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The distribution of pulmonary blood flow is uneven and can be described as a three-zone model, the West zones: zone 1 occurs whenever alveolar pressure exceeds arterial pressure; zone 2 when the arterial pressure is greater than alveolar but the alveolar pressure exceeds the venous pressure; and finally zone 3 when both arterial and venous pressures exceed alveolar pressure. Consequently, the blood flow is almost determined by the difference between the arterial and venous pressures in zone 3 and between arterial and alveolar pressures in zone 2 and ceases in zone 1. The understanding of this subject may be difficult to some medical students. Therefore, to improve the learning of this topic in our physiology course, we used a didactic model to demonstrate the core concept of flow down gradients and its application to pulmonary blood flow. We modeled a Starling resistor by placing a collapsible tube inside a hermetic chamber of variable pressure. Transparent turbine flowmeters were connected to the upstream and downstream extremities of the Starling resistor, and we generated a constant airflow with a brushless motor. By maintaining the input (arterial) pressure constant and varying the chamber (alveolar) pressure, we could simulate the three zones and demonstrate the resulting flow through the turbines. In conclusion, our demonstration using a Starling resistor model combined with visible turbine flowmeters can be used to facilitate comprehension of important concepts in physiology involving flow down gradients, such as pulmonary blood flow. NEW & NOTEWORTHY The understanding of respiratory physiology is a challenge to medical students. To improve the learning of pulmonary blood flow distribution through lung vessels in our physiology course, we modeled a Starling resistor model combined with visible turbine flowmeters. Our model can significantly improve the core concept of flow down gradients teaching and its application to West zones.

Objective: The biomechanics of upper airway collapse in obstructive sleep apnea (OSA) remains poorly understood. The goal of this study is to compare the area-pressure relationship (tube law) of the velopharynx at peak inspiration and peak expiration., Study Design: Cross-sectional., Setting: Academic tertiary medical center., Methods: The velopharyngeal tube law was quantified in a convenience sample of 20 OSA patients via step reductions in nasal mask pressure during drug induced sleep endoscopy (DISE). The velopharyngeal airspace cross-sectional area was estimated from endoscopy while luminal pressure was recorded with a catheter. The tube law was quantified for nasal mask pressures from 14 to 0 cmH 2 O at peak inspiration and at peak expiration in all patients. The tube law was also quantified during the breathing cycle at a constant nasal mask pressure of 4 cmH 2 O in 3 patients representing different phenotypes., Results: Velopharyngeal compliance (the slope of the tube law) was not statistically different in the peak inspiration versus peak expiration tube laws. Three phenotypes were observed, namely inspiratory collapse (phenotype 1), expiratory collapse (phenotype 2 = palatal prolapse), and a mostly stable airway during inspiration and expiration that collapsed as CPAP was reduced (phenotype 3)., Conclusion: Velopharyngeal compliance is not significantly different at peak inspiration and peak expiration, which suggests that muscle tone is low when luminal pressure is above the closing pressure. Additional studies are needed to investigate how different phenotypes of velopharyngeal collapse may affect therapeutic outcomes., (© 2024 American Academy of Otolaryngology–Head and Neck Surgery Foundation.)

The upper airway is often modeled as a Starling resistor, which predicts that flow is independent of inspiratory effort during flow limitation. However, while some obstructive sleep apnea (OSA) patients exhibit flat, Starling resistor-like flow limitation, others demonstrate considerable negative effort dependence (NED), defined as the percent reduction in flow from peak to mid-inspiration. We hypothesized that the variability in NED could be due to differences in phasic pharyngeal muscle activation between individuals. Therefore, we induced topical pharyngeal anesthesia to reduce phasic pharyngeal muscle activation to see if it increased NED. Twelve subjects aged 50±10 years with a BMI of 35±6 kg/m(2) and severe OSA (apnea-hypopnea index=52±28 events/h) were studied. NED and phasic genioglossus muscle activity (EMG(GG)) of flow limited breaths were determined before and after pharyngeal anesthesia with lidocaine. Pharyngeal anesthesia led to a 33% reduction in EMG(GG) activity (p

The upper airway is often modeled as a classical Starling resistor, featuring a constant inspiratory airflow, or plateau, over a range of downstream pressures. However, airflow tracings from clinical sleep studies often show an initial peak before the plateau. To conform to the Starling model, the initial peak must be of small magnitude or dismissed as a transient. We developed a method to simulate fast or slow inspirations through the human upper airway, to test the hypothesis that this initial peak is a transient. Eight subjects [4 obstructive sleep apnea (OSA), 4 controls] slept in an "iron lung" and wore a nasal mask connected to a continuous/bilevel positive airway pressure machine. Downstream pressure was measured using an epiglottic catheter. During non-rapid eye movement (NREM) sleep, subjects were hyperventilated to produce a central apnea, then extrathoracic pressure was decreased slowly (∼2-4 s) or abruptly (

A quarter of the world's population experience wheezing. These sounds have been used for diagnosis since the time of the Ebers Papyrus (ca 1500 BC). We know that wheezing is a result of the oscillations of the airways that make up the lung. However, the physical mechanisms for the onset of wheezing remain poorly understood, and we do not have a quantitative model to predict when wheezing occurs. We address these issues in this paper. We model the airways of the lungs by a modified Starling resistor in which airflow is driven through thin, stretched elastic tubes. By completing systematic experiments, we find a generalized ‘tube law’ that describes how the cross-sectional area of the tubes change in response to the transmural pressure difference across them. We find the necessary conditions for the onset of oscillations that represent wheezing and propose a flutter-like instability model for it about a heavily deformed state of the tube. Our findings allow for a predictive tool for wheezing in lungs, which could lead to better diagnosis and treatment of lung diseases.

This paper introduces a novel physical model of the intracranial system, which was built with the specific purpose of gaining a better insight into the fundamental mechanisms involved in the cerebral circulation. Specifically, the phenomena of passive autoregulation of the blood flow and the variation of the intracranial compliance as a function of the mean intracranial pressure have been investigated. The physical model allows to go beyond state-of-the-art mathematical models that are often based on strong assumptions or simplifications on the physical mechanisms governing the cerebral circulation. Indeed, the physical model based on passive components was able to correctly replicate some fundamental mechanisms of the blood flow autoregulation. In particular, it allows to highlight the role of the venous outflow, which behaves as a Starling resistor. The physical model can be employed as a demonstrator for educational purpose and to test the behavior of shunts for the therapy of hydrocephalus.

Headache is the most frequent and often the most severe symptom of idiopathic intracranial hypertension (IIH) clinical presentation, although pain characteristics are very variable among sufferers and the pain may even lack in some cases. Whatever the headache features, refractoriness to treatments, pain worsening in the recumbent position, and frequent awakenings with severe headache late in the night are the specific complains of such patients. However, a migraine or probable migraine headache, mostly with a chronic headache pattern, can be diagnosed in about 2/3 of the cases. In IIH cases without papilledema (IIHWOP), this leads to a high rate of misdiagnosis with primary chronic migraine (CM). Mechanisms responsible for the shared migrainous presentation of CM and IIH/IIHWOP may rely on a pathologic CGRP release from the rich trigemino-vascular innervated dural sinuses, congested in the course of raised intracranial pressure. The possible role of IIHWOP as a powerful and modifiable risk factor for migraine progression is discussed. Further studies investigating the possible efficacy of anti CGRP/receptor antibodies in IIH/IIHWOP headache treatment are needed. [ABSTRACT FROM AUTHOR]

We present a theoretical description of flow-induced self-excited oscillations in the Starling resistor--a pre-stretched thin-walled elastic tube that is mounted on two rigid tubes and enclosed in a pressure chamber. Assuming that the flow through the elastic tube is driven by imposing the flow rate at the downstream end, we study the development of small-amplitude long-wavelength high-frequency oscillations, combining the results of two previous studies in which we analysed the fluid and solid mechanics of the problem in isolation. We derive a one-dimensional eigenvalue problem for the frequencies and mode shapes of the oscillations, and determine the slow growth or decay of the normal modes by considering the system's energy budget. We compare the theoretical predictions for the mode shapes, frequencies and growth rates with the results of direct numerical simulations, based on the solution of the three-dimensional Navier-Stokes equations, coupled to the equations of shell theory, and find good agreement between the results. Our results provide the first asymptotic predictions for the onset of self-excited oscillations in three-dimensional collapsible tube flows. [ABSTRACT FROM AUTHOR]

Remote cerebellar hemorrhage (RCH) after intracranial surgery is a rare complication. Cerebellar hemorrhage is the most commonly described remote site hemorrhage after surgery for supratentorial pathologies. Although this is a rare complication 0.04% to 0.8%, it can be devastating in terms of patient outcome. There are various hypotheses to explain the occurrence of RCH. We report 6 cases of RCH after surgery for supratentorial lesions, discuss the pathophysiology, and review the pertinent literature. We retrospectively analyzed data of patients who underwent surgery for supratentorial lesions at our center between 2015 and 2017. We identified 6 patients who developed RCH among 1200 patients who underwent surgery and reviewed the demographic data, diagnosis, surgical procedure, and final outcome. A total of 1200 patients underwent surgery for supratentorial pathologies between 2015 and 2017. Six patients developed RCH (incidence, 0.5%); 5 were male and 1 was female, with a mean age of 46.4 years. One patient underwent suboccipital decompression for RCH; the rest 5 were managed with close observation and serial imaging. The Glasgow outcome scale (GOS) of 5 was observed in 4 patients, GOS of 4 in 1 patient at discharge, and GOS of 1 in 1 patient who succumbed to severe pulmonary infection after surgery. RCH is a rare complication but can lead to catastrophic results. Loss of large volumes of cerebrospinal fluid or sudden alteration in intracranial pressure due to removal of a mass lesion is the likely etiology. Although majority of cases may be managed conservatively, in a subset of cases with neurologic deterioration, surgery may be required as a life-saving procedure. [ABSTRACT FROM AUTHOR]

Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as "intracranial pressure sensor" played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM. [ABSTRACT FROM AUTHOR]

Introduction: Chronic overdrainage affects shunted patients producing a variety of symptoms that may be misdiagnosed. The best known symptoms are so-called shunt-related headaches. There is mounting evidence that changes in cerebrospinal venous system dynamics are a key factor to the pathophysiology of chronic overdrainage syndrome.Clinical presentation: We report the case of a 29-year-old woman with a shunt since the postnatal period suffering from chronic but the most severe intermittent headache attacks, despite an open shunt and with unchanged ventricular width during attacks. Intracranial pressure (ICP) recordings were performed during headache attacks and thereafter.Diagnosis and managment: Massively increased ICPs, a continuous B wave “storm,” and severely compromised intracranial compliance despite an open shunt were found, a scenario that was always self-limiting with the resolution of symptoms after several hours. When mobilized to the upright position, her ICPs dropped to − 17 mm Hg, proving shunt overdrainage.Outcome and conclusions: Symptomatology can only be explained by sudden venous entrapment following chronic venous distention as a result of chronic overdrainage. Subsequent therapeutic management with an overdrainage preventing shunt and satisfying clinical outcome with complete ceasing of headache attacks adds insight into the pathophysiology of chronic overdrainage syndrome. [ABSTRACT FROM AUTHOR]

We present a novel application of rotors in geometric algebra to represent the change of curvature tensor that is used in shell theory as part of the constitutive law. We introduce a new decomposition of the change of curvature tensor, which has explicit terms for changes of curvature due to initial curvature combined with strain, and changes in rotation over the surface. We use this decomposition to perform a scaling analysis of the relative importance of bending and stretching in flexible tubes undergoing self-excited oscillations. These oscillations have relevance to the lung, in which it is believed that they are responsible for wheezing. The new analysis is necessitated by the fact that the working fluid is air, compared to water in most previous work. We use stereographic imaging to empirically measure the relative importance of bending and stretching energy in observed self-excited oscillations. This enables us to validate our scaling analysis. We show that bending energy is dominated by stretching energy, and the scaling analysis makes clear that this will remain true for tubes in the airways of the lung.

Inspiratory flow limitation means that when the flowrate reaches a certain value, it no longer increases, or even decreases, which is called negative effort dependence flow limitation, even if the inspiration effort is increased. This occurs often in obstructive sleep apnea patients, but its mechanism remains unclear. To reveal the mechanism of inspiratory flow limitation, we constructed a unique partially collapsible in-vitro upper airway model of obstructive sleep apnea patients to observe the change of airway resistance with inspiratory driving pressure. The important findings demonstrate that with the increase of inspiratory effort, the driving pressure increases faster than the airway resistance in the early stages, and then the reverse occurs as the airway becomes narrower. The airway collapse caused by the transmural pressure can lead to a rapid increase in downstream resistance with the increase of inspiratory effort, which is the key reason causing the flow reduction and the formation of typical negative effort dependence flow limitation. The mechanical mechanism revealed in this study will lead to fully new insights into the study and treatment of obstructive sleep apnea. [ABSTRACT FROM AUTHOR]

Retinal vein pulsation was first noted soon after the invention of the ophthalmoscope 170 years ago and was seen to change with cerebrospinal fluid pressure (CSFP) variation in the 1920s. The classical explanation for vein pulsation was that the cardiac cycle induced systolic peak in intraocular pressure (IOP) tended to intermittently collapse the retinal vein close to its exit in the central optic disk, causing pulsation to be counter-phase to IOP. Recently, improved ophthalmodynamometry and video recording techniques have allowed us to explore the fundamentals of retinal vein pulsation. This demonstrates that retinal venous collapse is in phase with both IOP and CSFP diastole, indicating the dependence upon CSFP pulse. We describe in some detail the mathematical and physical models of Starling resistors and how their results can be applied to understand the physiology of retinal vein pulsation. We discuss various techniques for measuring retinal venous pulsation, including a novel modified photo-plethysmographic technique developed in our laboratory. With these techniques, non-invasive measurement of CSFP is beginning to look feasible. Venous pulsation properties also have significant prognostic value in predicting long-term outcomes for both glaucoma and central retinal vein occlusion, as well as utility in other retinal vasculopathies and orbital disease. We demonstrate the potential use of modified photo-plethysmographic images in assessing these various disorders. A revised understanding of retinal vein pulse wave transmission along with improved measurement techniques may generate useful clinical tools for assessing these disorders. [ABSTRACT FROM AUTHOR]

Experiments are performed for a rigid, high-aspect-ratio, rectangular channel with a portion of one wall replaced by a flexible membrane (a “2D” Starling resistor). The fluid is air, which is driven by a pressure drop up to 300 Pa, producing Reynolds numbers up to 22,000. The experiments include pressure measurements at 6 locations along the channel, 1 velocity measurement, and high speed video of the membrane which is analyzed to extract the membrane motion. The primary variables considered are membrane tension, inlet pressure, and area of the side-wall gap. Steady and unsteady behaviors are observed for the 3 membrane tensions considered. The unsteady behaviors are categorized as “traveling”, “mode 2”, or “complex” oscillations, which may be recognized by the spectral characteristics of their pressure signal. Hysteresis is clearly observed depending on how the inlet pressure is adjusted. The side-wall gap, which permits air leakage around the membrane, is an important factor, and is characterized as a function of membrane tension and inlet pressure. [ABSTRACT FROM AUTHOR]

A computational model of a morphologically-based alveolar capillary unit (ACU) in the rabbit is developed to relate lung fluid balance to mechanical forces between capillary surface and interstitium during development of interstitial edema. We hypothesize that positive values of interstitial liquid pressure P liq impact on capillary transmural pressure and on blood flow. ACU blood flow, capillary recruitment and filtration are computed by modulating vascular and interstitial pressures. Model results are compared with experimental data of P liq increasing from ~−10 (control) up to ~4 cmH 2 O in two conditions, hypoxia and collagenase injection. For hypoxia exposure, fitting data requires a linear increase in hydraulic conductivity L p and capillary pressure P C , that fulfils the need of increase in oxygen delivery. For severe fragmentation of capillary endothelial barrier (collagenase injection), fitting requires a rapid increase in both hydraulic and protein permeability, causing ACU de-recruitment, followed by an increase in P C as a late response to restore blood flow. In conclusion, the model allows to describe the lung adaptive response to edemagenic perturbations; the increase in P liq , related to the low interstitial compliance, provides an efficient control of extravascular water, by limiting microvascular filtration. [ABSTRACT FROM AUTHOR]

Loss of cerebrospinal fluid (CSF) occurs commonly in daily neurosurgical practice. Understanding the altered physiology following CSF loss is important for optimization of patient care and avoidance of complications. There is overwhelming evidence now that the cerebral venous system plays a major role in intracranial pressure (ICP) dynamics especially when one takes into account the effects of postural changes, atmospheric pressure, and gravity on the craniospinal axis as a whole. The CSF and cerebral venous compartments are tightly coupled in two important ways. CSF is resorbed into the venous system, and there is also an evolved mechanism that prevents overdrainage of venous blood with upright positioning known as the Starling resistor. With loss of CSF pressure, this protective mechanism could become nonfunctional which may result in posture-related venous overdrainage through the cranial venous outflow tracts leading to pathologic states. This review article summarizes the relevant anatomic and physiologic basis of the relationship between the craniospinal venous and CSF compartments in the setting of CSF diversion. It is hoped that this article improves our understanding of ICP dynamics after CSF loss, adds a new dimension to our therapeutic methods, stimulates further research into this field, and ultimately improves our care of these patients. [ABSTRACT FROM AUTHOR]

Simulation of disorders of respiratory mechanics shown by spirometry provides insight into the pathophysiology of disease but some clinically important disorders have not been simulated and none have been formally evaluated for education. We have designed simple mechanical devices which, along with existing simulators, enable all the main dysfunctions which have diagnostic value in spirometry to be simulated and clearly explained with visual and haptic feedback. We modelled the airways as Starling resistors by a clearly visible mechanical action to simulate intra- and extra-thoracic obstruction. A narrow tube was used to simulate fixed large airway obstruction and inelastic bands to simulate restriction. We hypothesized that using simulators whose action explains disease promotes learning especially in higher domain educational objectives. The main features of obstruction and restriction were correctly simulated. Simulation of variable extra-thoracic obstruction caused blunting and plateauing of inspiratory flow, and simulation of intra-thoracic obstruction caused limitation of expiratory flow with marked dynamic compression. Multiple choice tests were created with questions allocated to lower (remember and understand) or higher cognitive domains (apply, analyse and evaluate). In a cross-over design, overall mean scores increased after 1½ h simulation spirometry (43-68 %, effect size 1.06, P < 0.0001). In higher cognitive domains the mean score was lower before and increased further than lower domains (Δ 30 vs 20 %, higher vs lower effect size 0.22, P < 0.05). In conclusion, the devices successfully simulate various patterns of obstruction and restriction. Using these devices medical students achieved marked enhancement of learning especially in higher cognitive domains. [ABSTRACT FROM AUTHOR]

We developed electrical circuit based model for the different components of the cerebral circulation, what allowed us to simulate cerebral blood flow in a variety of cerebrovascular disorders. This approach allowed us to derive a set of equations by which relative maximum, or fractional flow reserve, can be defined and calculated in three relevant sites: the stenotic artery, in the veins related to the stenotic artery, and in the collateral circulation of the affected region of the brain. Our results create theoretical basis for the entirely new approach to cerebrovascular disorders that currently emphasise anatomical identification of the disease to guide the treatment, such as the degree of arterial luminal stenosis obtained from various imaging modalities. In doing so, we directly address an urgent need for stroke experts to advance the care of their patients, since current approach of stroke treatment has not been meaningfully successful. [ABSTRACT FROM AUTHOR]

The upper airway is often modeled as a Starling resistor, which predicts that flow is independent of inspiratory effort during flow limitation. However, while some obstructive sleep apnea (OSA) patients exhibit flat, Starling resistor-like flow limitation, others demonstrate considerable negative effort dependence (NED), defined as the percent reduction in flow from peak to mid-inspiration. We hypothesized that the variability in NED could be due to differences in phasic pharyngeal muscle activation between individuals. Therefore, we induced topical pharyngeal anesthesia to reduce phasic pharyngeal muscle activation to see if it increased NED. Twelve subjects aged 50±10 years with a BMI of 35±6kg/m² and severe OSA (apnea-hypopnea index=52±28 events/h) were studied. NED and phasic genioglossus muscle activity (EMGGG) of flow limited breaths were determined before and after pharyngeal anesthesia with lidocaine. Pharyngeal anesthesia led to a 33% reduction in EMGGG activity (p<0.001), but NED worsened only by 3.6±5.8% (p=0.056). In conclusion, phasic EMGGG had little effect on NED. This finding suggests that individual differences in phasic EMGGG activation do not likely explain the variability in NED found among OSA patients. [ABSTRACT FROM AUTHOR]

Here we extend the global, closed-loop, mathematical model for the cardiovascular system in Müller and Toro (2014) to account for fundamental mechanisms affecting cerebral venous haemodynamics: the interaction between intracranial pressure and cerebral vasculature and the Starling-resistor like behaviour of intracranial veins. Computational results are compared with flow measurements obtained from Magnetic Resonance Imaging (MRI), showing overall satisfactory agreement. The role played by each model component in shaping cerebral venous flow waveforms is investigated. Our results are discussed in light of current physiological concepts and model-driven considerations, indicating that the Starling-resistor like behaviour of intracranial veins at the point where they join dural sinuses is the leading mechanism. Moreover, we present preliminary results on the impact of neck vein strictures on cerebral venous hemodynamics. These results show that such anomalies cause a pressure increment in intracranial cerebral veins, even if the shielding effect of the Starling-resistor like behaviour of cerebral veins is taken into account. [ABSTRACT FROM AUTHOR]

The upper airway is a complex, multifunctional, dynamic neuromechanical system. Its patency during breathing requires moment-to-moment coordination of neural and mechanical behavior and varies with posture. Failure to continuously recruit and coordinate dilator muscles to counterbalance the forces that act to close the airway results in hypopneas or apneas. Repeated failures lead to obstructive sleep apnea (OSA). Obesity and anatomical variations, such as retrognathia, increase the likelihood of upper airway collapse by altering the passive mechanical behavior of the upper airway. This behavior depends on the mechanical properties of each upper airway tissue in isolation, their geometrical arrangements, and their physiological interactions. Recent measurements of respiratory-related deformation of the airway wall have shown that there are different patterns of airway soft tissue movement during the respiratory cycle. In OSA patients, airway dilation appears less coordinated compared with that in healthy subjects (matched for body mass index). Intrinsic mechanical properties of airway tissues are altered in OSA patients, but the factors underlying these changes have yet to be elucidated. How neural drive to the airway dilators relates to the biomechanical behavior of the upper airway (movement and stiffness) is still poorly understood. Recent studies have highlighted that the biomechanical behavior of the upper airway cannot be simply predicted from electromyographic activity (electromyogram) of its muscles. [ABSTRACT FROM AUTHOR]

Background: Brain arteriovenous malformations (AVMs) produce circulatory and functional disturbances in adjacent as well as in remote areas of the brain, but their physiological effect on the cerebrospinal fluid (CSF) pressure is not well known. Methods: The hypothesis of an intrinsic disease mechanism leading to increased CSF pressure in all patients with brain AVM is outlined, based on a theory of hemodynamic control of intracranial pressure that asserts that CSF pressure is a fraction of the systemic arterial pressure as predicted by a two‑resistor series circuit hydraulic model. The resistors are the arteriolar resistance (that is regulated by vasomotor tonus), and the venous resistance (which is mechanically passive as a Starling resistor). This theory is discussed and compared with the knowledge accumulated by now on intravasal pressures and CSF pressure measured in patients with brain AVM. Results: The theory provides a basis for understanding the occurrence of pseudotumor cerebri syndrome in patients with nonhemorrhagic brain AVMs, for the occurrence of local mass effect and brain edema bordering unruptured AVMs, and for the development of hydrocephalus in patients with unruptured AVMs. The theory also contributes to a better appreciation of the pathophysiology of dural arteriovenous fistulas, of vein of Galen aneurismal malformation, and of autoregulation‑related disorders in AVM patients. Conclusions: The hydraulic hypothesis provides a comprehensive frame to understand brain AVM hemodynamics and its effect on the CSF dynamics. [ABSTRACT FROM AUTHOR]

Objectives: A purely hydraulic mechanism consisting in the pulsatile cuff-compression effect, by the cerebrospinal fluid displacement induced by the arterial pulsation, on the final portion of the bridging veins, has recently been hypothesized. This mechanism is able to maintain the constancy of cerebral blood flow (CBF) within the autoregulatory range, thus implying an exact balance between arterial inflow and venous outflow. In this study, we correlated arterial inflow and venous outflow during an experimentally induced condition of intracranial hypertension in pigs. Methods: Mock cerebrospinal fluid (CSF) was progressively infused until a condition of brain tamponade was reached. Blood flow velocities at middle cerebral artery and sagittal sinus sites were evaluated simultaneously. Results: Mean intracranial arterial blood flow velocity (IABFV), mean sagittal sinus blood flow velocity (SSBFV), and pulsatile-IABFV remained almost constant until cerebral perfusion pressure (CPP) dropped below 60-70 mmHg; then, a progressive decrease in mean IABFV and SSBFV, together with an increase in pulsatile-IABFV, was evident. Conclusion: The strict similarity between mean IABFV and SSBFV patterns suggests that CBF decrement is mainly due to a decrease in the venous outflow, which, in turn, produces an obstacle to the arterial inflow. The correspondent increase in pulsatile-IABFV confirms the presence of a distal outflow obstruction. All these findings point towards a purely hydraulic mechanism underlying the cerebral autoregulation which acts at the level of the so-called Starling resistor. [ABSTRACT FROM AUTHOR]

We studied the impact of wall strain and surrounding pressure on the onset of airflow limitation in a thin-walled "floppy" tube model. A vacuum source-generated steady-state (baseline) airflow (0-350 ml/s) through a thin-walled latex tube (length 80 mm, wall thickness 0.23 mm) enclosed within a rigid, sealed, air-filled, cylindrical chamber while upstream minus downstream pressure, chamber pressure (Pc), and lumen geometry [in-line digital camera; segmentation (Amira 5.2.2) and analysis (Rhinoceros 4) software] were monitored. Longitudinal strain (S; 0-62.5%) and Pc (0-20 cmH2O) combinations were imposed, and Pc associated with onset of 1) reduced airflow and 2) fully developed airflow limitation recorded. At any strain, increasing Pc resulted in a decrease in airflow. Across all baseline airflow, threshold pressure was 1-7 cmH2O for S < 25%, 6-8 cmH2O at S = 25% and 37.5%, and 5-7 cmH2O at S = 50% and 62.5%. Pc associated with fully developed airflow limitation was 4-6 cmH2O for S < 25%, >20 cmH2O at S = 25% (i.e., no flow limitation), 18 cmH2O at S = 37.5%, and 8-12 cmH2O at S = 50% and 62.5%. Lumen area decreased with increasing Pc but was 1) larger at S = 25% and 2) characterized by bifold narrowing at S < 25% and trifold narrowing at S ≥ 25%. In conclusion, tube function was modulated by Pc vs. S interactions, with S = 25% producing trifold lumen narrowing, maximal patency, and no airflow limitation. Findings may have implications for understanding peripharyngeal tissue pressure and pharyngeal wall strain effects on passive pharyngeal airway function in humans. [ABSTRACT FROM AUTHOR]

In this paper, we re-propose the role of a hydraulic mechanism, acting where the bridging veins enter the dural sinuses in cerebral blood flow (CBF) autoregulation. We carried out an intraventricular infusion in ten albino rabbits and increased intracranial pressure (ICP) up to arterial blood pressure (ABP) levels. We measured CBF velocity by an ultrasound probe applied to a by-pass inserted in a carotid artery and recorded ICP by an intraventricular needle. Diastolic and pulsatile ICP and ABP values were analyzed from basal conditions up to brain tamponade and vice versa. A biphasic pattern of pulsatile intracranial pressure (pICP) was observed in all trials. Initially, until the CBF velocity remained constant, pICP increased (from 1.2 to 5.4 mmHg) following a rise in diastolic intracranial pressure (dICP); thereafter, in spite of a further rise in dICP, pICP decreased (2.87 mmHg) following CBF velocity reduction until intracranial circulation arrest (pICP = 1.2 mmHg). A specular pattern was observed when the intraventricular infusion was stopped and CBF velocity returned to basal levels. These findings can be interpreted as indicating a hydraulic mechanism. Initially, when CBF is still constant, pICP rise is due to an increase in venous outflow resistance; subsequently, when CBF decreases following a further increase in venous outflow resistance, the vascular engorgement produces an arteriolar vasodilation. This vasodilation determines an increase in vascular wall stiffness, thus reducing pulse transmission to surrounding subarachnoid spaces. [ABSTRACT FROM AUTHOR]

In central serous chorioretinopathy (CSC), the macula is detached because of fluid leakage at the level of the retinal pigment epithelium. The fluid appears to originate from choroidal vascular hyperpermeability, but the etiology for the fluid is controversial. The choroidal vascular findings as elucidated by recent optical coherence tomography (OCT) and wide-field indocyanine green (ICG) angiographic evaluation show eyes with CSC have many of the same venous patterns that are found in eyes following occlusion of the vortex veins or carotid cavernous sinus fistulas (CCSF). The eyes show delayed choroidal filling, dilated veins, intervortex venous anastomoses, and choroidal vascular hyperpermeability. While patients with occlusion of the vortex veins or CCSF have extraocular abnormalities accounting for the venous outflow problems, eyes with CSC appear to have venous outflow abnormalities as an intrinsic phenomenon. Control of venous outflow from the eye involves a Starling resistor effect, which appears to be abnormal in CSC. Similar choroidal vascular abnormalities have been found in peripapillary pachychoroid syndrome. However, peripapillary pachychoroid syndrome has intervortex venous anastomoses located in the peripapillary region while in CSC these are seen to be located in the macular region. Spaceflight associated neuro-ocular syndrome appears to share many of the pathophysiologic problems of abnormal venous outflow from the choroid along with a host of associated abnormalities. These diseases vary according to their underlying etiologies but are linked by the venous decompensation in the choroid that leads to significant vision loss. Choroidal venous overload provides a unifying concept and theory for an improved understanding of the pathophysiology and classification of a group of diseases to a greater extent than previous proposals. [ABSTRACT FROM AUTHOR]

In this paper, an experimental set-up for investigating airflow through collapsible tubes has been described in detail. The test rig is basically composed of an airtight chamber socalled ‘Starling resistor’, which includes a length of collapsible tube attached to rigid tubes at its ends, a compressor supplying steady airflow, and measuring devices. The self-excited oscillations that develop due to strong fluid-pipe interaction cause the flow to be time dependent. A data acquisition system is utilized to obtain the measurements. Therefore, it is possible to measure simultaneously the time-dependent parameters, which are upstream and downstream pressures, velocity downstream of the collapsible tube. It has been verified by referring to the experimental results that the calibration of the whole system is satisfied and the measuring instruments give sensible output in combination with the data acquisition system. The presented test rig should be useful in point of view for testing possibility of airflow in soft elastic tubes. [ABSTRACT FROM AUTHOR]

‘Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures’ by J. B. West, C. T. Dollery, and A. Naimark (J Appl Physiol 19: 7 13–724, 1964) is a classic paper, although it has not yet been included in the Essays on the American Physiological Society Classic Papers Project (http://www.the-aps.org/publications/classics/). This is the paper that originally described the ‘zones of the lung.’ The final figure in the paper, which synthesizes the RESULTS and DISCUSSION, is now seen in most textbooks of physiology or respiratory physiology. The paper is also a model of clear, concise writing. The paper and its final figure can be used to teach or review a number of physiological concepts. These include the effects of gravity on pulmonary blood flow and pulmonary vascular resistance; recruitment and distention of pulmonary vessels; the importance of the transmural pressure on the diameter of collapsible distensible vessels; the Starling resistor; the interplay of the pulmonary artery, pulmonary vein, and alveolar pressures; and the vascular waterfall. In addition, the figure can be used to generate discovery learning and discussion of several physiological or pathophysiological effects on pulmonary vascular resistance and the distribution of pulmonary blood flow. [ABSTRACT FROM AUTHOR]

Background and Objectives: Impressive quantities of fluid can be infused into the epidural space of the spine without causing dramatic or sustained increases in pressure. The epidural space is considered “leaky,” but questions remain about how fluid leaves the epidural space. We used constant-flow infusions of saline to gain insight into the hydrodynamics involved. Methods: We infused saline at a constant rate into the lumbar epidural space of 6 anesthetized pigs while measuring pressure at the adjacent interspace. Three or 4 infusions were performed at different flow rates in each animal. Results: Epidural space pressure in the absence of flow was consistently 2 to 3 mm Hg above right atrial pressure. During each infusion, pressure increased slowly to a steady plateau value between 15 and 70 mm Hg. When flow was stopped, pressure declined exponentially to the starting pressure. The presence of a plateau indicates that fluid leaving the epidural space ends up in a structure with high capacitance. Plateau pressures were linearly related to flow rate in each animal, indicating constant resistance to outflow. The flow-pressure relation showed neither a critical opening pressure nor moderating pressures with increased flow. Conclusions: Fluid leaves the porcine spinal epidural space through channels that are open at baseline rather than being recruited as epidural pressure increases. This behavior is inconsistent with the view that the epidural space behaves like a Starling resistor. [Copyright &y& Elsevier]

We determined effects of augmented inspiratory and expiratory intrathoracic pressure or abdominal pressure (Pab) excursions on within-breath changes in steady-state femoral venous blood flow (Qfv) and net Qfv during tightly controlled (total breath time = 4 s, duty cycle = 0.5) accessory muscle/"rib cage" (ΔPab <2 cmH2O) or diaphragmatic (ΔPab <5 cmH2O) breathing. Selectively augmenting inspiratory intrathoracic pressure excursion during rib cage breathing augmented inspiratory facilitation of Qfv, from the resting limb (69% and 89% of all flow occurred during nonloaded and loaded inspiration, respectively); however, net Qfv in the steady state was not altered because of slight reductions in femoral venous return during the ensuing expiratory phase of the breath. Selectively augmenting inspiratory esophageal pressure excursion during a predominantly diaphragmatic breath at rest did not alter within-breath changes in Qfv relative to nonloaded conditions (net retrograde flow = -9 ± 12% and -4 ± 9% during nonloaded and loaded inspiration, respectively), supporting the notion that the inferior vena cava is completely collapsed by relatively small increases in gastric pressure. Addition of inspiratory + expiratory loading to diaphragmatic breathing at rest resulted in reversal of within-breath changes in Qfv, such that <90% of all anterograde Qfv occurred during inspiration. Inspiratory + expiratory loading also reduced steady-state Qfv during mild- and moderate-intensity calf contractions compared with inspiratory loading alone. We conclude that 1) exaggerated inspiratory pressure excursions may augment within-breath changes in femoral venous return but do not increase net Qfv in the steady state and 2) active expiration during diaphragmatic breathing reduces the steady-state hyperemic response to dynamic exercise by mechanically impeding venous return from the locomotor limb, which may contribute to exercise limitation in health and disease. [ABSTRACT FROM AUTHOR]

Tackles the fundamental mechanics of flexible-tube flows and its physiological applications. Mathematical models for bounded flows; Importance of flow patterns in the development of arterial disease; Motion of long bubbles in flexible tubes and channels.

ABSTRACT Retinal venous pressure was examined in six pigs using a balanced servo-nulling micropuncture technique. The mean transmural venous pressure was 0.95 mmHg (SD 1.50 mmHg). The transmural venous pressure was lower at the optic disc than away from the disc (0.32 ± 1.46 mmHg vs 1.69 ± 1.19 mmHg, P < 0.01). At the disc a transmural pressure of zero or less (0 to –0.5 mmHg) was demonstrated in 10/21 (48%) of the disc readings. Over an intraocular pressure range of 15–26 mmHg there was a strong correlation between intraocular pressure and retinal venous pressure (Pearson coefficient r = 0.92). The results are compatible with the Starling resistor theory of venous outflow from the eye. [ABSTRACT FROM AUTHOR]

Obstructive sleep apnea (OSA) is a disease that results from loss of upper airway muscle tone leading to upper airway collapse during sleep in anatomically susceptible persons, leading to recurrent periods of hypoventilation, hypoxia, and arousals from sleep. Significant clinical consequences of the disorder cover a wide spectrum and include daytime hypersomnolence, neurocognitive dysfunction, cardiovascular disease, metabolic dysfunction, respiratory failure, and pulmonary hypertension. With escalating rates of obesity a major risk factor for OSA, the public health burden from OSA and its sequalae are expected to increase, as well. In this chapter, we review the mechanisms responsible for the development of OSA and associated neurocognitive and cardiometabolic comorbidities. Emphasis is placed on the neural control of the striated muscles that control the pharyngeal passages, especially regulation of hypoglossal motoneuron activity throughout the sleep/wake cycle, the neurocognitive complications of OSA, and the therapeutic options available to treat OSA including recent pharmacotherapeutic developments., (Copyright © 2022 Elsevier B.V. All rights reserved.)

The effect on pulmonary artery pressure of a rise in alveolar pressure differed in chronically hypoxic rats (10% O2 for 3-5 weeks) compared with control rats. Chronically hypoxic rats have newly muscularised walls in arterioles in the alveolar region. Isolated lungs of chronically hypoxic and control rats were perfused with blood under conditions in which alveolar pressure was greater than left atrial pressure during both normoxia and hypoxia. Alveolar pressure was the effective downstream pressure. Pressure-flow lines were measured at low and high alveolar pressure (5 and 15 rnmHg). During normoxia pressure-flow lines of chronically hypoxic rats had a steeper slope (higher resistance) and greater extrapolated intercept on the pressure axis (effective downstream pressure) than control rats. In both groups of rats the change from low to high alveolar pressure during normoxia caused an approximately parallel shift in the pressure-flow line similar to the change in alveolar pressure. During hypoxia, which led to an increase in slope and intercept in both groups of rats, the effect of a rise in alveolar pressure differed in chronically hypoxic from control rats. In control rats there was a small parallel shift in the pressure-flow line that was much less than the increase in alveolar pressure; in chronically hypoxic rats there was a large parallel shift in the pressure-flow line that was greater than the increase in alveolar pressure. Thus in chronically hypoxic rats hypoxic vasoconstriction probably occurred mainly in muscular alveolar vessels, whereas in control rats it probably occurred upstream in extra-alveolar vessels.At constant blood flow the relation between pulmonary artery pressure and alveolar pressure was measured while alveolar pressure was reduced from approximately 15 mmHg to zero during both normoxia and hypoxia. In control and chronically hypoxic rats the slope of this line was <1. At an alveolar pressure of 2-3 mmHg there was an inflection point below which the line was nearly horizontal in control but negative in chronically hypoxic rats. During hypoxia the inflection point increased in control but not in chronically hypoxic rats, whereas the preinflection slope became negative. Apart from a rise in pulmonary artery pressure at all values of alveolar pressure, which occurred in both groups of rats, there was no change in the form of the curve in chronically hypoxic rats during hypoxia. These results also suggest constriction of extra-alveolar vessels in control rats and alveolar vessels in chronically hypoxic rats during hypoxia. The inflection point and negative preinflection slope, however, indicate that there is also extra-alveolar muscular tone in chronically hypoxic rats both during normoxia and hypoxia. The results have implications for the hypoxic human lung, whose anatomy resembles that of the hypoxic rat. [ABSTRACT FROM PUBLISHER]

Background: The higher incidence of obstructive sleep apnea (OSA) in men than in women has been attributed to the upper airway being longer in men. The Starling resistor is the paradigm biomechanical model of upper airway collapse in OSA where a collapsible tube (representing the pharynx) is located between two rigid tubes (representing the nasal cavity and trachea). While the Starling resistor has been extensively studied due to its relevance to many physiological phenomena, the effect of tube length on tube collapsibility has not been quantified yet., Methods: Finite element analysis of a 3-dimensional collapsible tube subjected to a transmural pressure was performed in ANSYS Workbench. The numerical methods were validated with in vitro experiments in a silicone tube whose modulus of elasticity (361 ± 28 kPa) and dimensions (length = 100 mm, diameter = 22.2 mm, and wall thickness = 1.59 mm) were selected so that tube compliance was similar to pharyngeal compliance in humans during sleep. The buckling pressure (transmural pressure at which the tube collapses) was quantified in tubes of three different diameters (10 mm, 16 mm, and 22.2 mm) and ten length-to-diameter ratios (L/D = 4 to 13), while keeping the wall-thickness-to-radius ratio constant at 0.143., Results: The absolute value of the buckling pressure decreased from 4.7 to 3.3 cmH 2 O (461-324 Pa) when L/D increased from 4 to 13. The buckling pressure was nearly independent from tube length for L/D >10., Conclusions: Our finding that longer tubes are more collapsible than shorter tubes is consistent with the higher incidence of obstructive sleep apnea in males than females., (Copyright © 2021 Elsevier Ltd. All rights reserved.)