Section 5

Question 1

What is cardiac output (CO), and how is it calculated?

Answer 1

Cardiac output is the volume of blood pumped by each ventricle per minute. It is calculated by multiplying heart rate (HR) by stroke volume (SV):

CO = HR × SV

Question 2

How is stroke volume (SV) defined, and what is its approximate value at rest?

Answer 2

Stroke volume is the amount of blood ejected by a ventricle with each contraction. At rest, stroke volume is approximately 70 ml.

Question 3

What is the approximate cardiac output (CO) at rest, and how does it change during exercise?

Answer 3

At rest, cardiac output is almost 5 liters of blood per minute from each ventricle, roughly the entire blood volume of an average person (5-5.5L). During exercise, CO can exceed 20L/min, and this increase is due to an increase in either heart rate (HR), stroke volume (SV), or both.

Question 4

What is the primary pacemaker of the heart?

Answer 4

The primary pacemaker of the heart is the sinoatrial (SA) node.

Question 5

How many times does the SA node spontaneously depolarize per minute?

Answer 5

The SA node spontaneously depolarizes around 70 times per minute.

Question 6

How is heart rate regulated by the autonomic nervous system?

Answer 6

The autonomic nervous system regulates heart rate. The parasympathetic system, via the vagus nerve, slows down heart rate, while the sympathetic system innervates both atria and ventricles to increase heart rate.

Question 7

What is one effect of parasympathetic stimulation on the heart?

Answer 7

Parasympathetic stimulation slows down the heart rate.

Question 8

How does parasympathetic stimulation affect K+ permeability in atrial muscle cells?

Answer 8

Parasympathetic stimulation increases K+ permeability in atrial muscle cells, leading to faster repolarization during the action potential.

Question 9

What is the impact of increased K+ permeability in atrial muscle cells on the strength of contraction?

Answer 9

Increased K+ permeability shortens the plateau phase during the action potential, resulting in less Ca2+ entering the cells and reducing the strength of contraction.

Question 10

How does parasympathetic stimulation affect the excitability of the AV node?

Answer 10

Parasympathetic stimulation hyperpolarizes the AV node membrane, making it less excitable, similar to its effect on the SA node.

Question 11

What is the consequence of parasympathetic stimulation at the SA node?

Answer 11

Parasympathetic stimulation at the SA node decreases heart rate through multiple mechanisms.

• It increases the permeability of potassium ions (K+) in atrial muscle cells, leading to faster repolarization during the action potential. This hyperpolarizes the membrane potential, making it more challenging for the cell to reach the threshold for depolarization.
• Additionally, parasympathetic stimulation opposes the If current, a crucial component for pacemaker activity.

Acetylcholine release is a key mediator of these effects, contributing to the overall reduction in heart rate.

Question 12

What effect does parasympathetic stimulation have on ventricular muscle cells?

Answer 12

Parasympathetic stimulation has very little effect on ventricular muscle cells due to minimal innervation. The majority of parasympathetic innervation is on the SA node and AV node, not the ventricles.

Question 13

What are the four effects of sympathetic stimulation on the heart?

Answer 13

Sympathetic stimulation has four primary effects on the heart:

1. Increasing Heart Rate: Norepinephrine release at the SA node enhances pacing currents (If and T-type Ca2+ currents), leading to a faster membrane potential threshold. The slope of the pacing current is increased and the pacing rate of the heart is increased.
2. Increasing AV Node Excitability: Norepinephrine release at the AV node decreases the AV node delay, allowing faster transmission of excitation to the ventricles.
3. Enhancing Conduction Speeds: Conduction speed is increased in the cardiac conduction system, including the bundle of His and purkinje fibers, facilitating faster transmission of the excitation wave.
4. Increasing Contractility: Sympathetic stimulation increases the contractile strength of both atrial and ventricular muscle cells. This is achieved by enhancing Ca2+ permeability during the plateau phase of the action potential, leading to stronger contractions and increased blood ejection.

Question 14

How does sympathetic stimulation affect heart rate, and what mechanisms are involved?

Answer 14

Sympathetic stimulation increases heart rate by enhancing the pacing currents (If and T-type Ca2+ currents) at the SA node. Norepinephrine release boosts the strength of the pacing current, leading to a faster rise in the membrane potential, reaching the threshold more quickly and resulting in an increased heart rate.

Question 15

What is the impact of sympathetic stimulation on AV node excitability, and how is it achieved?

Answer 15

Sympathetic stimulation decreases AV node delay by releasing norepinephrine at the AV node. This reduction in delay allows for a faster transmission of the excitation wave from the atria to the ventricles, enhancing AV node excitability and speeding up the overall cardiac conduction.

Question 16

How does sympathetic stimulation enhance conduction speeds in the heart, and which components are affected?

Answer 16

Sympathetic stimulation increases conduction speeds throughout the cardiac conduction system, including the bundle of His and purkinje fibers. This effect is achieved by the release of norepinephrine, leading to faster transmission of the excitation wave and ensuring more efficient coordination of heart contractions.

Question 17

What is the impact of sympathetic stimulation on the contractility of cardiac muscles, and what mechanisms are involved?

Answer 17

Sympathetic stimulation enhances the contractile strength of both atrial and ventricular muscle cells. This is primarily accomplished by increasing Ca2+ permeability during the plateau phase of the action potential. The heightened Ca2+ influx directly strengthens contractions and enhances Calcium-Induced Calcium Release (CICR), leading to increased blood ejection and a lower end-systolic volume within the ventricles.

Question 18

How does injury to the vagus nerve affect heart rate, and what is the normal endogenous pacing rate of the SA node?

Answer 18

Injury to the vagus nerve, which normally exerts parasympathetic influence, results in the removal of this inhibitory effect. Consequently, the resting heart rate increases. The endogenous pacing rate of the SA node, in the absence of parasympathetic influence, is around 100 beats per minute, but under normal conditions, the parasympathetic system reduces it to around 70 bpm.

Question 19

How does physical activity influence heart rate, and what changes in autonomic input occur during exercise?

Answer 19

During physical activity, there is a decrease in parasympathetic input and an increase in sympathetic input, allowing the sympathetic system to dominate. This shift in autonomic balance raises heart rate, facilitating the delivery of oxygen to working muscles.

Question 20

Why does heart rate increase during fever, and what is the physiological purpose of this response?

Answer 20

During fever, the increase in core body temperature prompts an elevation in heart rate. This physiological response aims to enhance blood flow to the tissues, aiding in heat dissipation through the skin.

Question 21

What is the role of the cardiovascular control center in the brain in regulating heart rate?

Answer 21

The cardiovascular control center in the brain plays a crucial role in coordinating the relative activities of the parasympathetic and sympathetic branches of the autonomic nervous system. It modulates the balance between these two branches, adjusting their input to the heart and thereby regulating heart rate based on physiological needs and conditions.

Question 22

What is stroke volume (SV), and how is it controlled?

Answer 22

troke volume (SV) is the volume of blood pumped out of each ventricle during each heartbeat. It is controlled through extrinsic and intrinsic factors. Extrinsic control involves external factors, mainly influenced by the sympathetic nervous system. Intrinsic control also influences contractility but involves factors within the heart, contributing to the regulation of stroke volume.

Question 23

What is the relationship between end-diastolic volume (EDV) and stroke volume (SV)?

Answer 23

EDV and SV exhibit a direct correlation, meaning that as more blood returns to the heart, leading to increased EDV, a larger volume of blood is pumped out during systole, resulting in increased SV. It’s essential to note that the ventricles never completely empty during systole. The presence of more blood in the ventricle causes distension, stretching the cardiac muscle fibers and influencing the length-tension relationship. This alteration in muscle fiber length allows for a more effective contraction during systole.

Question 24

What you think would occur if the right ventricle was to pump an increased volume of blood into the pulmonary circulation? Would there be an increase or decrease in EDV in the left ventricle? What about the SV?

Answer 24

An increase of blood volume from the right ventricle would return to the left atria to be pumped to the left ventricle and increase end diastolic volume and thus stroke volume.

Question 25

What is preload, and how does it impact end-diastolic volume (EDV) and stroke volume?

Answer 25

Preload refers to the amount of blood returning to the ventricle, also known as venous return. An increase in preload, achieved by elevating venous return, leads to higher EDV and stroke volume. Preload involves stretching the right or left ventricles to their maximum dimensions, optimizing their ability to contract during systole.

Question 26

What is afterload, and how does increased pressure in the aorta affect stroke volume?

Answer 26

Afterload is the force opposing ventricular contraction. Increased aortic pressure requires the left ventricle to work against a greater load. This can cause premature closure of the aortic valve, reducing stroke volume. However, normal blood volume returning during diastole increases end-diastolic volume (EDV) and, consequently, the force of the next contraction.

Question 27

What is ejection fraction, and why is it clinically relevant?

Answer 27

Ejection fraction is the proportion of blood pumped out of the ventricles relative to the total volume before contraction during systole. Clinically, it’s a significant parameter, often measured by echocardiography or calculated. A normal ejection fraction at rest is approximately 60%, indicating that a considerable amount of blood remains in the ventricles post-systole, serving as a reserve for situations requiring increased cardiac output.

Question 28

What are some ways in which sympathetic stimulation stimulates the heart?

Answer 28

Some ways in which sympathetic stimulation regulates the heart are:
* Increase the force of contraction
* Increase stroke volume
* Shift the Frank-Starling curve upwards
* Increase AV node excitability
* Increase contractility of cardiac muscles

The effects of extrinsic and intrinsic control can occur at the same time for an even greater increase of
stroke volume

Question 29

Would increased parasympathetic activity result in INCREASED or DECREASED cardiac output?

Answer 29

Increased parasympathetic activity would result in decreased cardiac output.

Question 30

Would increased heart rate result in INCREASED or DECREASED cardiac output?

Answer 30

Increased heart rate would result in increased cardiac output.

Question 31

Would increased sympathetic activity result in INCREASED or DECREASED cardiac output?

Answer 31

Increased sympathetic activity would result in increased cardiac output.

Question 32

Would decreased stroke volume result in INCREASED or DECREASED cardiac output?

Answer 32

Decreased stroke volume would result in decreased cardiac output.

Question 33

Would decreased end-diastolic volume result in INCREASED or DECREASED cardiac output?

Answer 33

Decreased end-diastolic volume would result in decreased cardiac output.

Question 34

what is end-diastolic volume?

Answer 34

End-diastolic volume refers to the amount of blood present in a ventricle at the end of its relaxation phase, or diastole, just before the subsequent contraction (systole). It represents the maximum volume of blood that the ventricle holds during its filling phase.

Question 35

Would prolonged increases in heart rate have positive or negative effects on the heart?

Answer 35

Negative effects.

Explanation: Prolonged increases in heart rate reduce ventricular filling time, leading to insufficient blood filling, potential backup in the pulmonary system and organs, and eventually decreased cardiac output. This may weaken the heart muscles over time.

Question 36

What structural changes might occur in the heart when compensating for decreased cardiac output by increasing stroke volume?

Answer 36

Cardiac hypertrophy.

Explanation: Increased stroke volume may lead to cardiac hypertrophy, which initially allows the heart to pump harder. However, hypertrophy can strain the cardiovascular system, impair diastolic function, and limit the heart’s ability to fill properly, potentially leading to decreased cardiac output.

Question 37

How might a prolonged increase in heart rate impact cardiac function over time?

Answer 37

It may weaken the heart muscles and contribute to decreased cardiac output.

Question 38

What challenges may arise from long-term increases in stroke volume?

Answer 38

Challenges include increased workload, potential strain on the cardiovascular system, impaired diastolic function, and limitations in ventricular filling, all of which may contribute to decreased cardiac output.

Question 39

What might happen long term if the heart is forced to increase heart rate for a long period of time to
maintain cardiac output? What might happen if it was forced to increase stroke volume to
maintain cardiac output?

Answer 39

• Increased heart rate: A faster heart rate can weaken the heart muscles and be counterproductive as it
  allows less time for the ventricles to fill with blood after each heartbeat. This can eventually cause a backup of blood in the pulmonary system and the organs as well as decreased CO.
• Increased stroke volume: The heart can also compensate by pumping harder by developing stronger, thicker heart walls (cardiac hypertrophy). Hypertrophy, however, increases the heart’s need for nutrients and oxygen. It will also make the diastolic function worse by impairing the ability of the heart
  to relax properly. Finally, hypertrophy can limit the heart’s ability to fill with blood (i.e. further reducing cardiac output).