Cardiac / Vascular Function Curves - Cardiovascular - Medbullets Step 1
Tutorials/Quizzes These elegant studies led to a model of these relationships that could be graphically represented by plotting Cardiac function curves ( sometimes called cardiac output curves) are essentially Frank-Starling Systemic vascular function curves (sometimes called venous return curves) are generated by. Venous return is the rate of blood flow back to the heart. It normally limits cardiac output. Although the above relationship is true for the hemodynamic factors that determine the flow of blood from the veins back to the heart, it is important not to. Venous return is the principal regulator of cardiac output beasue the Frank- Starling What is the relationship between the two variables seen in these curves? .. hint and system to try to help us in solving the problems on the test he then says.
One primary criticism of Guyton's model is that the parameters describing venous return had not been measured in a functioning cardiovascular system in humans.
Frank–Starling law - Wikipedia
Thus, concerns have been expressed in regard to the ability of Guyton's simplistic model, with few parameters, to model the complex human circulation. Further concerns have been raised in regard to the artificial experimental preparations that Guyton used. Recently reported measurements in humans support Guyton's theoretical and animal work.
Introduction The support of blood flow is one of the central goals of clinical medicine, and the understanding of the regulation of blood flow is the sine qua non of cardiac physiology. Building on the foundational work of Frank and Starling, Arthur Guyton proposed that characteristics of the venous circulation were of fundamental importance in the regulation of cardiac output and thus blood flow.
However, several authors have raised strong objections to Guyton's model, and more than 50 years after the publication of his model, there is still debate about whether Guyton's ideas present a viable model of cardiac control or whether several fundamental misjudgments lie at the core of Guyton's conclusions [ 1 - 4 ].
A brief history of cardiac output Traditionally, the heart's accepted role has been that it not only provides the driving force for blood flow but also determines the total blood flow [ 5 - 7 ]. Simply stated, cardiac output is the product of stroke volume and heart rate.
In this view, all pressures in the heart and circulatory system for example, those measured in the large veins, in the cardiac chambers, and in the arteries are derivatives of the force generated by the heart rather than independent variables that might have an influence on the heart's function and thus cardiac output.
At the end of the 19th century, Frank [ 8 ] found that ventricular contractility was increased if the ventricle was stretched prior to contraction. Building on this observation, Starling and colleagues [ 910 ] found that increasing venous return increased stroke volume.
Cardiac / Vascular Function Curves
We therefore term the ability of the heart to change its force of contraction and stroke volume in response to changes in venous return the Frank-Starling mechanism. The ventricle does not operate on a single Frank-Starling curve. Any heart may operate on a family of curves, each of which is defined by the afterload, inotropic state, and diastolic compliance of the heart. Changes in venous return cause the ventricle to move along a single Frank-Starling curve that is defined by the existing conditions of afterload and inotropy and diastolic compliance.
Guyton's observations and model Guyton felt that three factors were central in the determination of cardiac output: The heart's permissive role in the determination of cardiac output If, Guyton reasoned, cardiac output is governed solely by heart function, then changing either heart rate or the heart's pumping ability should change cardiac output [ 12 ].
CV Physiology | Cardiac and Systemic Vascular Function Curves
Extending the observations of Brauwald and colleagues [ 13 ] that cardiac output was largely unaffected by heart rate when subjects were electrically paced, Guyton electrically paced the hearts of dogs that had a surgically created arteriovenous fistula between the aorta and the inferior vena cava [ 14 ].
Prior to the opening of this fistula, changes in heart rate had no effect on cardiac output. However, when the fistula was opened causing increased preload as evidenced by high right atrial pressure [PRA] valuescardiac output increased in proportion to heart rate changes. The advent of extra-corporeal circuits allowed Guyton to question whether the intrinsic pumping ability or contractility of the heart was the sole determinant of cardiac output [ 15 ].
When the pump speed of the extracorporeal circuit was increased, cardiac output did not increase significantly. During inspiration, the intrathoracic pressure is negative suction of air into the lungsand abdominal pressure is positive compression of abdominal organs by diaphragm.
This makes a pressure gradient between the infra- and supradiaphragmatic parts of v. 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 return. The effects of gravity on venous return seem paradoxical because when a person stands up, hydrostatic forces cause the right atrial pressure to decrease and the venous pressure in the dependent limbs to increase. This increases the pressure gradient for venous return from the dependent limbs to the right atrium; however, venous return actually decreases.
The reason for this is when a person initially stands, cardiac output and arterial pressure decrease because right atrial pressure falls. The flow through the entire systemic circulation falls because arterial pressure falls more than right atrial pressure; therefore the pressure gradient driving flow throughout the entire circulatory system is decreased.
Pumping action of the heart: During the cardiac cycle right atrial pressure changes alter central venous pressure CVPbecause there is no valve between the heart's atria and the large veins. CVP reflects right atrial pressure. Therefore, right atrial pressure also alters venous return. 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.
The effects of gravity on venous return seem paradoxical because when a person stands up hydrostatic forces cause the right atrial pressure to decrease and the venous pressure in the dependent limbs to increase.