1) Briefly explain why a larger-than-normal end-diastolic volume helps the heart
ID: 135418 • Letter: 1
Question
1) Briefly explain why a larger-than-normal end-diastolic volume helps the heart pump more blood out during that heart cycle (increase stroke volume) the list of statements below makes a step-by-step explanation? Make the answer look like that.
Higher EDV means more blood enters the ventricles
More blood means stretch of the ventricle wall _________
More stretch in ventricle wall means the sarcomeres __________
When the sarcomeres are more ______________, they are able to _____________________
Because the ventricle contracts more strongly, more blood is ________________
Therefore, an increase in EDV increases SV.
2). How does the parasympathetic nervous system affect heart rate? How does the sympathetic NS affect heart rate and stroke volume? Give cellular-level mechanism for each of these questions (ex: Channel X stays open longer. for this question make sure you talk about which ion channels in the SA node open earlier or later, be sure to then say what that means for membrane potential (does it become more depolarized? More hyper polarized?) and then what that means for reaching threshold in the SA node and what that means for the rate at which these cells can fire AP’s. So - this is like the first question - where you need to take the logic step by step.
3) In Q2 you summarized how the PNS affects heart rate (and thus CO) and how the SNS affects heart rate and stroke volume (and thus CO). For this question: summarize how the SNS affects venous return and arteriolar radius, and how these effects can change CO or TPR and then MAP. for this q , when addressing the the venous return, talk about what the SNS does to VEINS.When addressing resistance in the whole circuit, talk about what the SNS does to arterioles.
help with these 3 questions please clearly (prefer typed anwer !)
Explanation / Answer
Left ventricular end-diastolic volume is often considered to be the same as preload. This is the amount of blood the veins return to the heart before contraction. Because there is no true test for preload, doctors may calculate left-side end-diastolic volume as a way to estimate preload.
Doctors use end-diastolic volume plus end-systolic volume to determine a measurement known as stroke volume. Stroke volume is the amount of blood pumped from the left ventricle with each heartbeat.
The calculation for stroke volume is:
stroke volume = end-diastolic volume – end-systolic volume
For an average-sized man, the end-diastolic volume is 120 milliliters of blood and the end-systolic volume is 50 milliliters of blood. This means the average stroke volume for a healthy male is usually about 70 milliliters of blood per beat.
Total blood volume also affects this number. The body’s total blood volume varies depending on a person’s size, weight, and muscle mass. For these reasons, adult women tend to have a smaller total blood volume, which results in a slightly lower end-diastolic and end-systolic volume compared to adult men.
A person’s end-diastolic volume tends to decrease with age.
A doctor can calculate these volumes through a few diagnostic tests, such as the following:
Information from these tests can provide an understanding of how well the heart is working.
Stroke volume is part of another calculation of heart function known as cardiac output, or how much blood the heart is pumping out each minute. Cardiac output is calculated by multiplying the heart rate and the stroke volume.
The workings of end-diastolic volume are also described by a law known as the Frank-Starling mechanism: The more the heart muscle fibers are stretched, the harder the heart will squeeze. The heart can compensate for quite some time by squeezing harder. However, squeezing harder can cause the heart muscle to thicken over time. Ultimately, if the heart muscle gets too thick, the muscle can no longer squeeze as well
There are a number of conditions related to the heart that can cause increases or decreases in end-diastolic volume.
An overly stretched heart muscle, known as dilated cardiomyopathy, can affect a person’s end-diastolic volume. This condition is often the result of a heart attack. The damaged heart muscle can become larger and floppy, unable to properly pump blood, which can lead to heart failure. As the ventricle enlarges more, the end-diastolic volume goes up. Not all people with heart failure will have a higher-than-normal end-diastolic volume, but many will.
Another heart condition that changes end-diastolic volume is cardiac hypertrophy. This often occurs as a result of untreated high blood pressure. In this case, the chambers of the heart become thicker, having to work harder against high blood pressure. At first, the end-diastolic volume decreases because the thicker heart muscle squeezes more strongly. Eventually, the heart muscle can’t get any thicker, and it starts to wear out. This causes the end-diastolic volume to increase as heart failure develops.
Sometimes abnormalities of the heart’s valves can affect the end-diastolic volume. For example, if the aortic valve that controls blood flow from the left ventricle to the aorta (the large artery that pumps oxygenated blood to the body) is smaller than normal, the heart can’t move blood out of the heart as well. This can leave behind extra blood in the heart in diastole.
Another example is mitral regurgitation, in which the blood doesn’t flow as well to the left ventricle. This can be caused by mitral valve prolapse, a condition that occurs when the mitral valve flaps don’t close properly.
Left ventricular end-diastolic volume is one of several calculations that doctors use to determine how well the heart is pumping. This calculation, combined with other information, such as the end-systolic volume, can tell your doctor more about your overall heart health
(2)Heart rate is controlled by the two branches of the autonomic (involuntary) nervous system. The sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS). The sympathetic nervous system (SNS) releases the hormones (catecholamines - epinephrine and norepinephrine) to accelerate the heart rate. The parasympathetic nervous system (PNS) releases the hormone acetylcholine to slow the heart rate. Such factors as stress, caffeine, and excitement may temporarily accelerate your heart rate, while meditating or taking slow, deep breaths may help to slow your heart rate. Exercising for any duration will increase your heart rate and will remain elevated for as long as the exercise is continued. At the beginning of exercise, your body removes the parasympathetic stimulation, which enables the heart rate to gradually increase. As you exercise more strenuously, the sympathetic system “kicks in” to accelerate your heart rate even more. Regular participation in cardiovascular exercise over an extended period of time can decrease your resting heart rate by increasing the hearts size, the contractile strength and the length of time the heart fills with blood. The reduced heart rate results from an increase in activity of the parasympathetic nervous system, and perhaps from a decrease in activity of the sympathetic nervous system
(3)
Mechanisms of Long-Term Control of Arterial Pressure by the Sympathetic Nervous System
Sympathetic nervous system activity can elevate arterial pressure by augmenting the force and/or rate of cardiac contraction; decreasing the diameter of resistance arteries; and reducing sodium and water excretion by the kidneys. Within the conceptual framework of the Guyton-Coleman model, however, only 1 of these actions can exert a major effect on the long-term level of arterial pressure. Because pressure-natriuresis is presumed to have infinite gain over the long term within the hierarchy of circulatory control mechanisms,5 the ability of efferent renal sympathetic nerve activity to shift the pressure-natriuresis relationship to higher pressures,6 directly or indirectly (eg, through renin release), is of paramount importance. If this were the only physiological effect of sympathetic activation, the results would be sodium and water retention, blood volume expansion, and increased arterial pressure. There is good evidence supporting an important role for renal sympathetic activity in the pathophysiology of hypertension. Renal denervation lowers resting arterial pressure and also attenuates the development of hypertension in numerous experimental models.7–9Furthermore, sympathetic activity at rest is quite low and is only increased ?50% in hypertension4,10; and renal tubules and juxtaglomerular cells respond to significantly lower sympathetic firing rates than do resistance arteries.11 Thus, it is quite plausible that moderately increased sympathetic nerve activity causes hypertension by affecting renal sodium and water excretion.
Nevertheless, there are some problems with this concept. First, although the majority of published studies report an effect of renal denervation on hypertension development,7 this is not uniformly the case.12,13 Second, evidence linking renal sympathetic activity to chronic changes in sodium excretion or total circulating blood volume in hypertension is also conflicting.14–16 Third, although expansion of total blood volume alone can increase arterial pressure and account for chronic hypertension under some circumstances,17,18 in general there is an inverse relationship between arterial pressure and total blood volume, across the spectrum from abnormally low to abnormally high pressures.
Related Questions
Navigate
Integrity-first tutoring: explanations and feedback only — we do not complete graded work. Learn more.