5 Static and Steady Flow Models 5.1. INTRODUCTION In this chapter, we will discuss some applications of hydrostatics and steady flow models to describe blood flow in arteries. Even though the flow in the human circu- latory system is unsteady, particularly at the pre-capillary level, steady flow models do provide some insight into the aspects of flow through the arteries and some use- ful applications can be found using the steady flow models. As would be expected, steady flow models are also simpler to use because of the absence of time variations in the governing equations (cf. the equations of motion, Equations 1.43a through 1.43). Steady flow models also avoid the complexity of having a moving interface between the blood and the vessel wall as the artery distends in response to pulsatile pressure. 5.2. HYDROSTATICS IN THE CIRCULATION For a typical adult, the mean arterial pressure at the level of the heart is about 100mmHg. In the supine (ie., lying down) position, pressures in the blood vessels of the head and legs would be ~95 mmHg (Figure 5.1). However, when a person is standing up, the hydrostatic effects that were discussed in Section 1.3 must be taken into account. In order to assess the pressure differences due to gravitational effects, the force balance of Equation 1.12 can be applied as Ap=pgh (1.12) Using the previous equation and knowing the density of blood, the pressures in the blood vessels can be estimated as shown in the figure. Since arteries are relatively stiff vessels, the increase in pressure due to hydrostatic effects will only cause mini- mal alterations in the blood volume since the vessel cross section remains nearly constant, However, in the veins, the blood volume will be greatly affected because they are much thinner and can expand significantly (see Section 3.4). In fact, if the venous tone is low and a person suddenly stands up, they may actually faint because of the increased pooling of blood in the lower extremities which reduces blood flow back to the heart and, thus, flow to the brain, Moreover, due to the corresponding decrease of pressure in the head due to further increases in elevation, the veins in that region may be in a partially collapsed state. Typically, the veins take on an elliptical or dumb bell shape in which flow of blood still persists but against a much 155156 Biofluid Mechanics: The Human Circulation Arterial pressure Arterial FIGURE 5.1 Hydrostatic pressure differences in the circulation. (Redrawn from Burton, .C., Physiology and Biophysics of the Circulation, Yeat Book Medical Publishers, Chicago, IL, Copyright 1971, Elsevier.) higher resistance. A good way to prevent this is by flexing the muscles in the leg calf 80 as to effectively pump the blood out of the lower veins and back to the heart. In the event of fainting, however, the resultant change in posture from standing to supine is the ideal “remedy” for the effects of cerebral hypotension 5.3 APPLICATIONS OF THE BERNOULLI EQUATION The Bernoulli equation, derived in Section 1.6, was based upon the assumption of steady flow along a streamline in an incompressible, inviscid fluid (Figure 1.9) and is given by the relationship vy? pt+p- tpgc=H (1.62) where H is a constant and is referred to as the “total head” or total energy per unit volume of fluid. This equation can be applied to several disease conditions in the circulatory system such as flow through constrictions and across orifices, keeping in mind the assumptions used in deriving the equation. 5.3.1 Torat versus Hyprostatic Pressure MEASUREMENT The most common method for measuring intravascular blood pressure clinically is to insert a fluid-filled catheter into a vessel then externally connecting the catheter to a pressure transducer. The pressure measured is then that sensed at the tip of the catheter and transmitted along the fluid channel to the manometer (this device is known as a “fluid-filled catheter manometer"). In addition to the pressure energy, however, the effect of kinetic energy on the pressure measurement must also be taken into account, as seen in Equation 1.62.Static and Steady Flow Models 157 To pressure To pressure transducer transducer Flow aT side p = es) wf @) “Lateral pressure” “End pressure” FIGURE5.2 Schematic for the measurement of lateral and end pressure: (a) lateral opening in the catheter and (b) opening at the end of the catheter. ‘The hydrostatic pressure, p, would be best measured by the catheter shown in the configuration with a lateral port (Figure 5.2a). However, when the catheter opening faces the flow as shown in the configuration Figure 5.2b, the fluid that impinges against the catheter opening slows to zero velocity. When that happens, the kinetic energy in the fluid will be converted into pressure and will introduce a difference between the end pressure and the lateral pressure: -A=P 6.1) In this equation and in subsequent discussions on the application of Bernoulli equa- tion in biological flows, V will refer to the mean velocity over the cross section of the artery/conduit. This difference can be significant, especially in segments of nar- rowed vessels where velocities, and thus, the kinetic energy, become considerable. Thus, for normal physiological pressure measurements, openings are located at the sides of the catheter such that lateral pressures are measured. In the case of catheter- tipped pressure transducers where a sensor is directly placed on the catheter, these pressure-sensing elements are also mounted on the side of the catheter. 5.3.2 Arteria STENOSES AND ANEURYSMS In patients with vascular disease, segments of an artery may become narrowed due to fatty deposits and atherosclerosis, resulting in a stenosis. Here, the Bernoulli equa- tion can be applied to the flow conditions to estimate the effects of this narrowing. If, for example, a cross section of an artery is stenosed such that the diameter at that cross section is less than its normal value (Figure 5.3), then from the principle of conservation of mass A, = AbVe where subscript 1 denotes a cross section upstream to the stenosis subscript 2 at the narrowest site of the stenosis158 Biofluid Mechanics: The Human Circulation FIGURE 5.3. Application of Bernoulli equation to an arterial stenosis. If the cross sections under consideration are relatively close to each other, we can neglect the effect of viscous dissipation and apply the Bernoulli equation, Over a short distance, the gravitational changes will also be negligible and the relationship in Equation 1.62 will reduce to v2 pre 2 . +o (6.2) 2 2 Since p,, V;, and V, are known, the pressure at the site of constriction, p, can be computed, To express the kinetic energy per unit volume (also in terms of mmHg), the conversion factor 1 g/em-s? = 7.5 x 10-4 mmHg can be used. Example 5.1 Consider a case where there is a focal stenosis of a 6mm diameter femoral artery in which its cross-sectional diameter is reduced to one-third of normal. Then, the velocity at the stenosis, V,, will be nine times the upstream velocity, V;. Furthermore, if the flow rate through the artery were 50.cm*/min, then the veloci- ties, V, and V,, are V4 = (50cm*/min)/(60- (0.6 cm)? /4) = 2.95 crn/s Vz =9-Y4 = 26,5cm/s Therefore, if the pressure at the upstream is 100 mmHg, then the pressure at the stenosis will be reduced by p/2 [v2 -v?] = 9300g/cms? 0.29mmHg One result of a lower pressure at a constriction is that under severe conditions, the vessel walls may actually cave in under sufficient external pressure, even to the point of complete occlusion. In this case, the flow velocity will slow down due to frictionalStatic and Steady Flow Models 159 resistance and the kinetic energy will be converted to pressure. Then, the pressure at the constriction will once again increase, reopening the artery. This phenomenon will repeat itself cyclically, resulting in the phenomenon of arterial flutter. This is actually the mechanism behind the Korotkoff sounds that are used with the tradi- tional blood pressure measurement made with an inflated cuff around the arm and sensed by a stethoscope. A converse condition can occur where there is a weakening of the arterial wall and a corresponding increase in the lumen cross section which causes a bulge or an aneurysm to occur. It is thought that an aneurysm forms due to a weakening of the vessel wall, possibly because of an excess of a degradation enzyme known as elastase which acts to break down elastin, a normal load-bearing fiber in the artery wall. It is commonly seen in the distal, or abdominal, aorta where it is referred to as an abdominal aortic aneurysm (AAA). Analysis performed on the energy present in the flow similar to that mentioned earlier shows that the flow velocity is reduced at the cross section of the aneurysm and that some of the kinetic energy will, thus, be converted into pressure at that site. Although the increase in pressure may not be sig- nificant in the resting state (<5 mmHg), the corresponding conversion from kinetic energy to pressure may be substantial under exercise conditions when aortic velocity increases several fold. The increase in pressure will lead to a corresponding increase in wall stress (see Section 2.2), which may be sufficient to cause further expansion of the aneurysm cross section. This sequence of events acts as a positive feedback loop in that further enlargement of the artery reduces velocity and, again, increases static pressure. Ultimately, this process may result in the bursting of the vessel at that site. Obviously, this is never a desirable outcome, but when it occurs in the major outlet vessel from the heart, it is particularly critical, being fatal in ~50% of cases. 5.3.3 Carpiac VALVE STENOSES Another application of the Bernoulli equation is in the analysis of natural and pros- thetic heart valves. In traditional engineering applications, this analysis is based on flow through an orifice as used for flow meters placed in internal flows. An example of this is flow through a nozzle as shown schematically in Figure 5.4. As the fluid passes through the sharp edges of the nozzle, flow separation causes a recirculation region immediately downstream of the nozzle. The fluid in the core region continues to accelerate to form a contracted cross section (denoted by 2 in the figure) referred Dy Flow ROOT160 Biofluid Mechanics: The Human Circulation toas the vena contracta. At this cross section, the streamlines are parallel to the axis of the tube and the pressure over the cross section is uniform. Keeping in mind the assumptions used in deriving the Bernoulli equation and also neglecting the effect of gravity, the Bernoulli equation can be written as eae ee Also, from the continuity equation, we have (J -(4) Substituting this relation, we get Voideat The velocity computed using the previous expression is “ideal” because we used the Bernoulli equation and, thus, have neglected the effect of fluid viscosity. As can be observed from Figure 5.4, the area at position 2 where the streamlines are essentially parallel to the axis is smaller than that at the throat of the orifice. The area A, can be related to the throat area Ag by introducing a contraction coefficient, C,, such that Due to frictional losses, the velocity at position 2 will be less than the ideal value given by the previous expression. Hence, a velocity coefficient, Cy, is introduced such that Vactuat Gq VeeStatic and Steady Flow Models 161 ‘Then, the actual volume flow rate can be computed as CAoCwVaideai AxVractuat or Squaring the expression and rewriting, we obtain ponte [inca or where Cy = C,Cy, ih '1—C}(Ap/A;)” is defined as the discharge coefficient. ‘The discharge coefficient C, depends upon the geometry of the nozzle as well as the dimensions of the tube and the throat of the nozzle. In flow meter applications, the discharge coefficient is determined experimentally. In clinical practice, this expression is applied to determine the effective orifice area (EOA) of heart valves in the fully open position. In terms of the area at the throat, we get 63) where Q,, is the mean flow rate Ap = Pi-P2 In the case of the EOA for aortic valves, Q,, is replaced by the mean systolic flow (MSF) rate (as opposed to the cardiac output). Equation 5.3 was employed in the 1950s to estimate the orifice area of human heart valves and is commonly referred to as the Gorlin equation in the clinical literature. For the aortic valve, the Gorlin equation is given by AVA = —— 6.4) where AVA is the aortic valve area Ap, is the mean pressure drop across the valve162 Biofluid Mechanics: The Human Circulation The constant 44.5 (cm/s)(mmHg)') takes into account the conversion of units between the MSF (mL/s) and the mean systolic pressure drop (mmHg) and it also includes an assumed discharge coefficient to compute the orifice area in om?. The corresponding Gorlin equation for the mitral valve is given by MDF MVA = ———— 31.0 Ap, (6.5) where the mean diastolic flow (MDA) rate (mL/s) and the mean diastolic pressure gradient (mmHg) are used. Measurements of the flow rate and the pressure drop across the valves can be used to predict the effective valve orifice areas of the natural valves suspected of being stenotic. Such information is useful for cardiac surgeons in deciding when to replace diseased valves. For normal aortic and mitral valves, a discharge coefficient close to unity is assumed. In the case of natural heart valves with centralized flow and no obstructions, the analogy with the flow through a nozzle may be reasonable. This formula is also extensively used to predict the effective valve orifice area of pros- thetic valves. However, due to obstruction of the leaflets, especially with mechanical valves, the discharge coefficient can be expected to be significantly different from that of natural valves. The common practice is to perform in vitro experiments in which the actual EOA can be measured and to determine the discharge coefficient for each type of prosthetic valve. The expression for the EOA derived earlier is based on steady flow across a nozzle and is thus applied assuming constant systolic flow conditions. In reality, however, even during this period when the valve is fully open, the blood flow goes through acceleration and deceleration phases so that the flow is time dependent. Therefore, a more rigorous analysis should include the acceleration of the fluid as well as viscous dissipation. In one-dimensional analysis, the pressure drop across an orifice can be written as (Young, 1979) Af2 4 30? +CQ (5.6) dt where is the flow rate dQ/dt represents the temporal acceleration BQ? represents the convective acceleration CQ represents the viscous dissipation ‘The inertial term (time dependence) can be eliminated by averaging Equation 5.6 over the forward flow interval (time during which the valve is open), resulting in Pm = BQ, +CQn 67)Static and Steady Flow Models 163 or by taking the measurements at the time of peak flow when dO/dt will be idei cally equal to zero, which results in Ap, = BQ; +CQ, (5.8) In this relationship, the subscript “p” denotes that the values are measured at the instant of peak flow through the orifice. Performing a dimensional analysis on the important parameters for flow through an orifice—pressure p, flow rate Q, orifice area A, density p, and viscosity ji shows that the constants B and C can be related to a and L re respectively. Hence, the relationships for the peak and mean pressure drops can be rewritten as (5.9) and (5.10) Substituting typical physiological values for p, 1, A, and Q into the previous equa- tions and performing an order of magnitude study, it can be observed that the iner- tial term in both the equations (first term on the RHS) is three orders of magnitude larger than the viscous effect (second term on the RHS). Thus, the viscous effects can indeed be neglected in flow through the valves. By computing the mean values during the forward flow duration, the EOA relationship (Equation 5.3) will reduce to the form BOA = KQsns,| © GID164 Biofluid Mechanics: The Human Circulation ‘The difference between the previous relationship and the Gorlin equation derived earlier is the root mean square flow rate used here instead of the mean flow rate used in the Gorlin equation, The relationship using the peak flow will be given by EOA= 0, P- (5.12) Pp where Q, is the peak flow rate Ap, is the pressure drop across the valve at the instant of peak flow rate The use of the previous two relationships rather than the Gorlin equation provides more accurate values for the valve orifice area from the rigorous fluid mechanical analysis discussed earlier. A dimensional analysis of steady flow through an orifice has shown that c= 1( $e) where dis the orifice diameter Dis the diameter of the pipe Re is the Reynolds number (=pVD/j\) For a given valve geometry, the only variable in the aforementioned relationship is the flow rate and, hence, it has been proposed that EOA= 6.13) ko (Jap where CQ) is the discharge coefficient as a function of flow rate Q. Using an in vitro experimental setup in which the orifice areas of prosthetic valves of various geometries were measured using planimetry over a range of flow rates, studies have demonstrated that when the discharge coefficient was expressed as a linear function of flow rate such as Cu(Q) = CO+Cr (6.14) the prediction capability of the effective valve orifice areas was significantly improved.Static and Steady Flow Models 165 5.4 RIGID TUBE FLOW MODELS ‘The simplest model for blood flow through a vessel would be steady, fully developed flow of a Newtonian fluid through a straight cylindrical tube of constant circular cross section. Such flows are characterized as Poiseuille flow in the honor of J.L.M. Poiscuille (1799-1869) who performed experiments relating pressure gradient, fiow, and tube geometry in such a model. From his experiments, he empirically derived the relationship given as follows: _ KApD* caer 6.15) where Qis the flow rate Ap is the drop in pressure in a tube of length L and diameter D K denotes a constant that was found to be independent of the other variables. Hagenbach, working independently, arrived at the theoretical solution for the afore- mentioned problem that introduced fluid viscosity as follows _ BR py Oe UL z (5.16) where ris the coefficient of viscosity Ris the tube radius From Equations 5.15 and 5.16, it can be observed that K = x/128p. Thus, the relation- ship in Equation 5.2 is also referred to as the Hagen—Poiseuille law. We have already derived the aforementioned relationship in Chapter 1 from the Navier-Stokes equa- tion (Equation 1.53). We also utilized this relationship considering the forces acting on a volume element of the fluid in Chapter 4 in our discussions on the principles of the capillary viscometer. Several assumptions were made in deriving the relationship for the flow rate given in Equation 5.16 and we should critically examine the validity of these assumptions in models describing blood flow in arteries. The assumptions are as follows: 1. Newtonian fluid: The governing equations used in deriving the expression for the velocity profile assumed that the fluid is Newtonian with a constant viscosity coefficient. When we discussed the viscous behavior of blood in Section 4.1.3, we concluded that the rheology of blood can best be described by Casson relationship and that blood exhibits nonlinear shear stress ver~ sus rate of shear characteristics, especially at low rates of shear. However, it was also determined that at relatively high rates of shear, the viscosity coefficient asymptotically approaches a constant value. Thus, for flow in166 Biofluid Mechanics: The Human Circulation large blood vessels, where relatively large shear rates can be expected dur- ing systole, a Newtonian description appears to be reasonable, . Laminar flow: The governing equations also assume that the flow regime is laminar. For steady flow in cylindrical pipes, we can define a criti- cal Reynolds number, Re,, beyond which the flow can be considered to be turbulent. In a typical human aorta, one can estimate the Reynolds number assuming a diameter at the root of the aorta of 2.5em and a mean time-averaged flow velocity of 20mL/s (based on a cardiac out- put of 6Lpm) and compute a magnitude of about 1500. Whole blood density of 1.056 g/cc and a viscosity coefficient of 0.035P were used in this computation. Thus, the time-averaged Reynolds number is observed to be well below the critical value of about 2100. If a peak flow rate of 20.L/m is assumed during systole, then the Reynolds number during that part of the cardiac cycle is about 5100. However, the human aorta is a distensible vessel with a complex geometry so the critical Reynolds num- ber determined from experiments in rigid straight cylindrical pipes is not applicable in this situation. Jn vivo velocity measurements using hot film anemometry have indicated disturbed flow during the deceleration phase of the cardiac cycle although there is no experimental evidence of sustained turbulence in the human circulation (in the absence of any dis- eased states such as valvular or arterial stenoses). Thus, the assumption of laminar flow in the model also appears to be reasonable. No slip at the vascular wall: The innermost lining of the arterial wall in contact with the blood is a layer of firmly attached endothelial cells and it appears to be reasonable to assume no slip at the interface. . Steady flow: As pointed out earlier, the steady flow model is the simplest to deal with mathematically and, therefore, was used in deriving the afore- mentioned relationship. Based on this assumption, we neglected the inertial forces in the simplifications of the governing equations. However, as dis- cussed in the review of cardiovascular physiology (Chapter 3), flow through human arteries is clearly pulsatile, consisting of systolic and diastolic phases; therefore, the assumption of steady flow is not valid in the major part of the circulatory system. . Cylindrical shape: The tube model discussed earlier assumed a circular cross section and axisymmetry. Even though this geometry may be a good approximation for most of the arteries in the systemic circulation, the veins and the pulmonary arteries are more elliptical in shape. The arteries also have a taper with their cross sections narrowing with distance downstream, Thus, the general assumption of a circular cross section without taper is a deviation from reality. ». Rigid wall: As was discussed in Section 3.4, the arterial walls are viscoelas- tic and distend with the pulse pressure. The interaction between the flowing blood and the distensible arterial wall is an important factor in the descrip- tion of the flow dynamics. Thus, the assumption of rigid walls in the model is also not valid. However, for the special case of steady flow models in the circulatory system, distensibility of the vessels will not affect the solution,Static and Steady Flow Models 167 7, Fully developed flow: The model described earlier also assumes that the flow is fully developed, which implies that the velocity profile remains the same at any cross section with distance downstream. However, as the blood leaves the ventricle through the aortic valve, the velocity profile in the aorta, is relatively flat and a finite length is needed before the flow may become fully developed (as described in the next section). Similarly, even in the dis- tal arteries, flow passes through several branching points and curved arte- rial sections, At each location where the cross-sectional geometry deviates from a straight arterial segment, the flow will also be appropriately altered. Thus, the assumption of fully developed flow is also not valid. It can be observed that in applying the steady flow models to describe blood flow in the circulation, the assumptions of steady flow, wall rigidity, cylindrically shaped lumens, and fully developed flow are all clearly violated. We will discuss unsteady flow models in distensible vessels in the next chapter. In order to analyze the effect of complex noncylindrical geometry as well as the developing nature of flow, experi- mental measurements or use of computational fluid dynamic (CFD) simulations are necessary (see Chapter 11). At this point, however, we will use the basic relationship obtained with this simplified steady flow model in order to introduce some applic tions in the flow through the arterial system. 5.4.1 VASCULAR RESISTANCE We introduced the concept of resistance to flow in the chapter on cardiovascular physiology (Chapter 3). The vascular resistance is given by the relationship Ap 3.3) a G3) This expression is analogous to the electrical resistance given by (5.17) where Tis the current Eis the voltage across a segment of a circuit If the pressure drop is measured in terms of mmHg and the flow rate in terms of mL/s, then the resistance is expressed as mmHg - s/cm? or a peripheral resistance unit (PRU) and it is used in physiological literature. From the Poiseuille expression for flow rate through a tube (Equation 1.53), we obtained the relationship SL R, (3.4)168 U/Ry = UR, + Ry + UR FIGURE 5.5 Total resistance with tubes in series or parallel configuration. ‘When the vessels are in series, the total resistance will be the sum of the individual resistances. When the vessels are in parallel, the total resistance across the vessels can be computed using the relationship shown in Figure 5.5. ‘This formula for the vascular resistance, derived from the steady, fully devel- oped flow relationship can be used to estimate the resistance in segments of the vascular system. For example, the mean pressures at the aortic root and at the ter- minal end of the vena cava can be measured along with the time-averaged flow rate through the systemic circulation. These data can be used to compute the resistance in the systemic circulation as a measure of the functioning of the circulatory system. Similarly, the pulmonary vascular resistance can also be determined by measure- ment of the corresponding pressures. The expression for the resistance (Equation 3.4) shows that it is inversely proportional to the fourth power of the radius, and thus, a small change in the radius of the vessel will considerably affect the resistance to flow. The implication of this is that the autonomic nervous system in the body con- trols the tension of the smooth muscles in the vessel wall in the arterioles. Thus, with the alteration of the muscle tension, the arterioles can be distended or contracted selectively to control the amount of blood flow into the various segments of the body. Even though the measurement of vascular resistance yields information about the state of the circulatory system and, hence, can be used as a diagnostic parameter, several limitations must be kept in mind on the information provided: (1) It does not indicate which pathway between the two points of measurement is constricted or dilated; (2) it does not indicate the cause for the change (due to nervous stimulation, increased transmural pressure, or other causes); (3) it yields information only on net changes and does not indicate local changes; and (4) it does nor provide informa- tion to distinguish between dilation of the vessels or the opening of new vessels (angiogenesis). 5.4.2 REGIONAL ALTERATIONS IN VASCULAR RESISTANCE Due to the powerful effect of vessel radius upon flow (Q « R¢ under constant pres- sure drop), the body has the capability of widely altering the blood flow to various regions in the circulatory system by appropriate increases or decreases in the diam- eter of the arterioles supplying those regions. A typical example of such selectiveStatic and Steady Flow Models 169 regional alterations is that of heavy exercise when blood flow to the skeletal muscles can increase by as much as 20 times the baseline blood flow (see Problem 5.9). The effects of exercise on the circulatory system are (1) increase in mean arterial pressure and (2) increase in the cardiac output. These occur because the sympathetic nervous system stimulates the heart to increase the heart rate and the cardiac contraction forces in order to increase the cardiac output to several times the normal level. The muscles in the systemic veins are also contracted in order to increase the mean sys- temic filling pressure. Simultaneously, the arterioles of most of the peripheral circu- lation are contracted, thereby increasing the resistance to flow in those regions of the circulatory system, while the arterioles supplying the active muscles are dilated in order to decrease their resistance to blood flow, thereby providing increased perfu- sion to those muscles. In general, blood flow through the coronary arteries and the cerebral circulation are maintained at adequate rates since the arterioles in these regions are not subjected to vasoconstriction (Guyton and Hall, 2000). ‘Another example of regional alterations in blood flow is the decrease of flow experienced in vessels close to the skin surface on a cold day. This happens in order to reduce body heat loss and to sustain perfusion to the visceral organs such as the heart, liver, kidney, lungs, and the brain at a constant body temperature. Constriction of the arterioles near the skin increases the resistance to flow at the body surface and also causes blood flow to be diverted to the core region of the body. 5.5 ESTIMATION OF ENTRANCE LENGTH AND ITS EFFECT ON FLOW DEVELOPMENT IN ARTERIES ‘As pointed out in Section 1.8.1.3, as fluid enters a pipe from a reservoir, the velocity profile will be relatively flat and the fluid must pass through a finite length of the tube before the velocity profile attains a final shape. This observation is represented in Figure 5.6. At the tube entrance, the fluid coming in contact with the tube wall will be forced to have zero velocity—that is, the “no slip” condition, due to frictional forces and a gradient in velocity is established in the radial direction, Further downstream, more and more fluid is retarded due to the radial penetration of shearing effects of fluid adjacent to the wall. At the same time, the fluid in the core region is actually acceler- ated by the unbalanced pressure and viscous forces which then maintains a constant flow rate at all cross sections in the tube (ie., satisfies the continuity requirement) Consequently, the initially blunt profile is progressively modified and, ultimately, a parabolic velocity profile is established further downstream. Thus, very near the ima FIGURE 5.6 Concept of entry length before the flow becomes fully developed. ~~ Boundary-layer edge170 Biofluid Mechanics: The Human Circulation entrance, the radial distance in the fluid over which the viscous effects are present js very small. However, as we proceed downstream, the viscous effects have di fused further in the radial direction. The “thickness” within which this diffusion ppas occurred is referred to as the boundary layer. At some location downstream, the poundary layer grows to the point where it reaches the centerline of the tube and, at this point, the flow is said to become fully developed. In Chapter 1, we presented a relationship for the entrance length (Equation 1.78) in terms of tube diameter and the Reynolds number for laminar flow. We will now show the basis for such a relation- ship based on the effect of inertial and viscous drag forces within the boundary layer. ‘A small fluid element within the boundary layer is considered in Figure 5.7. Let the area A, and A, be equal to A. The tangential shear stresses in those areas are (du/dy), ‘and p(du/dy)l,, respectively. The net viscous force on the clement will be the area times the change in stress with the distance y from the wall and will be given by d {du w(t) s00-m) Inthe absence of flow acceleration, the viscous forces must be balanced by the iner- tial forces acting on the element. However, a solution of the governing equations in the boundary layer is too complicated to be solved analytically. By assigning suitable scales to the Variables representing the two forces, an estimate of the entrance length ‘can be obtained. To estimate the viscous forces, we use the boundary layer thickness § at a distance X from the entrance and the free stream velocity U in the previous equation. Then the viscous force is proportional to U AG») ‘The inertial force acting on the element is given by (Convective acceleration)(Volume of the element) FIGURE 5.7 A force balance on a fluid element in the boundary layer.Static and Steady Flow Models 1 If the boundary layer thickness is considered at a distance X from the entrance of the tube, then the time scale for the fluid to reach that distance (the convection time) is X/U. The convective acceleration at this location is then proportional to UM(X/U), or, U/X, Thus, the inertial force on the element will be given by Equating these two forces, we obtain uv u FT iy Py he where & is the proportionality constant that can be determined from experiments, Thus, the boundary layer thickness at any axial location can be written as oe [HX pu From the previous relationship, we can see that the boundary layer grows in propor- tion to the square root of the distance. Also, the boundary layer thickness decreases at any given location as the flow rate through the tube increases, producing a cor- responding increase in the free stream velocity. The boundary layer will fill the tube and the flow will become fully developed (ie., with no further convective accelera- tion in the fluid) when the boundary layer thickness equals the radius, or 8 = D/2, where D is the diameter of the tube. Then, the entrance length will be given by x, =e v or uD X= w(2) (5.18) where the terms in the parenthesis represent the Reynolds number. In this relation- ship, v= jp is referred to as the kinematic viscosity. Equation 5.18 can be used to predict the entrance length for steady laminar flow through a straight pipe of circular cross section. The magnitude for the constant k has been experimentally determined to be ~0.06. Thus, if an artery were assumed to be a straight cylindrical tube with steady and laminar flow, we would be able to estimate the distance at which the flow would become fully developed using the expression given in Equation 5.18. Note that this relationship is valid only for fiows with Reynolds numbers greater than 50.172 Biofluid Mechanics: The Human Circulation In cases where the Reynolds number is close to zero (e.g., in capillaries where th: Reynolds number is <0.01), the entrance length becomes a constant of 0.65 D. In arterial flow, flow development is affected by a number of factors. First, it large arteries, for example, the entrance length is relatively long since it depend not only on vessel diameter but also on the Reynolds number (Equation 5.18), bot! of which are large. This produces a situation in which a large portion of most majo arteries is exposed to developing flow with higher velocity gradients near the wall Second, the axial velocity profile becomes skewed at sites of curvature and bifurca tion of the arteries (see Section 6.6) with higher velocity (and, thus, a higher velocity gradient) toward one wall and a lower velocity toward the opposite wall. One of thi implications of this is that the intimal lining of arteries is exposed to higher shea forces proximally, and lower shear forces distally. Also, there is a general tendenc) for higher shear forces on the outer wall of curvatures and branch inlets and ot the flow divider of bifurcations. In terms of the boundary layer, it will be thinne in regions of high velocity compared with regions with a low velocity. The size 0 the boundary layer is also important in terms of mass transport of molecules (i.e. gas and nutrient) between the blood and artery wall since diffusive effects are mort important than convective effects in large boundary layer regions. This is the basi: for one theory of atherosclerosis (see Section 6.4) in that certain molecules, such a! LDL, may accumulate within regions of thicker boundary layers and tend to stay it that region for longer time, enhancing their diffusive transport to the subendothelia region and initiating atherosclerotic lesions. 5.6 FLOW IN COLLAPSIBLE VESSELS In the relationship derived for flow through conduits (Section 1.5.3.2), we observec that the flow through an individual conduit is proportional to the pressure drop across the system when the flow is laminar. Even when the flow is turbulent, the flow rate will monotonically increase with an increase in pressure drop but not in a lineal fashion. In the circulatory system, however, the conduits are flexible and, in some instances, the transmural (ie., across the vessel wall) pressure can cause significan collapse of the conduit. This is especially true downstream of a stenosis where the pressure in the conduit can drop below that of the extramural (ie., outside the vesse wall) pressure. In such cases, the flow through the conduit is no longer dependent upon the upstream, p,, and downstream, p,, pressure difference, but rather on the difference between the upstream pressure and the pressure surrounding the conduit, p, When that happens, flow through the conduit can remain relatively constant ever though the downstream pressure, p2, varies widely. This phenomena is variously described as flow limitation, Starling resistor phenomenon, sluice effect, and water: {fall effect. It has been observed in blood flow situations such as from extrathoracic to intrathoracic veins, diseased coronary arteries, pulmonary blood flow, and flow through cerebral vessels and in urine flow. Let us consider a system of blood vessels as shown in Figure 5.8 where all the vessels are assumed to be rigid. Pressure at the inlet of the channel is assumed to be 12mmHg and the pressure drop across the arteries, capillaries, and veins is assumed to be 3, 6, and 3mmHg, respectively. These pressure drops are due to viscousStatic and Steady Flow Models 173 hy pl (er) immu) to 10+4 ste oti Arteries Capillaries Veins FIGURE 5.8 Pressure and flow through rigid pipe segments. (Redrawn from Milnor, W.R., Hemodynamics, Williams & Wilkins, Baltimore, MD, 1989) dissipation as the fluid flows across the vessel. A total flow rate of 2mL/s is assumed to be evenly divided between the two segments. The vertical distance between the vessels and the corresponding hydrostatic pressure difference are also shown on the scale on the left of the figure. The resulting pressures that include the hydrostatic effect are given inside the vessels and the pressures due to the effects of viscous losses alone are given at the outside. If the vessel in the upper segment is not rigid but is made of a thin elastic material, it will collapse due to the low transmural pressure and, thus, the flow would cease in the upper segment. However, as soon as the flow ceases, the pressure would rise to 4mmHg due to the static conditions and the vessel would once again open. Thus, this sequence of events will be repeated continuously and has been demonstrated in in vitro experiments. However, in vivo, thin-walled vessels will tend to attain an equilibrium state as shown in Figure 5.9 (Milnor, 1989) Assume here that the capillary segments collapse to a narrow lumen at a transmu- ral pressure of 0.2mmHg and completely collapse at OmmHg. Pressure and flow through the upper channel will reach a state of equilibrium at about 0.1 mfg trans- mural pressure with a lower flow through the upper segment as shown in Figure 5.9. The phenomenon described earlier can be used to explain flow through the lung capillaries. When a person is standing, little flow occurs through the capillaries in the apices of the lung due to the collapse of the blood vessels. As discussed ear- lier, the flow rate through a rigid tube is dependent on the distal pressure which is not necessarily true in a collapsed vessel as discussed in the following. Figure 5.10 shows two rigid vessels connected by a collapsible vessel. The collapsible vessel is enclosed in a box so that the pressure outside the vessel can be independently set. This arrangement is also referred to as Starling's resistor. The collapsible segment is assumed to be fully open at a transmural pressure of 0.2mmHg and to be com- pletely closed at OmmHg. The pressures at various points in the system (in mmHg) are included in the figure. The flow through the vessel will reach equilibrium when174 Biofluid Mechanics: The Human Circulation hy pl | (em) enmigy +o — | 07) (@4)! +4 sts a= 143 ot 2 oh 12) ot FIGURE 5.9 Effect of vessel collapsibility on the pressure and flow. (Redrawn from Milnor, W.R., Hemodynamics, Williams & Wilkins, Baltimore, MD, 1989.) Pp h (em| ™H® (2, ~ P,mmig) 150 2» 6 WW 5 0 ya 15 Flow (mL/min) FIGURE 5.10 Pressure and flow through a collapsible tube. (Redrawn from Milnor, W.R., Hemodynamics, Williams & Wilkins, Baltimore, MD, 1989.) the pressure inside the vessel is 4.1 mmHg representing a transmural pressure of 0.1 mmHg. Changing the distal pressure at point “c” by raising or lowering the out- flow beaker will not alter the flow through the vessel provided it is not raised above 4.2mmHg. However, changing the pressure within the box will affect the flow. The interaction between the variables is represented in the curve shown on at the right half part of the figure. When the outlet pressure P, is equal to the inlet pressure P,, there is no flow through the vessel. Gradually decreasing the outlet pressure results in a linear increase in the flow through the vessel until the outlet pressure equals the pressure in the box surrounding the vessel. Further decrease in the outlet pressure does not increase the flow through the vessel even though the gradient P, ~ P, continues to increase.Static and Steady Flow Models 1 ‘The model described earlier is similar to that occurring in the lungs. Here, the pres- sure in the box would depict the alveolar pressure and, due to the low pressure in the vessels in the lung circulation combined with the hydrostatic effects, the capillary acts like a sluice gate controlled by the arterial pressure and the alveolar pressure. Such a phenomenon where the flow is independent of the downstream pressure is also described as the “vascular waterfall.” The physics of this phenomenon, in which the mechanism by which the flow becomes independent of the variation in the down- stream pressure, is explained by the “inertial” and “frictional” mode of flow limita tion. In the “inertial” mode explanation, the upstream and downstream pressure is assumed to be decoupled at a point in the converging (collapsed) conduit at which the flow has accelerated to a velocity that exceeds the pressure wave propagation velocity of the system at that point, Pressure disturbances distal to the “choke point” cannot be propagated upstream since the medium is moving in the opposite direction with a yelocity greater than the pressure wave propagation velocity. In the mechanism due to the “frictional” mode of flow limitation, it is suggested that changes in the upstream pressure alter the pressure distribution in the adjacent segment of the conduit to cause a compensatory change in the flow resistance in a direction to maintain a constant flow through the conduit 5.7. SUMMARY In this chapter, we used simple steady flow models to derive some relationships between the flow and pressure in the circulatory system and discussed some clini- cal applications based on the simplified models. We will now consider the effect of unsteady flow and the distensibility of the blood vessels as we proceed on to more realistic models to describe blood flow dynamics in the arterial system. PROBLEMS 5.1 For a typical human, the diameter at the root of the aorta is 2.5em, the time- averaged flow rate (cardiac output [CO}) is 5.5Lpm and the peak flow rate dur ing systole is 20Lpm. a. Calculate the Reynolds number based on the time-averaged flow rate as well as the peak flow rate assuming a Poiseuille flow relationship. b, Compute the corresponding wall shear stress in the aorta. c. Assuming time-averaged flow rates of 0.6L/min in the carotid artery (diameter = 0.8cm) and a flow rate of 0.3L/min for a femoral artery (diameter = 0.5cm), calculate the Reynolds number and wall shear rate in these vessels also. d. Do you think that the flow in the aorta becomes turbulent based on the calcu lated Reynolds numbers? 5.2 Assume that the blood is flowing through an aorta of 1,.0cm in diameter at an average velocity of 50cm/s. Let the mean pressure in the aorta be 100mmHg If the blood were to enter a region of stenosis where the diameter of the aorta is only 0.5cm, what would be the approximate pressure at the site of narrowing? (Assume blood density to be 1.056 g/em*: 1 g/em-s? = 7.5 x 10“* mmHg.)