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The first step to exercise is preceded by the required assumption of the upright body position, which itself involves physical activity. The gravitational displacement of blood from the chest to the lower parts of the body elicits a fall in central blood volume (CBV), which corresponds to the fraction of thoracic blood volume directly available to the left ventricle. The reduction in CBV and stroke volume (SV) in response to postural stress, post-exercise, or to blood loss results in reduced left ventricular filling, which may manifest as orthostatic intolerance. When termination of exercise removes the leg muscle pump function, CBV is no longer maintained. The resulting imbalance between a reduced cardiac output (CO) and a still enhanced peripheral vascular conductance may provoke post-exercise hypotension (PEH). Instruments that quantify CBV are not readily available and to express which magnitude of the CBV in a healthy subject should remains difficult. In the physiological laboratory, the CBV can be modified by making use of postural stressors, such as lower body "negative" or sub-atmospheric pressure (LBNP) or passive head-up tilt (HUT), while quantifying relevant biomedical parameters of blood flow and oxygenation. Several approaches, such as wearable sensors and advanced machine-learning techniques, have been followed in an attempt to improve methodologies for better prediction of outcomes and to guide treatment in civil patients and on the battlefield. In the recent decade, efforts have been made to develop algorithms and apply artificial intelligence (AI) in the field of hemodynamic monitoring. Advances in quantifying and monitoring CBV during environmental stress from exercise to hemorrhage and understanding the analogy between postural stress and central hypovolemia during anesthesia offer great relevance for healthy subjects and clinical populations. [ABSTRACT FROM AUTHOR]

Keywords: oxygen consumption; regulation of skeletal muscle mass; Parkinson's disease and autonomic function; artificial intelligence & hemodynamic monitoring; arterial thrombosis & exercise; atrial fibrillation & cognitive decline; breath-hold diving; T2DM & cerebral perfusion/sympathetic control EN oxygen consumption regulation of skeletal muscle mass Parkinson's disease and autonomic function artificial intelligence & hemodynamic monitoring arterial thrombosis & exercise atrial fibrillation & cognitive decline breath-hold diving T2DM & cerebral perfusion/sympathetic control 1 3 3 02/10/22 20220208 NES 220208 In 1993 the Swedish physiologist Björn Folkow (1921-2012) wrote " I .. in humans, it is particularly difficult to differentiate between manifestations of aging per se and symptoms of morbidity, especially at higher ages when morbidity is common i " (Folkow and Svanborg, [2]). Exercise training is a well-recognized tool in the management of T2D due to its many cardiometabolic benefits, however T2D may negatively affect cardiovascular responses to exercise. Oxygen consumption, regulation of skeletal muscle mass, Parkinson's disease and autonomic function, artificial intelligence & hemodynamic monitoring, arterial thrombosis & exercise, atrial fibrillation & cognitive decline, T2DM & cerebral perfusion/sympathetic control, breath-hold diving. [Extracted from the article]

The human brain is constantly active and even small limitations to cerebral blood flow (CBF) may be critical for preserving oxygen and substrate supply, e.g., during exercise and hypoxia. Exhaustive exercise evokes a competition for the supply of oxygenated blood between the brain and the working muscles, and inability to increase cardiac output sufficiently during exercise may jeopardize cerebral perfusion of relevance for diabetic patients. The challenge in diabetes care is to optimize metabolic control to slow progression of vascular disease, but likely because of a limited ability to increase cardiac output, these patients perceive aerobic exercise to be more strenuous than healthy subjects and that limits the possibility to apply physical activity as a preventive lifestyle intervention. In this review, we consider the effects of functional activation by exercise on the brain and how it contributes to understanding the control of CBF with the limited exercise tolerance experienced by type 2 diabetic patients. Whether a decline in cerebral oxygenation and thereby reduced neural drive to working muscles plays a role for "central" fatigue during exhaustive exercise is addressed in relation to brain's attenuated vascular response to exercise in type 2 diabetic subjects. [ABSTRACT FROM AUTHOR]

Heart rate (HR) has an impact on the central blood pressure (BP) wave shape and is related to pulse wave velocity and therefore to timing and duration of systole and diastole. This study tested the hypothesis that in healthy subjects both in rest and during sympathetic stimulation the relation between HR and pulse pressure (PP) is described by a linear effect model. Forty-four healthy volunteers were subjected to sympathetic stimulation by continuous lower body negative pressure (LBNP) until the onset of pre-syncopal symptoms. Changes in PP and HR were tracked non-invasively and modeled by linear mixed effect (LME) models. The dataset was split into two groups: the first was used for creating a model and the second for its evaluation. Models were created on the data obtained during LBNP. Model performance was expressed as absolute median error (1st; 3rd quantiles) and bias with limits of agreement (LOA) between modeled and measured PP. From rest to sympathetic stimulation, mean BP was maintained while HR increased (∼30%) and PP decreased gradually (∼20%). During baseline, PP could be modeled with an absolute error of 6 (4; 10) mm Hg and geometric mean ratio of the bias was 0.97 (LOA: 0.8-1.1). During LBNP, absolute median model error was 5 (4; 8) mmHg with geometric mean ratio 1.02 (LOA: 0.8-1.3). In conclusion, both during rest and during sustained sympathetic outflow induced by progressive central hypovolemia, a LME model of HR provides for an estimate of PP in healthy young adults. [ABSTRACT FROM AUTHOR]

Introduction: In the initial phase of hypovolemic shock, mean blood pressure (BP) is maintained by sympathetically mediated vasoconstriction rendering BP monitoring insensitive to detect blood loss early. Late detection can result in reduced tissue oxygenation and eventually cellular death. We hypothesized that a machine learning algorithm that interprets currently used and new hemodynamic parameters could facilitate in the detection of impending hypovolemic shock. Method: In 42 (27 female) young [mean (sd): 24 (4) years], healthy subjects central blood volume (CBV) was progressively reduced by application of -50 mmHg lower body negative pressure until the onset of pre-syncope. A support vector machine was trained to classify samples into normovolemia (class 0), initial phase of CBV reduction (class 1) or advanced CBV reduction (class 2). Nine models making use of different features were computed to compare sensitivity and specificity of different non-invasive hemodynamic derived signals. Model features included: volumetric hemodynamic parameters (stroke volume and cardiac output), BP curve dynamics, near-infrared spectroscopy determined cortical brain oxygenation, end-tidal carbon dioxide pressure, thoracic bio-impedance, and middle cerebral artery transcranial Doppler (TCD) blood flow velocity. Model performance was tested by quantifying the predictions with three methods: sensitivity and specificity, absolute error, and quantification of the log odds ratio of class 2 vs. class 0 probability estimates. Results: The combination with maximal sensitivity and specificity for classes 1 and 2 was found for the model comprising volumetric features (class 1: 0.73-0.98 and class 2: 0.56-0.96). Overall lowest model error was found for the models comprising TCD curve hemodynamics. Using probability estimates the best combination of sensitivity for class 1 (0.67) and specificity (0.87) was found for the model that contained the TCD cerebral blood flow velocity derived pulse height. The highest combination for class 2 was found for the model with the volumetric features (0.72 and 0.91). Conclusion: The most sensitive models for the detection of advanced CBV reduction comprised data that describe features from volumetric parameters and from cerebral blood flow velocity hemodynamics. In a validated model of hemorrhage in humans these parameters provide the best indication of the progression of central hypovolemia. [ABSTRACT FROM AUTHOR]

Renal hypoxia is thought to be an important pathophysiological factor in the progression of chronic kidney disease (CKD) and the associated hypertension. In a previous study among CKD patients, supplementation with 100% oxygen reduced sympathetic nerve activity (SNA) and lowered blood pressure (BP). We aimed to assess the underlying haemodynamic modulation and hypothesized a decreased systemic vascular resistance (SVR). To that end, 19 CKD patients were studied during 15-min intervals of increasing partial oxygen pressure (ppO2) from room air (0.21 ATA) to 1.0 ATA and further up to 2.4 ATA, while continuously measuring finger arterial blood pressure (Finapres). Off-line, we derived indexes of SVR, cardiac output (CO) and baroreflex sensitivity from the continuous BP recordings (Modelflow). During oxygen supplementation, systolic, and diastolic BP both increased dose-dependently from 128 ± 24 and 72 ± 19 mmHg respectively at baseline to 141 ± 23 (p < 0.001) and 80 ± 21 mmHg (p < 0.001) at 1.0 ATA oxygen. Comparing baseline and 1.0 ATA oxygen, SVR increased from 1440 ± 546 to 1745 ± 710 dyns/cm5 (p = 0.009), heart rate decreased from 60 ± 8 to 58 ± 6 bpm (p < 0.001) and CO from 5.0 ± 1.3 to 4.6 ± 1.1 L/min (p = 0.02). Baroreflex sensitivity remained unchanged (13ş13 to 15±12ms/mmHg). These blood pressure effects were absent in a negative control group of eight young healthy subjects. We conclude that oxygen supplementation in CKD patients causes a non-baroreflex mediated increased in SVR and blood pressure. [ABSTRACT FROM AUTHOR]

In healthy subjects, variation in cardiovascular responses to sympathetic stimulation evoked by submaximal lower body negative pressure (LBNP) is considerable. This study addressed the question whether inter-subject variation in cardiovascular responses coincides with consistent and reproducible responses in an individual subject. In 10 healthy subjects (5 female, median age 22 years), continuous hemodynamic parameters (finger plethysmography; Nexfin, Edwards Lifesciences), and time-domain baroreflex sensitivity (BRS) were quantified during three consecutive 5-min runs of LBNP at -50 mmHg. The protocol was repeated after 1 week to establish intra-subject reproducibility. In response to LBNP, 5 subjects (3 females) showed a prominent increase in heart rate (HR; 54 ± 14%, p = 0.001) with no change in total peripheral resistance (TPR; p = 0.25) whereas the other 5 subjects (2 females) demonstrated a significant rise in TPR (7 ± 3%, p = 0.017) with a moderate increase in HR (21 ± 9%, p = 0.004). These different reflex responses coincided with differences in resting BRS (22 ± 8 vs. 11 ± 3 ms/mmHg, p = 0.049) and resting HR (57 ± 8 vs. 71 ± 12 bpm, p = 0.047) and were highly reproducible over time. In conclusion, we found distinct cardiovascular response patterns to sympathetic stimulation by LBNP in young healthy individuals. These patterns of preferential autonomic blood pressure control appeared related to resting cardiac BRS and HR and were consistent over time. [ABSTRACT FROM AUTHOR]

A siphon is suggested to support cerebral blood flow but appears not to be established because internal jugular venous (IJV) pressure is close to zero in upright humans. Thus, in eleven young healthy males, IJV pressure was 9 ± 1mmHg (mean ± SE) when supine and fell to 3 ± 1mmHg when seated, and middle cerebral artery mean blood velocity (MCA Vmean; P < 0.007) and the near-infrared spectroscopy-determined frontal lobe oxygenation (ScO2; P = 0.028) also decreased. Another subject, however, developed (pre)syncopal symptoms while seated and his IJV pressure decreased to −17mmHg. Furthermore, his MCA Vmean decreased and yet within the time of observation ScO2 was not necessarily affected. These findings support the hypothesis that a negative IJV pressure that is a prerequisite for creation of a siphon provokes venous collapse inside the dura, and thereby limits rather than supports CBF. [ABSTRACT FROM AUTHOR]

The sitting beach-chair position is regularly used for shoulder surgery and anesthesia may be induced in that position. We tested the hypothesis that the cardiovascular challenge induced by induction of anesthesia is attenuated if the patient is placed in a reclining beach-chair position. Anesthesia was induced with propofol in the sitting beach-chair (n = 15) or with the beach-chair tilted backwards to a reclining beach-chair position (n = 15). The last group was stepwise tilted to the sitting beach-chair position prior to surgery. Hypotension was treated with ephedrine. Continuous hemodynamic variables were recorded by photoplethysmography and frontal cerebral oxygenation (ScO2) by near infrared spectroscopy. Significant differences were only observed immediately after the induction when patients induced in a reclining beach-chair position had higher mean arterial pressure (MAP) (35 ± 12 vs. 45 ± 15 % reduction from baseline, p = 0.04) and ScO2 (7 ± 6 vs. 1 ± 8% increase from baseline, p = 0.02) and received less ephedrine (mean: 4 vs. 13mg, p = 0.048). The higher blood pressure and lower need of vasopressor following induction of anesthesia in the reclining compared to the sitting beach-chair position indicate more stable hemodynamics with the clinical implication that anesthesia should not be induced with the patient in the sitting position. [ABSTRACT FROM AUTHOR]

Rationale: A critical reduction in central blood volume (CBV) is often characterized by hemodynamic instability. Restoration of a volume deficit may be established by goal-directed fluid therapy guided by respiration-related variation in systolic- and pulse pressure (SPV and PPV). Stroke volume index (SVI) serves as a surrogate end-point of a fluid challenge but tissue perfusion itself has not been addressed. Objective: To delineate the relationship between arterial pressure variations, SVI and regional brain perfusion during CBV depletion and repletion in spontaneously breathing volunteers. Methods: This study quantified in 14 healthy subjects (11 male) the effects of CBV depletion [by 30 and 70 degrees passive head-up tilt (HUT)] and a fluid challenge (by tilt back) on CBV (thoracic admittance), mean middle cerebral artery (MCA) blood flow velocity (Vmean), SVI, cardiac index (CI), PPV, and SPV. Results: PPV (103 ± 89%, p < 0.05) and SPV (136 ± 117%, p < 0.05) increased with progression of central hypovolemia manifested by a reduction in thoracic admittance (11 ± 5%, p < 0.001), SVI (28 ± 6%, p < 0.001), CI (6 ± 8%, p < 0.001), and MCAVmean (17 ± 7%, p< 0.05) but not in arterial pressure. The reduction in MCAVmean correlated to the fall in SVI (R2 = 0.52, p< 0.0001) and inversely to PPV and SPV [R2 = 0.46 (p < 0.0001) and R2 = 0.45 (p < 0.0001), respectively]. PPV and SPV predicted a ⩾15% reduction in MCAVmean and SVI with comparable sensitivity (67/67% vs. 63/68%, respectively) and specificity (89/94 vs. 89/94%, respectively). A rapid fluid challenge by tilt-back restored all parameters to baseline values within 1 min. Conclusion: In spontaneously breathing subjects, a reduction in MCAVmean was related to an increase in PPV and SPV during graded CBV depletion and repletion. Specifically, PPV and SPV predicted changes in both SVI and MCAVmean with comparable sensitivity and specificity, however the predictive value is limited in spontaneously breathing subjects. [ABSTRACT FROM AUTHOR]

Anesthesia was induced with propofol in the sitting beach-chair (n=15) or with the beach-chair tilted backwards to a reclining beach-chair position (n=15). The last group was stepwise tilted to the sitting beach-chair position prior to surgery. Hypotension was treated with ephedrine. Continuous hemodynamic variables were recorded by photoplethysmography and frontal cerebral oxygenation (ScO2) by near infrared spectroscopy. Significant differences were only observed immediately after the induction when patients induced in a reclining beach-chair position had higher mean arterial pressure (MAP) (35±12 vs. 45±15 % reduction from baseline, p=0.04) and ScO2 (7±6 vs. 1±8 % increase from baseline, p=0.02) and received less ephedrine (mean: 4 vs. 13 mg, p=0.048). The higher blood pressure and lower need of vasopressor following induction of anesthesia in the reclining compared to the sitting beach-chair position indicate more stable hemodynamics with the clinical implication that anesthesia should not be induced with the patient in the sitting position. [ABSTRACT FROM AUTHOR]