The discovery of Sanal flow choking is a scientific breakthrough and a paradigm shift in the diagnostics of the detonation/hemorrhage in real‐world fluid flow systems. The closed‐form analytical models capable of predicting the boundary‐layer blockage factor for both 2D and 3D cases at the Sanal flow choking for adiabatic and diabatic fluid flow conditions are critically reviewed here. The beauty and novelty of these models stem from the veracity that at the Sanal flow choking condition for diabatic flows all the conservation laws of nature are satisfied at a unique location, which allows for computational fluid dynamics (CFD) code verification. At the Sanal flow choking condition both the thermal choking and the wall‐friction‐induced flow choking occur at a single sonic fluid throat location. The blockage factor predicted at the Sanal flow choking condition can be taken as an infallible data for various in silico model verification, validation, and calibration. The 3D blockage factor at the Sanal flow choking is found to be 45.12% lower than the 2D case of a wall‐bounded diabatic fluid flow system with air as the working fluid. The physical insight of Sanal flow choking presented in this review article sheds light on finding solutions, through in silico experiments in base flow and nanoflows, for numerous unresolved problems carried forward over the centuries in physical, chemical, and biological sciences for humankind.

A closed-form analytical model is developed for estimating the 3D boundary-layer-displacement thickness of an internal flow system at the Sanal flow choking condition for adiabatic flows obeying the physics of compressible viscous fluids. At this unique condition the boundary-layer blockage induced fluid-throat choking and the adiabatic wall-friction persuaded flow choking occur at a single sonic-fluid-throat location. The beauty and novelty of this model is that without missing the flow physics we could predict the exact boundary-layer blockage of both 2D and 3D cases at the sonic-fluid-throat from the known values of the inlet Mach number, the adiabatic index of the gas and the inlet port diameter of the internal flow system. We found that the 3D blockage factor is 47.33 % lower than the 2D blockage factor with air as the working fluid. We concluded that the exact prediction of the boundary-layer-displacement thickness at the sonic-fluid-throat provides a means to correctly pinpoint the causes of errors of the viscous flow solvers. The methodology presented herein with state-of-the-art will play pivotal roles in future physical and biological sciences for a credible verification, calibration and validation of various viscous flow solvers for high-fidelity 2D/3D numerical simulations of real-world flows. Furthermore, our closed-form analytical model will be useful for the solid and hybrid rocket designers for the grain-port-geometry optimization of new generation single-stage-to-orbit dual-thrust-motors with the highest promising propellant loading density within the given envelope without manifestation of the Sanal flow choking leading to possible shock waves causing catastrophic failures.

The discovery of Sanal flow choking in the cardiovascular‐system calls for multidisciplinary and global action to develop innovative treatments and to develop new drugs to negate the risk of asymptomatic‐cardiovascular‐diseases. Herein, it is shown that when blood‐pressure‐ratio (BPR) reaches the lower‐critical‐hemorrhage‐index (LCHI) internal‐flow‐choking and shock wave generation can occur in the cardiovascular‐system, with sudden expansion/divergence/vasospasm or bifurcation regions, without prejudice to the percutaneous‐coronary‐intervention (PCI). Analytical findings reveal that the relatively high and the low blood‐viscosity are cardiovascular‐risk factors. In vitro studies have shown that nitrogen, oxygen, and carbon dioxide gases are dominant in fresh blood samples of humans/guinea pigs at a temperature range of 98.6–104 F. An in silico study demonstrated the Sanal flow choking phenomenon leading to shock‐wave generation and pressure‐overshoot in the cardiovascular‐system. It has been established that disproportionate blood‐thinning treatment increases the risk of the internal‐flow‐choking due to the enhanced boundary‐layer‐blockage‐factor, resulting from an increase in flow‐turbulence level in the cardiovascular‐system, caused by an increase in Reynolds number as a consequence of low blood‐viscosity. The cardiovascular‐risk can be diminished by concurrently lessening the viscosity of biofluid/blood and flow‐turbulence by raising the thermal‐tolerance‐level in terms of blood‐heat‐capacity‐ratio (BHCR) and/or by decreasing the systolic‐to‐diastolic blood‐pressure‐ratio.