Valsalayam Raghavapanicker Sanal Kumar

Waveriders achieve high aerodynamic efficiency by sustaining an attached shock along the lower surface. However, the proximity of the shock and sonic surface ([Formula: see text]) to the body results in significant thermal loading due to entropy confinement. This study investigated an integrated passive–active aerothermal control strategy for a hypersonic waverider at Mach 6 under high-altitude conditions using design-oriented Reynolds-averaged Navier–Stokes simulations. This approach combines blunt-nose shaping, sonic jet injection, and geometric surface modification to influence shock–entropy coupling and surface pressure distribution. A gas mixture with a high heat-capacity ratio (80% helium and 20% argon) was injected sonically through the nose to modify local thermoacoustic properties associated with Sanal flow choking, displace the sonic surface outward, and reduce entropy transport toward the wall. Surface shaping induced streamtube divergence, which led to controlled Prandtl–Meyer expansion and improved aerodynamic load distribution. Results show that increasing sonic-surface standoff distance is associated with increased shock standoff distance and reduced aerodynamic heating potential while maintaining or improving lift-to-drag ratio. The analysis includes quantitative evaluation of sonic-surface standoff distance and nondimensional Vinay-layer thickness. Although configuration-specific, the results establish a design-oriented framework linking thermoacoustic effects and surface shaping for coupled aerodynamic and thermal performance improvement.

Sudden cardiac arrest (SCA) in individuals without structural or electrical abnormalities remains an unresolved clinical problem. Here we report a pilot translational study investigating whether pressure-driven microbubble dynamics in human blood can generate physical conditions capable of destabilizing cardiovascular flow. Venous blood from healthy adult volunteers (n = 10) was subjected to controlled decompression (760→100 mmHg) at physiological temperature (37–40 °C), while high-speed imaging quantified microbubble nucleation, growth, coalescence and rupture. Microbubble formation consistently initiated below ~600 mmHg, followed by coalescence into transient gas cavities resembling vapor-lock structures. Increasing void fraction was associated with pronounced acoustic softening, with modeled effective sound speed decreasing from ~1500 m s⁻¹ to <100 m s⁻¹. Surface roughness significantly increased nucleation density (p < 0.05). Bubble rupture events produced localized transient pressure disturbances. Although bulk flow was not imposed, the observed acoustic-softening regime defines mechanical conditions permissive for multiphase flow choking in dynamic systems. These findings establish mechanistic feasibility for a physics-based cascade linking decompression-induced microbubble dynamics, acoustic softening and potential flow instability, motivating future in vivo and dynamic investigations into unexplained sudden cardiac collapse.

Background Many cases of sudden cardiac arrest (SCA) occur in individuals with normal coronary arteries and no detectable structural or electrical abnormalities. Mechanistic explanations for such events remain limited. We conducted a pilot translational study to evaluate whether pressure-driven microbubble dynamics can generate physical conditions capable of destabilizing cardiovascular flow. Methods In this pilot, proof-of-concept investigation, venous blood from healthy adult volunteers (n = 10; age 24–32 years) was subjected to controlled static decompression (760→100 mmHg) at physiological temperature (37–40 °C). Microbubble nucleation, growth, coalescence, and rupture were quantified using high-speed imaging. Smooth and rough metallic substrates were used to model vascular and biomaterial interfaces. Acoustic behavior was evaluated using Wood’s equation to estimate sound-speed reduction and identify acoustic-softening thresholds associated with theoretical multiphase flow choking. Effect sizes and confidence intervals were calculated for primary comparisons. Results Microbubble nucleation reproducibly initiated below ~600 mmHg, followed by bubble growth, coalescence, and formation of vapor-lock–like gas cavities. Increasing void fraction produced marked acoustic softening, with modeled effective sound speed decreasing from ~1500 m/s to <100 m/s. Rough surfaces demonstrated significantly higher nucleation density than smooth surfaces (p < 0.05; large effect size). Bubble rupture generated transient shock-like disturbances. Although bulk flow was not imposed, the observed acoustic-softening minimum defines mechanical conditions permissive for multiphase flow choking in dynamic systems. Conclusions This pilot study suggests a possible mechanistic pathway linking decompression-induced microbubble dynamics, acoustic softening, and theoretical flow instability, which requires validation in dynamic experimental and clinical studies. The findings demonstrate the physical feasibility of this cascade under controlled conditions and should be considered hypothesis-generating. They motivate future adequately powered, dynamic, and in-vivo investigations to assess clinical relevance in unexplained sudden cardiac arrest. Significance Statement This pilot translational study identifies a previously unrecognized, physics-based mechanistic framework by which decompression-induced microbubble dynamics may produce acoustic softening and flow instability in blood. By establishing mechanistic feasibility rather than clinical causality, the findings motivate future investigations into monitoring, prevention, and device design strategies for unexplained sudden cardiac collapse.

When astronauts or divers experience a rapid drop in surrounding pressure, tiny gas bubbles can form in their blood—a condition that can threaten heart and vessel function. In this study, we simulated such decompression using fresh, warmed blood samples (37–40 °C) placed in a vacuum chamber. Bubbles consistently appeared near 600 mmHg. Their formation led to acoustic softening, a sharp drop in the speed of sound through blood. As flow velocity remained unchanged, the rising local Mach number brought the system closer to Sanal flow choking, triggered at a critical pressure ratio. Once choking occurs, it can lead to localized supersonic zones and abrupt pressure jumps. Additionally, bubbles may coalesce and block narrow vessels—a phenomenon akin to vapor lock—further impeding circulation. These findings reveal a novel mechanistic link between microbubble formation, acoustic softening, and flow choking, offering valuable insights for protecting cardiovascular health during spaceflight and rapid decompression events.

Sanal flow choking, a groundbreaking concept rooted in the fundamental principles of fluid dynamics and thermodynamics, redefines our understanding of cardiovascular physiology, particularly in the context of multi-phase flows and shock waves [1-15]. Contrary to critiques labeling it as a fallacy [16], this theory provides a crucial framework for addressing flow dynamics in extreme physiological conditions, such as decompression sickness and microgravity, where blood compressibility and gas evolution become prominent [3]. Our extensive research—spanning analytical [3-7], in silico [8-11], in vitro [8-10], and in vivo [1,2,15] studies—demonstrates that under certain pathological or environmental circumstances, blood exhibits compressible flow behavior, leading to multi-phase flow choking and subsequent shock wave formation [1,2]. This paradigm shift challenges the traditional assumption of blood as an incompressible fluid, which has limited the medical understanding of high-speed cardiovascular flow and trauma. Through the introduction of critical indices, such as the Lower Critical Hemorrhage Index (LCHI) and Upper Critical Hemorrhage Index (UCHI), Sanal flow choking offers a robust method to predict cardiovascular risks, including embolisms and vascular damage, induced by rapid pressure changes and gas bubble formation. Furthermore, these phenomena are influenced by the thermodynamic properties of blood and the coexistence of liquid and gas phases. In this rebuttal, we clarify the misinterpretations presented in a recent correspondence [16] against our articles [1-15] and reaffirm the validity of Sanal flow choking in cardiovascular research. We argue that compressible flow theory is indispensable for accurately modeling blood behavior in extreme conditions, and our findings underscore the necessity of revisiting long-held assumptions to prevent significant cardiovascular risks in both clinical and aerospace environments. It is clear that the correspondence [16] misinterprets our detailed analytical, in silico, in vitro, and animal in vivo research, as outlined in our review article in Physics of Fluids [1]. We wish to reaffirm that Sanal flow choking in cardiovascular systems is not a scientific fallacy, but a revolutionary concept grounded in established thermodynamic and fluid dynamics principles [3]. This concept challenges traditional views and provides new insights into the behavior of multiphase flows and shock waves in biological systems as detailed below.

This manuscript1 and the corresponding erratum2 have been retracted by AIP Publishing, following an extensive investigation in line with the COPE guidelines. This manuscript1 and the corresponding erratum2 have been retracted by AIP Publishing, following an extensive investigation in line with the COPE guidelines.