Understanding Stroke Volume: 3 Key Factors Explained

what three factors mak up stroke volume

Stroke volume is the volume of blood pumped by the heart's ventricles per beat. It is an important determinant of cardiac output, which is the product of stroke volume and heart rate. The three factors that make up stroke volume are preload, contractility, and afterload. Preload refers to the filling pressure of the heart at the end of diastole. Contractility is the force of myocyte contraction, or the inherent vigour of contraction of the heart muscles during systole. Afterload is the pressure against which the heart must work to eject blood during systole.

Characteristics Values
Preload The filling pressure of the heart at the end of diastole
Contractility The inherent vigour of contraction of the heart muscles during systole
Afterload The pressure against which the heart must work to eject blood during systole

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Preload: the filling pressure of the heart at the end of diastole

Preload is a measure of the filling pressure of the heart at the end of diastole. It is one of the three main factors that influence stroke volume, which is the volume of blood pumped from the ventricle per beat. The other two factors are contractility and afterload.

Preload is the amount of stretch or tension on the ventricular wall before it contracts. It is also referred to as the end-diastolic volume or pressure of the ventricles. This is the volume in a ventricle just before the start of systole. Preload is best described as the amount of stretch of cardiac muscle fibre before myocardial contraction occurs. An optimal amount of stretch is necessary for the subsequent ejection force.

The Frank-Starling law describes the relationship between preload and stroke volume. This law states that the more the diastolic volume at the end of diastole, the greater the force of the next contraction during systole. In other words, as preload increases, stroke volume also increases. This is because the amount of muscle fibre that shortens during contraction increases, resulting in a more forceful contraction.

Preload is influenced by factors such as blood volume, venous return, intrathoracic pressure, and systolic and diastolic function of the heart. It can be estimated using a catheter by measuring the pulmonary capillary wedge pressure. This is done by advancing a catheter into the pulmonary artery and briefly blocking blood flow to measure the pressure in the left atrium, which is used to estimate the preload.

In summary, preload is the filling pressure of the heart at the end of diastole and is an important determinant of stroke volume. It is influenced by various factors and can be estimated using a catheter.

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Contractility: the force of myocyte contraction, or the inherent vigour of heart muscle contraction

Stroke volume is influenced by three primary factors: preload, afterload, and contractility. This response will focus on the third of these factors, contractility, which refers to the force of myocyte contraction, or the inherent vigour of heart muscle contraction.

Contractility is defined as the force of myocyte contraction, or the heart's inotropy. It is one of the most important determinants of stroke volume, which is the volume of blood pumped from the ventricle per beat. The average stroke volume of a 70 kg male is 70 mL, though this can vary depending on several factors, including contractility.

The inherent vigour of the heart muscle's contraction is influenced by both sympathetic and parasympathetic stimulation. Sympathetic stimulation increases contractility, while parasympathetic stimulation decreases it. Sympathetic stimulation triggers the release of norepinephrine at the neuromuscular junction from the cardiac nerves, which binds to beta-1 receptors and opens chemical- or ligand-gated sodium and calcium ion channels. This allows an influx of positively charged ions, shortening the repolarization period and thus speeding up the rate of depolarization and contraction, resulting in an increased heart rate. On the other hand, parasympathetic stimulation releases acetylcholine, which slows heart rate by opening chemical- or ligand-gated potassium ion channels, thereby slowing the rate of spontaneous depolarization.

The impact of sympathetic and parasympathetic stimulation on contractility is also influenced by the presence of certain hormones and drugs. For example, sympathetic stimulation also stimulates the adrenal cortex to secrete epinephrine and norepinephrine, which have a positive chronotropic effect, increasing heart rate. Additionally, synthetic drugs such as dopamine and isoproterenol mimic the effects of these hormones by stimulating the influx of calcium ions, leading to an increased strength of contraction. On the other hand, negative inotropic agents such as hypoxia, acidosis, hyperkalemia, and certain synthetic drugs like beta-blockers and calcium channel blockers decrease contractility.

In summary, contractility, or the force of myocyte contraction, is a critical factor in determining stroke volume. It is influenced by both sympathetic and parasympathetic stimulation, as well as the presence of certain hormones and drugs, which can either increase or decrease the vigour of the heart muscle's contraction.

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Afterload: the pressure against which the heart must work to eject blood during systole

Stroke volume is the volume of blood pumped from the ventricle per beat. It is calculated by measuring the volume of blood in the ventricle at the end of a beat (end-systolic volume) and subtracting this from the volume of blood just before the beat (end-diastolic volume).

Stroke volume is determined by three factors: preload, contractility, and afterload. This answer will focus on the third factor, afterload, which is the pressure against which the heart must work to eject blood during systole.

Afterload is the pressure that the heart must work against to eject blood during systole (ventricular contraction). It is proportional to the average arterial pressure. As aortic and pulmonary pressures increase, the afterload increases on the left and right ventricles, respectively. Afterload is also a determinant of cardiac output, which is the product of stroke volume and heart rate.

Afterload can be calculated by determining the wall stress of the left ventricle using the Young-Laplace equation:

> {\displaystyle \left({\frac {EDP\cdot EDR}{2h}}}\right)}

Where:

  • EDP is the end-diastolic pressure in the left ventricle, typically approximated by taking pulmonary artery wedge pressure
  • EDR is the end-diastolic radius at the midpoint of the left ventricle
  • H is the mean thickness of the left ventricle wall

The tension upon the muscle fibres in the heart wall is the pressure within the ventricle multiplied by the volume within the ventricle, divided by the wall thickness. This ratio is the other factor in setting the afterload.

When comparing a normal heart to a heart with a dilated left ventricle, if the aortic pressure is the same in both hearts, the dilated heart must create greater tension to overcome the same aortic pressure to eject blood. This is because it has a larger internal radius and volume. Thus, the dilated heart has a higher afterload.

Afterload is also influenced by aortic pressure (for the left ventricle) and pulmonic pressure or pulmonary artery pressure (for the right ventricle). The pressure in the ventricles must be greater than the systemic and pulmonary pressure to open the aortic and pulmonic valves, respectively. As afterload increases, cardiac output decreases.

Elevated afterload, commonly measured as aortic pressure during systole, reduces stroke volume. It usually does not affect stroke volume in healthy individuals, but it will hinder the ventricles in ejecting blood, causing reduced stroke volume. Increased afterload may be found in conditions such as aortic stenosis and arterial hypertension.

In summary, afterload is the pressure against which the heart must work to eject blood during systole, and it is influenced by aortic and pulmonary pressures, as well as the radius and volume of the ventricles. Afterload affects cardiac output and stroke volume, and it can be calculated using the Young-Laplace equation.

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Heart size: men's hearts are larger on average, so they have higher stroke volumes

The size of the heart is one of the three factors that determine stroke volume, with men's hearts being larger on average, resulting in higher stroke volumes.

Stroke volume is the volume of blood pumped from the ventricle per beat. It is calculated by measuring the volume of the ventricle using an echocardiogram and subtracting the volume of blood in the ventricle at the end of a beat (end-systolic volume) from the volume of blood at the beginning of a beat (end-diastolic volume). The stroke volume for a healthy 70-kg man is approximately 70 mL.

The size of the heart is a factor in determining stroke volume because a larger heart can hold more blood. Men's hearts are typically larger than women's, resulting in a higher stroke volume. Additionally, the force of contraction and duration of contraction also play a role in stroke volume. The force of contraction, or contractility, is the inherent vigour of the contraction of the heart muscles during systole. An increase in contractility, such as during exercise, generally leads to an increase in stroke volume. The duration of contraction, on the other hand, refers to the time it takes for the heart to fill with blood, known as the preload, and the time it takes for the heart to empty, known as the afterload. An increase in preload will result in an increase in end-diastolic volume and a larger stroke volume. Conversely, an increase in afterload will lead to a smaller stroke volume as it becomes more difficult for the heart to eject blood.

Prolonged aerobic exercise can also increase stroke volume by increasing the amount of blood the heart can hold and eject. This results in a lower resting heart rate, as the heart can pump more blood with each beat, reducing the number of beats needed to supply the body with sufficient blood.

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Heart rate: changes in heart rate can affect stroke volume

Stroke volume is the volume of blood pumped from the ventricle per beat. It is an important determinant of cardiac output, which is the product of stroke volume and heart rate.

Heart rate, one of the three factors that make up stroke volume, can affect stroke volume in the following ways:

Heart Rate and Stroke Volume

Changes in heart rate alone inversely affect stroke volume. When heart rate increases, stroke volume can be maintained if other mechanisms are activated. These mechanisms include increased venous return, venous constriction, increased atrial and ventricular inotropy, and an enhanced rate of ventricular relaxation. However, if these mechanisms fail, an elevated heart rate will lead to a decrease in stroke volume.

During exercise, for example, an increase in heart rate can lead to an increase in stroke volume due to the activation of these additional mechanisms. On the other hand, in situations where these mechanisms are not engaged, an elevated heart rate will result in a decline in stroke volume.

The Impact of Heart Rate on Stroke Volume in Clinical Settings

In clinical settings, such as surgery or critical illness situations, patients may require higher than normal stroke volume. In these cases, it may be more appropriate to aim for optimal rather than normal stroke volume. Additionally, in cases of hypovolemia, or inadequate blood volume, stroke volume optimization algorithms are used to monitor for early signs of blood volume loss. This involves assessing various physical examination findings, such as axillary hydration status, mucous membrane colour, and capillary refill time.

The Relationship Between Heart Rate, Stroke Volume, and Cardiac Output

Cardiac output, which is the amount of blood the heart pumps from each ventricle per minute, is influenced by both heart rate and stroke volume. Changes in either of these factors can impact cardiac output. Therefore, by manipulating heart rate and stroke volume, healthcare professionals can help maintain adequate perfusion and match the body's global metabolic needs.

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