In the interest of furthering the understanding of hemodynamics, this study has developed a method for modeling fluid mechanics behavior in individual human carotid arteries. A computational model was constructed from magnetic resonance (MR) data of a phantom carotid bifurcation model, and relevant flow conditions were simulated. Results were verified by comparison with previous in vitro experiments. The methodology was extended to create subject-specific carotid artery models from geometry data and fluid flow boundary conditions which were determined from MR and phase contrast MR (PCMR) scans of human subjects. The influence of subject-specific boundary conditions on the flow field was investigated by comparing a model based on measured velocity boundary conditions to a model based on the assumption of idealized velocity boundary conditions. It is shown that subject-specific velocity boundary conditions in combination with a subject-specific geometry and flow waveform influence fluid flow phenomena associated with plaque development. Comparing a model with idealized Womersley flow boundary conditions to a model with subject-specific velocity boundary conditions demonstrated the importance of employing inlet and flow division data obtained from individual subjects in order to predict accurate, clinically relevant, fluid flow phenomena such as low wall shear stress areas and negative axial velocity regions. This study also illustrates the influence of the bifurcation geometry, especially the flow divider position, with respect to the velocity distribution of the common carotid artery on the development of flow characteristics. Overall it is concluded that accurate geometry and velocity measurements are essential for modeling fluid mechanics in individual human carotid arteries for the purpose of understanding atherosclerosis in the carotid artery bifurcation.

Systemic cardiovascular effects of volatile and intravenous anesthetics :evaluation in the time domain, the frequency domain and the pressure-volume plane.<p>Cardiovascular stability is of prime importance in order to maintain homeostasis during anesthesia and intensive care, and to reduce cardiovascular perioperative morbidity and mortality.<p>General anesthesia does have profound cardiovascular effects, and the end result is usually a decrease in arterial pressure, with the potential of inadequate organ perfusion and consequently organ damage. Therefore, elucidation of the mechanisms of cardiovascular effects of general anesthesia is important in order to prevent and/or to treat adequately the cardiovascular perturbations, and to perform the optimal choice of the anesthetic management. Anesthetic management for the patient presenting with cardiovascular alterations relates essentially to the question of a volatile anesthetic based regimen versus a propofol based anesthetic regimen.<p>A traditional hemodynamic investigation includes the measurement of heart rate, systemic and pulmonary arterial pressure, the filling pressures of the heart and cardiac output. These measurements allows for the calculation of systemic vascular resistance in order to evaluate arterial tone. However, calculated systemic vascular resistance cannot discriminate between passive (flow-dependent) and active (tone-dependent) changes in arterial pressure. Changes in arterial tone must be assessed by constructing pressure-flow plots.<p>Neither calculated systemic vascular resistance nor pressure-flow plots takes into account the pulsatile nature of the circulation. In order to do so, one has to measure instantaneous pressure and flow waves, perform harmonic analysis on both waves and calculate vascular impedance spectra.<p>The cardiovascular system is a mechanical system in which two components are functionally coupled: there is an energy transfer between the energy source, i.e. the left ventricle, and its mechanical load, i.e. the arterial tree. An alteration in one of these components necessitates an appropriate alteration in the other component in order to maintain optimal coupling, i.e. maximal energy transfer between the two elements. In the pressure-volume plane the left ventricle and the arterial tree are considered to be two elastic chambers in series. The performance of the left ventricle is quantified by the end-systolic elastance, while the load of the arterial tree is quantified by the effective arterial elastance. The ratio of end-systolic elastance to effective arterial elastance relates ventricular-arterial coupling to either maximisation of stroke work or either to maximisation of mechanical efficiency (i.e. the ratio of mechanical power output to cardiac oxygen consumption).<p>In the first experiment we investigated the systemic vascular effects of isoflurane versus propofol anesthesia in dogs using a traditional hemodymamic approach, measurement of instantaneous aortic flow and pressure with subsequent calculation of aortic input impedance spectra, and construction of pressure-flow plots generated by gradual reduction of venous return. Calculated systemic vascular resistance could not detect differences in arteriolar tone between isoflurane and propofol, whereas pressure-flow plots did: compared with isoflurane, propofol better maintained aortic pressure at all levels of flow, except at the lowest level of flow. Impedance spectra demonstrated a decreased pulsatile load and less energy losses in pulsations with propofol as compared with isoflurane.<p>In the second experiment we investigated the effects of escalating doses of sevoflurane and propofol anesthesia on arterial mechanical properties and left ventricular-arterial coupling in the dog. Arterial mechanics were assessed by traditional hemodynamics, aortic input impedance spectra, and pressure-flow plots generated by rapid caval inflow reduction. Left ventricular-arterial coupling was assessed as the ratio of end-systolic elastance to effective arterial elastance. The end-systolic elastance and the effective arterial elastance were obtained from left ventricular pressure and aortic flow data using a ‘single-beat’ estimation method. Traditional hemodynamics and pressure-flow plots demonstrated that sevoflurane causes a limited arteriolar vasodilation and causes arterial hypotension essentially by a decrease of cardiac output. Propofol insignificantly decreases cardiac output, but is an “actual” arteriolar dilator. The impedance spectra demonstrated that sevoflurane and propofol do have different effects on the elastic properties of large conduit arteries. Sevoflurane increased the characteristic impedance and reduced arterial compliance, indicating an increased physical elastance of the arterial tree. Propofol caused an insignificant increase of the characteristic impedance and the arterial compliance remained unaltered, suggesting that propofol does have a beneficial effect on the elastic properties of the arterial tree, thereby confirming the conclusion of the first experiment (i.e. a decreased pulsatile load with propofol). Sevoflurane impaired ventricular-arterial coupling by decreasing end-systolic elastance and increasing effective arterial elastance. Propofol maintained left ventricular-arterial coupling: the end-systolic elastance and effective arterial elastance remained unchanged and as consequence the ratio of end-systolic elastance to effective arterial elastance did not change. All results taken together we conclude that sevoflurane decreases cardiac output and left ventricular contractility, and increases the pulsatile and total load to the left ventricle. Propofol maintains cardiac output and left ventricular contractility, induces an arterial dilatation but without affecting the pulsatile and total load to the left ventricle.<p>These results, obtained in dogs, suggest that propofol, compared to volatile anesthetics, is an anesthetic, which can better preserve hemodynamic stability and homeostasis in the cardiovascular compromized patient undergoing surgery.<p>/<p>Evaluation des effets cardiovasculaires systémiques des agents anesthésiques dans le domaine du temps, le domaine de la fréquence et le plan pression-volume.<p>La stabilité cardiovasculaire est d’une importance prioritaire pour maintenir l’homéostasie pendant l’anesthésie et le séjour aux soins intensifs, et pour réduire la morbidité et mortalité cardiovasculaire pendant la période péri-opératoire.<p>L’anesthésie générale exerce des effets marqués sur le système cardiovasculaire. Généralement une hypotension artérielle systémique est observée, avec la possibilité d’une hypoperfusion des organes vitaux et ultérieurement des lésions de ces mêmes organes. Donc l’éclaircissement des mécanismes des effets cardiovasculaires de l’anesthésie générale est important pour prévenir et traiter les perturbations cardiovasculaires, et pour effectuer le choix optimal de la gestion anesthésique.<p>La question de la gestion anesthésique chez le patient présentant une fonction cardiovasculaire altérée se traduit essentiellement par le choix de l’anesthésie soit basée sur un agent volatile soit basée sur le propofol intraveineux.<p>Une exploration traditionnelle de l’hémodynamique comprend le mesure de la fréquence cardiaque, des pressions artérielles systémique et pulmonaire, des pressions de remplissage et du débit cardiaque. Ces mesures permettent de calculer la résistance vasculaire systémique de manière à évaluer le tonus artériel. Cela dit, la résistance vasculaire systémique calculée ne peut pas faire la différence entre des changements actifs (changements du tonus artériel) ou passifs (changements des débits) de la pression artérielle systémique. Les changements du tonus artériel doivent être évalués par des courbes pression - débit.<p>Ni les résistances vasculaires systémiques ni les courbes pression débit ne tiennent compte de la nature pulsatile de la circulation. L’exploration des effets pulsatiles<p>requiert tout d’abord la mesure des pressions instantanées et des débits instantanés. En seconde lieu, ces signaux doivent subir une décomposition harmonique (analyse de Fourier), pour afin de pouvoir calculer le spectre d’impédance vasculaire.<p>Le ventricule gauche et le système artériel sont deux éléments d’un système mécanique, dans lesquels il y a un transfert d’énergie entre la source d’énergie et sa charge. Une modification dans un des éléments nécessite une modification appropriée dans l’autre élément pour maintenir un couplage optimal entre les deux éléments, c'est-à-dire un transfert maximal d’énergie. Dans le plan pression volume, le ventricule gauche et l’arbre artériel sont considérés comme deux chambres élastiques en série.<p>La performance du ventricule gauche est quantifiée par l’élastance ventriculaire télésystolique, et la charge du système artériel est quantifiée par l’élastance artérielle effective. Le rapport entre l’élastance ventriculaire télésystolique et l’élastance artérielle effective permet de situer le « couplage ventriculo-artériel » soit en termes de maximisation du travail ventriculaire ou soit en termes d’ efficience mécanique. L’efficience myocardique est définie comme un rapport entre la puissance ventriculaire produite et l’oxygène consommé.<p>Dans la première expérimentation, nous avons étudié les effets vasculaires sur la circulation systémique du chien d’une anesthésie inhalatoire à l’isoflurane versus une anesthésie au propofol, ceci au moyen d’une exploration hémodynamique traditionnelle, les spectres d’impédance aortique et les courbes pression débit étant générées par une réduction graduelle du retour veineux. Les résistances vasculaires systémiques calculées n’ont pas décelé de différences de tonus artériolaire entre les effets d’une anesthésie inhalatoire à l’isoflurane et les effets d’une anesthésie intraveineuse au propofol. Par contre les courbes pression-débit démontrent une différence :comparé à l’anesthésie à l’isoflurane, l’anesthésie au propofol maintientt mieux la pression aortique à tous les niveaux de débit sanguin sauf aux débits les plus bas. Les spectres d’impédance démontrent une charge pulsatile réduite et des pertes d’énergie réduites avec le propofol par rapport à l’isoflurane.<p>Dans la seconde expérimentation chez le chien, nous avons étudié les effets de doses croissantes de deux agents anesthésiques généraux, le sevoflurane et le propofol, sur les caractéristiques mécaniques du système artériel et le couplage ventriculo- artériel systémique. La mécanique artérielle était étudiée par une exploration hémodynamique traditionnelle, les spectres d’impédance aortique et les courbes pression-débit étant générées par une réduction rapide du retour veineux. Le couplage ventriculo-artériel systémique était calculé par le rapport entre l’élastance ventriculaire télésystolique et l’élastance artérielle effective. L’élastance ventriculaire télésystolique et l’élastance artérielle effective ont été estimées à partir de la pression ventriculaire gauche et du débit aortique instantané en appliquant une méthode dite de « single beat ». L’hémodynamique traditionnelle et les courbes pression - débit démontrent que le sevoflurane provoque une vasodilatation artériolaire limitée et que la cause principale de l’hypotension artérielle est une réduction du débit cardiaque. Le propofol réduit le débit cardiaque d’une manière non significative, mais est un vasodilatateur artériolaire réel. Les spectres d’impédance montrent que le sevoflurane et le propofol ont des effets différents sur les caractéristiques élastiques des grosses artères à conduction. Le sevoflurane augmente l’impédance caractéristique et réduit la compliance artérielle, indiquant une augmentation de l’élastance physique de l’arbre artériel. Le propofol provoque une augmentation non significative de l’impédance caractéristique, mais la compliance artérielle reste inchangée. Ces résultats suggèrent que le propofol aurait un effet favorable sur les propriétés élastiques de l’arbre artériel, et donc confirment les conclusions de la première expérimentation, c’est-à-dire une charge pulsatile réduite avec le propofol. Le sevoflurane dégrade le couplage ventriculo-artériel à la suite d’une réduction de l’élastance ventriculaire télésystolique et d’une augmentation de l’élastance artérielle effective. Le propofol maintient le couplage ventriculo-artériel. L’élastance ventriculaire télésystolique et l’élastance artérielle effective restent par contre inchangées. Par conséquent, le rapport entre les deux élastances ne change pas. Sur base de ces résultats, nous concluons que le sevoflurane réduit le débit cardiaque et la contractilité du ventricule gauche, et augmente la charge pulsatile et totale sur le ventricule gauche. Le propofol maintient le débit cardiaque et la contractilité du ventricule gauche, et induit une dilatation artérielle sans altérer la charge pulsatile et totale sur le ventricule gauche.<p>Ces résultats, obtenus chez le chien, suggèrent que le propofol, comparé aux anesthésiques volatiles, est un anesthésique qui permet de mieux préserver la stabilité hémodynamique et l’homéostasie chez le patient présentant une fonction cardiovasculaire restreinte et devant bénéficier d’un acte chirurgical.<p> / Doctorat en Sciences médicales / info:eu-repo/semantics/nonPublished

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Cardiovascular disease, mostly atherosclerosis, is responsible for one third of all deaths globally, rising to more than 50% in the Western World. Risk factors include smoking, diet, and familial history. Doppler ultrasound can provide estimates of blood velocity and wall shear rate. Clinically, maximum velocity is used to categorise patients for surgery, although Doppler velocity measurement is prone to errors and in need of validation. Wall shear stress—which can be derived from wall shear rate—plays a role in disease initiation and progression, although its clinical utility is unclear due to difficulties associated with its measurement. This thesis investigates the use of Doppler ultrasound as a tool to estimate blood velocity and wall shear rate. A simplified method for estimation of wall shear rate in healthy arteries is developed that uses spectral Doppler ultrasound. This method is based upon the theory of oscillatory flow in rigid pipes, requiring two measurements that are readily available with clinical ultrasound machines. This method is compared to a similar method based on colour flow imaging. The spectral Doppler method underestimated the theoretic value of wall shear rate by between 7 and 22%, with results varying between phantoms. Errors for the colour method were on average 35% greater. Test measurements from one healthy volunteer demonstrated that this method can be applied in-vivo. In more advanced stages of disease, peak velocity distal to a stenosis is of clinical interest and the simplified method for wall shear rate estimation is invalid. Steady flow in a series of simplified stenosis geometries was studied using a dual-beam Doppler system to obtain velocity vectors. These measurements were compared with data from an equivalent system that used particle image velocimetry (PIV) and was considered the gold standard. For Reynolds numbers at the stenosis throat of less than 800, flow remained laminar over the region studied, although distal flow separation did occur. For higher throat Reynolds numbers—corresponding to more severe stenoses or increased flow rates—asymmetric recirculation regions developed; the transition to turbulence occurred more proximally, with a corresponding reduction in stenotic jet and recirculation length. Qualitative agreement was observed in the velocity profile shapes measured using ultrasound and PIV at throat Reynolds numbers less than 800. Above this threshold the qualitative agreement between the velocity profiles became poorer as both downstream distance and the degree of stenosis increased. Peak axial velocity distal to the stenosis was underestimated, on average, by 15% in the ultrasound system. Estimation of shear rate remained difficult with both experimental techniques. Under a Newtonian approximation, the normalised wall shear stresses agree qualitatively. Under pulsatile flow conditions using an idealised flow waveform, superior qualitative agreement was observed in the velocity profiles at diastole than at systole. Similar to the steady flow behaviour, this agreement deteriorated with stenosis severity. The current generation of clinical ultrasound machines are capable of estimating the wall shear rate in healthy arteries. In the presence of significant arterial disease, errors in the peak velocity may result in mis-selection of patients for surgery, while estimation of the wall shear stress remains extremely problematic; particularly with identifying the wall location and measuring velocities close to the wall.

The analysis of hemodynamic parameters and functional reactivity of cerebral capillaries is still controversial. The detailed mapping of tissue oxygen levels on the scale of micrometers cannot be obtained by means of an experimental approach, necessitating the use of theoretical methods in this investigating field. To assess the hemodynamics and oxygen transport in the cortical capillary network, 2D and 3D generic models are constructed (non-tree like) using random voronoi tessellation in which each edge represents a capillary segment. The modelling presented here is based on morphometric parameters extracted from physiological data of the cortex in which the spatial distribution of the diameter of the capillary is based on a Modified Murray method. This method led to a proper link between the diameter topology and flow pattern such that the maximum efficiency for flowing blood is concluded in the model of cortical capillary network. The approach is capable of creating an appropriate generic, realistic model of a cerebral capillary network relating to each part of the brain cortex because its geometrical density is able to vary the capillary density. The pertinent hemodynamic parameters are obtained by numerical simulation based on effective blood viscosity as a function of hematocrit and microvessel diameter, ESL (endothelial surface layer) effect, phase separation and plasma skimming effects. Using a solution method of the Green's function, the model is numerically developed to provide different simulations of oxygen transport for varying perfusion and metabolism in a mesoscale model of the cortical capillary network, bridging smaller and larger scale phenomena. The analysis of hemodynamic parameters (blood flow rate, velocity and hematocrit) demonstrates a consistency with the experimental observation. The distribution pattern of wall shear stress (WSS) in the network model supports the physiological data which in turn represents a proper matching between the hemodynamics and morphometrics in the cerebral capillary network. The distributions of blood flow throughout the 2D and 3D models seem to confirm the hypothesis in which all capillaries in a cortical network are recruited at rest (normal condition). The predictions showed a heterogeneous distribution in the flow pathways (aspect of length and inflow) and the pertinent transit time of red blood cell (RBC) in the network model which is dependent on varying perfusion rates. The analyses of oxygen transport in the model has demonstrated that oxygen levels in the tissue are sensitively dependent on the microvascular architecture and flow distribution. Unlike the homogeneous compartmental models, the mesoscale model presented in this study led to a prediction of tissue PO2 gradients throughout the tissue and a spatial distribution of tissue PO2 on the micron-scale for varying perfusion and metabolism. The predicted nonlinear changes in the oxygen extraction fraction (OEF) of the model as a function of the perfusion rate provide a basis for the quantitative interpretation of functional magnetic resonance imaging (fMRI) studies in terms of changes in local perfusion. The model is capable of predicting the brain oxygen metabolism under both normal and disease states, particularly, local hypoxia and local ischemia caused by misery perfusion syndrome. The hypoxic states for different perfusion rates and oxygen consumption rates demonstrated that in a significant decrease in brain perfusion (as can occur in stroke), the tissue hypoxia can be avoided by a moderate reduction in oxygen consumption rate. Increasing oxygen consumption rates (a realization of spatiotemporal stimulation of neural tissue) with respect to maintaining the tissue PO2 in the model led to a predicted flow-metabolism coupling in the model which supports the experimental studies of somatosensory and visual stimulation in humans by positron emission tomography (PET) and functional MRI (magnetic resonance imaging). A disproportionately large increase in blood supply is required for a small increase in the metabolic utilization (oxygen consumption rate) which in turn, is strongly dependent on the resting OEF such that the magnitude of the blood flow increases in the higher resting OEF.

Three investigations were conducted using pulsed Doppler echocardiography (PDE) and oxygen consumption to non-invasively determine the relationship between hemodynamic and metabolic variables from rest through submaximal and maximal exercise in early adolescent males. In the first study, interinvestigator and day-to-day variability of cardiac output measurements at rest and during exercise determined by PDE were analyzed in six junior high school age boys. Four Doppler-derived variables (cardiac output, cardiac index, stroke volume, and stroke index) were not different when calculated by independent investigators and showed the same interinvestigator variability from rest through submaximal and maximal exercise as has been reported at rest in previous validation studies. There was a slight but statistically significant increase in the absolute values of the above hemodynamic variables and simultaneously collected metabolic variables during a second identical test conducted approximately nine days later. A faster adjustment to increasing workrates in the second test could explain this latter finding since supine cycle ergometry is not as familiar an activity as more frequently used modes of exercise testing. It is concluded that hemodynamic measurements using PDE exhibit the same acceptable variability throughout exercise as has been previously demonstrated at rest. In the second study, PDE was used to determine rapid serial measurements of cardiac output during a rapid loading supine cycle ergometer exercise test in twenty-two junior high school age boys. These measurements were compared to simultaneoulsy determined measurements of oxygen consumption. Cardiac output adjusted faster to each new workrate than oxygen consumption. Further analysis of these responses revealed that increases in heart rate (as opposed to stroke volume) were responsible for this rapid adjustment. It is concluded that there is an uncoupling and recoupling of these normally closely related hemodynamic and metabolic variables during the transitional periods between increasing levels of steady-state supine exercise. In the final study, gradual loading and rapid loading supine cycle ergometer protocols were compared in fifteen junior high school age boys. Maximal metabolic measurements and heart rate from each test were not different. Maximal PDE-derived measurements of cardiac output, cardiac index, stroke volume, and stroke index were slightly, but significantly, higher in the gradual loading protocol. It is concluded that a more complete adjustment of cardiac output (reflected by stroke volume) to maximal supine exercise occurs in a more gradual loading protocol than in a rapid loading protocol.

Pump thrombosis is the epitome of left ventricular assist device dysfunction for end-stage heart failure patients. With the increased utilization of implantable, long-term, left ventricular assist devices (LVADs), understanding the implications associated with device orientation and interaction with the body is exceedingly important. Components associated with pump thrombosis in the Thoratec© HeartMate II™ (HMII) and the HeartWare© HVAD® devices include the inflow cannula, the outflow graft, and the pump elements as well as pump pocket depth for the HMII specifically. Several studies have been conducted to analyze these interactions with the HMII, however there is minimal to no data available analyzing how the device orientation of the HeartWare HVAD affects hemodynamics and a patient’s risk for developing pump thrombosis. Therefore, the purpose of this pilot study is the simulate the hemodynamic implications associated with Sub-optimal cannula angulation of the HVAD. Using Solidworks 2016 Ed., a simplified, hemo-static model of the left side of the heart was created. Dimensions for the atria, ventricle, and mitral valve were determined through the combination of Trans-Esophageal Echo cardiogram data as well as literature references. Three different inflow cannula angle scenarios were developed including a Control, a Clinically Optimal, and a Sub-optimal. Assumptions included body temperature, no accumulation within the ventricle, and no ejection or contraction. The model consists of static continuous flow set to 5 liters per minute with the assumption that the HeartWare HVAD is completely supporting the left ventricle. The results include both qualitative and quantitative data. Flow trajectory plots for each cannula scenario depict the hemodynamic flow patterns for different time points. Results show visible changes in the Sub-optimal orientation when compared to both the Control and the Clinically Optimal scenario. Additionally, it was determined that there were no statistically significant differences in the velocity vectors for any of the scenarios however, the shear stress values were determined to be significantly different for all time points, p < 0.001 for all scenarios when compared to Control. Though there are several limitations of this study, with sub-optimal inflow cannula angulation, there is a potential increased risk of hemolysis due to increased shear stress.

Understanding cardiac pumping function is crucial to guiding diagnosis, predicting outcomes of interventions, and designing medical devices that interact with the cardiovascular system.  Computer simulations of hemodynamics can show how the complex cardiovascular system is influenced by changes in single or multiple parameters and can be used to test clinical hypotheses. In addition, methods for the quantification of important markers such as elevated arterial stiffness would help reduce the morbidity and mortality related to cardiovascular disease. The general aim of this thesis work was to improve understanding of cardiovascular physiology and develop new methods for assisting clinicians during diagnosis and follow-up of treatment in cardiovascular disease. Both computer simulations and medical imaging were used to reach this goal. In the first study, a cardiac model based on piston-like motions of the atrioventricular plane was developed. In the second study, the presence of the anatomical basis needed to generate hydraulic forces during diastole was assessed in heathy volunteers. In the third study, a previously validated lumped-parameter model was used to quantify the contribution of arterial and cardiac changes to blood pressure during aging. In the fourth study, in-house software that measures arterial stiffness by ultrasound shear wave elastography (SWE) was developed and validated against mechanical testing. The studies showed that longitudinal movements of the atrioventricular plane can well explain cardiac pumping and that the macroscopic geometry of the heart enables the generation of hydraulic forces that aid ventricular filling. Additionally, simulations showed that structural changes in both the heart and the arterial system contribute to the progression of blood pressure with age. Finally, the SWE technique was validated to accurately measure stiffness in arterial phantoms. / <p>QC 20161115</p>

A monitorização após o parto é necessária a manutenção da vida nos bezerros clonados. É imperativo que os protocolos e procedimentos, bem como a avaliação clínica dos sistemas cardiovascular e respiratório sejam aprimorados para a sobrevida dos clones. As avaliações que permitam averiguar a capacidade de oxigenação dos pulmões são de crucial importância na assistência ao neonato, sendo que para essa finalidade tem-se recomendado a utilização da hemogasometria. O estudo foi dividido em quatro capítulos, sendo o 1 º Capítulo: Comparação das diferenças da adaptação neonatal de bezerros da raça Nelore(n=10) e de bezerros da raça Holandesa(n=10) nas trocas gasosas e nos parâmetros hemodinâmicos obtidos por meio do cateter de Swan-Ganz, o 2 º Capítulo: Avaliação da hemodinâmica e da hemogasometria de bezerros clonados(n=3), e o 3º Capítulo: Relato da utilização da ventilação mecânica não invasiva - modo CPAP- no tratamento de hipóxia neonatal em 10 bezerros e o 4º Capítulo: Avaliação hemodinâmica e hemogasométrica de bezerros neonatos com distúrbios respiratórios submetidos a ventilação mecânica não invasiva com mascara facial modo ventilatório CPAP (n=12). O objetivo deste trabalho será padronizar a utilização de ventiladores em bezerros neonatos dando o suporte respiratório necessário, avaliando hemodinâmicas da pressão da artéria pulmonar, freqüência cardíaca, débito cardíaco por meio da utilização do cateter de Swan-Ganz, a hemogasometria de sangue arterial para avaliação dos distúrbios respiratórios e obtenção dos valores de normalidade dos parâmetros, além de conhecer a adaptação neonatal das raças Nelore e holandesa. Foram determinadas média pressão artéria pulmonar, pressão artéria pulmonar ocluída, pressão ventrículo direito, pressão átrio direito, temperatura, pH, pCO2, pO2, HCO3, BE, SO2. Os animais foram ventilados modo CPAP- ventilação mecânica não invasiva com mascara facial com pressão positiva no final da expiração(PEEP). / Monitoring after calving is required for the maintenance of life in cloned calves. It is imperative that protocols and procedures, as well as the clinical assessment of cardiovascular and respiratory systems are improved for the survival of clones. Evaluations in order to verify the oxygenation capacity of lungs are crucial in neonatal care, and for this purpose has recommended the use of blood gas analysis. The study was divided into four chapters, the 1st chapter: Comparison of differences in neonatal adaptation of Nellore calves (n = 10) and Holstein calves (n = 10) in gas exchange and hemodynamic parameters obtained by through the Swan-Ganz, the 2nd Chapter: hemodynamic evaluation and blood gas analysis of cloned calves (n = 3), and the 3rd Chapter: Reporting the use of noninvasive mechanical ventilation - CPAP- in the treatment of neonatal hypoxic 10 calves and Chapter 4: hemodynamic evaluation and hemogasometric of newborn calves with respiratory disorders underwent noninvasive ventilation with face mask ventilation mode CPAP (n = 12). The purpose of this study is to standardize the use of mechanical ventilators in newborn calves giving the required respiratory support, evaluating hemodynamic pulmonary artery pressure, heart rate, cardiac output by using of the Swan-Ganz catheter, arterial blood gas analysis to evaluation of respiratory disorders and obtaining the parameters normal values, and know the neonatal adaptation of Nellore and Hostein Frisian races. They were determined means of pulmonary artery pressure, pulmonary artery wedge pressure, right ventricular pressure, right atrial pressure, temperature, pH, pCO2, pO2, HCO 3, BE, SO 2. The animals were ventilated CPAP- noninvasive ventilation mode with face mask with positive pressure at the end of expiration (PEEP)

Contexto: Existem controvérsias na literatura médica sobre potenciais alterações da hemodinâmica venosa dos membros inferiores durante a gravidez. Objetivo: Estudar a drenagem venosa em membros inferiores e suas alterações na gestação (1º, 2º e 3º trimestres) e pós-parto mediante Mapeamento Dúplex (MD) das veias profundas e superficiais e a Pletismografia a Ar (PGA). População: Foram recrutadas vinte mulheres primigestas, sem doença venosa prévia, junto aos Núcleos de Saúde da Família ligados ao Centro de Saúde Escola da FMRP-USP. Métodos: O estudo hemodinâmico venoso nos membros inferiores foi realizado empregando-se dois métodos não invasivos: o MD e a PGA. Foram registrados os diâmetros e os refluxos das principais veias (femoral comum, femoral, poplítea, safena magna e parva) dos membros inferiores por meio do MD. Foram avaliados pela PGA: o índice de enchimento venoso (IEV), a fração de ejeção (FE), a fração de volume residual (FVR) e o esvaziamento venoso (OF-outflow). Todos os registros foram obtidos em 3 diferentes períodos da gestação e no pós-parto. Os dados foram estatisticamente analisados e considerou-se p?0,05. Resultados: Houve aumento do diâmetro venoso no território da femoral comum e da safena magna infravalvar bilateralmente, nos 2º e 3º trimestres. Na PGA, registrou-se diminuição da FVR bilateral, elevação do IEV à direita e aumento do OF bilateral no decorrer da gestação. Observou-se edema em 4 (15%) gestantes no segundo trimestre e 11 (55%) no terceiro trimestre. Quanto ao refluxo, documentouse um caso no 2º trimestre no território da safena magna supravalvar esquerda (5%) e mais dois casos no 3º trimestre (15%), sendo uma no território da safena magna infravalvar esquerda e outra gestante com refluxo nos territórios de safena magna infravalvar e safena parva esquerdas. Após o parto, houve regressão de todas essas alterações anatômicas e hemodinâmicas da drenagem venosa dos membros inferiores. Conclusão: Apesar do aumento significativo dos diâmetros das veias femorais comuns e safenas magnas infravalvares bilateralmente, diminuição da FVR bilateral, elevação do IEV à direita, aumento do OF durante a gestação, todas essas alterações retornaram aos parâmetros anatômicos e hemodinâmicos venosos iniciais, após o parto / Background: The relation between pregnancy and venous reflux is still misunderstood and some authors question if pregnancy is the main cause of venous reflux and venous disease. Objective: analyze venous hemodynamics in healthy primigravidae during the first, second and third trimester of pregnancy and in the puerperium. Methods: prospective study with 20 primigravidae evaluated in the first, second and third trimester of pregnancy and postpartum. Duplex scan evaluated venous diameters and reflux; air plethysmography evaluated venous filling index (VFI), ejection fraction (EF), residual volume fraction (RVF), outflow fraction (OF )in both limbs. OF in the right limb while the patient was in left lateral decubitus position was also evaluated. Results: During pregnancy, there was bilateral increase in venous diameters in common femoral and infravalvar great saphenous veins; occurrence of reflux in the left surpravalvar great saphenous vein in one patient (5%) in the second trimester; and occurrence of reflux more other two patents (15%) in the third trimester: one in the left infravalvar great saphenous vein, and other in the left popliteal and small saphenous vein. All these alterations observed during pregnancy disappeared after delivery. VFI decreased after delivery in the left limb, but increased progressively in the right limb, returning to basal level after delivery; EF did not change; RVF decreased during pregnancy, mainly in left limb, and returned to basal level after delivery; OF increased during pregnancy and returned to basal levels after delivery; OF in left lateral decubitus did not change. Conclusion: pregnancy caused a diameter increase in bilateral common femoral and great saphenous veins, unilateral right increase in VFI, bilateral decrease in the RVF and bilateral increase in OF. All these parameters returned to initial status after delivery