In vitro prediction of the lower/upper-critical biofluid flow choking index and in vivo demonstration of flow choking in the stenosis artery of the animal with air embolism

Diagnostic investigations of aneurysm, hemorrhagic stroke, and other asymptomatic cardiovascular diseases and neurological disorders due to the flow choking (biofluid/boundary layer blockage persuaded flow choking) phenomenon in the circulatory system of humans and animals on the Earth and in the human spaceflight are active research topics of topical interest {Kumar et al., “boundary layer blockage persuaded flow choking leads to hemorrhagic stroke and other neurological disorders in earth and human spaceflight,” Paper presented at the Basic Cardiovascular Sciences Conference, 23–25 August 2021 (American Stroke Association, 2021) [Circ. Res. 129, AP422 (2021)] and “Lopsided blood-thinning drug increases the risk of internal flow choking and shock wave generation causing asymptomatic stroke,” in International Stroke Conference, 19–20 March 2021 (American Stroke Association, 2021) [Stroke 52, AP804 (2021)]}. The theoretical concept of flow choking [Kumar et al., “Lopsided blood-thinning drug increases the risk of internal flow choking leading to shock wave generation causing asymptomatic cardiovascular disease,” Global Challenges 5, 2000076 (2021); “Discovery of nanoscale boundary layer blockage persuaded flow choking in cardiovascular system—Exact prediction of the 3D boundary-layer-blockage factor in nanotubes,” Sci. Rep. 11, 15429 (2021); and “The theoretical prediction of the boundary layer blockage and external flow choking at moving aircraft in ground effects,” Phys. Fluids 33(3), 036108 (2021)] in the cardiovascular system (CVS) due to gas embolism is established herein through analytical, in vitro (Kumar et al., “Nanoscale flow choking and spaceflight effects on cardiovascular risk of astronauts—A new perspective,” AIAA Paper No. 2021-0357, 2021), in silico (Kumar et al., “Boundary layer blockage, Venturi effect and cavitation causing aerodynamic choking and shock waves in human artery leading to hemorrhage and massive heart attack—A new perspective,” AIAA Paper No. 2018-3962, 2018), and in vivo animal methodology [Jayaraman et al., “Animal in vivo: The proof of flow choking and bulging of the downstream region of the stenosis artery due to air embolism,” Paper presented at the Basic Cardiovascular Sciences Conference, 25–28 July 2022 (American Heart Association, 2022)]. The boundary layer blockage persuaded flow choking phenomenon is a compressible viscous flow effect, and it arises at a critical pressure ratio in continuum/non-continuum real-world yocto to yotta scale flow systems and beyond [Kumar et al., “Universal benchmark data of the three-dimensional boundary layer blockage and average friction coefficient for in silico code verification,” Phys. Fluids 34(4), 041301 (2022)]. The closed-form analytical models, capable of predicting the flow choking in CVS, developed from the well-established compressible viscous flow theory are reviewed and presented herein. The lower-critical flow-choking index of the healthy subject (human being/animal) is predicted through the speciation analysis of blood. The upper-critical flow-choking index is predicted from the specific heat of blood at constant pressure (C_p) and constant volume (C_v), estimated using the Differential Scanning Calorimeter. These flow-choking indexes, highlighted in terms of systolic-to-diastolic blood pressure ratio (SBP/DBP), are exclusively controlled by the biofluid/blood heat capacity ratio (BHCR = C_p/C_v). An in vitro study shows that nitrogen (N₂), oxygen (O₂), and carbon dioxide (CO₂) gases are predominant in fresh-blood samples of the healthy humans and Guinea pigs at a temperature range of 37–40 °C (98.6–104 °F) causing gas embolism. In silico results demonstrated the existence of the biofluid/boundary layer blockage persuaded flow choking, stream tube flow choking, shock wave generation, and pressure overshoot in the downstream region of simulated arteries (with and without stenosis), at a critical pressure ratio, due to gas embolism. The flow choking followed by aneurysm (i.e., bulging of the downstream region of the stenosis artery due to shock wave generation) due to air embolism is demonstrated through small animal in vivo studies. We could corroborate herein, with the animal in vivo and three-dimensional in silico studies, that flow-choking followed by shock wave generation and pressure overshoot occurs in arteries with stenosis due to air embolism at a critical pressure ratio. Analytical models reveal that flow-choking occurs at relatively high and low blood viscosities in CVS at a critical blood pressure ratio (BPR), which leads to memory effect (stroke history/arterial stiffness) and asymptomatic cardiovascular diseases [Kumar et al., “Lopsided blood-thinning drug increases the risk of internal flow choking leading to shock wave generation causing asymptomatic cardiovascular disease,” Global Challenges 5, 2000076 (2021)]. We concluded that an overdose of drug for reducing the blood viscosity enhances the risk of flow choking (biofluid/boundary layer blockage persuaded flow choking) due to an enhanced boundary layer blockage (BLB) factor because of the rise in Reynolds number (Re) and turbulence. An analytical model establishes that an increase in Re due to the individual or the joint effects of fluid density, fluid viscosity, fluid velocity, and the hydraulic diameter of the vessel creates high turbulence level in CVS instigating an escalated BLB factor heading to a rapid adverse flow choking. Therefore, prescribing the exact blood-thinning course of therapy is crucial for achieving the anticipated curative value and further annulling adverse flow choking (biofluid/boundary layer blockage persuaded flow choking) in CVS. We could conclude authoritatively herein, with the animal in vivo studies, that flow choking occurs in the artery with stenosis due to air embolism at a critical BPR (i.e., SBP/DBP = 1.892 9), which is regulated by the heat capacity ratio of air. The cardiovascular risk due to boundary layer blockage persuaded flow choking could be diminished by concurrently reducing the viscosity of biofluid/blood and flow-turbulence. This comprehensive review is a pointer toward achieving relentless unchoked flow conditions (i.e., flow Mach number < 1) in the CVS for prohibiting asymptomatic cardiovascular diseases and neurological disorders associated with flow choking and shock wave generation followed by pressure overshoot causing arterial stiffness. The unchoked flow condition can be achieved in every subject (human/animal) by suitably increasing the thermal-tolerance-level in terms of BHCR and/or by reducing the BPR within the pathophysiological range of individual subjects through the new drug discovery, the new companion drug with the conventional blood thinners and/or proper health care management for increasing the healthy-life span of one and all in the universe.