Regulation of Stroke Volume & Heart Rate Flashcards

1
Q

Describe the role of the pacemaker cells in regulating heart rate.

A

Pacemaker cells, typically found in the sinoatrial node, depolarize to threshold first, initiating an action potential that spreads through the heart to cause contractions.

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2
Q

How does the sympathetic nervous system affect heart rate?

A

The sympathetic nervous system, responsible for the fight or flight response, increases heart rate by releasing noradrenaline and adrenaline, which act on adrenergic receptors to increase the slope of the pacemaker potential.

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3
Q

Define tachycardia.

A

Tachycardia is the technical term for an increased heart rate, often caused by factors like sympathetic nervous system activation.

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4
Q

What is the role of the parasympathetic nervous system in heart rate regulation?

A

The parasympathetic nervous system, responsible for rest and digest functions, decreases heart rate by releasing acetylcholine, which acts on muscarinic receptors to hyperpolarize pacemaker cells.

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5
Q

Describe the influence of preload on stroke volume.

A

Preload, a term coined by Starling, refers to the initial length of the cardiac muscle and influences the energy of contraction, as per Starling’s law.

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6
Q

How does the parasympathetic nervous system affect heart rate?

A

The parasympathetic nervous system decreases heart rate by releasing acetylcholine, which hyperpolarizes pacemaker cells and slows down the firing of action potentials.

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7
Q

What is bradycardia?

A

Bradycardia refers to a decreased heart rate, often caused by factors like parasympathetic nervous system activation.

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8
Q

Define stroke volume.

A

Stroke volume is the amount of blood pumped by the heart in one contraction, influenced by factors like preload, afterload, and contractility.

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9
Q

Define the term ‘preload’ in the context of muscle physiology.

A

Preload refers to the initial resting length of the muscle before contraction, which is correlated with the tension or strength of the subsequent muscle contraction.

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10
Q

How does the number of crossbridges between actin and myosin filaments affect muscle contraction strength according to the Starling curve?

A

Optimal crossbridge formation at peak tension results in a strong muscle contraction. Fewer crossbridges at larger muscle lengths lead to weaker contractions, while excessive overlap hinders crossbridge formation, reducing efficiency.

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11
Q

Describe the application of the length-tension relationship from skeletal muscle to cardiac muscle.

A

The length-tension relationship, commonly applied to skeletal muscle, is also relevant to cardiac muscle. In cardiac muscle, the end diastolic volume, which stretches the muscle, influences the strength of contraction and stroke volume.

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12
Q

Do changes in venous return affect cardiac muscle contraction and stroke volume?

A

Yes, increasing venous return stretches the cardiac muscle more, leading to a stronger contraction and increased stroke volume. Conversely, decreasing venous return results in less muscle stretching, weaker contractions, and lower stroke volume.

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13
Q

Explain the significance of end diastolic volume in relation to cardiac muscle contraction.

A

End diastolic volume represents the volume of blood filled into the ventricles before contraction. It influences the stretching of cardiac muscle, affecting the strength of contraction and stroke volume in the heart.

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14
Q

Describe the importance of the mechanism discussed in the content.

A

The mechanism ensures self-regulation and closely matched stroke volumes of the left and right ventricles to prevent blood accumulation on one side.

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15
Q

Define afterload in the context of the content.

A

Afterload is defined as the load against which the muscle tries to contract, particularly referring to the pressure the ventricle must overcome to push the aortic valve open.

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16
Q

How does the mitral valve influence stroke volume during systole?

A

The mitral valve stops the ventricle from shortening during systole, requiring the ventricle to build up pressure to push the mitral valve closed.

17
Q

Describe the role of the aortic valve in relation to the left ventricle.

A

The aortic valve being closed stops the left ventricle from shortening during systole, requiring the left ventricle to build up enough pressure to push the aortic valve open.

18
Q

What is the major factor influencing total peripheral resistance?

A

The major factor is how constricted or dilated the arterioles are, which affects the resistance vessels and consequently the total peripheral resistance.

19
Q

How does increased total peripheral resistance impact stroke volume?

A

Increased total peripheral resistance leads to a decrease in stroke volume, as more energy is spent in building up pressure in the left ventricle to overcome the resistance.

20
Q

Describe the relationship between arterial pressure, afterload, and stroke volume.

A

Arterial pressure determines afterload, which in turn affects total peripheral resistance. Increased total peripheral resistance due to higher arterial pressure results in decreased stroke volume.

21
Q

Explain the impact of constricted arterioles on the left ventricle.

A

Constricted arterioles increase total peripheral resistance, requiring the left ventricle to work harder to push the aortic valve open, leading to decreased stroke volume.

22
Q

How does the content explain the relationship between energy expenditure and stroke volume?

A

The content suggests that more energy is wasted in building up pressure in the left ventricle to overcome resistance, resulting in decreased stroke volume as less energy is available for ejecting blood effectively.

23
Q

Describe the relationship between heart and stroke volume when heart rate is increased in isolation.

A

Increasing heart rate in isolation can lead to a decrease in stroke volume due to cutting into the rapid filling phase, reducing end diastolic volume, and subsequently decreasing preload and force of contraction.

24
Q

Define Starling’s law in the context of cardiac physiology.

A

Starling’s law states that the force of cardiac muscle contraction is directly proportional to the initial length of the muscle fibers before contraction, emphasizing the relationship between preload and stroke volume.

25
Q

How does decreasing vagal tone affect heart rate during exercise?

A

Decreasing vagal tone during exercise allows for an increase in heart rate by reducing the inhibitory effect of acetylcholine on the pacemaker cells, leading to a higher heart rate.

26
Q

Describe the role of sympathetic tone in increasing heart rate during exercise.

A

Increased sympathetic tone during exercise stimulates the heart to beat faster, contributing to the overall increase in heart rate observed during physical activity.

27
Q

What effect does increased sympathetic tone have on the contractility of the heart during exercise?

A

Increased sympathetic tone during exercise enhances the contractility of the heart, leading to stronger and more forceful contractions of the cardiac muscle.

28
Q

Explain how increasing heart rate during exercise differs from increasing heart rate in isolation.

A

During exercise, increasing heart rate is accompanied by other compensatory mechanisms such as increased contractility and decreased vagal tone, which offset the decrease in stroke volume that occurs when heart rate is increased in isolation.