**5. In silico methodology**

Over the decades, bio-medical researchers have been relying on *in silico* simulation to model and cognize the natural mechanisms behind the creation and evolution of hemodynamic disorders. It has been recognized that the *wall-shear-stress* exerted on the walls of the blood vessel due to the flow of blood/biofluid is one of the main pathogenic factors leading to the occurrence of such disorders. The magnitude and distribution of the *wall shear stress* in a blood vessel can provide an insight into the locations of possible aneurysm growth. Furthermore, blockages that build up over time can be predicted by having a qualitative understanding of the flow profile. *In silico* methods can be used for modeling and understanding such vital internal flows. Obviously, the insights gained from the three-dimensional (3D)

**331**

**Figure 6.**

*embolism and without any plaque [5]).*

*Internal Flow Choking in Cardiovascular System: A Radical Theory in the Risk Assessment…*

multi-phase *in silico* simulation can help design patient-specific treatments and forecast asymptomatic cardiovascular risk. In this book chapter, as a proof of the concept of fluid-throat persuaded shock waves, we are highlighting the single phase *in silico* results (**Figure 6**) demonstrating the Sanal flow choking phenomenon followed by pressure-overshoot in an idealized physical model of a blood vessel with divergent region (see **Figure 3**) with working fluid as gas. The modeling of non-Newtonian behavior of blood flow is an important task in any *in silico* simulation with fluid-structural interaction for forecasting asymptomatic cardiovascular diseases. Additionally, a realistic time-varying boundary condition need to be implemented in order to mimic the pulsatile nature of diabatic flow (flow involves

The in silico result presented in **Figure 6** is clearly demonstrating the phenomenon of the Sanal-flow-choking and the shock-waves generation at the subsonic inflow condition (creeping flow) leading to the transient pressure-overshoots (stroke) in the downstream region of an artery with divergent port. **Figure 6** provides the proof of the concept of fluid-throat persuaded flow choking in the CVS. The closed-form analytical prediction of the 3D blockage factor [1] at the sonic-fluid-throat location is a useful tool for the *in vitro* and *in silico* experiments in both the continuum and non-continuum flows with due consideration of heat transfer effects (real-world fluid flow effect). Note that the phenomenon of Sanal flow choking is a paradigm shift in the diagnostic sciences of asymptomatic CVD. Therefore, development of a multi-phase, multispecies, viscoelastic fluid-structural interactive *in silico* model capturing the memory effect (stroke history) is a meaningful objective for predicting *a priori* asymptomatic cardiovascular diseases with credibility [2]. Such an effort will be helpful for the diagnosis, prognosis, treatment and prevention of the hemorrhagic

stroke and the acute heart failure of each and every subject with confidence.

*Single phase* in silico *result is demonstrating the transient pressure-overshoot (stroke) at 12 milli-second from Sanal flow choking time, after reaching the lower critical hemorrhage index (LCHI), in a simulated artery with the boundary layer blockage (a case of an internal flow choking and shock wave generation due to gas* 

*DOI: http://dx.doi.org/10.5772/intechopen.96987*

transfer of heat) of blood in a thermo-viscoelastic vessel.

#### *Internal Flow Choking in Cardiovascular System: A Radical Theory in the Risk Assessment… DOI: http://dx.doi.org/10.5772/intechopen.96987*

multi-phase *in silico* simulation can help design patient-specific treatments and forecast asymptomatic cardiovascular risk. In this book chapter, as a proof of the concept of fluid-throat persuaded shock waves, we are highlighting the single phase *in silico* results (**Figure 6**) demonstrating the Sanal flow choking phenomenon followed by pressure-overshoot in an idealized physical model of a blood vessel with divergent region (see **Figure 3**) with working fluid as gas. The modeling of non-Newtonian behavior of blood flow is an important task in any *in silico* simulation with fluid-structural interaction for forecasting asymptomatic cardiovascular diseases. Additionally, a realistic time-varying boundary condition need to be implemented in order to mimic the pulsatile nature of diabatic flow (flow involves transfer of heat) of blood in a thermo-viscoelastic vessel.

The in silico result presented in **Figure 6** is clearly demonstrating the phenomenon of the Sanal-flow-choking and the shock-waves generation at the subsonic inflow condition (creeping flow) leading to the transient pressure-overshoots (stroke) in the downstream region of an artery with divergent port. **Figure 6** provides the proof of the concept of fluid-throat persuaded flow choking in the CVS. The closed-form analytical prediction of the 3D blockage factor [1] at the sonic-fluid-throat location is a useful tool for the *in vitro* and *in silico* experiments in both the continuum and non-continuum flows with due consideration of heat transfer effects (real-world fluid flow effect). Note that the phenomenon of Sanal flow choking is a paradigm shift in the diagnostic sciences of asymptomatic CVD. Therefore, development of a multi-phase, multispecies, viscoelastic fluid-structural interactive *in silico* model capturing the memory effect (stroke history) is a meaningful objective for predicting *a priori* asymptomatic cardiovascular diseases with credibility [2]. Such an effort will be helpful for the diagnosis, prognosis, treatment and prevention of the hemorrhagic stroke and the acute heart failure of each and every subject with confidence.

#### **Figure 6.**

*Cardiac Diseases - Novel Aspects of Cardiac Risk, Cardiorenal Pathology and Cardiac Interventions*

Over the decades, bio-medical researchers have been relying on *in silico* simulation to model and cognize the natural mechanisms behind the creation and evolution of hemodynamic disorders. It has been recognized that the *wall-shear-stress* exerted on the walls of the blood vessel due to the flow of blood/biofluid is one of the main pathogenic factors leading to the occurrence of such disorders. The magnitude and distribution of the *wall shear stress* in a blood vessel can provide an insight into the locations of possible aneurysm growth. Furthermore, blockages that build up over time can be predicted by having a qualitative understanding of the flow profile. *In silico* methods can be used for modeling and understanding such vital internal flows. Obviously, the insights gained from the three-dimensional (3D)

**Batch No. Blood Group SBP/DBP BPR BHCR UCHI @ 37.5o**

 O+ 150/90 1.666 3.500 3.110 A+ 120/70 1.714 2.760 2.691 B- 150/90 1.666 2.7292 2.709 O+ 150/90 1.666 2.9935 2.824 A+ 140/96 1.458 2.6759 2.640

*Demonstrating the percentage variations of evolved gases (viz., N2-m/z = 28, O2 m/z = 32, CO2-m/z = 44, Ar-m/z = 40, an unknown composite gas - m/z = 28.5) from the blood samples of four different healthy human* 

*beings and one Guinea pig during the hyphenated technique at a blood temperature of 40 °C (104o*

*Prediction of the UCHI from the heat capacity ratio of fresh blood samples of healthy human being of* 

 **C**

 *F) [2].*

**330**

**Table 1.**

**Figure 5.**

*age 23–56 [2].*

**5. In silico methodology**

*Single phase* in silico *result is demonstrating the transient pressure-overshoot (stroke) at 12 milli-second from Sanal flow choking time, after reaching the lower critical hemorrhage index (LCHI), in a simulated artery with the boundary layer blockage (a case of an internal flow choking and shock wave generation due to gas embolism and without any plaque [5]).*
