**1. Introduction**

The cardiovascular system (blood circulatory system) is an internal fluid flow loop with multiple branches, transport nutrients and oxygen to all cells in the body. The center of the cardiovascular system (CVS) is the heart, which is accountable to pump blood through the complex network of viscoelastic vessels, viz., arteries, veins and capillaries. Blood flow in CVS is inherently an unsteady phenomenon experiencing with transient events. Blood flow begins when the heart relaxes between two heartbeats. Due to the cyclic nature of the heart the velocity and pressure of the internal fluid (blood/biofluid) circulating through the viscoelastic vessels varies with time. Blood flow in CVS is typically laminar but due to its pulsatile nature makes possible the flow transition to turbulent. Furthermore, the variations in the fluid flow properties and vessel geometry due to pathophysiological reasons, including the seasonal effects, contribute for the transition of laminar flow to turbulent.

Diseases of the CVS are manifold in gravity and microgravity environment (human spaceflight) and afflict millions of patients worldwide including cases of: coronary artery disease (CAD), ischemic gangrene, abdominal aortic aneurysms, moyamoya disease, and stroke. A few of these dysfunctions are reported to be the end result of atherosclerosis, characterized by plaque accumulation within the walls of the arteries. Atherosclerotic cardiovascular disease (CVD) is the leading cause of death for both men and women. There is no clear age cut point for defining the onset of risk for CVD, which is corroborated from the clinically detected elevated risk factor levels and subclinical abnormalities of adolescents as well as young adults. The hemodynamic characteristics of blood flow have long been thought to play an important role in the pathogenesis of atherosclerosis. In light of the discovery of internal flow choking in CVS [1, 2], the hemodynamic characteristics of blood flow need to be examined in detail for exploring the causes and effects of flow choking in gravity and microgravity environment for an authentic conclusion in the risk assessment of asymptomatic cardiovascular diseases.

Heart failure (HF) is the cardiovascular epidemic of the 21st century [2]. Although there has been significant advancement in the diagnosis, prognosis, treatment and prevention of HF with reduced ejection fraction (EF), the morbidity and mortality are still extensive. This is particularly true due to the Covid-19 pandemic (www.escardio.org). The EF is a blood flow measurement in percentage (%), specifying how much blood the left ventricle pumps out with each contraction. The EF measurement under 40% may be an indication of HF or cardiomyopathy. An EF from 41–49% may be considered as "borderline" cases having the history of stroke (memory effect). A normal heart's EF may be between 50–70%. An EF value higher than 75% generally indicates hypertrophic cardiomyopathy (HCM), which could affect people of any age [2]. HCM is reported as a cause of acute HF particularly in young people, including young athletes. Although all these percentage demarcations of the EF are meaningful for the diagnosis, until the discovery of the Sanal flow choking the EF estimations were not supported by any closed-form analytical model for taking brilliant clinical decisions case by case. The recent theoretical discovery of the Sanal flow choking [1, 2] provides an insight for the risk assessment of asymptomatic cardiovascular diseases. Moreover, the Sanal flow choking model could generate universal benchmark data for predicting the condition of internal flow choking in CVS for taking an authentic conclusion on the desirable EF in terms of blood flow percentage for healthy subjects for reducing the risk of acute-heart-failure. The European Society of Cardiology (ESC) reported (2020) that patients with cardiovascular risk factors and established cardiovascular disease (CVD) represent a vulnerable population when suffering from the Covid-19. It is important to note that patients with cardiac injury in the context of Covid-19 have an increased risk of morbidity and mortality.

The acute-heart-failure is an event rather than a disease [3, 4]. Therefore, many researchers argued for a radical change in thinking and in therapeutic drug

**321**

blockage [6].

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

development through multidisciplinary research [1–6]. Of late, Kumar et al. [2] reported conclusively that the transient event causing the acute-heart-failure is due to the phenomenon of internal flow choking (biofluid/Sanal flow choking) at a critical total-to-static pressure ratio. Internal flow choking is a compressible fluid flow effect caused by the blockage factor, which occurs at a critical blood-pressureratio (BPR), irrespective of the incoming flow velocity. In the CVS, the total pressure is considered as systolic blood pressure (SBP) and the static pressure is denoted as diastolic blood pressure (DBP). The physical situation of internal flow choking in the micro/nanoscale fluid flows in the circulatory system is more susceptible at microgravity condition due to altered variations of blood viscosity, turbulence and the BPR (SBP/DBP). During a long-term human spaceflight mission, the major factor that affects cardiovascular dysfunctions is the absence of gravity [6]. Cardiovascular changes in actual spaceflight differ from those in stimulations such as head-down bedrest or dry immersion [7]. The changes in the cardiovascular system begin solely with the fluid shift associated with microgravity, followed by the decreased circulatory blood volume, cardiac size, and aerobic capacity, and the most prominent symptom, postflight orthostatic intolerance. These symptoms are generically known as "cardiovascular deconditioning" [7–11]. Microgravity environment decreases plasma volume and increases the hematocrit compared with the situation on the earth surface, which increases the relative viscosity of blood. Since blood viscosity strongly depends on hematocrit there are possibilities of an early flow choking in microgravity environment due to an enhanced boundary layer

Human blood is a compressible fluid with different degrees of the compressibility percentage because the specific volume (or density) of blood does change with temperature and/or pressure [1, 2]. Therefore, the specific heat at the constantpressure (Cp) is always higher than the specific heat at the constant-volume (Cv) of all human blood. The ratio of Cp and Cv is defined as the blood-heat-capacity-ratio (BHCR), which is an important parameter determining the thermal-tolerance level of blood [2]. The specific heat capacity depends on the number of degrees of freedom and each independent degree of freedom permits the particles to store thermal energy and as a result the BHCR will be always greater than one. It corroborates that blood is a compressible fluid and internal flow choking in CVS could occur at a critical BPR irrespective of hypertension or hypotension. Traditionally hypertension is considered as a cardiovascular-risk-factor in patients with systemic autoimmune and chronic inflammatory diseases. Until the theoretical discovery of the internal flow choking in CVS there were no authentic conclusions to support whether hypertension or hypotension is more risk with regards to the hemorrhagic stroke and acute myocardial infarction [1, 2]. The fact is that an acute-heart-failure could occur in both hypertension or hypotension patient because the controlling parameter of this event is the blood-pressure-ratio (BPR). In brevity, attaining the critical BPR is considered as the risk factor for asymptomatic cardiovascular diseases. At the threshold of the internal choking condition, a minor oscillation in BPR for both *hyper* and *hypo* subjects is likely to aggravate the cardiovascular risk. In light of the discovery of internal flow choking in CVS [1, 2], the classic definition of the hypertension causing cardiovascular risk is largely arbitrary [SBP ≥140 and/ or DBP ≥90 mmHg]. The prevailing cardiovascular risk data remains challenging owing to the fact that the internal flow choking could occur in both hypertension or hypotension subjects once SBP/DBP reaches the critical BPR. The internal flow choking could happen anywhere in CVS including capillaries, vasa vasorum and/ or nanoscale vessels. Capillaries are tiny blood vessels connecting arteries to veins. These blood vessels carry oxygen and nutrients to individual cells throughout the body. The vasa vasorum is a network of small blood vessels that are found in large

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

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

development through multidisciplinary research [1–6]. Of late, Kumar et al. [2] reported conclusively that the transient event causing the acute-heart-failure is due to the phenomenon of internal flow choking (biofluid/Sanal flow choking) at a critical total-to-static pressure ratio. Internal flow choking is a compressible fluid flow effect caused by the blockage factor, which occurs at a critical blood-pressureratio (BPR), irrespective of the incoming flow velocity. In the CVS, the total pressure is considered as systolic blood pressure (SBP) and the static pressure is denoted as diastolic blood pressure (DBP). The physical situation of internal flow choking in the micro/nanoscale fluid flows in the circulatory system is more susceptible at microgravity condition due to altered variations of blood viscosity, turbulence and the BPR (SBP/DBP). During a long-term human spaceflight mission, the major factor that affects cardiovascular dysfunctions is the absence of gravity [6]. Cardiovascular changes in actual spaceflight differ from those in stimulations such as head-down bedrest or dry immersion [7]. The changes in the cardiovascular system begin solely with the fluid shift associated with microgravity, followed by the decreased circulatory blood volume, cardiac size, and aerobic capacity, and the most prominent symptom, postflight orthostatic intolerance. These symptoms are generically known as "cardiovascular deconditioning" [7–11]. Microgravity environment decreases plasma volume and increases the hematocrit compared with the situation on the earth surface, which increases the relative viscosity of blood. Since blood viscosity strongly depends on hematocrit there are possibilities of an early flow choking in microgravity environment due to an enhanced boundary layer blockage [6].

Human blood is a compressible fluid with different degrees of the compressibility percentage because the specific volume (or density) of blood does change with temperature and/or pressure [1, 2]. Therefore, the specific heat at the constantpressure (Cp) is always higher than the specific heat at the constant-volume (Cv) of all human blood. The ratio of Cp and Cv is defined as the blood-heat-capacity-ratio (BHCR), which is an important parameter determining the thermal-tolerance level of blood [2]. The specific heat capacity depends on the number of degrees of freedom and each independent degree of freedom permits the particles to store thermal energy and as a result the BHCR will be always greater than one. It corroborates that blood is a compressible fluid and internal flow choking in CVS could occur at a critical BPR irrespective of hypertension or hypotension. Traditionally hypertension is considered as a cardiovascular-risk-factor in patients with systemic autoimmune and chronic inflammatory diseases. Until the theoretical discovery of the internal flow choking in CVS there were no authentic conclusions to support whether hypertension or hypotension is more risk with regards to the hemorrhagic stroke and acute myocardial infarction [1, 2]. The fact is that an acute-heart-failure could occur in both hypertension or hypotension patient because the controlling parameter of this event is the blood-pressure-ratio (BPR). In brevity, attaining the critical BPR is considered as the risk factor for asymptomatic cardiovascular diseases. At the threshold of the internal choking condition, a minor oscillation in BPR for both *hyper* and *hypo* subjects is likely to aggravate the cardiovascular risk. In light of the discovery of internal flow choking in CVS [1, 2], the classic definition of the hypertension causing cardiovascular risk is largely arbitrary [SBP ≥140 and/ or DBP ≥90 mmHg]. The prevailing cardiovascular risk data remains challenging owing to the fact that the internal flow choking could occur in both hypertension or hypotension subjects once SBP/DBP reaches the critical BPR. The internal flow choking could happen anywhere in CVS including capillaries, vasa vasorum and/ or nanoscale vessels. Capillaries are tiny blood vessels connecting arteries to veins. These blood vessels carry oxygen and nutrients to individual cells throughout the body. The vasa vasorum is a network of small blood vessels that are found in large

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

The center of the cardiovascular system (CVS) is the heart, which is accountable to pump blood through the complex network of viscoelastic vessels, viz., arteries, veins and capillaries. Blood flow in CVS is inherently an unsteady phenomenon experiencing with transient events. Blood flow begins when the heart relaxes between two heartbeats. Due to the cyclic nature of the heart the velocity and pressure of the internal fluid (blood/biofluid) circulating through the viscoelastic vessels varies with time. Blood flow in CVS is typically laminar but due to its pulsatile nature makes possible the flow transition to turbulent. Furthermore, the variations in the fluid flow properties and vessel geometry due to pathophysiological reasons, including the seasonal effects, contribute for the transition of laminar

Diseases of the CVS are manifold in gravity and microgravity environment (human spaceflight) and afflict millions of patients worldwide including cases of: coronary artery disease (CAD), ischemic gangrene, abdominal aortic aneurysms, moyamoya disease, and stroke. A few of these dysfunctions are reported to be the end result of atherosclerosis, characterized by plaque accumulation within the walls of the arteries. Atherosclerotic cardiovascular disease (CVD) is the leading cause of death for both men and women. There is no clear age cut point for defining the onset of risk for CVD, which is corroborated from the clinically detected elevated risk factor levels and subclinical abnormalities of adolescents as well as young adults. The hemodynamic characteristics of blood flow have long been thought to play an important role in the pathogenesis of atherosclerosis. In light of the discovery of internal flow choking in CVS [1, 2], the hemodynamic characteristics of blood flow need to be examined in detail for exploring the causes and effects of flow choking in gravity and microgravity environment for an authentic conclusion

in the risk assessment of asymptomatic cardiovascular diseases.

an increased risk of morbidity and mortality.

Heart failure (HF) is the cardiovascular epidemic of the 21st century [2]. Although there has been significant advancement in the diagnosis, prognosis, treatment and prevention of HF with reduced ejection fraction (EF), the morbidity and mortality are still extensive. This is particularly true due to the Covid-19 pandemic (www.escardio.org). The EF is a blood flow measurement in percentage (%), specifying how much blood the left ventricle pumps out with each contraction. The EF measurement under 40% may be an indication of HF or cardiomyopathy. An EF from 41–49% may be considered as "borderline" cases having the history of stroke (memory effect). A normal heart's EF may be between 50–70%. An EF value higher than 75% generally indicates hypertrophic cardiomyopathy (HCM), which could affect people of any age [2]. HCM is reported as a cause of acute HF particularly in young people, including young athletes. Although all these percentage demarcations of the EF are meaningful for the diagnosis, until the discovery of the Sanal flow choking the EF estimations were not supported by any closed-form analytical model for taking brilliant clinical decisions case by case. The recent theoretical discovery of the Sanal flow choking [1, 2] provides an insight for the risk assessment of asymptomatic cardiovascular diseases. Moreover, the Sanal flow choking model could generate universal benchmark data for predicting the condition of internal flow choking in CVS for taking an authentic conclusion on the desirable EF in terms of blood flow percentage for healthy subjects for reducing the risk of acute-heart-failure. The European Society of Cardiology (ESC) reported (2020) that patients with cardiovascular risk factors and established cardiovascular disease (CVD) represent a vulnerable population when suffering from the Covid-19. It is important to note that patients with cardiac injury in the context of Covid-19 have

The acute-heart-failure is an event rather than a disease [3, 4]. Therefore, many researchers argued for a radical change in thinking and in therapeutic drug

**320**

flow to turbulent.

veins (e.g., the venae cavae) and arteries such as the aorta and its branches. These small vessels serve to provide blood supply and nourishment for tunica adventitia and outer parts of tunica media of large vessels. Arteries deliver blood from the heart to the rest of the body and Veins return the blood back to the heart from the rest of the body. It is important to note that the pressure inside of arteries is very different from the pressure inside of veins. The pressure created by the heart pushes the blood through the arteries and the pressure inside the arteries is directly related to the blood pressure. The pressure in the veins is very low. Of late Kumar et al. [2, 3] reported that not the pressure but the magnitude of the bloodpressure-ratio (BPR) is the risk factor for acute-heart-failure and the brain hemorrhage because at the choked flow condition there are possibilities of the occurrence shock wave and pressure-overshoot in any vessel with divergent and/or bifurcation region causing aneurysm or wall tearing.

A brain hemorrhage is a type of stroke. It is caused by an artery in the brain bursting and causing localized bleeding in the surrounding tissues. Brain arteriovenous malformations (AVMs) are abnormal connections of arteries and veins [12]. An AVM can develop anywhere in the body, but occurs most often in the brain. Brain AVMs are a leading cause of the hemorrhage in children and young adults, although they can cause other morbidities such as seizures, focal neurological deficits, and headaches. There is usually high flow through the feeding arteries, nidus, and draining veins, which may result in rupture and intracranial hemorrhage, the most severe complication of an AVM. Clinically, brain AVMs are technically challenging and resource-intensive to manage with the available therapeutic modalities and often require multi-modal therapy. The factors influencing risk of hemorrhage associated with sporadic brain AVM is still poorly understood. It has already been established that blood/biofluid is a compressible viscous fluid and internal flow choking can occur anywhere in CVS at a critical BPR causing asymptomatic hemorrhage. In light of the theoretical discovery of the phenomenon of internal flow choking in nano scale fluid flows [1, 2], further studies on the pathogenesis of asymptomatic intracranial hemorrhage is envisaged [13]. Briefly, the concept of internal flow choking in blood circulatory system provides an insight for the diagnosis, prognosis, treatment and prevention of the asymptomatic coronary artery disease (CAD) and peripheral artery disease (PAD).
