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-Ensherah Mokheemer

- ABDULLAH ZREQAT

-Faisal Mohammad

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In the previous lecture we talked about:

- cardiac index: we use the cardiac index to compare the cardiac output

between different individuals, and we said that the cardiac index equals

the cardiac output divided by body surface area, so cardiac index unit

will be L/min/𝑚2.

- You should know that there are differences in the basic cardiac output values between individuals, since it is affected by the size and weight so to solve this there is what we call the cardiac index

- We also said that the cardiac

output is proportional to oxygen

consumption, the higher the

oxygen consumption is the

higher the cardiac output.

- The cardiac output is the sum of all tissues’ blood flow, during exercise

there is more oxygen consumption and more blood flow to skeletal

muscles so the cardiac output increases during exercise.

- Flow (cardiac output)= ∆𝑝/𝑅 (Ohm’s law):

*∆𝑝: is the pressure difference between the aorta and the right atrium.

The aortic pressure that we use on the equation is the mean arterial

pressure (MAP) which is affected by systole and diastole. The mean

arterial pressure= 1/3 systolic pressure+ 2/3 diastolic pressure. Why we

took 2/3 of the diastolic pressure and only 1/3 of systolic pressure? that

is because the duration of diastole equals 0.5s while the duration of the

systole is 0.3s so diastole contributes more to the MAP.

so ∆𝑝= 1/3 systolic pressure+2/3 diastolic pressure – right atrium

pressure (which is almost zero).

* R is the total peripheral resistance: which equals all the resistance in all

the vessels from aorta until reach the right atrium.

If we rewrite the equation in another form it will be like this:

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Flow (CO)=The mean arterial pressure (MAP)/ the total peripheral

resistance.

MAP= CO* total peripheral resistance.

- MAP of any person should always stay constant (homeostasis), if it

increases our system will try to decrease it and vice versa.

- From the previous equation we can conclude that we can change

the MAP by changing CO or by changing Total peripheral

resistance:

1- you can change the cardiac output by changing the stroke volume

or heart rate or both.

2- You can change total peripheral resistance by vasodilation

(decrease resistance) or vasoconstriction (increases resistance).

-Normally the cardiac output is almost 5L, when during exercise there is

an increase in the cardiac output and this increase in the cardiac output

is mainly due to the increase in the blood flow to the cardiac muscles.

Note : exercise can increase CO up to 700% ( almost 35 L).

Note: the skeletal muscles usually constitute 40% of our weight and they

normally receive about 1 L of blood/min, so 20% of our cardiac output

goes to 40% of out body. But during exercise the blood flow reaches 8L

per min.

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-Also, during exercise, the blood flow to the skin increases due to water

loss. And the blood flow to the digestive system is reduced.

-There are variations in tissue blood flow. And that the heart has one of

the highest blood flow

relative to its body

weight (around

70ml/min/100gm).

-Other tissues have

higher blood flow but

this is not for oxygen

consumption, it's for

filtration like in the

kidney. While the heart

receives good amount

of blood flow only for

oxygen consumption.

-Other tissues like adrenal and thyroid glands have very high blood flow,

they are small glands, the blood that is going to them is much higher

than they need.

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- Cardiac output= Stroke volume* Heart Rate:

Heart rate is controlled by sympathetic (positive chronotropic)

and parasympathetic (negative chronotropic).

Stroke volume is controlled intrinsically by End diastolic volume

(Frank starling law) (increase venous returnincrease

EDVcontractility stroke volume), or extrinsically by

sympathetic stimulation (positive inotropic).

Now let’s talk about the cardiac output curve:

-The cardiac output curve relates the right atrium pressure to the cardiac

output, and it is a mathematical representation of Frank-starling law.

-The right atrium pressure is an indicator for EDV, the higher the EDV is,

the higher the right atrium pressure.

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-The cardiac output is an indicator for the intraventricular pressure

-keep this in your mind

When the pressure in the

right atrium equals zero

the cardiac output will be

5L.

* Cardiac reserve :

Maximal % increase in CO

in response to increase

body needs

-Normally, according to

this curve the cardiac

reserve is 10L.

Remember: cardiac reserve= maximum CO- normal CO (15-

5=10L).

- The cardiac output curve might be shifted upward to the left:

positive inotropic effect which is usually due to sympathetic

stimulation, so very high sympathetic stimulation might shift the

curve upward to the left and the is what we call HYPEREFFECTIVE

HEART.

Note: Athletes might have hyper effective heart, in this case they

have hypertrophy of ventricles.

-HYPOEFFECTIVE HEART the curve shifted downward to the right

and it might occur because of sympathetic inhibition or

myocardial infarction.

- Hence that the normal curve represents normal sympathetic

stimulation, the hypereffective curve represents maximum

sympathetic stimulation and hypoeffective represents minimal

(Zero) sympathetic stimulation.

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Maximum sympathetic stimulation: shifted upward to the left.

Zero sympathetic stimulation: Shifted downward to the right.

Parasympathetic stimulation: not very important because usually

it does not affect.

Effect of the intra-plural pressure on the cardiac output:

-The heart is in the chest and it is surrounded by the lungs, and

the lungs is surrounded by the pleura.

-The pressure inside the pericardium is equal to the pressure

inside the pleura.

- The intra-plural pressure is always negative** around”-5mmHg”

that’s why the lungs are distended and there is a vacuum

around them.

** remember that we considered the atmospheric pressure zero,

so a negative pressure will be less than the atmospheric pressure.

The atmospheric pressure is our reference point that is why it is

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considered zero, but it does not equal zero it equals 760mmHg so

the pressure in the pleura will be 760-5= 755mmHg.

- Normally the right atrium pressure is zero (760mmHg)

when the pleural pressure around it is -5 (755mmHg).

- In case of pleural effusion, the pleural pressure increases

from -5 to -3(-5+2), this increase in the intra-pleural

pressure will be reflected on the heart and the pressure will

change in the right atrium from zero to +2 (zero+2) and this

means that in order to fill the atrium we will need higher

pressure gradient. This will shift the cardiac output curve to

the right.

- If the pleural pressure increases from -5 to zero ( -5+5) the

right atrium pressure will become +5 (Zero+5), shifted to

the right.

- If the intra pleural pressure decreases, a decrease in the

right atrial pressure is seen.

- It is important to notice that in case of increase/decrease in

IPP the whole curve will be shifted to the right/left and the

maximum cardiac output according to Frank-Starling will

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be the same it will not be affected!! But it is shifted.( very

important)

- According to the figure above:

1- Let’s consider the normal intrapleural pressure is (-4

mmHg) at this value the right atrium pressure (RAP) will

be zero and the cardiac output at that pressure equals

5L and the maximum cardiac output is 15L.

2- When the intrapleural pressure is decreased to -

5.5mmHg the pressure in the right atrium will be

reduced to -1.5mmHg and the cardiac output at that

pressure will be equal to 5L and the maximum CO will

be 15L. (shifted to the left). in this case the heart is

working at less pressure

3- When the IPP increases to 2 (like in the case of pleural

effusion) the pressure in the right atrium will be +6 and

the CO at that pressure will be 5L and the maximum CO

will remain 15L. (shifted to the right) in this case the

heart is working on higher pressure.

Hence that the normal CO and the maximum CO did not

change they were only shifted!! That is because the

Cardiac muscle is not affected directly because the

pleura is far from the heart muscle (not on direct contact

with it).

- In the case of Cardiac tamponade “pericardial effusion”: The

increase in the pericardium pressure will directly affect the heart

muscle and it will prevent filling of the blood, thus reaching the

maximum CO will become very difficult (we will need very high

pressure to reach the maximum CO).

From the figure above:

-When the interpleural pressure was -4 mmHg we

needed almost 2 mmHg to reach the maximum cardiac

output. “less severe”.

- However, when the interpleural was -4 mmHg and

there was pericardial effusion we needed almost 8

mmHg to reach the maximum Co. “more severe”.

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As a conclusion because the pleural is not in direct contact with

the heart muscle (far from it ), in case of pleural effusion the

effect will not be severe. But because the pericardium is in direct

contact with the heart muscle the pericardial effusion will have

more sever effect.

- If the cardiac tamponade becomes very severe, the cardiac

output might not reach the maximum CO and it might reach

0 since the heart is unable to pump blood anymore and this

eventually will cause heart failure.

- So cardiac tamponade is an emergency case and it needs to

be relieved by cutting through the chest using a sharp

object.

- cardiac tamponade --- increase RIGHT ATRIAL PRESSURE---

-- shift the curve to the right and sometimes downward

Returning to our main subject which is the cardiac output

curve:

- Plateau of CO curve determined by heart strength

(contractility + HR):

1- sympathetic stimulation raises the plateau up and shifts the

curve to the left. hypereffective heart.

2-parasympathatic mostly does not have any significant effect.

3-Heart hypertrophy raises the plateau up and shifts the curve

to the left. Hypereffective heart.

4- Myocardial infarction lowers the plateau and shifts the curve

to the right due to mass decrease. Hypoeffective heart.

5- Valvular disease lowers the plateau and shifts the curve to

the right due to decrease in the cardiac output, examples

are stenosis or regurgitation, in case of regurgitation

because of the valve (AV valve) incompetence some of the

blood goes back to the atria from the ventricle, in case of

semilunar valve incompetence some of the blood returns

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from the aorta to the ventricle in the case of aortic stenosis

is a narrowing of the aortic valve opening. Aortic stenosis

restricts the blood flow from the left ventricle to the aorta

“you can consider it as an increase in the resistance to

blood flow due to the narrowing of the orifice” and this

leads to decrease in stroke volume and eventually decrease

in cardiac output.

6- Myocarditis lowers the plateau because it affects the

myocardium leading to reduction in the function of the

myocardium (contractility).

7- Cardiac tamponade (pericardial effusion) it will prevent the

filling of the ventricle, so it decreases cardiac output and

thus lowers the plateau of the curve.

8- Metabolic damage also lowers the plateau.

Factors that affects cardiac output:

Cardiac output=Heart rate * stroke volume

*Heart rate is controlled by the Autonomic nervous system

(sympathetic or parasympathetic) or Hormones (Thyroxin

and catecholamines).

*Stroke volume =End diastolic volume-End systolic volume

1-The increase in the End diastolic volume is called increase

in preload and this is Frank-Starling law.

2-The decrease in the End systolic Volume is mainly due to

positive inotropic and the increase in ESV in due to negative

inotropic.

a- EDV is mainly affected by:

-The venous return (how much blood return back to the

heart). Increase in venous return increases EDV increases

preload.

--The venous return = CO= RAP ( under physiological

conditions)

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-Filling time, which is affected by the heart rate, increasing

the heart rate leads to decrease in the cardiac output due to

the decrease in the duration of ventricular diastole and this

reduces the filling time of the ventricle.

During exercise the heart reaches to its maximum heart

rate and this is dangerous, you should not exceed 80% of

your maximum heart rate, because the increase in heart rate

leads to reduced stroke volume and thus decrease in cardiac

output and eventually might lead to myocardial ischemia.

There is a test called exercise stress test which is used to

determine how well your heart responds during times when

it’s working its hardest.

During the test, you’ll be asked to exercise — typically on

a treadmill — while you’re hooked up to an

electrocardiogram (EKG) machine. This allows your doctor to

monitor your heart rate.

If the ECG showed depression in the ST segment, the

doctors will tell you to stop running and this depression is

due to coronary obstruction (stenosis) which might lead to

ischemia.

b- ESV is affected by:

- Contractility: Decrease in contractility increases ESV.

- Vasoconstriction, increases the pressure, increases the

resistance and thus decreasing the blood flow (cardiac

output) by decreasing stroke volume. Vasoconstriction

causes an increase in the afterload and increase in the ESV.

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*vasodilation decreases the afterload.

- Contractility is increased by Epinephrine, Norepinephrine,

Glucagon, Thyroid hormone. ** These figures are very

important

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Regulation of Preload:

-Increase in the venous pressure means increase in ∆𝑝: The

difference between the venous pressure and the right atrium

pressure.

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Regulation of afterload (contractility):

- Main factor that controls contractility is sympathetic

stimulation or inhibition.

-Cardiac contractility is measured by measuring the

maximum change in pressure per time (dP/dt).

-Excess K+ decreases contractility.

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- Excess Ca++ increases contractility.

Measurement of cardiac output:

Direct methods:

1- - In animals you cut the aorta, collect the blood ejected

per min, this gives you cardiac output. Obviously, we

can't do this in humans.

Indirect methods:

1- Electromagnetic flowmeter it is indirect but is done directly

in heart surgery.

2- Indicator dilution (dye such as cardiogreen)

3- Thermal dilution

4- Oxygen Fick Method CO = (O2consumption / (A-V O2

difference)

**remember that the cardiac output is the amount of blood

ejected from the aorta per min.

1- Electromagnetic flowmeter: We have two poles of

magnate (north and south). When a charged flow passes

between the two poles, an electrical current is formed

and it is proportional to the flow, the current can be

followed up by a calibrated galvanometer. Because blood

is full of electrolytes, It is a charged flow, and the current

that would be formed (we can also call it voltage

difference or potential difference) between the magnate

is proportional to the flow. If we measure this flow per

min, we can calculate the cardiac output. This method can

be used around any artery, and many times, (only used

during cardiac surgery).

2- Fick Method (oxygen consumption):

-The blood coming from the right ventricle to the lungs

through pulmonary artery. And it is deoxygenated.

-The amount of blood that comes from the right ventricle

to the lungs through the pulmonary artery per min is

called Cardiac output.

- The blood that come to the left ventricle by pulmonary

veins is equal to CO.

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- the amount of oxygen that comes to the lung per minute

equals cardiac output multiplied by oxygen concentration

in the blood.

- The amount of oxygen that come to left ventricle from

the lungs by pulmonary veins = the cardiac output* the

concentration of oxygen in the arterial blood.

Which equals the concentration of oxygen in the blood

that entered the lungs + the amount of oxygen which

was up taken by the lungs.

-Q1= Cardiac output*concentration of O2 in venous

blood.

-Q2= amount of Oxygen uptake by the lungs which can

be measured by spirometer.

-Q3= Cardiac output * (The concentration of O2 in the

venous blood+ The concentration of oxygen uptake). Or

the Cardiac output * the concentration of O2 in arterial

blood.

-Oxygen uptake= CO *(C arterial O2 – C venous O2).

-Cardiac output= Oxygen uptake/ (C arterial O2 – C venous O2).

THE END

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