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CVS & IBL - Physiology 🫁 > L4: Cardiac output and its regulatory mechanisms > Flashcards

L4: Cardiac output and its regulatory mechanisms Flashcards

1
Q

What is cardiac output?

A

The is the volume of blood pumped by each ventricle per minute, It is also called minute volume.

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2
Q

What does cardiac output normally equal?

A

Normally, it is about 5 liters/minute during rest and is equal for both ventricles.

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3
Q

What is the definition of end-diastolic volume? And what does it equal?

A

Is the volume of blood in the ventricle at the end of diastole, it is about (110-130 ml).

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4
Q

What is the definition of end-systolic volume and what is its value?

A

Is the volume of blood in the ventricle at the end of the systole, is about (40-60 ml).

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5
Q

What is the definition of stroke volume and what is its value?

A
  • It is the volume of blood pumped by each ventricle per beat.
  • SV = EDV (130) – ESV (60) = 70 ml.
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6
Q

What is the formula used to calculate cardiac output or minute volume?

A

The COP = SV x HR. = 70 x 70 = 4900 ml/minute, at rest.

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7
Q

What is the definition of the cardiac index?

A

Is the volume of blood pumped by each ventricle/square meter of body surface area/minute.

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8
Q

What does cardiac index equal?

A

about 3.2 litres/m2/min.

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9
Q

What is the importance of cardiac index? (CI)

A

It is used to compare the COP between the different individuals.

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10
Q

What is the definition of ejection fraction? (EF)

A

Is the percentage ratio of the SV to the EDV.

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11
Q

What is the formula used to calculate ejection fraction? and what it is normally equal to?

A
  • EF = SV / EDV x 100

- Normally, it is about 65%.

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12
Q

What is ejection fraction considered an indicator for?

A

It is a sensitive indicator of myocardial contractility.

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13
Q

What is ejection fraction directly related to? And when does it decrease?

A

ventricular contractility, in Heart failure

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14
Q

How is cardiac output determined clinically?

A

by echocardiography.

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15
Q

What are the factors affecting cardiac output?

A

Venous return (preload)
Arterial blood pressure (afterload)
Heart rate (HR)
Strength of ventricular contraction

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16
Q

What mainly determines cardiac output?

A
  • the volume of blood returned by the veins from the tissues i.e. by the metabolic activity of the tissues, particularly the voluntary muscles.
  • So, VR → ↑COP
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17
Q

What are the factors that affect venous return?

A

1) The pumping action of the heart (most important)
2) Pressure gradient
3) Respiratory movements
4) Gravity
5) Vascular system
6) Skeletal muscle contraction (a muscular pump)
7) Blood volume

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18
Q

how does the pumping of action of the heart affect venous return?

A

forcing blood into the blood vessels.

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19
Q

What is the effect of pressure gradient in Venous return?

A
  • The pressure gradient for venous return is the difference between the mean circulatory pressure (MCP) and the right atrial pressure (RAP).
  • In the recumbent position, (MCP ) is 7-8 mm Hg and (RAP) is 2 mm Hg, this leads to a venous return of about 5 liters/minute.
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20
Q

What is the mean Circulatory pressure and what does it equal?

A

Is the blood pressure in peripheral venules and veins in the recumbent position and is normally about 7-8 mm Hg.

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21
Q

What is the right atrial pressure and what does it equal?

A

It is the pressure in the right atrium, In the recumbent “patients are carried in this position” position it is 2 mmHg.

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22
Q

What is the effect of respiratory movements on venous return?

A

Venous return increases with inspiration and decreases with expiration.

23
Q

How does venous return increase during inspiration?

A

Normal inspiration makes the intrathoracic pressure more negative and the intraabdominal pressure more positive → blood is sucked from extra to intrathoracic veins → VR.

“Breathe to let blood in”

24
Q

How does venous return decrease during expiration?

A

During normal expiration, the negativity inside the thorax is decreased, and so the VR is less than during inspiration.

25
Q

How does gravity affect Venous return?

A
  • Gravity influences VR in a mechanical way.
  • In the recumbent position, gravity has no effect on VR.
  • In the erect position, gravity helps the VR from parts above the level of the heart but reduces it from parts below the level of the heart.
26
Q

How does the diameter of arterioles affect venous return?

A
  • Normally, the tone of the arterioles leads to partial VC.

- VD of arterioles →↑VR.

27
Q

How does the diameter of capillaries affect venous return?

A
  • If all the capillaries of the body are widely dilated, as by injection of histamine, the whole blood volume will be retained in them → no VR, no COP, ➔shock and death i.e., “Histamine shock”.“No use of vasodilators in case of decreased cardiac output”
  • Thus, VD of capillaries → ↓VR →↓ COP.
28
Q

Normally, how many capillaries are open during rest?

A
  • About 10% only of the capillaries are opened and the other 90% are collapsed during the rest.
29
Q

How does the diameter of veins affect venous return?

A
  • Venous tone prevents full distension of veins with blood, So, it maintains VR.
  • VD of veins → stagnation blood into veins →↓ VR and COP and vice versa.
30
Q

How does skeletal muscle contraction affect venous return?

A
  • During muscular contraction, the muscle fibers compress the blood vessels lying in between them, squeezing the blood into veins towards the heart, so increasing the VR and COP.
  • During muscular relaxation, the blood does not regurgitate back to the muscles because the veins possess very efficient valves which direct the bloodstream towards the thoracic veins.
31
Q

How does blood volume affect venous return?

A
  • Increased blood volume (e.g. during muscular exercise due to contraction of blood reservoirs →↑VR and COP.
  • Decreased blood volume →↓VR, COP.
32
Q

How does arterial blood pressure afterload affect cardiac output?

A

Changes in ABP have no effect on the COP provided the VR is kept constant.

1) When the blood pressure rises suddenly, the first systole will not be strong enough to pump all the blood received during diastole and some blood remains in the
ventricle, This residual blood is added to the diastolic filling→↑EDV of the next systole→↑force of myocardial contraction (according to Starling’s law).

2) When the ABP is lowered the opposite occurs, The first few beats expel more blood than that received during diastole→↓ ESV→↓EDV→↓force of myocardial contraction
(according to Starling’s law).

33
Q

What influences the change of COP by heart rate?

A

both the amount of VR and the extent of changes in heart rate.

34
Q

What happens in the case of mild to Moderate changes in heart rate with constant VR? (Physiological or moderate changes of HR)

A
  • If the venous return is kept constant, moderate changes in HR have no effect on COP, it affects only the SV.
  • The SV increases when the heart slows (as it has enough time to fill with more blood) and decreases when the heart accelerates, So, the COP remains constant in both instances
35
Q

What happens in case of excessive changes in heart rate with constant VR?

A

If the venous return is kept constant marked acceleration or slowing of the heart decreases the COP.

36
Q

What are examples of excessive or physiological changes in heart rate with constant VR?

A

In paroxysmal tachycardia: (HR 200 beats/min or more).
- The diastolic period will be greatly shortened with no sufficient time for filing of the heart and so the COP decreases.
▪ e.g. COP = SV x HR = 20 x 200 = 4000 ml/min.

In complete heart block: COP= SV x HR = 130 x 30 = 3900 ml/min

37
Q

What are the cases in which heart rate changes with the change of VR?

A
  • When the VR is increased, the acceleration of the heart becomes of fundamental importance in increasing the COP.
38
Q

Why does COP increase with increased venous return of the heart?

A

This is because:

  • Increased EDV
     With an enhanced rate of blood flow, the heart can be filled to a maximum in a short diastolic period leading to an increase in the EDV.
  • Decreased ESV
     Also, sympathetic stimulation during exercise → forced ventricular contraction →↓ESV.
  • These factors lead to a marked increase of the SV and so the COP increases 7-8 folds.
39
Q

The factor: Strength of ventricular contraction in maintaining COP

A
  • when the ventricles contract more strongly, they pump more blood.
  • Starling’s law of the heart represents an important mechanism of cardiac reserve power.
  • In a normal heart within limits, when the VR increases as in muscular exercise, → the ventricle dilates i.e. increases the initial length of the cardiac muscle fiber during diastole →↑force of ventricular contraction →↑SV and COP.
40
Q

What are the methods of measurement of COP?

A

1) The direct Fick’s principle

2) Echocardiography

41
Q

What does direct Fick’s principle state?

A

This principle states that: The amount of a substance taken up by an organ or by the whole body/min
= arterial content – venous content X blood flow/min.

42
Q

What are the requirements for direct Fick’s principle?

A
  • The O2 consumption/min
  • The O2 content in the mixed venous blood (from the pulmonary trunk by a cardiac catheter).
  • The O2 content in the arterial blood
  • Therefore, the COP = 250/ (190-140) = 250/ 50 = 5 liters/min.
43
Q

What is the regulation of COP?

A

Is the ability of the cardiac muscle to change its COP to meet the body requirements under different situations.

  • COP may be changed by changing the SV or HR or both.
44
Q

How is intrinsic regulation (autoregulation) studied?

A

Studied by the heart-lung preparation that allows the study of the cardiac muscle independent of nervous or hormonal factors in experimental animals.

45
Q

What are the stages of intrinsic regulation?

A

Heterometric and homeometric

46
Q

compare between Heterometric and homeometric regulations Acc to:-

A 
Definition
Nature
Cause
Starts
Lasts
EDV
ESV
SV 
Explained by
47
Q

compare between Heterometric and homeometric regulations Acc to:-

Definition
Nature
Cause
Starts
Lasts
EDV
ESV
SV 
Explained by
A
  • Is the regulation of COP with the change of the initial length.
  • Intrinsic
  • ↑Preload (VR)
  • Within 30 sec.
  • Few minutes (Transient mechanism)
  • Marked ↑↑ “sudden return of blood”
  • Slight ↑
  • ↑
  • Is the regulation of COP without change of the initial length.
  • Intrinsic
  • ↑Afterload (ABP)
  • Within 5 min.
  • Continues as long as after-load is ↑ (Steady-state mechanism).
  • returns to normal “blood is pumped”
  • ↓below normal “due to better contraction”
  • ↑ “due to better contraction”
48
Q

What explains heterometric regulation of COP?

A

↑ the initial length of the ventricle (EDV)

i.e starling‘s law.

49
Q

What explains homeometric regulation of COP?

A

1) The preceding heterometric stage ➔ better metabolic state i.e. More warmth and Ca++ etc.
▪ This leads to forceful contraction.

2) Pressure-induced regulation: The rise in the aortic pressure will increase the coronary blood flow that will provide more O2 to the contracting myocardium.
3) Release of myocardial catecholamines.

50
Q

When is the heterometric autoregulation observed?

A

Physiologically, the heterometric autoregulation is observed when a person goes from the standing position to the recumbent position, a relatively large volume of blood shifts from the veins of the lower limbs to the heart →↑ EDV →↑SV → ↑COP.

51
Q

What is the extrinsic regulation of COP?

A

The autonomic nerve supply of the heart and the circulating blood hormones regulate the COP by adjusting both the heart rate and the stroke volume.

52
Q

How does the autonomic nervous system regulate COP extrinsically?

A

Sympathetic stimulation increases the COP by:

1) +ve chronotropic effect, it increases the heart rate.

2) It increases the strength of ventricular contraction, by:
✓ The increased forces of ventricular contraction, decrease the ESV –> increase SV
✓ Also forceful ventricular contraction →rapid relaxation acts as suction force ↑ filling of the ventricles at the short diastole.

3) It increases the mean circulatory pressure ➔ increases the pressure gradient of VR ➔ increase VR and increases COP.

Parasympathetic stimulation decreases the COP by slowing the heart. (HR)

53
Q

How do hormones and drugs regulate COP?

A

Inc COP by Inc Both: Catecholamines, Thyroxine

Inc COP by Inc SV “force of contraction”: Digitalis, Xanthine derivatives e.g. caffeine, theobromine, and theophylline, Glucagon, and corticosteroids

Dec COP by dec HR “chronotropic effect”: Acetylcholine and other parasympathomimetic drugs such as methacholine, carbachol, and pilocarpine

CVS & IBL - Physiology 🫁 (12 decks)

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