rfumsphysiology / Control of Cardiac Output
Download this guide for some hard learned lessons that just might Venous vasodilation decreases cardiac output and venous return at a. THE CARDIAC OUT PUT AND VENOUS RETURN. The vascular function ( venous return) curve depicts the relationship between blood flow. 1) where the cardiac output and right atrial pressure (RAP) are determined at the As can be deducted from the venous return equation and curve, venous return static cardiac filling pressure is still the most often used parameter to guide.
Such a measure is the Cardiac Index, defined as cardiac output divided by body surface area. Body surface area normalizes for different shapes, heights and weights. Tables are available that estimate body surface area from weight and height. An average surface area is 1. A cardiac index less than 2. Shock is suggested by a cardiac index less than 1. Although the heart is driven by tissue demand, it can only pump the amount of blood that returns to it. Cardiac output is, therefore, limited by venous return.
To make sense of this rather circular-seeming argument, a series of diagrams relating venous return and cardiac output have been developed. Relationship of right atrial pressure and venous return. The major determinant of venous return is the systemic filling pressure PSF.
Retention of salt and water, with its resulting increase of PSF, would increase the pressure difference and increase venous return noted on the upper dotted line. On the other hand, hemorrhage would reduce peripheral venous pressure and reduce venous return for a given right atrial pressure noted in the lower dotted curve. Further, if the ventricles failed to pump all the blood delivered to them, blood would accumulate in the atria thereby raising atrial pressure.
The resulting increase in right atrial pressure would reduce the pressure difference between peripheral veins and the heart and reduce venous return. Relationship of right atrial pressure and cardiac output. Right atrial pressure determines the extent of ventricular filling during diastole preload. The relationship between preload, afterload and contractility can be understood by overlaying cardiac function curve Fig. These curves demonstrate the relationship between contractility and preload and cardiac output venous return.
Reading from the normal contractility curve Fig. Assuming a constant systemic filling pressure an increase in cardiac contractility should increase stroke volume and cardiac output Fig.
- Control of Cardiac Output
- Venous Return - Hemodynamics
Two results of this change are noted on the upper curve above. First, cardiac output has increased with increased contractility. Blood volume remained unchanged, while mean systemic pressure rose from 9. The effect of the hormone was to increase the vascular tone, causing an increase in filling pressure at a constant blood volume.
Right atrial pressure is normally approximately 0 mm Hg or atmospheric pressure. At a normal level of right atrial pressure, venous return will be normal as long as mean systemic pressure and resistance are normal.
Volume and its relationship to cardiac output and venous return.
Each additional 1 mm Hg increase resulted in a similar decrease in venous return, until atrial pressure reached 7 mm Hg, the mean systemic pressure, at which point flow into the heart ceased. The results of their study are plotted in Figure 2. As atrial pressure is raised from the normal value of 0 to 7 mm Hg, venous return falls from the normal level to 0.
The slope of the relationship is the inverse of the more When right atrial pressure is reduced below the normal value of 0 mm Hg, a different venous return response pattern is observed. But with subsequent 1 mm Hg increments in pressure reduction, the rate of rise in venous return falls progressively less until it reaches a steady level at pressures below —4 mm Hg.
Further right atrial pressure reductions below —4 mm Hg will not increase venous return further. The negative right atrial pressure and venous return data are presented in Figure 2. The relationship becomes curved as pressure falls to approximately —2 to —3 mm Hg as the slope decreases progressively with additional reductions in atrial pressure. At approximately —4 mm Hg, the slope becomes 0, and further reductions do not cause additional increases in venous return.
The relationship is curvilinear between —2 and —4 mm Hg due to progressively increasing resistance to venous return resulting from collapse of more The explanation for the nonlinear nature of the relationship in the negative pressure range of the right atrial pressure and the plateau below —4 mm Hg is the progressive collapse of veins as the luminal pressure falls below extramural pressure.
Within the chest, the pressure averages approximately —4 mm Hg but cycles between values more negative during inspiration to slightly positive during expiration. As right atrial pressure, which is equal to venous pressure anywhere within the thorax, falls below atmospheric pressure, some veins just outside their point of entry into the thorax may collapse during inspiration, as their intraluminal pressure falls below atmospheric pressure.
As central venous pressure falls lower, more veins may collapse for longer portions of the respiratory cycle, while below —4 mm Hg, essentially, all veins in the chest remain collapsed until the buildup of upstream blood increases their intraluminal pressure to —4 mm Hg or greater.
The collapse of the veins increases resistance to venous return, which is the inverse of the slope of the relationship between flow and right atrial pressure. Ultimately, resistance becomes infinite below —4 mm Hg, preventing any increase in flow above that present at —4 mm Hg. The resistance increases progressively as right atrial pressure falls from approximately —2 to —4 mm Hg, causing the plotted relationship between pressure and flow to be curvilinear in this range.
The pulsations of the right atrium cause a retrograde pressure wave that may progress through the central veins to varying distances.
These pulses contribute to the fluctuations in venous closure that occur in the negative right atrial pressure range that are reflected in the curve or splay of the pressure—flow relationship. Changes in arterial as well as venous resistances affect venous return. In Chapter 1the progressive blood pressure reductions throughout the vascular system were presented in Table 1.
The greatest segmental pressure reduction occurs at the arterioles, indicating that arterioles contribute the largest portion of total systemic vascular resistance. Furthermore, the resistance of the arterioles is highly dynamic, capable of increasing or decreasing several folds in a few seconds.
The smooth muscle in the arteriole walls responds rapidly to changes in concentrations of circulating vasoactive hormones, local metabolically linked mediators, and input from fibers of the sympathetic nervous system.
Angiotensin II and catecholamines in the blood and locally produced endothelin are powerful arteriolar smooth muscle agonists, significantly affecting resistance to venous return. In the experiment referred to above, in which angiotensin II was infused into dogs for 7 days, venous return remained unchanged while mean systemic pressure increased from 9.
During this period, right atrial pressure increased slightly from 1.
Calculating resistance to venous return during the control period from the pressure gradient for venous return mean systemic pressure—right atrial pressure and the rate of venous return cardiac output yields a value of 2. After 7 days of angiotensin infusion, resistance to venous return increased to 3.
In a study on dogs, after a 7-day control period, angiotensin II was infused intravenously for an additional 7 days.
Locally produced and circulating nitric oxide, prostacyclin, and prostaglandin E2 are vascular smooth muscle antagonists, producing arteriolar dilation and reduction of resistance to venous return. Local tissue metabolism, in particular, aerobic metabolism, strongly affects arteriolar resistance. Activity that reduces tissue pO2 especially elicits significant arteriolar dilation and reduction in resistance to venous return.
The linkage between total body tissue oxygen demand and resistance to venous return is a fundamental mechanism governing control of cardiac output. This is the basic mechanism by which the cardiovascular system responds to changes in demand for cardiac output as metabolic rate changes. Other means of cardiovascular control may take part in responses to metabolic changes, but this connection of tissue oxygen demand to resistance to venous return is of overriding significance.Cardiac Output, Stroke volume, EDV, ESV, Ejection Fraction
Oxygen demand is a strong determinant of resistance to venous return over periods ranging from seconds to hours and in long-term and steady-state conditions. If demand is elevated for extended periods of days or weeks, new microvascular vessels grow through the tissue in need, decreasing local vascular resistance and increasing blood flow. Conversely, if blood flow exceeds demand for periods of several days or more, microvascular vessels will degenerate, reducing vascular density and increasing resistance.
This process is termed rarifaction and normally normally takes place in tissues whose use and metabolic activity are reduced. Rarifaction also may occur if arterial blood pressure increases.
CV Physiology | Venous Return - Hemodynamics
For example, in the angiotensin II infusion experiment, the infusion resulted in a steady-state increase in arterial blood pressure of 60 mm Hg by affecting renal function, and the peptide had an immediate direct constrictor effect on the arterioles throughout the body. But during the 7-day course of the study, the sustained increase in arterial pressure may have induced microvascular rarifaction throughout the body.
The immediate and delayed increases in tissue resistance throughout the body may both have contributed to the increase in observed resistance to venous return during the infusion period. The relatively large diameter of central veins presents little resistance to flowing blood, although they are easily compressed and flattened by surrounding tissue.
When they are compressed, they create significant resistance. For example, many veins entering the thorax over the first ribs are partially compressed by the sharp angle of the path over the bone. In the abdomen, the weight of the viscera may flatten the great veins, and in the neck, atmospheric pressure prevents the jugular veins from assuming a rounded shape when a person is upright.
Within the thorax, the veins may collapse if central venous pressure falls much lower than the atmospheric pressure. Even considering these impediments to blood flow, venous resistance is a relatively minor component of resistance to venous return. Arterial resistance, especially that portion resulting from the arterioles, makes up the greatest portion of total vascular resistance. It is this portion that is most actively regulated in response to changes in demand of the circulatory system.
The Venous Return Curve If right atrial pressure were changed in steps over the entire range of possible atrial pressures and venous return were measured at each point, plotting the data set would yield a complete venous return curve, which is presented in Figure 2.
For example, during lung expansion inspirationPRA can transiently fall by several mmHg, whereas the PV in the abdominal compartment may increase by a few mmHg. These changes result in a large increase in the pressure gradient driving venous return from the peripheral circulation to the right atrium.
Therefore, one could just as well say that venous return is determined by the mean aortic pressure minus the mean right atrial pressure, divided by the resistance of the entire systemic circulation i.
There is much confusion about the pressure gradient that determines venous return largely because of different conceptual models that are used to describe venous return.
Furthermore, although transient differences occur between the flow of blood leaving cardiac output and entering the heart venous returnthese differences when they occur cause adjustments that rapidly return in a new steady-state in which cardiac output flow out equals venous return flow in. Sympathetic activation of veins decreases venous complianceincreases central venous pressure and promotes venous return indirectly by augmenting cardiac output through the Frank-Starling mechanismwhich increases the total blood flow through the circulatory system.
During respiratory inspirationthe venous return transiently increases because of a decrease in right atrial pressure. An increase in the resistance of the vena cava, as occurs when the thoracic vena cava becomes compressed during a Valsalva maneuver or during late pregnancy, decreases venous return.