Venous return becomes limited when the pressure inside the great veins is less than the pressure outside their walls because the floppy walls of veins collapse and produce what is called a vascular waterfall or a flow limitation Fig. This occurs at atmospheric pressure when breathing spontaneously. When venous collapse occurs, further lowering right atrial pressure does not increase venous return [ 31 ]. This means that the best the heart can do to increase cardiac output is lower right atrial pressure to zero Fig.
Maximum venous return and cardiac output are defined by the MSFP, which is determined by stressed volume in the veins and venules and the compliance of these structures and by the resistance to venous return.
Maximum flow would occur, albeit for an instant, if the heart were suddenly taken out of the circulation, indicating that the heart gets in the way of the return of blood by creating a downstream pressure greater than zero. In patients mechanically ventilated with positive end-expiratory pressure, flow limitation occurs at a positive value and not zero [ 32 ].
When venous return is limited, cardiac output can only be increased by increasing MSFP by a volume infusion, by decreasing capacitance and recruiting unstressed into stressed volume without a change in total volume Fig. Limit of the return function. When the pressure inside the great veins is less than the surrounding pressure which is zero when breathing at atmospheric pressure , the vessels collapse and there is flow limitation.
Lowering right atrial pressure Pra further does not increase flow. The heart cannot create a flow higher than this value. Change in cardiac output and venous return with an increase in capacitance. An increase in capacitance is the same as lowering the opening on the side of a tub for it allows more volume to flow out, which is the equivalent of more volume being stressed.
Graphically it results in a leftward shift of the volume—pressure relationship of the vasculature upper left. This shifts the venous return curve to the right and increases cardiac output through the Starling mechanism lower left. This effect is identical to giving volume to expand stressed volume. Pra right atrial pressure. The cardiac function curve, too, has a limit.
This occurs because of the limit to cardiac filling due to restraint by the pericardium [ 33 ] or, if there is no pericardium, by the cardiac cytoskeleton itself. In pathological situations mediastinal structures can also impose limits on cardiac filling. When cardiac filling is limited, increasing diastolic filling pressure does not increase stroke volume because there is no change in end-diastolic volume and thus no increase in sarcomere length.
Under this condition cardiac output can only be increased by an increase in heart rate or cardiac contractility or by a decrease in afterload. When cardiac filling is limited, cardiac output is independent of changes in the venous return function. Blood flows down an energy gradient, which generally means that blood flows from an area of high pressure to an area with a lower pressure. As already discussed, pressure in each compartment is determined by the compliance of the wall of the compartment and the volume it contains.
As discussed elsewhere in this series, ejection of blood by the heart occurs by what is called a time-varying elastance, which means that the elastance of the walls of the cardiac chambers markedly increase during systole.
Conversely, the compliance of the heart markedly decreases during systole. This greatly increases the pressure in the volumes contained in the ventricles. The peak pressure achieved in the ventricle by the cyclic decreases in compliance depends upon where the volume is along the ventricular end-systolic volume—pressure line, the pressure in the aorta at the onset of ventricular contraction, and how easy it is for blood to flow out of the aorta, which is dependent upon the downstream arterial resistance and critical closing pressures [ 34 ].
This produces a pulse pressure which is determined by the elastance of the aorta [ 35 ]. The increase in aortic volume stretches its walls and creates a pressure gradient from the arteries to the veins. The consequent change in volume in the veins minimally increases the pressure in that region i.
During diastole the compliance of the right and left heart markedly increase and the pressures in the ventricles markedly fall because there is much less volume than before the systolic decrease in compliance. Since there is little change in MSFP and a marked drop in the downstream right atrial pressure, it is evident that the major factor affecting the return of blood to the heart is the lowering of right atrial pressure by the action of the right heart and not the trivial change in MSFP or the pressure in the aorta.
The rhythmic pulsations produced by the time-varying elastances of the ventricles produce important limitations to blood flow. When a step increase is made in flow to a compliant system with an outflow resistance, the pressure does not increase with a step change but rather rises to the new value exponentially. This means that if there is not enough time in the cycle to reach the new steady state, volume will be trapped in the upstream compartment.
Thus, besides just pressure gradients, heart rate becomes a factor in cardiac filling and emptying. The equation for venous return VR is:. This can be substituted into Eq. This indicates that venous return is determined by stressed volume and the time constant of venous drainage.
All this assumes that the limit is due to too short a filling time and that there is not already a limit imposed by the steep portion of the diastolic filling curve. During normal circulatory adjustments to high flow needs, as occur during aerobic exercise, reduction in venous resistance and the distribution of flow as described in the Krogh model below are necessary to allow greater rates of venous return. These occur by matching changes in regional resistances to metabolic activity.
This co-ordination of resistances does not occur properly in sepsis and could explain why volume needs to be used to increase MSFP in sepsis to allow for a sufficient cardiac output to match the fall in arterial resistance during distributive shock. So far in this review cardiac function has been considered as one unit starting from the right atrium and exiting from the aortic valve. Pulmonary vessels and independent functions of the right and left ventricle have not been considered.
This simplification normally produces a small error because total pulmonary compliance is only one-seventh of total systemic vascular compliance [ 11 ] and the pulmonary circuit does not contain a lot of volume that can be shifted to the systemic circulation.
It also cannot take up a lot of volume without causing a large increase in pulmonary venous pressure and a major disturbance to pulmonary gas exchange. Even maximal sympathetic stimulation results in only a small shift from the pulmonary circuit to the systemic circulation [ 36 ]. However, the small volume reserves in the pulmonary vasculature become important during the variation in pulmonary flow during ventilation, especially during mechanical ventilation and increases in pleural pressure.
The normal gradient for venous return is only in the range of 4 to 8 mmHg. Because the heart is surrounded by pleural pressure and not atmospheric pressure, an increase in pleural pressure of 10 mmHg during a mechanical breath would cut the inflow to the heart to zero and there would be no stroke volume on beats at peak inspiration [ 37 ]. One would thus expect marked variations in left-sided output and arterial pressure during mechanical ventilation, but normally they are moderate.
This is because the volume in the compliant component of the pulmonary vasculature provides a reservoir that can sustain left heart filling for the few beats that are necessary during the peak inspiratory pressure. This can be called pulmonary buffering [ 37 ]. The compliant compartment of the pulmonary circulation is also important under two pathological conditions. When there is a disproportionately greater decrease in left heart function than right heart function, stressed volume accumulates in the pulmonary circuit because higher filling pressures are needed by the left heart to keep up with the output of the more efficient right heart [ 11 , 38 ].
In modeling studies without reflex adjustments and failure of the right heart, this leads to a rise in pulmonary venous pressure, which is the upstream reservoir for the left ventricle, and a decrease in MSFP [ 37 ]. The fall in MSFP reduces venous return and cardiac output. This would be hard to detect in a patient because fluid retention by the kidney, reflex adjustments, or exogenous fluid administration increase total blood volume and restore MSFP and cardiac output.
Accumulation of volume in the pulmonary vasculature is especially a problem in patients with marked left ventricular diastolic dysfunction. In these cases the left-sided filling pressure needs to be higher than normal to maintain adequate stroke volume and cardiac output to perfuse vital organs such as the kidney. However, the higher left ventricular filling pressure increases pulmonary capillary filtration and leads to pulmonary edema and respiratory failure.
If volume is removed to treat the respiratory failure, cardiac output deceases and the kidneys fail. If volume is then added to improve renal perfusion, respiratory failure occurs. There is no obvious solution to this clinical problem.
A second mechanism that can increase the proportion of vascular volume in the pulmonary compartments is an increase in the proportion of the lung in West zones 1 and 2 [ 37 , 39 ]. Under these conditions alveolar pressure becomes the downstream pressure for pulmonary flow instead of left atrial pressure. When this happens, pulmonary venous pressure rises one-to-one with an increase in alveolar pressure and provides a considerable load for the right ventricle.
The increased pressure is also downstream of pulmonary capillaries and will increase pulmonary capillary filtration. Another factor that is not often taken into account when considering the distribution of volume and maintenance of normal pressure gradients for venous return is the size of the heart. In someone who has very dilated ventricles this could be an even higher proportion of total blood volume, although presumably most of it is unstressed. Excess accumulation of the volume in the heart is prevented by the characteristics of the passive filling curves of the ventricles, which become very steep at a value appropriate for a normal stroke volume.
If the capacity of the ventricles is too large for the volume reserves of the body, accumulation of volume in the ventricles could take up a significant proportion of systemic venous volume, which would decrease MSFP and limit cardiac output. So far in this review the systemic vascular compliance has been lumped into one region with a large compliance.
Early in the last century August Krogh [ 5 ] indicated that if the vasculature consists of an area with a high compliance in parallel with an area with much lower compliance, the fractional distribution of flow between these two regions affects venous return Fig.
This can be understood by the previous discussion on time constants of drainage. As indicated above, a sink has less compliance than a bathtub, so these two parallel compliances can be considered as a bathtub and sink in parallel. Because of its smaller surface area, a smaller amount of volume is needed to raise the height of water in the sink and to increase the outflow; a sink thus has a fast time constant compared with a bathtub, which has a large surface area and requires a large amount of volume to go through the outflow resistance to change the height of water.
Permutt and colleagues demonstrated that the splanchnic vasculature has a time constant of drainage in the range of 20 to 24 s [ 26 , 40 , 41 ], whereas that of the peripheral vasculature bed has a time constant of 4 to 6 s.
In this two-compartment model the venous return equation can be written as follows:. The two-compartment Krogh model. In this model the systemic circulation has a large compliant region such as the splanchnic vasculature in parallel with a low-compliance region equivalent of the peripheral vasculature.
A shift in the fractional flow to the low-compliance region by decreasing the arterial resistance Ra-p into this region decreases venous resistance upward shift of the slope in b compared with a but does not change MCFP. Rv-s is splanchnic venous resistance, Rv-p is peripheral venous resistance.
Used with permission from reference [ 5 ]. Note that if F per were 0 and F sp were 1, this equation is the same as Eq. The vasculature could be subdivided into smaller regions and, by specifying their drainage characteristics, the analysis could be refined, but use of two groups is sufficient to understand the broad consequences.
I will thus simply refer to the splanchnic bed as the high-compliance region and the peripheral region, which is composed primarily of muscle, as the low-compliance regions.
These also could be considered as the slow and fast time constant beds, respectively. Distribution of flow between the two is determined by regional arterial resistances. Importantly, it is the fraction of total cardiac output to each region that is important and not actual flow.
This is because total blood volume is constant. A good example of how this functions is the defense against a fall in blood pressure by the baroreceptors [ 9 ]. We analyzed this in an animal model in which we controlled the baroreceptor pressures in what is called an open-loop model. This means that the sensor for the perturbation, in this case blood pressure, is separated from the response.
We isolated the outflow from the splanchnic and peripheral beds and controlled cardiac output with a pump. This allowed us to assess the venous resistances, compliances, regional flows, and stressed volumes in all compartments. As expected, a decrease in baroreceptor pressure from to 80 mmHg produced a marked rise in arterial resistance. However, the increase in arterial resistance was greater in the peripheral region than the splanchnic region, which redistributed blood flow to the slow time constant splanchnic bed.
This makes sense from an evolutionary point of view for it would protect delicate abdominal structures [ 23 ], but the consequence of increasing the fraction of flow to the slow time constant bed is a decrease in cardiac output and this would decrease blood pressure further.
Other adaptations are thus necessary. There was no change in capacitance in peripheral beds for they have a smaller volume reservoir. Strikingly, at the same time that arterial resistance to the splanchnic bed increased, the venous resistance draining this bed decreased.
This decreased the time constant of drainage from the splanchnic bed. In this two-compartment model the time constants of flow into and out of each region become important because they affect the distribution of flow and emptying of the regions with changes in heart rate and blood pressure and this adds a further complexity to the analysis.
These factors are likely important for the responses to vasopressors and inotropic agents. The change in capacitance was an important part of the reflex response but this only can occur if there is adequate unstressed volume to recruit.
Unfortunately, unstressed volume cannot be measured in an intact person and thus clinicians must think about the potential unstressed reserves. The existence of unstressed volume and the ability to adjust stressed volume by changes in capacitance introduces a role for volume infusions that is not simply to increase cardiac output but rather to ensure reserves. Patients who have had volume losses and whose MSFP is being supported by a reduction in vascular capacitance by recruitment of their unstressed reserves no longer can use this mechanism to rapidly adjust stressed volume as needed.
Volume infusion could potentially restore these reserves without producing much change in cardiac output, although there might be some decrease in heart rate because of a decrease in sympathetic activity. However, the response to the next stress would be very different. Note that this would likely not produce much change in any measureable hemodynamic values, including ventilation-induced variations in arterial pressure or stroke volume. Although use of volume boluses to increase cardiac output is one of the most common clinical interventions in patients in shock, increasing preload is not the major way that the body normally produces large changes in cardiac output [ 42 ].
Under normal conditions the Frank—Starling mechanism primarily provides fine adjustment to cardiac function by making sure that the same volume that fills the ventricles on each beat leaves them. For example, during peak aerobic exercise there is very little change in right atrial pressure with the very large increases in cardiac output [ 43 ]. The increase in cardiac output occurs by increases in heart rate, contractility, and peripheral mechanical adaptations that allow more venous return.
This is not to say that fluids should not be used for resuscitation of patients in shock. Use of fluids can avoid the need for central venous cannulation and the need for drug infusion but it is necessary to understand the limits of what fluids can do.
In a 70 kg man with a stressed volume of ml and a MCFP of 10 mmHg, an infusion of a fluid that increased stressed volume by 1 L would increase MCFP to 17 mmHg and likely produce a significant increase in vascular leak.
More than likely the liter of fluid would not stay in the vasculature and the effect would be transient. If there is left ventricular dysfunction or non-West zone 3 conditions in the lungs, a greater than normal proportion of the fluid would be distributed to the pulmonary compartments [ 37 ].
When the two-compartment Krogh model is considered, the effect of the volume becomes even more complicated. The effect of the increase in stressed volume will be much greater if a greater fraction of the blood flow goes to the fast time constant muscle bed because this region is much less compliant and the increase in volume produces a greater increase in the regional elastic recoil pressure.
However, this also means that the equivalent of MSFP in the muscle region will be even higher than the estimate given above and be an even greater force for capillary filtration.
The study on the effect of the baroreceptor response to hypotension discussed above [ 9 ] gives insight into the response of the peripheral circulation to infusions of norepinephrine. Besides the expected increase in systemic arterial resistance, norepinephrine constricts the splanchnic venous compartment and increases stressed volume.
It potentially dilates or at least does not constrict the venous drainage from the splanchnic bed. This is because activation of alpha-adrenergic receptors constricts the venous drainage of the splanchnic vasculature whereas beta-adrenergic receptors dilate it [ 41 ]. Through its beta-adrenergic activity norepinephrine increases cardiac function and has little effect on pulmonary vessels [ 44 ]. The increase in precapillary resistance vessels and the decrease in right atrial pressure with the improvement in cardiac function could potentially decrease capillary filtration and thus could reduce edema formation.
However, it is possible that very high levels of norepinephrine compromise the normal distribution of flow and compromise organ function. Epinephrine likely works in the same way [ 26 ] except that it generally produces a greater increase in heart rate, which could produce problems by shortening diastole and producing unexpected changes in distribution of flow due to the limits of time constants in different vascular beds, on both the arterial and venous side.
The response of the circuit to phenylephrine is very different from the response to norepinephrine because it only has alpha-adrenergic activity [ 45 , 46 ]. Although phenylephrine can constrict the splanchnic capacitance vessels, it increases the venous resistance draining this region and the net effect on venous return depends upon how much volume is recruited versus how much the downstream resistance increases.
In most critically ill patients capacitance reserves are reduced so that the net effect with phenylephrine is decreased splanchnic drainage and decreased venous return. Phenylephrine also does not increase cardiac function so that cardiac output most often falls [ 47 ]. The net result of the capillary microcirculation created by hydrostatic and osmotic pressure is that substances leave the blood at one end of the capillary and return at the other end. Blood flow refers to the movement of blood through the vessels from arteries to the capillaries and then into the veins.
Pressure is a measure of the force that the blood exerts against the vessel walls as it moves the blood through the vessels. Like all fluids, blood flows from a high pressure area to a region with lower pressure.
Blood flows in the same direction as the decreasing pressure gradient: arteries to capillaries to veins. The rate , or velocity, of blood flow varies inversely with the total cross-sectional area of the blood vessels.
As the total cross-sectional area of the vessels increases, the velocity of flow decreases. Blood flow is slowest in the capillaries, which allows time for exchange of gases and nutrients. Resistance is a force that opposes the flow of a fluid. Click here for information on Cardiovascular Physiology Concepts, 3rd edition, a textbook published by Wolters Kluwer Klabunde Venous return VR is the flow of blood back to the heart. Under steady-state conditions, venous return must equal cardiac output CO when averaged over time because the cardiovascular system is essentially a closed loop see figure.
Otherwise, blood would accumulate in either the systemic or pulmonary circulations. Although cardiac output and venous return are interdependent, each can be independently regulated. The circulatory system is made up of two circulations pulmonary and systemic situated in series between the right ventricle RV and left ventricle LV as depicted in the figure. Balance is achieved, in large part, by the Frank-Starling mechanism.
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