Lecture 1:

• Systole: period of contraction

• Diastole: period of relaxation

First portion:
• Volume of ventricle is close to its indiastolic volume —> volume prior to contracting
• Pressure in the ventricle (red) is less than the pressure in the atria & also a lot less than the pressure in the
aorta
• Pressure in ventricle < pressure in atria —> mitral valve open
• Pressure in ventricle <<< pressure in aorta —> aortic valve shut —> ventricle can’t be ejecting blood because
it doesn’t have the pressure gradient to open the valve
• P wave associated with the depolarization of the atria
• After depolarization of atria —> it will then contract —> pressure in atria increases —> increases the pressure
gradient between the atria & ventricle —> more drive in force for ow —> push extra blood into the ventricle

Second portion: (Isovolumic contraction)

• After P wave —> QRS spike —> electrical signals come from the SA node to the AV node where it is held o
for a little while
• Ventricle begins to depolarize
• As the ventricle is depolarizing it begins to contract —> as it begins to contract the pressure in the ventricle
rises
• Pressure in the ventricle > pressure in the atria —> mitral valve shuts
• When mitral valve shuts we hear the rst sound (lub)
• First heart sound begins at the beginning of the isovolumetric contraction —> because as the ventricle is
contracting & generating more pressure there is a period of time where the pressure in the ventricle > pressure
in the atria —> mitral valve is shut
• But the pressure in the ventricle isn’t greater than the pressure in the aorta —> aortic valve is shut
• Both valves are shut —> there is no where for the blood to go —> the ventricles contract & increase pressure
—> volume stays the same —> hence isovolumic (same volume) contraction —> at line
• Depolarization of the septum rst —> associated with the early part of the QRS
• Hyper (peak) —> associated with depolarization of the apex
• Last part —> depolarization of the sides of the ventricle wall
• Depolarization & contraction occuring at the same time (why?) —> because you depolarize the tissue in series

Third portion: (Ejection)

• Reach a stage where the ventricular contraction is so great as well as the pressure —>
pressure in the ventricle > pressure in aorta —> aortic valve opens
• You begin to eject blood —> blood is getting forced out of the ventricle into the aorta —> aorta swells
• Aorta already has blood when this happens
• As you increase the pressure of the aorta —> aortic pressure rises
• Ventricular action potential depolarizes (plateau period) —> Ca ions coming into the cell & K is leaving
• Ca coming in —> causes ca release from the SR —> Ca binds to troponin C —> open up active sites & get
contraction

• T wave —> ventricular repolarization —> di erent areas of the ventricle is beginning to relax
• After repolarization the ventricles relax (why?)—> because Ca channels are shut (plateau phase) —> Ca is
taken up by the SR & ejected by the Ca pump on the sarcolemma —> force of ventricle begins to decrease
• Pressure in the ventricle decreases until it becomes less than the aortic pressure —> eventually the aortic
shuts —> mitral valve shut —> no change in volume —> & muscles relax, pressure in the ventricle is dropping
• When aortic valve shuts we hear the second sound (dub)
• This is the period of isovolumic relaxation
Fourth portion: (Rapid in ow)
• The volume begins to increase in the rapid in ow stage
• As soon as the pressure in the ventricle drops below the atria —> mitral valve opens —> pressure in the atria has
increased while the ventricle is ejecting blood & lling the atria —> increasing pressure
• In ECG it is isoelectric (why?) —> past repolarization —> the heart is at rest

• Filling then slows down eventually

• Second period —> diastasis —> the ventricle is directly receiving blood coming from the veins

In summary:
• The heart needs to generate pressure greater than the aortic pressure to open the aortic valve & push blood
out
• In order to ll pressure in the ventricle < pressure in the atria
 Recitation:

• Value for cardiac output = volume per unit time

• Average cardiac output - 70kg = 5 liters per minute
• Each ventricle pumps 5 liters of blood per minute at rest
• If you’re an athlete cardiac output may increase to 50
liters per minute —> 10 times at rest
• If cardiac output decreases —> not enough blood
pumped to meet the demands of the body
• If your blood level drops below the normal cells —>
su ering from heart failure —> acute or chronic

• HR —> Heart rate: how many beats the heart beats

per minute
• SV —> stroke volume: the amount of blood you
pump at each beat —> approx 70 ml
• Eg: Average person lying down—> heart rate 72,
stroke volume 70 —> CO = 5 Liters per minute
• Changes in HR & SV —> will change cardiac output
• When we exercise —> HR increases (why?) —> to
increase our CO —> SV increases as well
• Increasing both SV & CO —> will lead to greater CO

• Change in CO can be produced by change in HR

 • The normal pacemaker potential in SA cells reaches thershold —> Ca channels open & opening of Ca dependent
channels —> repolarize —> slowly depolarize —> funny leaky Na channels open as well
• If we have sympathetic stimulation —> it makes the leaky channels more leaky —> Na moves into the cells at a faster
rate —> Na depolarizes at a faster rate —> which means you reach threshold quicker —> you get more beats over a
certain time frame —> therefore heart rate increase
• Parasympathetic system —> when acetylcholine is released on the SA node cells —> it inhibits these channels —> less
Na comes in —> you depolarize a lot slower —> takes a lot longer to reach threshold —> therefore the number of beats
per minute is slow
• Parasympathetic system will decrease heart rate

• We are talking about Sinoatrial cells —>

since they control our heart rate
• Everytime SA cells re —> ventricle will
contract & eject blood —> we will have
a heart beat

• CO can be changed by changing our SV as well

• SV refers to how hard the cardiac muscle is contracting that is going to e ect
how much blood ejects
• If you increase the force of contraction —> you are going to increase the
amount of blood you pump out
• If we increase Ca levels —> will increase the stroke volume

• Increasing the end-diastolic volume up to a open will increase the SV

• Any further increases —> will decrease SV
• Decrease end-diastolic volume —> SV will become less
• What determines how much blood enters the heart? The amount of blood that returns
to the heart
• How much blood is returning to the heart will determine how much your end-diastolic
volume is
• For example: if you increase the amount of blood the left ventricle is pumping —> the
amount of blood that returns to the right atrium will increase —> more amount of
blood returned to the right ventricle
• This means the right ventricle is stretched —> will pump with more power & eject
more blood
• If it ejects more blood —> the amount of blood that gets to the left ventricle will
increase
• The CO of the right ventricle = the CO of the left ventricle —> they have to be the
same (how?) —> due to the end-diastolic volume
 • Afterload —> associated with the pressure that the
ventricle has to produce in order to begin ejecting
blood —> the pressure the ventricle has to reach to
start ejecting blood is equal to the pressure in the aorta
at the end of diastole (diastolic pressure in aorta)
• If we increase the afterload —> the ventricle has to
produce more force/pressure in order to open the
Aortic valve —> less actin-myosin interaction to eject
the blood —> decrease the SV
• The heart has to work harder to pump the same
amount of blood —> harder to get blood to all the
muscle —> causes hypertension

• One of the ways to increase contractility —> increase

intracellular Ca when the heart is beating

• If we increase end-diastolic volume —>

we shift to the right —> SV has increased
• End-diastolic volume: the amount of
blood in the heart before it starts
contracting

• If we increase the amount of Ca in the cell we have more Ca

bound to troponin C —>more active sites open + more actin-
myosin interaction —> greater sV
• If we are exercising we are going to increase both end-diastolic
volume (why?) —> norepinephrine will increase the amount of
blood returned to the heart —> stretch it + increase diastolic
volume
• Norepinephrine also increases the amount of intracellular Ca
every beat + also increase contractility
• Norepinephrine causes the veins to constrict —> increases the
amount of blood returning to the heart —> end-diastolic volume
increases —> more blood returning to the heart —> shifting to
the right
 • We need to be able to control where the
blood ow goes —> this is associated with
hemodynamics

• If we want to increase blood ow through our circulatory

system —> we can increase the pressure driving that ow

• P2 must be less than P1 in order for there

to be ow
• What will decrease the ow of blood as it
moves through? Resistance of ow
• P1= our systemic
circulation begins with the
blood we eject into the
aorta —> pressure=
120/80 mmHg
• P2 = pressure in the right
atrium —> pressure= 0

• Diastolic pressure = 80
• Systolic pressure = 120
• The pressure in the aorta rises when we eject —> reaches a pick
—> slowly drops down during diastole—> ventricle contract
again —> pushes the blood out —> diastole slowly drops
• Mean arterial pressure (MAP) = DP + 1/3 PP (systolic pressure -
diastolic pressure)
• P1 = MAP
• PP —> pulse pressure
 • Flow = pressure/resistance
• Change in pressure —> MAP
• Resistance to the ow —> TPR

• P1-P2 = MAP
• TPR = R

• If we increase MAP (pressure gradient from left ventricle to

the right atria) —> CO increases
• Decrease MAP —> CO decreases
• If we increase TPR —> CO decrease

• It is easier to measure MAP —> from that you can make

predictions about CO
• If CO is too low —> problem
• If viscosity is increased —> resistance increases
• If length is increased —> resistance increases
• If radius is increased —> resistance decrease
• A small change in radius is going to produce a large change in
resistance
• What happens to the length of the vascular tube when you put on
weight? Increases —> resistance to ow increases —> high blood
pressure
• If we double the radius —> the ow increases by 16 times
• If we narrow it by half —> decrease blood ow by1/16 to what it was originally
• By dilating we are increasing the blood ow
• Let’s say we want to increase the blood ow to our leg but we don’t want increase the ow to our kidney, what
would we do?
Dilate blood vessels going to the leg
Constrict the blood vessels going to the kidneys
• Why? Because this is associated with the gradient pressure developed by the heart
• Blood will always go to the path with the least resistance

• If we increase TPR —> this will decrease CO —> body will increase MAP —>
in order to bring CO back to normal
• We can maintain CO by changing the MAP
Lecture 2:
• Right atrium pressure is zero
• Any pressure in the veins —>
help drive blood back to the
atria
• Can you control venous
return? Yes by ANS —>
norepinephrine will act on
receptors in the vein —
squeezing them —> help
push blood back to the heart
—> increase venous return
• Venous return is the amount of blood returned to the heart
• The volume in the right ventricle must equal the volume in
the left ventricle —> pressure is di erent
• In order to maintain an adequate CO & V1 —> we must
have enough blood returning to the heart —> this is known
as venous return
• Increase VR —> stretch the heart
— more blood return to the heart
in the ventricle —> increase SV —>
increase cardiac output
• Veins —> low pressure
• Pressure in thoracic cavity < pressure in • When skeletal muscle
head & abdomen contract —> veins
• Pressure gradient favoring movement of squeezed —> pushes
blood from above or below thoracic cavity blood to the heart (one
to the heart direction)
• Breathe in —> increase volume in
thoracic cavity —> decrease pressure —>
increases blood ow from the abdomen
—> pressure di erence
• Negative pressure with relation to the
atmosphere
• The rst way we can increase CO is by increasing blood volume —> increase amount of blood returned to the heart
- increase venous return —>increase SV — because heart is stretched —> increase CO —> increase MAP
• If we increase sympathetic impulses —> increase HR (why?) —> because epinephrine is released which binds to SA
cells —> steepen pacemaker potential —> heart rate increases —> increase CO —> increase MAP
• Hormone from adrenal medulla increase SV —> because they increase contractility —> increase amount of Ca
inside the heart —> contract with a greater force —> therefore increase SV
• Decrease parasympathetic out ow —> less inhibition —> steepen it —> more action potential per minute —>
increase HR

• Increase in blood cells —> increase in blood viscosity —> increase SVR
• Increased body size (i.e obesity) —> increase total blood vessel length —> increase
resistance —> increase MAP
• Anything that causes vasoconstriction (i.e anything that blocks the arteries or makes
them narrower) —> increase SVR —> increase MAP

• How to control blood ow? Organ itself regulate blood

ow
• You diverate blood ow to di erent areas by dilating yo
the areas you want blood to ow & —> constricting to
areas you want to control/decrease blood ow
• Increase blood ow —> dilate
• Decrease blood ow —> constrict
• Increase rate of metabolism of an organ —> blood
ow increases —> vasodilation of arteries to supply
that organ —> HR increases
• Increasing metabolism —> more metabolites
released —> pH decreased —> cause vasodilation
—> more you work —> more stimulation for
vasodilation —> more blood ow
• Exercise —> sympathetic nervous system activated
—> causes constriction of vessels to the brain —>
to maintain our brain output
• Overwhelms the norepinephrine e ect
• How to change blood ow to speci c organs?
Through metabolism

• HBP —> pushing blood through the organs too much —>
damages capillaries —> also narrow blood vessels
• High perfusion is damaging especially for the brain & kidneys
 • If the activity coming in is suggesting not getting enough blood ow —> activates sympathetic nervous
system —> increase blood ow & contractility
• If the information coming in is suggesting that things are too high —> decrease activity of sympathetic
& increase activity of parasympathetic nervous system

• Baroreceptors are found in carotid artery

(blood ow to brain) & aortic arch

• Baroreceptors send information that goes to

the CV center in medulla —> sends its
output through the ANS
• If you increase blood pressure —>
baroreceptors get stretched —> increase
action potential ring to the medulla —>
increase in blood pressure
• Baroreceptors re continuously
• Baroreceptors send input into the CV center —> increase
sympathetic system —> SV of heart increases & construct blood
vessels —> bring blood pressure to normal rate
Lecture 3:

• Decrease in BP is going to lead to an inhibition of baroreceptors —> less stretch —> less baroreceptor ring —> this
decrease goes to the cardiovascular control centers —> control centers inhibit parasympathetic out ow —> heart
rate increases
• There will we a + e ect on sympathetic out ow —> overall e ect on HR is + —> increase HR & contractility —>
increase CO
• Norepinephrine will vasoconstrict the arterioles —> increase TPR —> increase MAP & bring BP back to normal

• Lying down —> standing up —> gravity shifts

from high to low —> increase blood volume to
the veins of the legs —> decreases venous
return —> decreases EDV (end-diastolic
volume) —> decreases CO —> decrease MAP
—> ring rate of baroreceptors gets slow —>
we are going to pump out sympathetic
out ow in order to get MAP back to normal
• Baroreceptor re ex kicks in —> gets MAP
back to normal

• ANP —> makes you get rid of more Na —> water follows —> you excrete more uid
• ADH —> inhibits the amount of urine you produce —> it is a water conserving hormone —> keeps blood
volume up
• ANP —> increases urine volume —> decreases blood volume
• Both ANP & ADH control our blood volume — & by controlling our blood volume they control blood
pressure
• This diagram talks about the e ect of renin angiotensin system on the blood volume
• Blood volume is decreased due to hemorrhage or Na de ciency or dehydration
• Decrease in blood volume —> decrease in blood pressure (why?) —> less blood less pressure
• Decrease in BP —> Juxtaglomerular cell produces more renin
• Renin acts as an enzyme or catalyst for causing the conversion of peptide called angiotensinogen (produced by
liver) —> to angiotensin I —> it travels to the lungs & nds an enzyme called angiotensin-converting enzyme — ACE
—> ACE changes angiotensin I into angiotensin II —> which increase BP
• Angiotensin II will vasoconstrict your arterioles —> total peripheral resistance increases —> MAP is brought back to
normal
• Angiotensin II will go to the adrenal cortex —> & cause the release of aldosterone —> goes to the kidney &
stimulates the kidney to take the Na from inside the kidney & move it back into the blood —> water follows —>
blood volume increases —> pressure goes back to normal
• ADH allows for the movement of water NOT ALDOSTERONE
• ADH works with aldosterone to help with the movement of water from the kidney back into the blood —> & so
increase volume

• To maintain blood pressure we need to make sure we have enough

uid in our blood (plasma) — circulating blood volume —> long term
control of blood pressure
• Short term blood pressure —> ANS + baroreceptor re ex
• Long term blood pressure —> blood volume
• Diuretics decrease blood volume —> used to treat high blood
pressure (why?) —> because they decrease blood volume
 • Low BP/vol activates the renin-angiotensin system
• Decreased BP —> Decreased volume —> causes
release of renin —> leads to elevated levels of
angiotensin II —> causes vasoconstriction
• How does angiotensin II cause vasoconstriction?
Arterioles have angiotensin II receptors —> when
angiotensin II binds to these receptors it causes elevated
levels of Ca —> smooth muscle contracts —> blood
vessels constrict —> which increases TPR
• Angiotensin II also causes secretion of aldosterone —>
which increases Na reabsorption by the kidney —> Na
moves —> water follows
• Angiotensin II directly stimulates the release of ADH
• Angiotensin II Directly a ects the kidney —> increases Na
reabsorption by the kidney
• All these things work together to increase the blood
volume

• There are di erent types of shocks:

Anaphylactic shock: immune response in which all blood vessels dilate —> blood
gets stuck
Hemorrhagic shock: where you lose a leg —> bleed out —> blood volume drops
Cardiogenic shock: heart hardly beats with any force —> can’t generate enough
pressure to drive blood around our system
• When you get a shock —> you will need to increase blood volume & increase
CO to maintain blood supply
• Hypovolemic shock —> lost a lot blood due to hemorrhage —> baroreceptors
ring rate is going to decrease —> this is going to our cardiovascular control
centers in our medulla & say increase sympathetic activity to get pressure back
up to normal
• This response in the baroreceptors is going to tell the hypothalamus to release
ADH —> which will help get our blood volume back up
• Decrease in BP —> stimulate secretion of renin —> which is going to produce
angiotensin II

• There are a couple of things can stimulate renin secretion:

1. Sympathetic out ow associated with drop in blood pressure
2. Decrease blood ow in kidney —> drop in blood ow —> decrease in blood
volume
• Angiotensin & norepinephrine constrict blood vessels —> both work together to
increase our TPR & try to get our BP back to normal
• ADH will cause our kidneys to conserve water —> bring blood volume up —>
ADH can also constrict blood vessels —> which will help maintain blood
pressure
• To treat shocks in patients:
Hurry the situation by epinephrine (epipen) —> to help this system along the way
Give patients intravenous uids to bring blood volume up