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Movement of skeletalmuscles is also important in preventing orthostatic hypotension. During walking, for example, movement of leg musclescompresses veins and augments venous return, because veinsoutside the central venous system contain one-way valves thatprevent backflow of blood.Effect of RespirationAnother factor affecting venous return is the effect of respiration. During inspiration, as the rib cage expands and the diaphragm moves down, negative pressure is created in thethorax. Simultaneously, pressure in the abdominal cavityrises, due to the downward movement of the diaphragm.Thus, veins in the abdomen are subjected to a positive pressure, which augments venous return toward the negative pressure in the thorax.
During expiration, the gradient is reduced.With increased depth and frequency of respiration, forexample during exercise, there is a pulsatile increase in venousreturn.Cardiac Function and Vascular Function CurvesThe interactions between vascular function and cardiac function can be illustrated by the simultaneous consideration oftwo relationships: the cardiac function curve (previously considered) and the vascular function curve (Fig.
11.7). Thecardiac function curve illustrates the Starling relationship, inwhich right atrial pressure is the independent variable andcardiac output is the dependent variable. A rise in right atrialpressure (preload) produces a rise in cardiac output. The vascular function curve as illustrated is an unconventional graph,in which the independent variable (cardiac output) is plottedon the y-axis, and the dependent variable (right atrial pressure) is on the x-axis. This is an inverse relationship: a rise incardiac output produces a fall in right atrial pressure (orpreload).
In other words, greater cardiac output will result inredistribution of blood volume, with reduction of preload.Note that the x intercept of the vascular function curve is themean circulatory pressure. This is the pressure in the systemwhen cardiac output is zero, and is dependent on bloodvolume and the compliance of the vascular system as a whole.Thus, if the heart is stopped, pressure equilibrates across theentire cardiovascular system. A positive mean circulatorypressure is necessary for the heart to effectively pump blood.Mean circulatory pressure is the residual pressure thatwould exist throughout the cardiovascular system (afterequilibration) if the heart were suddenly stopped and vasculartone throughout the system were to remain the same.
Thenormal value for mean circulatory pressure is about 7 mm Hgand is a function of vascular tone (particularly venous tone) andblood volume. Without positive mean circulatory pressure, efficient circulation of blood would not be possible, becausepreload would be compromised at even a very low cardiacoutput.Integration of the Cardiac and VascularFunction CurvesWhen the cardiac function and vascular function curves areplotted on the same graph, the two curves intersect at onepoint, the resting cardiac output and right atrial pressure(normally about 5 L/min and 2 mm Hg); in other words, thisis the steady-state or equilibrium point for normal restingcardiovascular function. When one of the curves is altered, anew equilibrium point is reached.
For example, an increase inblood volume (hypervolemia) will shift the vascular functioncurve upward and to the right (Fig. 11.7B). At the new equilibrium point for the two curves (point B), cardiac output isincreased, due to higher preload. Venous constriction wouldhave the same effect as increased volume. On the other hand,hypovolemia will shift the vascular function curve to the leftand downward, and the new equilibrium point A representslower cardiac output at rest. The cardiac mechanism resultingThe Cardiac Pump10ACardiacFunction Curve86CardiacOutput(L/min) 4Cardiac output = 5 L/minXVascularFunctionCurveMeancirculatorypressure2Changes invascularvolume021064Right AtrialPressureBX4ACardiacOutput(L/min)54MCP0462Right Atrial Pressure10Norepinephrine (sympathetic stimulation)76C6Heart failureXX A B C D2BChanges incontractility8Hypovolemia(hemorrhage)( preload/cardiacoutput)6810Hypervolemia( preload/ cardiac output)812344D2MCPC8100246Right Atrial Pressure81010TPR8B6CardiacOutput(L/min) 4XAX45B CardiacOutput7 (L/min)ATPR2MCPD0246Right Atrial Pressure810Figure 11.7 Cardiac Function and Vascular Function Curves A, In the cardiac function curve,right atrial pressure is the independent variable and cardiac output is the dependent variable.
A rise in rightatrial pressure produces a rise in cardiac output, as predicted by the Frank-Starling relationship. In thevascular function curve, the independent variable is cardiac output, plotted unconventionally on the y-axis,and the dependent variable is right atrial pressure. This is an inverse relationship; a rise in cardiac outputproduces a fall in right atrial pressure. The x-intercept of the vascular function curve is the mean circulatorypressure (MCP), the pressure throughout the system when cardiac output is zero.
The two curves intersectat point X, the resting cardiac output and right atrial pressure. This is the normal resting steady state forcardiovascular function. When one of the curves is displaced, for example by a change in (B) blood volume,(C) contractility, or (D) total peripheral resistance (TPR), a new steady state is reached.in these changes in cardiac output with changes in the vascularfunction curve is the Frank-Starling relationship.Similarly, changes in the cardiac function curve also producenew equilibrium points between the two curves (Fig.
11.7C).An increase in contractility, for example due to sympatheticstimulation of the heart, will increase the slope of the cardiacfunction curve, with higher cardiac output at the new equi-librium. Heart failure is associated with a lower slope in thecardiac function curve, and cardiac output is reduced as aresult.Changes in total peripheral resistance (TPR) affect both thevascular function and cardiac function curves (Fig. 11.7D).
Inthis analysis, it is assumed that arterial resistance (specifically,resistance in small arteries and arterioles) is altered, while124Cardiovascular Physiologyvenous tone is unchanged. Thus, if TPR is diminished, thevascular function curve rotates up and to the right, becausevenous and right atrial pressure will be raised as a result of thelower arterial resistance. Note that mean circulatory pressureis unchanged, because total compliance of the vascular systemis not significantly affected. The cardiac function curve shiftsupward, as stroke volume is ejected against lower arterial pressure (reduced afterload) due to reduced TPR.
Thus, the equilibrium point for the system moves from point X to point B,at which cardiac output is elevated from the original steadystate. Opposite changes occur when TPR is elevated. The vascular function curve rotates downward and to the left, and thecardiac function curve shifts downward, due to the effects ofincreased afterload. The equilibrium shifts from point X topoint A, at which cardiac output is reduced from the originalsteady state.CLINICAL CORRELATEVenous Pressure in Heart FailureIn right-heart failure, contractility of the right ventricle isreduced, often due to myocardial infarction.
As a result, cardiacoutput will be reduced and venous pressure will be elevated.This knowledge can be useful diagnostically. If a normal individual is lying in bed with his upper body tilted up 30 to 60degrees on a pillow, the external jugular vein is ordinarily collapsed just above the level of the clavicle.
The height of thecolumn of blood in the external jugular vein is a measure ofcentral venous pressure or right atrial pressure. If a patient is inheart failure and the central venous pressure is elevated, the veinwill be distended significantly above the clavicle.125CHAPTER12The Peripheral CirculationThe peripheral circulation consists of the systemic arteries,veins, and microcirculation.
The structures of arteries andveins include three tissue layers (Fig. 12.1):■■■Tunica intima: This innermost layer consists of a singleendothelial cell layer forming the inner lining of thevessel; these cells rest on a basement membrane thatseparates the intima from the media.Tunica media: The media consists mainly of smoothmuscle and is the contractile portion of the vascularwall.Tunica adventitia: The adventitia consists mainly ofconnective tissue.There is variation in the absolute and relative thickness ofmedia and adventitia between arteries and veins, as well asbetween small and large vessels; differences are also observedbetween vessel types in the connective tissue and cellular constituents of these layers. For example, the walls of large arterialvessels are rich in elastic tissue and have a relatively thickadventitia compared with smaller arteries.
On the other hand,smaller arteries have a relatively more dominant, muscularmedial layer. Capillaries, unlike other vessels, have no mediaor adventitia. Their vascular walls consist simply of endothelial cells and basement membrane.THE MICROCIRCULATION AND LYMPHATICSThe microcirculation consists of vessels less than 100 micrometers (μm) in diameter and includes arterioles, metarterioles, capillaries, and venules (Fig.
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