• Because depolarization works in that way

• When we’re doing an ECG —> we’re looking at the charge

di erence atrial-atrial & ventricle-ventricle NOT BETWEEN
THEM —> because between these is the brous skeleton
which separates the atria from the ventricle —> it’s neutral
—> no charge moving between the atria & ventricle —>
isoelectric period
• Depolarization owing through the septum
• You’re measuring Lead I, II & III
• Lead I —> moving a little bit to the left —> signal is + but quite low
• Lead II —> big de ection —> signal higher
• Lead III —> perpendicular —> de ection
 • Now there is a larger amount of cells —>
depolarized —> + on the outside & - on the
inside
• Lead I —> going in the same direction but
going a longer way —> higher
• Lead II —> response is even higher
• Lead III —> went longer

• Now vector is not as big because there is

less cell-cell interaction —> wave from the
apex —> less cells available —> less - & +
cell interaction —> goes in the same
direction but not as big
• Lead II —> smaller but it’s still + —>
because the response is smaller it’s the
signal is coming down
• Lead I —> slightly smaller —> coming
down
• Lead III —> also smaller —> coming down

• Now we’ve depolarized all the right ventricle & a

little bit of the left ventricle left to depolarize
• Signal + for lead I —> going towards the
electrode —> above the line
• Lead II & III —> pointing towards the - electrode
—> value below the baseline
• QRS depolarization spike shows us what’s
happening overtime with the positioning &
magnitude of the + & - interactions on the
outside of the cell

• Now everything is depolarized —> there is no

charge di erence —> everything ends up back to
where we started —> at line
• If you’re su ering from left or right bundle branch
block —> the QRS wave will be wider
• Symptoms —> heart failure/shock