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Factors Effecting Cardiac Output Physical Education Essay

Info: 1568 words (6 pages) Essay
Published: 1st Jan 2015 in Physical Education

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Inotropy can have positive or negative effect on the heart, especially the ventricles. There are few factors that can influence inotropy; this can either be neuronal, hormonal. The neuronal influence is predominately from the autonomic nerves, either the parasympathetic or the sympathetic nerves and these have both negative and positive effect on inotropy. However, other influences come from some drugs which have positive or negative effect on inotropy. This will consequently affect the cardio output by changing the state of for example ESV, preload, stroke volume and heart rate. All of these factors are related and depend on each other.

Section A:

The autonomic nerves are divided into two, parasympathetic and sympathetic nerves. The sympathetic nerves cause a positive inotropy. It does this by releasing norpinephrine by the postganlionic fibers and the secretion of epinephrine from adrenal medulla. These hormones, norpinephrine and epinephrine, causes the cardiac muscle cell metabolism. Hence, the contraction and the force of contraction in the cardiac muscle increase. This increases because of special types of receptors called adrenergic receptors found on the plasma membrane of the cardiac muscle cells. There are two types; one is called the alpha receptors and the other type is called the beta receptors. These receptors bind to and recognise both norepinephrine and epinephrine. Because of the cardiac muscle cells contraction increases this will cause the ventricles to contract harder. This will decrease the end systolic volume, because the amount of blood ejected from the ventricles increases.

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The other types of nerves that influence the inotropy are called parasympathetic nerves. The parasympathetic stimulation from the vagus causes the release of acetylcholine (ACh), which is a neurotransmitter. The ACh binds to two types of receptors; they are known as the muscarinic and nicotinic cholinergic receptors. There are different types of mascarinic receptors; and the M2 muscarinic receptors are specific for the heart. These receptors work by maintaining the heart to stay at its constant state. When the ACh is released it binds to M2 mascurinic receptors. Therefore, after the reactions occur between the M2 mascurinic receptors and the ACh, the effect it has on the heart is that it reduces the heart rate; it also reduces the action potential produced by the SA node and the AV node. However, it also affects the heart’s ability to contract. Both the arterial and ventricular muscle cells are innervated by the sympathetic and parasympathetic nerves. However, in the ventricular muscle cells, the parasympathetic nerves have more compact than the sympathetic nerves. For these reasons the parasympathetic stimulation has a negative effect on the inotropy.

Beside the parasympathetic and sympathetic stimulations having influence on the inotropic state; there are few hormones, described above, and drugs that can also influence the inotropic state of the heart. As mentioned above, epinephrine, which is released from the adrenal gland, and norepinephrine, which is released from the sympathetic nerves, increases the heart rate. This has a positive effect on the inotropic state of the heart. However, there are few drugs that have the opposite effect of the norepinephrine and epinephrine; these drugs are known as antagonist, because they block the action of the hormones. Some examples of such drugs are propanolol and digoxin. Propranolol works by blocking the beta adrenergic receptors that binds with epinephrine. This means that epinephrine cannot longer bind to these receptors, so therefore its effects are no longer seen and blocked. This is why propranolol and drugs similar to it are called beta-blockers. The actions seen by these drugs on the heart is that it slows down the heart rate.

When the ventricles contract with great deal of force, the ventricles have to overcome some sort of tension; this tension is known as afterload and comes from the aorta pressure. Therefore, if the afterload is increased, this will mean the ventricular muscle cells will contract for longer period. Hence, the greater the end systolic volume will be; this is because the blood ejected is less and this will reduce the stroke volume, which means cardiac output will decrease as well. This mechanism only happens when the inotropy is increased and this can be done by hormonal or anatomic stimulation influence. On the other hand, a reduced inotropic sate, in this case the afterload is increased as well, will have the opposite effect on the end systolic volume.

Section B:

The preload is directly proportional to the end diastolic volume; therefore if there is an increase in the preload, there is an increase in the end diastolic volume. Basically what preload does is that it affects the cardiac muscle cell’s ability of creating tension. So this means during systole, during the contraction of the ventricular muscle cells, the force produced increases and is forceful. Therefore increasing inotropy, by hormones such as epinephrine or stimulation from the autonomic nervous system, will increase in the force of contraction of the ventricles. Another way the inotropy can be increased depends on the amount of blood that is returned to the heart, which is known as the venous return. This can for example be caused by excise; this will increase the venous return and which will increase the end diastolic volume. Hence the increase of end diastolic volume will cause the increase of both stroke volume and cardiac output. What the venous return does is that it stretches the ventricular muscle cells because of the more blood. So this means the sacromere length will increase so does the tension. This results in the contraction of the ventricular muscle cells with greater force and the ejection of more blood. Thus, an increase in the preload will cause an increase in end diastolic volume; so therefore stroke volume is increased and cardiac output. This mechanism is known as the Frank-Starling law; this law basically states that the more the heart is stretched, the harder the heart contracts to eject more blood.

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When the ventricles contract with great deal of force, the ventricles have to overcome some sort of tension; this tension is known as afterload and comes from the aorta pressure. Therefore, if the afterload is increased, this will mean the ventricular muscle cells will contract for longer period. Hence, the greater the end systolic volume will be; this is because the blood ejected is less and this will reduce the stroke volume, which means cardiac output will decrease as well. This mechanism only happens when the inotropy is increased and this can be done by hormonal or anatomic stimulation influence. On the other hand, a reduced inotropic sate, in this case the afterload is increased as well, will have the opposite effect on the end systolic volume.

The contractility of the heart can, especially the ventricles, can have a great deal on the pressure and the development tension on the ventricles. This has an effect on the ejection fraction, because the inotropy changes the amount of blood ejected from the ventricles. There are two types of factors that increase the inotropic state. The types are either said to have positive inotropic or negative inotropic.

In order for the cardiac muscles cells to contract, the sarcoplasmic reticulum has to release Ca2+ .What causes the contraction of the cardiac cells are the entry of Ca2+ into the cells. Therefore what the positive inotropic does is that it increases the amount of Ca2+ that enter into the cardiac muscle cells. This increases the stroke volume and lowers the ESV which in return increases the cardiac output. An example of this is the sympathetic stimulation on the heart. However, the negative inotropic has the opposite effect. This can for example be the parasympathetic stimulation; basically this will block the entry of the Ca2+ into the cardiac muscle cells. Thus the ejection fraction is reduced which leads to an increase on the ESV; hence the stroke volume decrease and cardiac output as well.

The heart rate is defined as the number of times the heart beats in one minutes. In a normal person at rest beats as 70 beats per minutes. The body controls the heart rate different ways that might increase or decrease heart rate. Activities from the parasympathetic nerves decreases the heart rate, basically what happens is that stimulations sent from the parasympathetic nerves to the heart decreases heart rate; whereas the sympathetic nerves have the opposite effect. The effect seen from this is that the pacemaker potential decreases due to a decrease in the F-type sodium ions. This means the threshold is reached more slowly than it is normally, thus heart rate decreases and consequently the cardiac out decreases as well.

Heart rate can also be affected by hormonal influence. One primarily example is the release of epinephrine which is released from adrenal medulla. This hormone basically acts on the receptors found on beta-adrenergic receptors in the SA node. These receptors normally accept norepinephrine, which is released from the neurons. The effect of these hormones is that it increases the heart rate, hence the cardiac output.

 

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