7&8

Malak Salameh & Aya Qurini

Asma’a Abu-Qtaish & Rubba Alshouani

Faisal Mohammaed
 atrioventricular

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D II
Eicuspid Mitral
 Heart Pump and Cardiac Cycle
- Cardiac cycle refers to all events associated with blood flow through the heart.
- We considered the cardiac cycle 0.8 (sec) for teaching purposes, but it can be
different from one person to another.
During the 0.8 (sec) these events happen:
1. Systole of ventricles
2. Diastole of ventricles
3. Systole of atria
4. Diastole of atria Before ventricular systole we have to record QRS
which is (ventricular depolarization) Always the electrical
precedes the mecanicl.

Systole of the atria has to be produced

by P-wave, so the P-wave will be
recorded before the atrial systole. Atrial systole = 0.1 sec
Atrial diastole = 0.7

1. Rapped filling

2. Slow filling

2
1 1
2 1. Rapped ejection of blood

2. Slow ejection of blood

- Ventricular diastole= 0.5 seconds

- Ventricular systole= 0.3 second
- Isovolumic relaxation 0.02 seconds
- Isovolumic contraction 0.01 seconds
- Rapid filling & Slow filling (Diastasis)
- Rapid ejection period & Slow ejection period
- Atrial contraction
 Dicrotic notch: brief rise in aortic pressure
caused by backflow of blood rebounding off
semilunar valves

Atrial pressure:
V-wave A-wave =atrial systole
C-wave= ventricular
C-wave contraction (AV closure)
A-wave V-wave= ventricular
diastole (Av opening).

- The volume of right and left ventricles are the same, the difference is in their
pressure.

- We considered that the volume of left ventricle before the atrial systole = 100,
but it dosen’t mean anything, it is just for teaching purposes (in the exam it can
be different)
‫(غير مطالبين بحفظ أرقام الحجوم ألنها افتراضية فقط‬
- When the atria contracts it pushes certain amount of the blood into the
ventricles very fast, so its volume will become ~ 125 mm  that means the atria
systole doesn’t contribute more than 25%  it’s not more than that because
during the atrial systole the AV valve was open  if AV valve is open, the blood
comes to the ventricles  so the maximum contribution of atrial systole is 25%

End-diastolic volume (EDV): the maximum diastolic volume of the ventricle

(before the heart contracts during systole)
- The pressure of the atria = 0 (compared to atmospheric pressure)

1- Systole of ventricles: pressure increase too much, reach more than 80

(which is the pressure in aorta during diastole) or more than 8 (which is the
diastolic pressure in pulmonary artery)
 the seminary valve opens  the rapid ejection phase will happen  most of
the blood moves from the ventricles to aorta or to pulmonary artery  so the
slow ejection phase will happen (it’s slow because the majority of the blood
moves in the fast phase -rapid-, so the conductance of the blood decrease)

- When systole ends, the ventricles won’t completely empty, because it’s a hollow
organ, no matter how much you compressed it, small volume will remain in it.

End-systolic volume (ESV): the volume that stays in the ventricles at the end of
systole.

2- Diastole of ventricles: After the ventricles have constricted, the blood will flow
into the aorta (in the left ventricle), and the pulmonary (in the right ventricle),
now the ventricles will relax and the pressure in them will decrease gradually till
a point where its less than the pressure in the aorta and pulmonary.
- As we know the blood flows from a high-pressure area to a low pressure one,
but we don’t want the blood to go back to the ventricles, so the semilunar valves
will close to prevent the blood from going back to the ventricles.
- The blood remain in the aorta and pulmonary for short period called isovolumic
relaxation (0.02sec) which all valves are closed  the pressure decrease (less
than 0) in ventricles  AV valves open  the blood come from atrial to the
ventricles  blood collects rapidly in ventricles  Rapid filling phase will happen
 then the Slow filling phase will happen.

3- Pressure changes in left ventricle: considered the pressure = 0 (it’s -1 because

it’s pressure less than atrial pressure, but we considered it = 0)
 during the atrial systole, the atria contracts  pushes certain amount of blood
to the ventricles very fast  the pressure in left ventricle increases  the systole
of ventricle starts  as the pressure increase more than 0  AV valves closes
which is the beginning of isovolumic contraction pressure increased very fast.
- When the pressure reach more than 80 in left ventricle  the aortic valve open,
why? because the pressure in the aorta = 80 so when the ventricle exceeds 80
gradient in pressure make the blood moves from high to low pressure, so even if
the blood moves out from the ventricles, the P still increases
Why? because the contraction force is more than output blood volume, so there
is increasing in blood pressure of ventricles.

- The max pressure in left ventricle is around 120mmHg (it should be more than
the aortic pressure as it moves from the ventricle to the aorta)

4- Isovolumic relaxation: (the V in right = the V in left)

the pressure change from 80 to less than 0  AV valve opens.
✓ the Pressure of left ventricles varies between 0-120
✓ the Pressure of right ventricles varies between 0-25
✓ the Pressure of aorta varies between 80-120
✓ the pulmonary artery pressure varies between 8-25
✓ Diastolic pressure in pulmonary artery = 8
✓ Diastolic pressure in aorta = 80
✓ the pulmonary artery systolic pressure = 25
(all of them in mmHg)

‫( اذا بدنا رسمة‬80-120) ‫ الي بيتراوح بين‬left ventricle ‫ اللي فوق فيه رسمة ال‬diagram ‫( ال‬
)left ‫ وبتطلع نفس رسمة ال‬120 -> 25 ‫ و‬8 80 ‫ بنبدل‬right ventricle ‫ال‬

- when we measure the person’s pressure we say for example (120\80)

Systolic pressure in LV Diastolic pressure in

aorta

- Atrial depolarized  atrial systole  P increase  make A wave  AV valve

close  blood tries to go away from Atria.

- P in ventricles too high  pushes the AV valve toward the Atria  make C-wave
AV valve opens at the end of isovolumic relaxation  P decrease and make
V-wave.
 ▪ End diastolic volume (EDV) – End systolic volume (ESV) = Stroke volume (SV)
▪ SV X heart rate (HR) = cardiac output (CO)
▪ Ejection fraction = SV/EDV (without unit), it must be more than 0.56 if its
less, we call it weak heart.

SV: Volume of blood ejected from ether the right ang left ventricles ml/beat.

CO: Volume of blood ejected from ether the right ang left ventricles ml/minute.

……………………………………………………………………………………………………………………………
Changes in heart sounds
- Heart sounds (lub-dup) are associated with closing of heart valves
- Auscultation – listening to heart sound via stethoscope
 S1: “lubb” caused by the closing of the AV valves
- turbulence of blood around AV valve. NOTE:

 S2: “dupp” caused by the closing of the semilunar valves

We usually don’t hear S3 &
S4, if you hear them, it might
be something abnormal.

- turbulence of blood around a closed semilunar valves.

 S3: a faint sound associated with blood flowing into the ventricles.
 S4: another faint sound associated with atrial contraction.

We will take each period separately and look at it from all angles, let’s start with
 Atrial systole:
- When the atrial is depolarized it makes a P-wave, at this moment the atrial
systole.
- It systole = contraction so the pressure in it will increase (notice that the atrial
pressure curve has risen slightly in this period)
- When the atrial systole it will pump the blood to the ventricles so the
ventricular volume will increase (notice that the ventricular volume curve has
risen slightly)

 Isovolumetric contraction (very short period 0.01 sec - QRS): the volume in
each ventricle stays the same  the amount of the blood in them remains
the same  (look at the ventricular volume curve in this short period it’s a
straight line) that’s because when the ventricles start contracting it closes all
the valves (There is no difference in ventricular volume, but the difference in
their pressure), this period ends with the semilunar valve opening.

^ when are all valves open at the same time?

- It’s impossible for that to happen

 Ventricular systole:
- Before ventricular systole we have to record QRS which is a ventricular
depolarization  ventricular contraction  ventricular pressure will increase
dramatically results in closing of AV valves

 Ventricular ejection: this phase opens semilunar valves  so the Aortic

pressure increase. (notice the curve)
- this event is included in the ventricular systole period

- T-wave shows ventricular repolarization

 Isovolumetric relaxation – early diastole:

- Ventricles relax.
- Backflow of the blood in aorta and pulmonary trunk closes semilunar valves.

 Dicrotic notch: brief rise in aortic pressure caused by backflow of blood

rebounding off semilunar valves.

Very helpful video

https://youtu.be/KmNHqqrFqG8?si=glGv6rxnp4o14e0z
 Cardiac output and reserve
● Cardiac output (CO) is the amount of blood pumped by each ventricle in
one minute, which is normally around 5 Liters/min, in some cases it reach
15 Liters/min (maximum CO by Frank-Starling law without stimulation).

- Skeletal muscle length can be measured, on other hand cardiac muscle

length can’t, so we measure it by proportion to the volume that is found in
the ventricle.  EDV increase, resting tension increase, length
increase, CO increase.

- Frank-starling law: within physiological limit an increase in the initial

length or resting length or resting tension will lead to INCREASE the force
of contraction.

● Cardiac reserve is the difference between resting and maximal CO.

For example, 15 L/min – 5 L/min = 10 L/min

CO = HR × SV

HR (heart rate)  is the number of heart beats per minute.

SV (stroke volume)  is the amount of blood pumped out by a ventricle

with each beat.

For example:

CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)

CO= 5250 ml/min (5.25 l/min)

- We already discussed how to measure the HR in the previous sheets,
now we will learn the way we use to know the SV.

SV = EDV – ESV

End Diastolic Volume (EDV)  is the amount of blood collected in a

ventricle during diastole (at the end of diastole)
End Systolic Volume (ESV)  is the amount of blood remaining in a
ventricle after contraction (at the end of the systole)
 Factors affecting stroke volume
● Preload (EDV): is the amount ventricles stretched by contained
blood, in other word we can say it is the amount of tension before
contraction that’s why we call it Preload.

Increase EDV  Increases preload  Increases CO

● Contractility: cardiac cell contractile force due to factors other than

EDV. With fixed EDV there is an increase in SV.

- It can be measured using ejection fraction: EF = SV/EDV

● Afterload: is the back pressure exerted by blood

in the large arteries leaving the heart, it is also the Remember: pressure of aorta
during diastole = 80 mmHg
amount of tension which ventricle must develop in
order to eject blood.

If afterload increases SV decreases unless you develop more

energy.

- Hypertension means increasing in the blood pressure, if it’s

happened we will need more energy to deliver blood to aorta from
left ventricle. Blood pressure should be lowered in order to prevent
ischemia or infarction from occurring.

……………………………………………………………………………

Frank-starling law of the heart

● Preload or degree of stretch of cardiac muscle cells before they
contract is the critical factor controlling stroke volume.
● Slow heart beat and exercise increase venous return to the haert,
increasing SV.

● Blood loss and extremely rapid heartbeat decrease SV.

IMPORTANT NOTE:

- When the HR is slow there will be more time for filling which increases SV.

- When the HR is fast there will be less time for filling which decreases SV.
 The preload  The ventricles are dilated and full with
blood.

Increase of muscle’s length will lead to increase force of

contraction (Frank-Starling low)

The afterload  Increase afterload will lead to decrease SV.

NOTE:

Increased HR is not always lead to increase the CO; in certain condition it may lead to
decrease it. For example, in exercise the HR shouldn’t be higher than certain limit, if it
does be higher the SV will decrease which lead to decrease the CO.
 Extrinsic factors influencing STROKE VOLUME
● Contractility is the increase in contractile strength, independent of stretch and
EDV.

● Increase in contractility comes from:

-Increased sympathetic stimuli

-Certain hormones (epinephrine, norepinephrine)

-Ca+2 and some drugs

● Agents/factors that decrease contractility include:

-Acidosis (low PH)

-Increased extracellular K+ (affect resting membrane potential)

-Calcium channel blockers (decrease contractility)

‫ال تنسوا غزة من دعائكم‬

THE END OF SHEET #7&8