CV Physiology | Venous Return - Hemodynamics
Cardiac output (CO) is a measurement of the amount of blood pumped by It can be represented mathematically by the following equation: . Increased venous return stretches the walls of the atria where specialized baroreceptors are located. . and cardiac disease have resulted in warning labels on cigarette packages. Disease processes that alter either of these factors may alter cardiac output ( unless the disease . Cardiac output may be reduced by poor venous return and end-diastolic ventricular These relationships are expressed by the Fick equation. Venous return; Cardiac output; Skeletal muscle atrophy; Biomarkers; Reactive [ ] further explored the venous system control and its relationship with right atrial pressure. .. () The hemodynamics and diagnosis of venous disease.
The most important blood reservoir within the venous system is the splanchnic region liver, spleen, and small and large intestine for two reasons: The hemodynamic mechanism that involves the rate of venous blood return to the right heart through the venous system is defined as Venous Return, and is equivalent to the Cardiac Output at steady-state conditions [ 131417 ].
The functionality of the venous system depends on valves or valve-like structures, which are more prominent in deep limb veins and in the legs [ 1819 ]. Skeletal muscles surround these structures, and, therefore, serve as an external pump that compresses the veins to ensure the unidirectional blood flow back to the heart [ 131420 ].
Venous Return Determinants Hemodynamic parameters that determine venous return and, consequently determine cardiac output include: Furthermore, venous return from lower extremities can be profoundly influenced by the skeletal muscle pump and by valve function; these are important mechanisms during exercise performance [ 1920 ].
Thus, effective venous return depends on adequate interactions between the central pump, the pressure gradient peripheral and central pressurea peripheral venous pump, and on competent venous valves [ 19 ].
Hemodynamic factors affect or can be affected by vascular capacity. Since the venous system is the body's main blood reservoir, any change in its capacity greatly influences venous return altering preload and, in turn, affects cardiac output and blood pressure [ 131422 ]. Therefore, in physiological conditions, we can assume that cardiac output depends entirely on venous return and on all its determining factors [ 1521 ].
Unstressed and Stressed Volume The total blood volume contained in the circulation at a specific distending pressure, e. This volume can be divided into unstressed and stressed volumes [ 13142223 ]. Conversely, the latter is the volume of blood that stretches the vessels and generates a positive transmural pressure [ 91422 ]. Despite unstressed volume not being considered hemodynamically active, in some situations, e.
The unstressed volume can be reduced by venoconstriction through diminished inflow or decreased transmural pressure; on the contrary, it can be increased by venodilatation through increased inflow or augmented transmural pressure [ 14 ].
Unstressed volume can become stressed volume, acting as a blood volume reserve, which is quite important under various conditions such as hemorrhage and exercise [ 13 - 15 ].
Therefore, alterations in stressed volume can directly affect cardiovascular hemodynamics through changes in venous pressure and, consequently, in venous return and cardiac output [ 15 ]. Mean Circulatory Filling and Right Atrial Pressures The mean circulatory filling pressure is the hypothetical mean vascular pressure in the systemic circulation that would be observed if the heart were stopped and the pressure in all parts of the circulation, from the aorta to the right atrium, were equilibrated [ 141725 ].
Weber [apud 21 ] and was further linked to the cardiovascular system by Bayliss and Starling [ 3 ]. After having performed a sympathectomy to induce cardiac arrest, by vagal stimulation in a dog model through the insertion of a cannula in the femoral artery and vein, portal vein, inferior vena cava and aorta, Bayliss and Starling [ 3 ] demonstrated that under these circumstances, the pressure at these points reached an equilibrium with values about 5 to 10 mmHg.
Additional studies have observed that the mean circulatory filling pressure measured in patients in the intensive care unit is approximately 18 mmHg or 12 mmHg, considering central venous pressure zero [ 26 ]. Therefore, it can be assumed that this pressure is a reflection of how tightly the blood volume fills the venous and arterial systems [ 23 ].
There was a problem providing the content you requested
Normally, when the heart pumps blood, the arterial pressure rises and the venous pressure reduces compared to the mean pressure of the system. This pressure gradient between the vessels allows that blood to be pushed through the arterial system, capillaries and venous systems and, subsequently, back to the heart.
Nevertheless, the pressure within venules and small veins, the primary sites of compliance, is the same during active circulation and cardiac halt [ 1525 ]. For this reason, this pressure is considered to be the equivalent of mean circulatory filling pressure. Therefore, it can be postulated that, under normal conditions, mean circulatory filling pressure resides in small venous territory, and is the main driving force the upstream pressure that determines the rate of venous return and thus cardiac output [ 45222325 ].
The total stressed blood volume primarily determines the mean circulatory filling pressure. Other factors, however, such as venous compliance, ventricular contraction and relaxation, venous valve function and skeletal muscles can alter it as well [ 1415 ]. Similarly, a reduction in venous compliance, in the absence of a change in blood volume, also evokes an increase in mean circulatory filling pressure and in venous return [ 14 ].
For this reason, the mean circulatory filling pressure is considered to measure the effective volume status theoretically independently from cardiac function [ 22 ]. The cardiac function can only affect venous return indirectly by changing right atrial pressure the downstream pressureand consequently altering the driving pressure gradient [ 9 ].
Guyton et al extensively demonstrated this relationship through the venous return curve [ 457 ]. This curve represents the steady-state relationship between stepwise changes in right atrial pressure and the resulting changes in venous return, which is a function of the circulating blood volume, vasomotor tone and blood flow distribution [ 22 ].
When the right atrial pressure is 0 mmHg, the gradient between the upstream and downstream pressures is the greatest and the venous return reaches a maximum. If the right atrial pressure falls below 0 mm Hg, it produces a suction force that initially increases venous flow but, shortly after, limits the venous return at a plateau due to extrathoracic veins collapse [ 27 ].
On the other hand, if right atrial pressure rises, venous return is reduced. It is noteworthy that venous returns can only be zero when there is no pressure gradient between the upstream and downstream pressures. This occurs when the venous return curve intercepts the X-axis and, at this point, right atrial pressure reflects the mean circulatory filling pressure [ 25 ]. Furthermore, the derivative of any point of this curve describes the resistance for venous return, also referred to as venous resistance [ 922 ].
Venous Resistance Different from arterial resistance, venous resistance is lower, but is an important determinant of venous return due to the low pressure and the high capacity of the venous circulation. Whereas altering the tone of arterioles mostly affects resistance, in veins it mostly affects capacity. Thus, it is volume rather than resistance that is controlled in order to regulate the circulation [ 28 ]. In this context, it is postulated that venous resistance depends on the combination of resistance and capacitance the relationship between contained volume and distending pressure of a segment in different portions of the peripheral circulation.
Small veins and venules have very large cross-sectional areas with high capacitance and, thus, they have little contribution to venous resistance, serving mainly as a blood reservoir. On the other hand, large central veins such as the vena cava, and peripheral large and medium-sized veins have small cross-sectional areas with little capacitance, acting primarily as a conduit and having small contribution to the blood reservoir.
Therefore, venous resistance is mainly determined by these conducting veins, which can be passively affected by blood volume alterations in the reservoir compartment, by autonomic stimulation, and by vasoactive mediators [ 91421 ]. Many factors, such as the diameter of vessels and blood viscosity can alter venous resistance [ 922 ].
Constriction of conducting veins can directly increase venous resistance, although it causes only a minimal effect when compared to the arterial side as mentioned before.
An increase in blood viscosity polycythemia can also increase venous resistance. Nevertheless, the main mechanism by which venous resistance is altered is by redistribution of blood between different vascular beds through vasoconstriction mainly in the splanchnic region [ 2122 ].
These alterations evoke a brief rise in upstream pressure and expel blood into the systemic circulation [ 22 ]. Most of the venoconstriction occurs in the splanchnic circulation due to a more prominent innervation and a greater sensitivity to sympathetic stimulation than arterial resistance vessels [ 151921 ].
Still, it is important to point out that the splanchnic venoconstriction does not significantly affect venous resistance, but has a great capability to increase mean circulatory filling pressure secondary to an increase in stressed volume [ 1522 ]. Although in accordance to the classic muscle pump hypothesis, increased venous pressure caused, for example, by a head upright tilt, would produce increased blood flow, different insights about skeletal muscles have been brilliantly elucidated [ 31 ].
The authors also established the duration of muscle contraction as an important determinant of venous outflow dynamics. Both the amount of venous outflow per contraction and the time course of outflow during contraction are altered by changes in stimulation patterns. Competent venous valves, that divide the hydrostatic column of blood into segments, assist the muscle pump to avoid gravitational venous reflux [ 3033 ].
It happens mainly during walking and dynamic exercise when the rhythmic contraction of the peripheral skeletal muscles increases and causes intramuscular veins to suffer greater compression [ 203435 ]. In turn, this compression increases the mean circulatory pressure about three times the normal value and expels large amounts of blood from the venous vasculature toward the heart.
Thus, this muscle pump mechanism is one of the main factors that increases the cardiac output at the onset of muscular activity in conformity to Frank-Starling mechanismand it is mostly dependent upon muscle mass and pump activity intensity [ 32343637 ]. The ability of the skeletal muscle pump to empty the venous vessels has been widely demonstrated in animal and human studies [ 203234 - 38 ].
The main skeletal muscles responsible for this pump function are the lower limb muscles including those of the feet, calves, and thighs.
- Volume and its relationship to cardiac output and venous return
- Cardiac / Vascular Function Curves
- Venous Return - Hemodynamics
Among these, the most important is the calf muscle pump due to its large capacitance, and to the highest pressure generated [ 1935 ]. At least two mechanisms are responsible for this circulatory pump role played by lower limb muscle contraction. First, during muscular compression of intramuscular venous vessels, a considerable amount of kinetic energy is transmitted to the venous blood that facilitates its return to the heart assisted by the venous valves. Second, during muscular contraction, venous pressure is reduced to very low values or even negative values, which generates a greater arterial-venous gradient just after the end of muscle contraction that contributes to the venous flow.
As a result, venous return is augmented, and it contributes to most of the increase in cardiac output during exercise [ 172032 ]. Whereas the practice of physical exercise positively associates venous return and cardiac output, the disuse is the main mechanism to a negative relationship.
Other causes of skeletal muscle atrophy may include: Among chronic diseases related to skeletal muscle there are: A decrease in strength muscle will cause venous blood pooling which favors an increase in the unstressed volume and a decrease the stressed volume. As a result, the mean circulatory filling pressure will decrease producing a reduction in right atrium filling Figure 1.
Moreover, as consequence of muscle atrophy and extensive physical deconditioning, the demand of oxygen to the muscle is reduced leading to vascular atrophy [ 44 ]. This compensatory mechanism will increase vascular resistance and contribute to a reduction in venous return [ 45 - 47 ]. Thus, in the absence of skeletal muscle venous pumps, these hemodynamic changes promote an abnormal venous return that could compromise stroke volume and cardiac output [ 47 - 49 ].
Indeed, some studies have reported cardiac output to be reduced after periods of inactivity induced by bed rest, spinal cord injury, and spaceflight [ 4650 - 52 ]. Further, after 2 weeks of bed rest, Levine et al. Despite some studies not reporting a decrease in cardiac diastolic and systolic function after spinal cord injury [ 45 ], it has been discovered that left ventricle mass index and cardiac dimensions were reduced by prolonged inactivity and short-term spaceflight [ 455053 ].
Unquestionably, muscle atrophy caused by several conditions can impair cardiovascular hemodynamics and promote cardiac alterations. Some important genetic muscle atrophy disorders, like Becker and Duchenne diseases [ 5455 ], show progressive cardiac dysfunction.
Both are clinically characterized by progressive muscle weakness, whose implications are [ 56 ] attributed as a cause or a consequence of cardiovascular complications and are thought to, directly or indirectly, affect the cardiac output and, consequently, the venous return. These dystrophies generally develop during the second decade of the patient's life [ 57 - 60 ]. Although cardiac dysfunction originates due to specific myocardial loss of dystrophin, extrinsic hemodynamic parameters may impact the development, as well.
In Becker muscular dystrophy patients, there is no correlation between cardiac involvement [ 61 ] and the severity of the cardiomyopathy. Cardiac involvement may manifest as electrocardiographic abnormalities, hypertrophic cardiomyopathy, dilation of the cardiac cavities with preserved systolic function, dilative cardiomyopathy, and cardiac arrest. On the other hand, taking [ 62 ] the organ into account, myocardial damage increases with age through progressive reduction of left ventricular ejection fraction as observed in patients over The authors reported evolution of systolic impairment appearing somehow to be associated with the development of autonomic imbalance, a condition that contributes to increase ventricular propensity to arrhythmias.
Further investigations, nonetheless, demonstrate no autonomic nervous system involvement as a key finding in Becker muscular dystrophy [ 65 ]. To maintain the cardiac output, their hearts are forced to increase beating frequency to compensate reductions in left ventricle size. Consequently, the cardiac muscle encounters two major threats, i. Further, independent from additional genetic alterations in cardiac tissue, the widespread dystrophic damage of skeletal muscle concurrent with postural adaptation may also result in hemodynamic adaptation, which has been established as a risk factor for the development of cardiomyopathy [ 6667 ].
Therefore, progressive skeletal muscle degeneration and weakness most likely contributes to progressive cardiac dysfunction. Interestingly, animal studies with knockout mice have already demonstrated a potential causal link between skeletal muscle disease and cardiomyopathy.
Normally, the mdx mice, a mouse model of Duchenne muscular dystrophy, do not show characteristic dystrophic cardiomyopathy until they reach 21 or more months of age [ 6869 ]. Using this mice model, Megeney et al. As MyoD is not expressed in the heart and plays no role in heart development, any myocardial changes evident in mdx: MyoD2y2 mice would be directly attributable to the level of skeletal muscle damage.
Hence, the author suggested the progression of skeletal muscle damage as a significant contributing factor leading to the development of cardiomyopathy. Since in Becker and Duchenne muscular dystrophy cardiac impairment is not directly correlated with the severity of skeletal muscle involvement [ 71 ], the venous return is not directly a subject, but it is indirectly involved in cardiac manifestations. Cardiac involvement has been confirmed in cases preceding the onset of skeletal muscle manifestation and in cases of wheelchair-bound patients who did not develop cardiac dysfunctions.
Because of this, small changes of only a few mmHg pressure in either PV or PRA can cause a large percent change in the pressure gradient, and therefore significantly alter the return of blood to the right atrium. 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.
Cardiac / Vascular Function Curves - Cardiovascular - Medbullets Step 1
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. This increases the pressure gradient for venous return from the dependent limbs to the right atrium; however, venous return paradoxically decreases.
The reason for this is when a person initially stands and before the baroreceptor reflex is activated, cardiac output and arterial pressure decrease because right atrial pressure and ventricular preload falls, which decreases stroke volume by the Frank-Starling mechanism.