Venous return and cardiac output relationship advice

Venous Return - Control of Cardiac Output - NCBI Bookshelf

venous return and cardiac output relationship advice

These elegant studies led to a model of these relationships that could be graphically Cardiac function curves (sometimes called cardiac output curves) are Systemic vascular function curves (sometimes called venous return curves) are purposes only, and are not a source of medical decision-making advice. Study 22 Relationship between Cardiac Output and Venous Return flashcards from Kim L. on StudyBlue. Pulse can be palpated manually by placing the tips of the fingers across an artery that The relationship between blood volume, blood pressure, and blood flow is . the veins, the rate of velocity increases, as blood is returned to the heart.

Experimentally, if cardiac output is stopped by fibrillating the heart, aortic pressure falls and PRA increases to a common value of about 8 mmHg x-intercept of black curve in figure if the baroreceptor reflex is blocked. This pressure, which is recorded shortly after the heart is stopped, is called the mean circulatory filling pressure Pmc.

This pressure is not midway between the mean arterial pressure and the PRA because venous compliance is times greater than arterial compliance; therefore, as the volume of blood decreases in the arterial vessels and increases in the venous vessels, the arterial pressure typically falls at least fold more than the venous pressure rises. If the heart is restarted, then PRA decreases as the CO increases moved upward and leftward on black curve.

As the PRA starts to fall below zero, the increase in CO begins to plateau because the vena cava collapses, thus limiting venous return to the heart. There is no single systemic vascular function curve, but instead there is a family of curves that are determined by the blood volume Volvenous compliance CV; inverse of venous tone and systemic vascular resistance SVR; primarily arterial resistance. If, for example, blood volume is increased due to renal retention of sodium and water, or venous compliance is decreased due to sympathetic activation of the veins Panel Athere is a parallel shift to the right in the vascular function curve, which leads to an increase in the Pmc when the heart is stopped.

The opposite shift occurs with decreased blood volume or increased venous compliance. If SVR is increased Panel B by administering an arterial vasoconstrictor drugthe slope of the systemic vascular function curve decreases, but there is little or no change in the Pmc.

The opposite occurs with a decrease in SVR. The Pmc does not change appreciably with arterial constriction or dilation because arterial diameter changes required to change resistance causes only a small change in total vascular compliance. On the other hand, it both arteries and veins are constricted during sympathetic activation, then the curve will shift to the right as shown in Panel C increased Pmc due to decreased CV and the slope will decrease due to the increase in SVR.

The PRA increases because the decrease in SVR would decrease arterial pressure and arterial blood volume thereby shifting blood volume to the venous side. The CO increases primarily because stroke volume is enhanced by the Frank-Starling mechanism in response to the increase in preload, and because ventricular afterload is reduced as represented by the small shift to the left in the cardiac function curve.

If cardiac function were enhanced not shownthe cardiac function curve would shift up and to the left along the vascular function curve. There would only be, however, a very small increase in CO because decreasing the PRA below zero causes venous collapse, which impedes venous return and hence filling of the ventricle. If cardiac function is depressed e.

venous return and cardiac output relationship advice

This shows that depressing the heart leads to an increase in PRA and venous pressures along with the decrease in CO. A variety of commercial electronic devices are also available to measure pulse. The pulse is most readily measured at the radial artery, but can be measured at any of the pulse points shown.

Measurement of Blood Pressure Blood pressure is one of the critical parameters measured on virtually every patient in every healthcare setting. The technique used today was developed more than years ago by a pioneering Russian physician, Dr.

Turbulent blood flow through the vessels can be heard as a soft ticking while measuring blood pressure; these sounds are known as Korotkoff sounds.

The technique of measuring blood pressure requires the use of a sphygmomanometer a blood pressure cuff attached to a measuring device and a stethoscope. The technique is as follows: Although there are five recognized Korotkoff sounds, only two are normally recorded. Initially, no sounds are heard since there is no blood flow through the vessels, but as air pressure drops, the cuff relaxes, and blood flow returns to the arm.

As shown in Figure As more air is released from the cuff, blood is able to flow freely through the brachial artery and all sounds disappear. When pressure in a sphygmomanometer cuff is released, a clinician can hear the Korotkoff sounds.

venous return and cardiac output relationship advice

In this graph, a blood pressure tracing is aligned to a measurement of systolic and diastolic pressures. The majority of hospitals and clinics have automated equipment for measuring blood pressure that work on the same principles. The patient then holds the wrist over the heart while the device measures blood flow and records pressure. Cardiac output Volume of the blood Resistance Recall that blood moves from higher pressure to lower pressure. It is pumped from the heart into the arteries at high pressure.

Since pressure in the veins is normally relatively low, for blood to flow back into the heart, the pressure in the atria during atrial diastole must be even lower. It normally approaches zero, except when the atria contract see Figure Cardiac Output Cardiac output is the measurement of blood flow from the heart through the ventricles, and is usually measured in liters per minute. Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow.

These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels. Conversely, any factor that decreases cardiac output, by decreasing heart rate or stroke volume or both, will decrease arterial pressure and blood flow. These factors include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis.

Compliance Compliance is the ability of any compartment to expand to accommodate increased content. A metal pipe, for example, is not compliant, whereas a balloon is. The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure.

Veins are more compliant than arteries and can expand to hold more blood. When vascular disease causes stiffening of arteries, compliance is reduced and resistance to blood flow is increased.

CV Physiology | Venous Return - Hemodynamics

The result is more turbulence, higher pressure within the vessel, and reduced blood flow. This increases the work of the heart. Blood Volume The relationship between blood volume, blood pressure, and blood flow is intuitively obvious. Water may merely trickle along a creek bed in a dry season, but rush quickly and under great pressure after a heavy rain. Similarly, as blood volume decreases, pressure and flow decrease.

As blood volume increases, pressure and flow increase. Under normal circumstances, blood volume varies little. Low blood volume, called hypovolemia, may be caused by bleeding, dehydration, vomiting, severe burns, or some medications used to treat hypertension. It is important to recognize that other regulatory mechanisms in the body are so effective at maintaining blood pressure that an individual may be asymptomatic until 10—20 percent of the blood volume has been lost.

Treatment typically includes intravenous fluid replacement. Hypervolemia, excessive fluid volume, may be caused by retention of water and sodium, as seen in patients with heart failure, liver cirrhosis, some forms of kidney disease, hyperaldosteronism, and some glucocorticoid steroid treatments.

Restoring homeostasis in these patients depends upon reversing the condition that triggered the hypervolemia. Resistance The three most important factors affecting resistance are blood viscosity, vessel length and vessel diameter and are each considered below.

Blood viscosity is the thickness of fluids that affects their ability to flow. Clean water, for example, is less viscous than mud. The viscosity of blood is directly proportional to resistance and inversely proportional to flow; therefore, any condition that causes viscosity to increase will also increase resistance and decrease flow. For example, imagine sipping milk, then a milkshake, through the same size straw. You experience more resistance and therefore less flow from the milkshake.

Conversely, any condition that causes viscosity to decrease such as when the milkshake melts will decrease resistance and increase flow. Normally the viscosity of blood does not change over short periods of time. The two primary determinants of blood viscosity are the formed elements and plasma proteins.

Since the vast majority of formed elements are erythrocytes, any condition affecting erythropoiesis, such as polycythemia or anemia, can alter viscosity.

Since most plasma proteins are produced by the liver, any condition affecting liver function can also change the viscosity slightly and therefore decrease blood flow. Liver abnormalities include hepatitis, cirrhosis, alcohol damage, and drug toxicities. While leukocytes and platelets are normally a small component of the formed elements, there are some rare conditions in which severe overproduction can impact viscosity as well. Blood vessel length is directly proportional to its resistance: As with blood volume, this makes intuitive sense, since the increased surface area of the vessel will impede the flow of blood.

Likewise, if the vessel is shortened, the resistance will decrease and flow will increase. The length of our blood vessels increases throughout childhood as we grow, of course, but is unchanging in adults under normal physiological circumstances.

Cardiology - Cardiac Output

Further, the distribution of vessels is not the same in all tissues. Adipose tissue does not have an extensive vascular supply. One pound of adipose tissue contains approximately miles of vessels, whereas skeletal muscle contains more than twice that.

Overall, vessels decrease in length only during loss of mass or amputation. An individual weighing pounds has approximately 60, miles of vessels in the body. Gaining about 10 pounds adds from to miles of vessels, depending upon the nature of the gained tissue. One of the great benefits of weight reduction is the reduced stress to the heart, which does not have to overcome the resistance of as many miles of vessels.

In contrast to length, the blood vessel diameter changes throughout the body, according to the type of vessel, as we discussed earlier.

The diameter of any given vessel may also change frequently throughout the day in response to neural and chemical signals that trigger vasodilation and vasoconstriction.

The vascular tone of the vessel is the contractile state of the smooth muscle and the primary determinant of diameter, and thus of resistance and flow. The effect of vessel diameter on resistance is inverse: Given the same volume of blood, an increased diameter means there is less blood contacting the vessel wall, thus lower friction and lower resistance, subsequently increasing flow.

A decreased diameter means more of the blood contacts the vessel wall, and resistance increases, subsequently decreasing flow. The influence of lumen diameter on resistance is dramatic: A slight increase or decrease in diameter causes a huge decrease or increase in resistance.

This means, for example, that if an artery or arteriole constricts to one-half of its original radius, the resistance to flow will increase 16 times. A Mathematical Approach to Factors Affecting Blood Flow Jean Louis Marie Poiseuille was a French physician and physiologist who devised a mathematical equation describing blood flow and its relationship to known parameters.

The same equation also applies to engineering studies of the flow of fluids.

Cardiac and Systemic Vascular Function Curves

Although understanding the math behind the relationships among the factors affecting blood flow is not necessary to understand blood flow, it can help solidify an understanding of their relationships. Please note that even if the equation looks intimidating, breaking it down into its components and following the relationships will make these relationships clearer, even if you are weak in math. Focus on the three critical variables: It may commonly be represented as 3.

One of several things this equation allows us to do is calculate the resistance in the vascular system. Normally this value is extremely difficult to measure, but it can be calculated from this known relationship: The important thing to remember is this: Two of these variables, viscosity and vessel length, will change slowly in the body. Only one of these factors, the radius, can be changed rapidly by vasoconstriction and vasodilation, thus dramatically impacting resistance and flow.

Further, small changes in the radius will greatly affect flow, since it is raised to the fourth power in the equation. The Roles of Vessel Diameter and Total Area in Blood Flow and Blood Pressure Recall that we classified arterioles as resistance vessels, because given their small lumen, they dramatically slow the flow of blood from arteries.

Arterial Blood Pressure

In fact, arterioles are the site of greatest resistance in the entire vascular network. This may seem surprising, given that capillaries have a smaller size. How can this phenomenon be explained? Although the diameter of an individual capillary is significantly smaller than the diameter of an arteriole, there are vastly more capillaries in the body than there are other types of blood vessels.

Part c shows that blood pressure drops unevenly as blood travels from arteries to arterioles, capillaries, venules, and veins, and encounters greater resistance. However, the site of the most precipitous drop, and the site of greatest resistance, is the arterioles. This explains why vasodilation and vasoconstriction of arterioles play more significant roles in regulating blood pressure than do the vasodilation and vasoconstriction of other vessels.

Part d shows that the velocity speed of blood flow decreases dramatically as the blood moves from arteries to arterioles to capillaries. This slow flow rate allows more time for exchange processes to occur.

venous return and cardiac output relationship advice

As blood flows through the veins, the rate of velocity increases, as blood is returned to the heart. The relationships among blood vessels that can be compared include a vessel diameter, b total cross-sectional area, c average blood pressure, and d velocity of blood flow.

Disorders of the…Cardiovascular System: Arteriosclerosis Compliance allows an artery to expand when blood is pumped through it from the heart, and then to recoil after the surge has passed. This helps promote blood flow. In arteriosclerosis, compliance is reduced, and pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to generate a pressure great enough to overcome the resistance.

Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors.

Artery walls that are constantly stressed by blood flowing at high pressure are also more likely to be injured—which means that hypertension can promote arteriosclerosis, as well as result from it.

Recall that tissue injury causes inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff sclerotic. As a result, compliance is reduced. Moreover, circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where they are frequently joined by leukocytes, calcium, and cellular debris.