Week 5: The Cardiac Cycle and the Regulation of Cardiac Output Flashcards

1
Q

What is ventricular diastole and ventricular systole

A
  1. Ventricular diastole
    - is the period of filling, when the ventricles are relaxed
  2. Ventricular systole
    - Is the period when the ventricles contract, and eject the blood out the pulmonary trunk and aorta
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2
Q

Define preload

A
  • Is the resting length of the sarcomeres (z line to z line) within the contractile myocytes (degree of stretch of the ventricular wall by blood filling the ventricle)
  • As the ventricles fill with blood, they dilate passively to accommodate the greater volume of blood within the chambers

The more these chambers dilate, the more they will stretch the sarcomeres within the myocytes

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3
Q

Explain how an increase in preload increases the force of contraction

and what law this is called?

A

Due to length tension relationship

  • Stretching the sarcomeres increases the overlap of thin and thick filaments at rest
  • If you increase the overlap of these thin and thick filaments it increases the amount of cross-bridges that can form, which produces more force, increasing contractility
  • Thus, an increase in preload will increase the force of contraction of the heart
  • If we start exercising, we would have increased venous return (as a result of exercise) which will increase the preload which will increase the force of contraction resulting in an increased stroke volume
  • This is known as the Frank Starling Law
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4
Q

Define afterload and what it depends on

A
  • Is the resistance that the ventricles must overcome to eject blood
  • This depends on arterial pressure and ease of blood flow through the pulmonary and aortic valves (obviously if they don’t open completely, the afterload will increase like in those patients with stenotic valves)
  • In order to eject the blood, the ventricles must overcome the diastolic pressure which is forcing the pulmonary and aortic valves closed
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5
Q

What is the pressure in the aorta and pulmonary trunk respectively, (this is the afterload)

A

80mmHg in the aorta and 8mmHg in the pulmonary trunk

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6
Q

define end diastolic volume

A

blood volume in the ventricle at the end of diastole

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7
Q

define end-systolic volume

A

blood volume in the ventricle at the end of systole

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8
Q

what is the formula for stroke volume

A

SV = EDV - ESV

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9
Q

What are the 5 main steps in the cardiac cycle and explain what each of them are?

A
  1. Late diastole
    - Where the heart is entirely repolarised, all the contractile myocytes are relaxed
    - Diastolic filling is passively filling the ventricles
  2. Atrial Systole
    - This stage is basically the contraction of the atria’s
    - Excitation of the contractile myocytes within the atria has occurred forcing a small, final amount of blood into the ventricles. This is known as atrial kick
    - The AV node is sitting on the message and has yet to depolarise the ventricles (meaning they are still relax)
  3. Isovolumic ventricular contraction
    - Pressure within the ventricles is now higher than within the atria, which forces the atrioventricular valves shut
    - Despite this, the pressure within the aorta and pulmonary trunk is still to great for the pressure of the ventricles to overcome (the afterload is still higher) meaning the aortic and pulmonic valves stay closed (no blood moves anywhere)
  4. Ventricular ejection/ventricular systole
    - As a result of contraction, the pressure within the ventricles rises and eventually exceeds the pressure in the arteries
    - The semilunar valves open and blood is ejected
  5. Early Diastole/Isovolumic ventricular relaxation
    - Once the ventricles have contracted and forced the blood out, they relax
    - This results in a drop-in pressure within the ventricles, forcing blood to flow back in closing the semilunar valves
    - The ventricular pressure is still greater than the atrial pressure which is enough to hold closed the tricuspid and mitral valves
    - Once the pressure in the atria overcomes the ventricular pressure, we start again at the passive filling stage
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10
Q

Does isovolumic ventricular contraction occur before or after the QRS complex

A

after

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11
Q

What does point E and F represent on the wiggers diagram?

A

E = end diastolic volume

F = end systolic volume

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12
Q

What do points A, B, C, D, E represent in the wiggers diagram

A

A = the opening of the semilunar valves. You can see an increase in aorta presssure as the blood rushes through the aorta increasing pressure. Also as the ventricles contract it continues to increase the pressur in the ventricles.

B= Closing of the semi-lunar valves - pressure of the aorta exceeds that of the ventricles hence blood flows back closing the valves.

C = closing of the AV valves as blood pressure in the ventricles exceeds that of the atrium hence blood flow going back.

D = opening of the AV valves as atrial pressure exceeds that of the ventricles and thus filling of the ventricles (late diastole)

E = the rebound of the blood when the valves close (hence a quick spike in pressure)

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13
Q

What is a way to

increase EDV

Decrease ESV

Increase heart

and what will this result in?

A
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14
Q

Where does sound 1 and 2 occur on the wiggers diagram and what do these sounds represent?

A
  • Sound 1 occurs at point C when the mitral and tricuspid valves close (the atrioventricular valves)
  • Sound 2 occurs at point B when the pressure within the ventricle drops below the pressure with the great vessels resulting in closure of the pulmonic and aortic valves
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15
Q

Where are the baroreceptors located

A

In the carotid bodies (in the carotid arteries) and aortic bodies (in the aorta)

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16
Q

Explain the baroreceptor reflex

A
  • This stretching of the baroreceptors increases the rate of AP’s it shoots off which does a number of things;
    1. Causes activation of the parasympathetic nervous system, known as the cardioinhibitory centre (negative chronotropic and dromotropic effects)
    2. Inhibits the sympathetic nervous system affecting the heart, known as the cardioaccelatory centre (decreased inotropy and lusitropy meaning cardiac output is decreased)
    3. Inhibits the sympathetic nervous system affecting the blood vessels, known as the vasomotor centre (leading to vasodilation)
17
Q
  1. What is occuring during the portion lavelled V
  2. what is the reason for the change in atrial pressure curve just before AV valves close at the region lavelled a
  3. During the AV valves close, why is there a second surge in pressure (labelled C)
  4. What does the dicrotic notch repsent
A
  1. AV valves are open so the ventricles can fill diastole
  2. contraction of atria begins which increase pressure (atrial systole)
  3. During the isovolumeric ventricular contraction, the AV valves slightly move out into the atrium and slightly increase the pressure
  4. Bit of rebound of blood of the semilunar valves close
18
Q

A patient has had a number of myocardial infarctions which has resulted in dead myocytes which have been replaced by scarr tissue. How mightt this change the ventricular pressure curve?

A

The rate of rise of pressure will be slower due to loss of muscle mass. If severe enough the macimal force wil also be reduced (increasing end systolic volume).

Hence the isovolumic ventricular contraction period would be a lot longer as it would take longer for the heart to over come the afterload period.

19
Q

Why is ‘a’ component of the atrial pressure curve mirrored on the ventricular pressure curve? and what effect does this have on ventricular volume?

A

because the atria are contracting which increases pressure in the atria and blood is being forced into the ventricles increase blood volume and thus increasing pressure in the ventricles.

20
Q

How would the ventricular pressure curve change if there was an increase in sympathetic activity?

A

the pressure curve would increase quicker due to increase in ionotropic contraction and also decrease quicker due to increase luistopic effect

max pressure may also increase

21
Q

Why don’t the AV valves open immediately following hte closing of the aortic semi-lunar valves?

A

THe ventricle pressure is still too high and the blood therefore is moving back closing the AV valves. Hence need to wait until the pressure decreases enough until atrial pressure is higher.

22
Q

During which pahse of the cardiac cycle are the coronary arteries distributing their blood?

A

Diastole

This is because during diastole, when the blood goes up the aorta just after systole, some falls back down which causses the closing of the semi-lunar valves. The cusps of these valves fill with blood and the coronary ostium are located here. The blood is then drained through these into coronary arteries.

23
Q

Be able to draw the wiggers diagram

A
24
Q

A patient is distressed that he fainted after standing up from a hot bath. He’d been enjoying a long hot soak to ease muscle pain. He stood up rapidly and fainted. Why did he faint?

How could this be avoided?

A

When sitting, the parasympathetic nervous system dominant and plus heat vasodilates blood vessels. Therefore when someone jumpts to their feet rapidly, the blood pruessure drops significantly. This could be enough to decrease CNS blood pressure and faint. Not enough blood to brain

Short time bfore the baroreceptors kick in and compensate. –> inhbit parasympathetic nervous system which inhibits the cardioinhibitory centre. Stimulate vasomotor reflex which causes vasoconstriction. Stimulate cardioaccelatory system by stimulating sympathetic nervous system.

Could be avoided by standing up slowly enough for baroreceptors to kick in.

25
Q

Where are the chemoreceptors located?

A

Located in the aortic bodies in the arch of the aorta and int he carotid bodies in the carotid arteries.

26
Q

A patient is suffering from congestive heart failure, in which his ventricles are damaged and too weak to contract effectively.

How will this affect CO2? How will this affect tissue carbon dioxide levels.

How does the chemoreceptor response attempt to modulate CO to overcome the changes in tissue carbon dioxide levels?

A

Weak ventricles and therefore cannot generate much pressure so stroke volume is reduced –> reducing cardiac output. This decreases circulation throughout body –> decreasing bodies ability to remove CO2.

Will get increase CO2 levels in tissue and therefore increase pH in tissue.

Chemoreceptors will be activated - inhit cardioinhibitory system, stimulate cardioaccelatory system, stimulate vasmotor centre causing vaso constriction –> this all increases cardiac output.

It also increases respiratory centre.

Also remember because you have decrease circulating volume, the renal system will be triggered activating (juxtaglomerular apparatus (increasing RAAS), low volume receptors (releases ADH), high volume receptors (stimulate sympathetic nervous system).