1,721,224 research outputs found
Coupling arterial windkessel with peripheral vasomotion : modelling the effects on low frequency oscillations
No full textArterial pressure (AP) and heart rate (HR) waves have long been recognized as an important sign of cardiovascular regulation, however, the underlying interactions involving vasomotion, arterial mechanisms and neural regulation have not been clarified. With the aid of simple dynamical models consisting of active peripheral vascular districts (PVDs) fed by a compliant/resistant arterial tree, the relationship between local AP and flow and systemic AP waves were analyzed. A PVD was described as a nonlinear flow regulation loop. Various feedback dynamics were experimented and general properties were focused. The PVDs displayed a region of active flow compensation against pressure changes, in which self-sustained low-frequency (LF, 0.1 Hz) appeared. Oscillations critically depended on parameter, Teq, analogous to a windkessel time constant, proportional to arterial compliances: a value of about 2 s (consistent with a normal pulse pressure) performed a buffering effect essential for LF oscillations in peripheral flow; conversely, stiffer arteries damped LF vasomotion. Two PVDs fed by a common compliance oscillated in phase opposition; the consequent negative interference cancelled systemic AP waves, even in presence of large peripheral oscillations. The partial disruption of phase opposition by a common neural drive oscillating at a LF proximal to that of the PVDs unveiled LF waves in AP. Also, several PVDs with randomly different natural frequencies displayed a tendency to reciprocal cancellation, while a limited neurally induced phase alignment unmasked LF oscillations at systemic level. It is concluded that vasomotion, arterial compliances and, neural drives are all elements which may cooperate in forming AP waves
Simulating the interactions among vasomotion waves of peripheral vascular districts
No full textSimulations are performed in order to analyze the tendency of oscillating peripheral vascular districts (PVDs) to maintain equal phases thus inducing low frequency (LF) waves in systemic arterial pressure (AP). A PVD model regulating the local flow by means of a delayed non-linear feedback displayed spontaneous oscillations with a 12 sec period in the pressure range (40-150 mmHg) of active flow compensation. Two identical PVDs loading the same windkessel compartment could oscillate in phase inducing significant (10% of mean) AP waves: however, this behavior was unstable. On the contrary, phase opposition (without AP waves) was stable and corresponded to an energetic minimum (-9 % compared to the unstable solution). The introduction of either baroreflex mechanisms or a central drive was able to steadily align the PVD phases. Vasomotion synchronization can be a powerful modulation mechanism of LF waves in systemic AP
Spontaneous baroreflex sensitivity estimates during graded bicycle exercise : a comparative study
No full textIn the literature, several methods have been proposed for the assessment of the baroreflex sensitivity from spontaneous variability of heart period and systolic arterial pressure. The present study compares the most utilized approaches for the evaluation of the spontaneous baroreflex sensitivity (i.e. sequence-based, spectral, cross-spectral and model-based techniques) over a protocol capable of inducing a progressive decrease of the baroreflex sensitivity in the presence of a relevant respiratory drive (i.e. a stepwise dynamic bicycle exercise at 10%, 20% and 30% of the maximum nominal individual effort) in 16 healthy humans. Results demonstrated that the degree of correlation among the estimates is related to the structure of the model explicitly or implicitly assumed by the method and depends on the experimental condition (i.e. on the physiological mechanisms contemporaneously active with baroreflex, e. g. cardiopulmonary reflexes). However, even in the presence of a significant correlation, proportional and/or constant biases can be present, thus rendering spontaneous baroreflex estimates not interchangeable. We suggest that the comparison among different baroreflex sensitivity estimates might elucidate physiological mechanisms responsible for the relationship between heart period and systolic arterial pressure
Multi-channel parametric analysis of the coupling between respiration and cardiovascular variabilities
No full textRelationship between RR and RT variability. A measure of dispersion of ventricular repolarisation
No full textThe influence of exercise intensity on the power spectrum of heart rate variability
No full textThe power spectral analysis of R-R interval variability (RRV) has been estimated by means of an autoregressive method in seven sedentary males at rest, during steady-state cycle exercise at 21 percent maximal oxygen uptake. (% V O 2max), SEM 2%, 49% VO 2max, SEM 2% and 70% VO 2max, SEM 2% and during recovery. The RRV, i.e. the absolute power of the spectrum, decreased 10, 100 and 500 times in the three exercise intensities, returning to resting value during recovery. In the RRV power spectrum three components have been identified: (1) high frequency peak (HF), central frequency about 0.24 Hz at rest and recovery, and 0.28 Hz, SEM 0.02, 0.37 Hz, SEM 0.03 and 0.48 Hz, SEM 0.06 during the three exercise intensities, respectively; (2) low frequency peak (LF), central frequency about 0.1 Hz independent of the metabolic state; (3) very low frequency component (VLF), <0.05 Hz, no peak observed. The HF peak power, as a percentage of the total power (HF%), averaged 16%, SEM 5% at rest and did not change during exercise, whereas during recovery it decreased to 5%–10%. The LF% and VLF% were about 50% and 35% at rest and during low exercise intensity, respectively. At higher intensities, LF% decreased to 16% and VLF% increased to 70%. During recovery a return to resting values occurred. The HF component may reflect the increased respiratory rate and the LF peak changes the resetting of the baroreceptor reflex with exercise. The hypothesis is made that VLF fluctuations in heart rate might be partially mediated by the sympathetic system
Multivariate parametric model for the identification of diastolic pressure and pulse components
No full textAssessing baroreflex gain from spontaneous variability in conscious dogs : role of causality and respiration
No full textA double exogenous autoregressive (XXAR) causal parametric model was used to estimate the baroreflex gain (alpha(XXAR)) from spontaneous R-R interval and systolic arterial pressure (SAP) variabilities in conscious dogs. This model takes into account 1) effects of current and past SAP variations on the R-R interval (i.e., baroreflex-mediated influences), 2) specific perturbations affecting R-R interval independently of baroreflex circuit (e.g., rhythmic neural inputs modulating R-R interval independently of SAP at frequencies slower than respiration), and 3) influences of respiration-related sources acting independently of baroreflex pathway (e.g., rhythmic neural inputs modulating R-R interval independently of SAP at respiratory rate, including the effect of stimulation of low-pressure receptors). Under control conditions, alpha(XXAR) = 14.7 +/- 7.2 ms/mmHg. It decreases after nitroglycerine infusion and coronary artery occlusion, even though the decrease is significant only after nitroglycerine, and it is completely abolished by total arterial baroreceptor denervation. Moreover, alpha(XXAR) is comparable to or significantly smaller than (depending on the experimental condition) the baroreflex gains derived from sequence, power spectrum [at low frequency (LF) and high frequency (HF)], and cross-spectrum (at LF and HF) analyses and from less complex causal parametric models, thus demonstrating that simpler estimates may be biased by the contemporaneous presence of regulatory mechanisms other than baroreflex mechanisms
Multivariate parametric model for the identification of diastolic pressure and pulse pressure components = Modèle paramétrique multivarié pour l'identification del composantes de pression diastolique et pulsée
No full textArterial pressure variability is a relatively unexplored topic among the various and detailed studies of cardiovascular variability. A deeper analysis of components and contributions carried by diastolic and pulse pressure may provide a unique insight on the potential systemic effects due to vasomotor activity and response at the level of microcirculation, whose dynamics are either driven by neural and vascular modulations. The aim of the present work is to develop a multivariate parametric model for the identification of the main components of diastolic and pulse pressure in order to investigate all the potential correlations between systemic arterial pressure variability and peripheral sources of oscillations and to analyse their interactions with the most known mechanisms of cardiovascular regulation
Multimodal signal processing for the analysis of cardiovascular variability
No full textCardiovascular (CV) variability as a primary vital sign carrying information about CV regulation systems is reviewed by pointing out the role of the main rhythms and the various control and functional systems involved. The high complexity of the addressed phenomena fosters a multimodal approach that relies on data analysis models and deals with the ongoing interactions of many signals at a time. The importance of closed-loop identification and causal analysis is remarked upon and basic properties, application conditions and methods are recalled. The need of further integration of CV signals relevant to peripheral and systemic haemodynamics, respiratory mechanics, neural afferent and efferent pathways is also stresse
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