16 research outputs found
Baroreflex sensitivity variations in response to propofol anesthesia: comparison between normotensive and hypertensive patients
The aim of this paper is to compare baroreflex sensitivity (BRS) following anesthesia induction via propofol to pre-induction baseline values through a systematic and mathematically robust analysis. Several mathematical methods for BRS quantification were applied to pre-operative and intra-operative data collected from patients undergoing major surgery, in order to track the trend in BRS variations following anesthesia induction, as well as following the onset of mechanical ventilation. Finally, a comparison of BRS trends in chronic hypertensive patients (CH) with respect to non hypertensive (NH) patients was performed. 10 NH and 7 CH patients undergoing major surgery with American Society of Anesthesiologists classification score 2.5 ± 0.5 and 2.6 ± 0.5 respectively, were enrolled in the study. A Granger causality test was carried out to verify the causal relationship between RR interval duration and systolic blood pressure (SBP), and four different mathematical methods were used to estimate the BRS: (1) ratio between autospectra of RR and SBP, (2) transfer function, (3) sequence method and (4) bivariate closed loop model. Three different surgical epochs were considered: baseline, anesthetic procedure and post-intubation. In NH patients, propofol administration caused a decrease in arterial blood pressure (ABP), due to its vasodilatory effects, and a reduction of BRS, while heart rate (HR) remained unaltered with respect to baseline values before induction. A larger decrease in ABP was observed in CH patients when compared to NH patients, whereas HR remained unaltered and BRS was found to be lower than in the NH group at baseline, with no significant changes in the following epochs when compared to baseline. To our knowledge, this is the first study in which the autonomic response to propofol induction in CH and NH patients was compared. The analysis of BRS through a mathematically rigorous procedure in the perioperative period could result in the availability of additional information to guide therapy and anesthesia in uncontrolled hypertensive patients, which are prone to a higher rate of hypotension events occurring during general anesthesia induction
Physiology and Pathophysiology of Venous Flow
International audienceVeins provide heart filling flow with lower velocity and pressure than those in arteries. The right heart receives systemic venous blood and pumps blood into the pulmonary circulation that returns oxygenated blood into the left heart for its ejection at high velocity and pressure into the systemic circulation.Whereas systemic veins carry deoxygenated blood from cells to the right cardiac pump, oxygenated blood flows in pulmonary veins running to the left cardiac pump, although pulmonary veins receive a part of the systemic venous blood that is drained from the lung tissue.Usually, one or two veins run with an artery, collecting lymphatic vessel, and nerve packaged in a sheath. In the head, veins follow paths that differ from those of arteries.Whereas venous flow in the standing position in veins below the heart level is supported by the hydrostatic pressure, blood flow in veins situated above this level must struggle against the gravity effect.Veins constitute the major blood storage compartment. They accommodate blood volume changes by dilating and shrinking to possibly reach a collapsed state. Veins, into which blood pressure is relatively small, are usually more deformable than accompanying arteries subjected to the same external pressure. However, deep veins embedded into skeletal muscle are less deformable than superficial veins close to the skin. Although both types for a given merging generation have similar wall thickness, they behave as thick- and thin-walled conduit, respectively. However, deep veins embedded into skeletal muscle are less deformable than superficial veins close to the skin. Although both types for a given merging generation have similar wall thickness, they behave as stiff and and soft conduit, respectively. In other words, deep and superficial veins can be represented by thin-walled veins in a gel and air, respectively, the former being mush less collapsible than the latter. Compression stocking (or supportive hose) diverts superficial venous flow of legs to deep veins that are less subjected to chronic venous insufficiency, as it collapses superficial veins without deforming deep veins.Similar to arterial flow, venous flow is unsteady, especially in abdominal and thoracic veins that experience both breathing and cardiac pumping. In addition, veins of the inferior and superior limbs undergo more or less transient external compression by contracting skeletal muscles. During walking, venous valves prevent backflow to the feet, whereas muscles ensure an additional pumping that favors venous return
Physiology and Pathophysiology of Arterial Flow
International audienceArterial flow is a three-dimensional unsteady process that is analyzed by measurements as well as physiological, biological, and mechanical experiments and numerical simulations. Few quantities can be noninvasively measured; they encompass cardiac frequency and peripheral arterial blood pressure as well as velocity and flow rate in given arterial stations by functional imaging. The central arterial blood pressure, from which clinicians derive several indices that are related to the physiological state of compartments of the cardiovascular apparatus, is measured using catheter-based transducers. Research is carried out to adequately infer the aortic pressure from measures in peripheral arteries using efficient signal processing.Blood flows through deformable arteries that dilate and constrict. The expansion of elastic arteries (Windkessel effect) that constitute the upstream compartment of the arterial tree transforms the systolic bolus into a pulsatile flow. Furthermore, the perfusion of the cardiac pump by coronary arteries benefits from the backflow generated by the wall recoil in elastic arteries. However, the arterial deformation is not only passive but also active. Mural cells sense and react to the stress field and adjust the caliber of the arterial lumen accordingly using intra-, auto-, juxta-, and paracrine signaling. The arterial wall is innervated and perfused from the lumen and vasa vasorum, hence receiving nervous and endocrine cues that are transduced for appropriate outputs. The vasomotor tone determines the level of the flow resistance.The regulation of the arterial flow has been widely investigated by physiologists, exhibiting the intricated and complex mechanisms that control the body’s homeostasis and adapt the local blood supply to the needs. At lower length scales, biologists describe the entire set of regulators and demonstrate their respective role and the functioning of signaling pathways in normal and pathological conditions. Biomechanicians develop new methods to assess the rheology and behavior of living tissues and, in collaboration with applied mathematicians, model physiological and pathophysiological processes. Some mechanical aspects that are easily handled in mechanics (e.g., applied to civil engineering and aeronautics) cannot be directly used in biomechanics. First, the architecture and the structure are much more complicated. Second, blood is carried in arterial lumens surrounded by three-layered walls made of composite materials. Both blood and wall are biological tissues, water being a major component. Hence, the fluid–structure interaction problem requires specific numerical treatment and elaboration of proper algorithms and multiphysics coupling softwares. Numerical tests are nevertheless carried out using simplifying assumptions and can be useful in medical practice