PHYSIOLOGY - Cardiac Output

Question 1

What is cardiac output (CO)?

Answer 1

Cardiac output is the volume of blood ejected by the left ventricle in one minute (l/min)

Question 2

How is cardiac output calculated?

Answer 2

Heart rate (HR) x Stroke volume (SV)

Question 3

What is heart rate (HR)?

Answer 3

Heart rate is the number of heartbeats per minute

Question 4

What is stroke volume (SV)?

Answer 4

Stroke volume is the volume of blood ejected by the left ventricle during ventricular systole

Question 5

How is stroke volume (SV) calculated?

Answer 5

End-diastolic volume - End-systolic volume

Question 6

What is preload?

Answer 6

Preload refers to the length of the ventricular cardiomyocytes at the end of ventricular diastole (i.e. length before contraction)

Question 7

What is afterload?

Answer 7

Afterload refers to the resistance that the ventricular cardiomyocytes must overcome to eject blood during ventricular systole

Question 8

What is the isometric length-tension relationship?

Answer 8

The isometric length-tension relationship states that an increase in muscle length to an optimum will increase the muscle tension. When this optimal length is exceeded, the tension will actually begin to decrease

Question 9

What is the afterload-shortening relationship?

Answer 9

The afterload-shortening relationship states that an increased afterload will reduce muscle shortening during isotonic contraction

Question 10

How is the isometric length-tension relationship related to the afterload-shortening relationship?

Answer 10

Increased muscle length will increase muscle tension, allowing the muscle to generate a greater force of contraction to overcome the resistance caused by afterload

Question 11

What is central venous pressure (CVP)?

Answer 11

The measure of the pressure exerted by the blood within the cranial and caudal vena cavae (central veins)

Question 12

What is the Frank-Starling Mechanism?

Answer 12

The Frank-Starling Mechanism is the heart’s physiological ability to change its force of contraction, and therefore stroke volume, in response to changes in the central venous pressure (CVP)

Question 13

Describe how an increase in central venous pressure (CVP) would affect cardiac contraction and stroke volume

Answer 13

An increase in central venous pressure (CVP) will increase the volume of blood entering the atria and thus the ventricles during ventricular filling. This will increase the length of the ventricular cardiomyocytes (preload), leading to an increase in muscle tension at the end of ventricular diastole. This increased tension will allow for a greater force to be generated by the ventricular cardiomyocytes during ventricular systole, in order to overcome the resistance (afterload) by increasing the ventricular pressure beyond aortic pressure to stimulate the opening of the aortic valve to achieve ventricular ejection - this increases the stroke volume and thus the cardiac output

Question 14

How would an increase in central venous pressure (CVP) effect the end-diastolic volume?

Answer 14

Increase central venous pressure (CVP) will increase the preload and volume of blood entering the ventricles during ventricular diastole leading to an increased end-diastolic volume

Question 15

How would an increase in central venous pressure (CVP) effect a pressure-volume (p-v) curve?

Answer 15

Increase central venous pressure (CVP) would shift a pressure-volume (p-v) curve upwards and to the right to indicate an increase in end-diastolic pressure and stroke volume

Question 16

What are the six factors that can affect central venous pressure (CVP)?

Answer 16

Low blood volume
Sympathetic nervous system activation
Venous muscle pump
Increased cardiac output
Respiration
Increased extramural pressure

Question 17

How does low blood volume affect central venous pressure (CVP) and stroke volume?

Answer 17

When the blood volume is low, this will decrease central venous pressure, decreasing the volume of blood that reaches the heart, decreasing the stretch of the cardiomyocytes (preload) and thus the tension generated by the cardiomyocytes. This results in decreased contractile force during ventricular ejection
resulting in a decrease in stroke volume

Question 18

How does the sympathetic nervous system activation affect central venous pressure (CVP) and stroke volume?

Answer 18

When the sympathetic nervous system is activated, this causes vasoconstriction of the veins leading to an increase in central venous pressure, increasing the volume of blood that reaches the heart, increasing the stretch of the cardiomyocytes (preload) and thus the tension generated by the cardiomyocytes. This results in increase contractile force during ventricular ejection resulting in an increase in stroke volume. Furthermore, the sympathetic nervous system will increase heart rate meaning the heart will be pumping blood more frequently, leading to a greater volume of blood reaching the heart and being ejected from the ventricles, increasing stroke volume

Question 19

What is the venous muscle pump?

Answer 19

The physiological mechanism in which skeletal muscles help to propel blood through the veins to assist in the venous return of blood to the heart

Question 20

How does the venous muscle pump affect central venous pressure (CVP) and stroke volume?

Answer 20

When the venous muscle pump is activated, this helps with venous return to the heart, which increases central venous pressure (CVP), increasing the volume of blood returning to the heart, increasing the stretch of the cardiomyocytes (preload) and thus the tension generated by the cardiomyocytes. This results in increase contractile force during ventricular ejection resulting in an increase in stroke volume

Question 21

How does the increased cardiac output affect central venous pressure (CVP) and stroke volume?

Answer 21

With increased cardiac output, more blood is being ejected from the heart per minute which means there is less time for blood to accumulate within the ventricles, reducing filling pressure. This will lead to a decrease in stroke volume

Question 22

How does respiration affect central venous pressure (CVP) and stroke volume?

Answer 22

During inhalation, the expansion of the lungs and thoracic cavity causes a decrease in the intrathoracic pressure, which helps to facilitate the return of venous blood to the heart (liquid moves from high pressure in the periphery to low pressure in the thoracic cavity), increasing central venous pressure and thus stroke volume. During exhalation, the recoil of the lungs causes the intrathoracic pressure to increase which can impede venous return to the heart (liquid moves from high pressure in the thoracic cavity to low pressure in the periphery), causing a decrease in central venous pressure and thus stroke volume

Question 23

What is extramural pressure?

Answer 23

Extramural pressure refers to the pressure exerted onto the walls of the heart

Question 24

How does the increased extramural pressure affect central venous pressure (CVP) and stroke volume?

Answer 24

Increased extramural pressure can put external pressure on the walls of the heart, affecting the heart’s ability to expand and contract which will reduce stroke volume as the ventricles will not be able to fill with and eject blood as efficiently. This increased pressure will also compress the veins that bring venous blood back to the heart, decreasing the central venous pressure and further decreasing the stroke volume

Question 25

What is arterial pressure?

Answer 25

The measure of the pressure exerted by the blood agaisnt the walls of the arteries

Question 26

Describe how an increase in arterial pressure would affect cardiac contraction and stroke volume

Answer 26

An increase in arterial pressure increases the resistance (afterload). Because of this increased arterial pressure, a higher ventricular pressure must be achieved to exceed the aortic pressure to open the aortic valve for ventricular ejection. However, because the aortic pressure is already high, the ventricular ejection phase will not last as long because the aortic pressure will quickly exceed to ventricular pressure. This causes the aortic valve to close earlier, resulting in a reduced stroke volume as less blood has been ejected

Question 27

How would an increase in arterial pressure effect the end-systolic volume?

Answer 27

An increase in arterial pressure will make it harder for the ventricles to eject blood into the aorta during ventricular systole. The ventricular ejection phase will not last as long because the aortic pressure will quickly exceed to ventricular pressure, leading to an increased end-systolic volume

Question 28

How would an increase in arterial pressure effect a pressure-volume (p-v) curve?

Answer 28

An increase in arterial pressure would cause a pressure-volume (p-v) loop to move upward and to the left, indicating a decrease in stroke volume and an increase in end-systolic volume

Question 29

What is the common consequence of a chronic increase in arterial pressure?

Answer 29

Cardiomyocyte hypertrophy

Question 30

What is the difference between intrinsic and extrinsic alterations in cardiac contractility?

Answer 30

Intrinsic alterations refer to changes in cardiomyocyte length whereas extrinsic alterations refer to factors external to the heart such a hormones, neural signals or drugs

Question 31

What is the inotropic effect?

Answer 31

The inotropic effect refers to changes in the force of cardiac contraction

Question 32

List three extrinsic factors which have a positive inotropic effect on the heart?

Answer 32

Sympathetic nervous system activation
Adrenaline
β-agonists

Question 33

List six extrinsic factors which have a negative inotropic effect on the heart?

Answer 33

Parasympathetic nervous system
β-blockers
Calcium channel blockers
Barbiturates
Many anaesthetics
Hyperkalaemia